Pahs emergency protocol [2016 ed.]

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Emergency

Patan Academy of Health Sciences Department of General Practice and Emergency Medicine November, 2015

Content Title

Page Number

Communicaiton skills

1-4

Clinical examinations

5-25

Emergency structure and operation

26-32

Resuscitation

33-67

Cardiac emergencies

68-79

Respiratory emergencies

80-97

Abdominal emergencies

98-119

Neurological emergencies

120-131

Metaboic emergencies

132-147

Toxicology

148-167

Common problems

168-180

Environmental injuries

181-184

Orthopedic injuries

185-192

Obstetrics and Gynecology emergencies

193-197

Psychiatry emergencies

198-199

Police cases

200-202

Procedures

203-221

Paediatric emergencies

222-284

If there are any corrections or updates in the protocol please send mail at [email protected]

Communication Skills Contents Communication in crisis ..................................................................................................................................... 2 Crisis Resource management (CRM).............................................................................................................. 2 Three big CRM skills are ................................................................................................................................. 2 Close loop communication ........................................................................................................................ 2 Sharing information (SBAR) ....................................................................................................................... 2 Reassess ..................................................................................................................................................... 2 Delivering death notification ............................................................................................................................. 3 Griev_ing method .......................................................................................................................................... 3 What reaction to expect? .............................................................................................................................. 3 Medical Ethics .................................................................................................................................................... 4

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Communication in crisis

“Communiation errors kill patients.”

Crisis Resource management (CRM) Crisis Resource Management is the skill of managing the human and physical resources in a stressful, highstakes environment.

Three big CRM skills are 1. Uses closed-loop communication 2. Shares information 3. Reassesses

Close loop communication “What is thought is not said, what is said is not heard, what is heard is not understood, what is understood is not done, what is done is not confirmed.” So close the loop by speaking up and confirming that the person you want to communicate has understood. Sharing information (SBAR) • • • •

Situation Background Assessment Recommendation

Reassess Ferquent reassessment is the key to success.

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Delivering death notification Griev_ing method Gather Resources Identiry Educate Verify Space Inquire Nuts and bolts Give

Collect family in quiet, respectful place Call for any additional support to assist the family with their grief Identiry yourself, identify deceased patient by name, identify state of knowledge of the family pertraining to the evens of the day. Are they aware of possible death or will this be a completely unexpected event for them? Educate about event occurred in ED Suggest to them that you are bringing a very bad news Verify that a family member had died Give family member personal space and time for emotional moment Ask them if they have any question Allow relatives to see deceased Take care of personal belongings Give documents, express condolence

What reaction to expect? Families may go into denial, anger or guilt. Family anger is not uncommon so prepare to react supportively. Do not be defensive or judgemental if faced with statement of negligency or what should have been done. Allow survivors to express their feelings. Remain clam and silent.

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Medical Ethics

Medical ethics for practice: Ethics is set of principles, values with the help of which we can arrive in right decision. Nothing in right or wrong in ethics but it all depends on the situation. Something may be right for a person may not be right for the other. There are few principles in ethics which we can utilize to get right decisions. 1. Autonomy: We should respect patients’ decision in every step. If the patient is incompetent or minor (less than 16 years to give consent), we can seek help from surrogate decision makers. 2. Beneficence: Do good to the patient. Our every activity should be guided with this principle. 3. Non Maleficence: Do no harm to patient. 4. Justice: We should be guided with equitable distribution of resources. Besides these principles, we can use some other theories like • Consequentialism: If the result of the action is beneficial to the patient, we can do it. • Utilitarian: The action should be guided with positive effect to everyone not only to the person. • Deontology: every action should be guided by duty and if you are doing an action, you should think that this action can be done to you or not. • Confidentiality: we should maintain the confidentiality of the patients’ information as far as possible. In case of written order from court of law, we can give information to the court only. Sometimes, to protect society and other people, this principle is waived but we should inform patient before breaching it. • Medical Professionalism is a desire to help people and to help society as a whole with quality healthcare. We should be guided by professionalism to provide good care to the patient. • Informed Consent: There are three important component of informed consent. o Information- we should provide adequate comprehensible information to the patient. We should provide pros and cons of the procedure and consequences of not giving consent to patient. o Voluntariness – the consent should be given voluntarily without coercion. o Competency: the person giving consent should be competent to give consent. They should have good higher mental function without use of drugs that influence his competency. In case of life saving and emergency procedure, we can take consent from the surrogate decision makers if the patient is not competent.

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Clinical Examination Contents General Examination.......................................................................................................................................... 5 Respiratory System ............................................................................................................................................ 8 Cardiovascular System ..................................................................................................................................... 13 Abdomen.......................................................................................................................................................... 18 Approach to Coma ........................................................................................................................................... 22 Neurological Examination ................................................................................................................................ 25

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General Examination Skin •

• • • • • • •

•

•

Generalized absence of skin pigmentation occurs in albinism. Syndrom with features of albinism are – Chediak Higashi syndrome – Phagocytic deficiency disease, Phenylketonuria (Inborn error of amino acid metabolism) Patchy absence of skin pigmentation may be due to vitiligo Circumscribed hypopigmentation of lesion of skin occurs in – Hansen’s disease, Tenia vesicolor Generalized hyperpigmentation – Hemochromatosis, Addison’s, Cushing’s Patchy hyperpigmentation – Pellagra, Scleroderma Yellow pigmentation of skin: Jaundice, Carotenemia, Long standing severe anemia Bluish discolourisation: Cyanosis; Ruddy complexion: Polycythemia; Pallor: Decrease in Hb Diabetes Mellitus o Necrobiosis lipodica diabetocorum – Papulo nodular lesion enlarging to form brownish yellow plaque with waxy surface over front of leg. o Diabetic dermopathy – Dull, red, oval, flat topped o Diabetic bulla – over legs, hands, feets bilaterally healing with atrophic scars o Diabetic rubeosis – flushed skin of face o Carotenoderma – yellowish tint of skin due to deposition of carotene o Granuloma annulare – popular lesion over central area of body and flexures of neck, arm and thing o Sclerederma diabeticorum – diffuse waxy, non pitting, induration of skin particularly over back of neck and upper trunk o Infection like furuncle, carbuncle Chronic renal failure o Uraemic frost o Erythema papulatum uraemicum – erythematous nodules over palm, soles and forarm o Generalised puritis o Metastatic calcification o Kyrle’s disease – multiple discrete or confluent hyeperleratotic follicular papules over lower extrimities o Nail change – proximal white and distal half pink o Oral manifestations – coating of tongue, xerostomia, ulcerative stomatitis Internal malignancy o Acanthosis nigricans – adenocarcinoma of GIT o Plamo planter keratoderma – Ca bronchus and oesophagus o Nectolytic migratory erythema – glucagonoma o Pityriasis rotunda – hepatocellular Ca o Sign of Leser Trelat – sudden eruption of intensely pruritic multiple seborrhoeic keratosis in Ca stomach

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o Migratory thrombophlebitis in Ca panceas o Cutaneous hamartoma – Ca breast, thyroid, GI polyposis = cowdens disease Face Forehead • Prominent forehead: Acromegaly, Chronic Hyerocephalus, Rickets, Thalassemia • Wrinkling of forehead: o Bilateral: Anxiety, Bilateral ptosis as in Myasthenia Gravis, Bilateral III nerve palsy, Bilateral Horner’s syndrome o Unilateral: Unilateral ptosis as in unilateral III nerve palsy, Horner’s syndrome • Absence of wrinkling of forehead o Unilateral: Bell’s palsy o Bilateral: Myotonic dystrophy, hyperthyroidism (Joffroy’s sign) Eyes •

Ptosis, Pallor, Icterus, Bitot’s spot (Vitamin A deficiency), Arcus senilis

Tongue • Macroglossia: Acromegaly, Down’s syndrome. Tumors • Microglossia: Pseudobulbar palsy, Facial hemiatrophy • Fissured tongue: Down’s, Vitamin B deficiency, Acromegaly, Congenital malformation • Hairy leukoplakia: EB virus, typically seen in lateral margin of tongue Stature • Stature is total height measured from vertex of head to sole of feet. Upper segment is vertex of head to symphysis pubis. Lower segment is from symphasis pubis to sole of foot. • Stature > Arm span: Adrenal cortex tumor, precocious puberty • Arm span > stature: Hypogonadism, Marfan’s syndrome, Klinefelter’s syndrome • Upper segment > lower segment: Adrenal cortex tumor, precocious puberty • Lower segment > Upper segment: Hypogonadism, Marfan’s syndrome, Klinefelter’s syndrome • Gigantism: Height more than six feet six inch. Dwarfism is height less than four feet. Obesity • Generalised obesity: Uniform distribution of fat throughout the body. • Android obesity: Obesity characterized by excess deposition of fat over region of waist. • Gynoid obesity: Characterised by excess deposition of fat over region of hip and thigh. • Superior or central obesity: Excess fat deposition over face, neck and upper part of trunk – cushing’s syndrome Posture • Parkinsonian posture: Universally flexed posture • Cerebellar posture: Stands with feed wide apart and is unable to maintain a steady posture while standing. Patient is ataxic on sittine (trunkal ataxia) when vermis of cerebellum is affected.

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• • Nail • • • • • • •

Decrebrate posture: Extension of elbows and wrist with pronation of arm. Lesion is at brainstem disconnecting the cerebral hemispheres from the brainstem. Decorticate posture: Flexion of elbows and wrist with supination of the arms. It suggest severe bilateral hemispherical damage above the midbrain. Koilonychia – spoon shaped: Iron deficiency, IHD, Syphillis, Hemochromatosis Beau’s line – Transverse ridge in the nail plate due to temporary alteration of nail growth rate: Acute febrile illness, Pneumonia, MI Plummer nail – Onycholysis of nail: Hypothyroidism, Raynaud’s disease Lindsay nail – Proximal dull white portion and a distal pink or brown with a well demarcated transvere line: Uraemia White nail (Terry Nail) – White color in the nail bed than nailplate: Anaemia, CCR, DM, Malignancy Red nail: CCF, Blue nail: Wilson’s disease Black nail: Peutz Jeghers syndrome, Cushing’s syndrome, Addison’s disease

Fever • Maximum normal oral temperature: 6 am – 98.6, at 6 pm – 99.6 • Normal diurnal variation is 1 degree F, rectal temperature is 1 degree F more than oral. Oral temperature is 1 degree F more than axillary Fever with relative bradycardia • Typhoid Fever, Meningitis, Viral fever (Influenza), Brucellosis, Leptospirosis, Drug induced fever Fever with exanthema • Rash appearing on first day of fever – Chicken pox • Rash appearing on fourth day of fever – Measles • Rash appearing on seventh day of fever – Typhoid Patterns of fever • Continuous: The temperature remains elevated above normal without touching the baseline and the fluctuation does not exceed 1 degree F. E.g. Lobar pneumonia, infective endocarditis, enteric fever • Remittent: Temperature fluctuation exceeds 1 degree F but without touching baseline: abscess • Intermittent: Temperature touches the baseline in between. E.g. sepsis. Quotidian fever is a hectic fever occurring daily • Relapsing: Febrile episodes are separated by normal temperature for more than one day. o Tertian fever: Occuring alternate days, Pl vivax, Pl falciparum, Pl ovale o Quartan fever: Occuring every two ays, Pl malariae o Pel Ebstein fever: Lasting 3-10 days followed by afebrile period of 3-10 days. Hodgkins o Saddle back fever: Initially fever lasts 2-3 days followed by a remission lasting for 2 days and then fever reappears and continues for 2-3 days. Dengue fever o Cyclic neutropenia: Fever occurs every 21 days. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Respiratory System General Examination Built, Nourishment, Dyspnoea, Cyanosis Clubbing • Normal angle of nail and nail bed in 160 degree and is known as Lovibond angle. • Grading of clubbing: • Grade I: Obliteration of the angle between the nail and the nail bed and positive fluctuation test • Grade II: Parrot beak appearance • Grade III: Drumstick appearance • Grade IV: Hypertrophic osteoarthopathy – Painful swelling of wrist, elbow, knee, ankle with radiographic evidence of subperiosteal new bone formation. • Scharmroth’s sign: When the dorsum of the distal phalanges of the fingers of both hands are approximated to each other, a diamond shaped gap is made. This gap disappears with clubbing. • Causes of clubbing Pulmonary CVC GI Miscellaneous o Bronchogenic carcinoma o Cyanotic o Cirrhosis of o Syphillis o Metastatic lung disease congenital heart liver o Syringomyelia o Suppurative lung disease disease o Ulcerative o Acromegaly o Bacterial colitis (Bronchiectasis, cystic fibrosis, o Thyrotoxicosis endocarditis lung abscess, empyema) o Chron’s o ILD o Atrial myxoma disease o Longstanding PTB o Eisenmenger’s o GIT malignancy o Chronic bronchitis syndrome o Mesothelipma o Neurogenic diaphragmatic tumor o Pulmonary AVM Scaroidosis Inspection Inspection of upper respiratory tract Oral cavity, nose, pharynx Inspection of lower respiratory tract Supraclavicular area, Infraclavicular area, Mammary region, Axillary region, Infra axillary region, Suprascapular region, Interscapular region, Infrascapular region Position of Trachea Trial Sign: Prominence of clavicular head of sternocleidomastoid on the side to which trachea is deviated. Position of Apex beat Symmetry of Chest • Drooping of shoulder • Hollowness or fullness in supraclavicular and infraclavicular fossa DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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•

Crowding of ribs, Kyphosis or Scoliosis

Chest Deformities • Flat Chest: Anterior posterior and transverse diameter ratio 1:2 (Normally 5:7) – TB, Fibrothorax • Barrel Chest: Anterior posterior to transverse diameter 1:1 – COPD (Emphysema) • Pigeon Chest: Forward protusion of sternum and subcoastal cartilage – Marfan’s syndrome, Childhood asthma, Rickets • Pectus Excavatum (Funnel chest, cobbler’s chest): Hollowness of lower end of sternum – Marfan’s syndrome • Harrison’s sulcus: Indrawing of ribs to form symmetrical horizontal grooves above the costal margin, along the line of attachment of diaphragm due to hyperinflation of lungs and repeated strong contraction of the diaphragm – Chronic respiratory disease on childhood, Childhood asthma, Rickets, Blocked nasopharynx due to adenoid enlargement. • Ricket rosary: Bead like enlargement of costochondral jounction – rickets • Scorbutic rosary: Sharp angulation with or without beading or rosary formation of the ribs arising as a result of backward displacement of pushing of sternum – Vitamin C deficiency Overlying skin • Engorged veins and subcutaneous nodules – Sarcoid and malignancy • Intercostal scar – Drained pleural effusion, empyema or pheumothorax • Discharging sinus – TB • Empyma nessitans – Intercoastal swelling close to sternum Chest movement • Rate: Normal is 14-18 per minute. Tachypnoea is more than 20 per minute. Bradypnoea is decrease in respiratory rate. Hyperponea is increase in depth of respiration (Acidosis, Brain stem lesion, Anxiety). Rhythm Regular abnormal breathing patterns • Chyne stokes breathing: Hyperpnoea followed by apnoea failure, Renal failure, Narcotic drug poisoning and raised • Kassmaul’s breathing: Increased rate and depth of Metabolic acidosis, pontine lesion.

– Cardiac ICP breathing –

Irregular Abnormal Breathing Pattern deep • Biots breathing: Apnea between several shallow or few inspiration – Meningitis • Ataxic breathing: Irregular breathing where deep or shallow breathing occurs randomly – Brainstem lesion • Cogwheel breathing: Interrupted breathing seen in nervous individual. • Pursed lip breathing: Breaths against pursed lip to increase endobronchial pressure above the surrounding alveoli and prevents its collapse – COPD DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Palpation Trachea • Position of trachea is confirmed by slightly flexing the neck so that chin remains in the midline. The index finger is then inserted in the suprasternal notch and tracheal ring felt. Slight shift of trachea to the right is normal. Tracheal Tug – Olliver’s sign • This sign is elicited by standing behind patient. The chin of the patient is raised and cricoid cartilage is held up on deglutition on either side with finger of both hands. The sign is said to be positive when downward tug is belt by the fingers during cardiac systole. o Positive: Aortic arch Aneurysm o False Positive: Mediastina tumor attached to aortic arch o False negative: Non pulsatile aortic aneurysm (Thrombosed) Inspiratory Tracheal descent • Tracheal decent with inspiration – COPD Confirmation of Apical impulse Measurement of Chest Expansion In male at the level of nipple, in female below breast. Measured with measuring tape. Normal expansion is 5-8 cm. In severe emphysema it is less than 1 cm. Non respiratory cause - Ankylosing spondylitis. Assessing symmetry of chest expansion • Upper thorax: Examiner facing patient’s back and placing hand over the patient’s supraclavicular fossa. The extent of upward movement in quiet respiration is compared on both sides. • Anterior thorax: Both hand placed by the side of rib cage with thumb towards midline. After a deep breath, the degree of expansion is compared on both sides by movement of thumb away from the midline. • Posterior thorax: Similar posteriorly Tenderness over chest wall • Empyema; Local inflammation of parietal pleura, soft tissue and osteomyelitis; Infiltration with tumor; Amoebic liver abscess Detection of subcutaneous emphysema • Injury to chest wall and rib, pneumothorax, rupture oesophagus Others • Vocal fremitus: Felt over chest wall on asking patient to speak (99-99 or 1-1-1). Increased in consolidation, decreased in pleural effusion. Percussion Anterior chest wall • Supraclavicular region (Kronig’s Isthmus): Band of resonance 5-7 cm above supraclavicular fossa. Bounded medially by scalenus muscle, laterally by acromion process, anteriorly by clavical and

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•

posteriorly by trapezius. Percussion is done by standing behind patient. Hyper resonance – Emphysema; Impaired resonance – Pulmonary TB, Malignancy in apex Clavicle: Directly over medial 1/3rd of the clavicle

Lateral chest wall • 4th to 7th intercostal spaces Posterior chest wall • Suprascapular – above spine of scapula • Interscapular • Infrascapular up to eleventh rib Percussion on right side • Liver dullness from right 5th ICS up to right costal margin • Tidal percussion: To differentiate upward enlargement of liver or subdiaphragmatic abscess. If on deep inspiration, the previous dull note in the fifth right intercostal space on the mid clavicular line becomes resonant, it indicated dullness was due to liver, if persists it is due to lung pathology. Percussion on left side • Traub’s space: o Surface anatomy:Two parallel vertical lines are drawn from 6th costochondral junction and 9th rib in mid axillary line. These two lines are connecte with a horizontal line from 6th ICS above an costal margin below. o Boundaries: Right side – Left lobe of liver, Left side –Spleen, Above – Left lung resonance, Below – Left costal margin, Content – Fundus of stomach o Traube’s space is obliterated in: Left pleural effusion, massive splenomegaly, enlarged left lobe of liver, full stomach, fundal growth, and massive pericardial effusion. o Traube’s space is shifted upward in: Left diaphragmatic paralysis, Left lower lobe collapse, Fibrosis of left lung. Others • Percussion tenderness: Present in empyema and inflammation of parietal pleura. • Straight line dullness: Present in hydropneumothorax • Shifting dullness: Dull area percussed in axilla in sitting position becomes resonant in lying. Shifting occurs immediately in hydropneumothorax and very slowly in pleural effusion. • S shaped curve of ellis: In moderate pleural effusion, the uppermost level of dullness in highest in the axilla and lowest in the spine and tend to assume the shape of S. Auscultation General principles • Diaphragm is preferred. • Patient should breath with mouth open to prevent sound being produced from a partially closed nose.

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• • •

Avoid auscultation 2-3 cm from midline in the upper part of chest – bronchial breathing is normal here Hairy chest should be moistened. Auscultation after coughing is a useful procedure. It helps differentiate coarse crepitation and low pitched ronchi from pleural rub. Coughing does not alter pleural rub but alters ronchi and crackles.

Breath Sounds • Vesicular breath sound: Low pitched, Inspiration longer than expiration (3:1), no pause in between. Breath sound is decreased in: Asthma (Silent chest), Tumor, Pleural effusion, Pleural thickening, Collapse lung with occluded bronchus, Emphysema. • Bronchial breath sound: Loud, high pitched, prolong expiration with pause between inspiration and expiration. o Tubular: High pitched – Consolidation, Collapse, Above pleural effusion o Cavernous: Low pitched – Thickened wall cavity with communicating bronchus o Amphoric: Low pitched with high tone and a metallic quality – Smooth walled cavity, Broncho-pleural fistula, tension pneumothorax • Crackles: Nonmusical, interrupted added sounds of short duration. Fine Crackles: Less loud and arise from Alveoli. Coarse Crackles: Low pitched and arise from bronchioles and bronchus. o Early inspiratory – chronic bronchitis, Mid Inspiratory – Bronchiectasis, Late inspiratory – Asbestosis, pulmonary fibrosis, pneumonitis, interstitial lung disease, pulmonary edema, Expiratory - chronic bronchitis, pulmonary edema. • Wheeze o Fixed monophonic: Single note of constant pitch, timing and site. Results from air passage through localized narrowing of airway. Seen in – Tumors, Foreign body, Bronchial stenosis, Intrabronchial granuloma. o Random polyphonic: Scattered in inspiration and expiration. E.g. Bronchial asthma o Expiratory polyphonic: Complex musical sound continuing finally to end in expiration due to expiratory compression of large central airways. E.g. Emphysema o Sequential inspiratory wheeze: Opening of distal airway which has become abnormally opposed during previous expiration. E.g. pulmonary fibrosis, fibrosing alveolitis, asbestosis. • Sounds o Bronchophony: Appears to be heard near earpiece – consolidation, cavity communicating with bronchus, above level of pleural effusion o Aegophony: Nasal or bleating quality. On saying E it will be heard as A – consolidation, above level of pleural effusion. o Whispering pectoriloquy: Whispering voice at the end of respiration is transmitted without distortion – consolidation. o Pleural rub: Superficial, localized grating sound best heard with firm pressure with stethoscope and not altered by coughing, associated with pain. o Pleuro – pericardial rub: Adjacent to pericardium being moved across on another by cardiac pulsation. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Cardiovascular System General Examination Pulse Rate, Rhythm, Volume, Character Pulse Hypokinetic pulse Hyperkinetic pulse Anacrotic pulse (Pravus et Tradus) Pulsus Dicroticus Pulsus Bisfreiens Pulsus Bigeminus Pulsus alternans Pulsus paradox

Description

Example

Small volume pulse with narrow pulse pressure Large volume and wide pulse pressure Low amplitude pulse with slow rising and late peak Single pulse wave with one peak in systole and one peak in diastole Single pulse wave with two peak Normal beat followed by premature beat and compensatory pause Alternating large and small volume pulse Fall in systolic BP more than 10mm hg during inspiration

Cardiac failure, Shock, MS, AS High output – Anaemia, fever, beriberi; MR, VSD Severe AS LVF, Dehydration, DCM, Cardiac temponade AS, Severe AR, HOCM Digatilis toxicity LVF Cardiac temponade, constrictive pericarditis, airway obstruction, SVC obstruction

Pulsus paradoxus: Inflate the BP cuff to suprasystolic level and deflate at the rate of 2 mmHg per beat, The peak systolic pressure during expiration is noted. The cuff is then deflated even more slowly and the pressure is again noted when Koratkoff sound becomes audible throughout the respiration Blood Pressure • Korotkoff sounds • Phase 1: First appearance of clear, tapping sound. It represents the systolic BP • Phase 2: Tapping wounds are replaced by murmur • Phase 3: Murmurs become louder • Phase 4: Muffling of sounds • Phase 5: Disappearance of sounds Jugular Venous Pressure When measure with the patient reclining at 45 degree it is normally about 4-5 cm. Right atrial pressure is 0-8mmHg and at SVC it is 1-6mmHg. The measured JVP can be converted to mmHg by multiplying with 0.736. In JVP: a wave is due to atrial contraction, c wave is doe to closure of mitral and tricuspid valve, x descent is due to atrial relaxation, v wave is due to venous filling right ventricular contraction, y descent is due to atrial emptying. Causes of elevated JVP DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Unilateral non pulsatile Bilateral non pulsatile

Innominate vein thrombosis SVC obstruction, Massive right sided pleural effusion Bilateral pulsatile Cardiac: HF, TR, TS, Constrictive pericarditis, Cardiac temponade Pulmonary: COPD, Corpulmonale Abdominal: Ascities, Pregnancy Iatrogenic: Excessive iv fluid Kussmaul’s sign: Inspiratory rise in JVP: Constrictive pericarditis, restrictive pericarditis, RV infract, RF failure Friederich’s sign: Rapid fall and rise of JVP: Constrictive pericarditis, TR Abdominal jugular reflex: Pressing periumbilical area transiently raises JVP by 3 cm and falls down even when pressure is continued, whereas in patents with right or left hart failure, the JVP remains elevated. Systemic Examination Inspection Precordium bulge suggests LVH since child hood Visible Pulsation Carotid artery pulsation Hyperdynamic states, AR, Coarctation of aorta, HTN Aortic pulsation Dilation of ascending aorta, Aortic aneurysm, AR Pulmonary artery pulsation Pulmonary artery dilatation, High output states, Pulmonary HTN, Pulmonary hypercirculation (ASD) Suprasternal pulsation AR, Aortic arch aneurysm, Thyrotoxicisis, Coarctation of aorta Supraclavicular pulsation AR, Subclavian artery aneurysm Sternoclavicular pulsation AR, Aortic dissection, Aortic aneurysm Left parasternal pulsation RVH, MR Apical pulsation LV or RV hypertrophy Ectopic pulsation IHD, Left ventricular dysfunction, Aneurysm, Cardiomyopathies Inter and infra scapular pulsation Coarctation of aorta – Suzman’s sign Epigastric pulsation Aortic aneurysm, RVH Hepatic pulsation TS, TR Chest wall defects: Pectus excavatum, Pectus carinatum Costal cartilages: Costochondritis Spine: Kyphosis, scoliosis, ankylosing spondylitis. Palpation Apical impulse: 1 cm medial to mid clavicular line or 10 cm lateral to midsternal line in 5th intercoastal space. Normal displacement is 1 cm in lateral decubitus position. Normal apical impulse DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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is confined to one intercoastal space and has an area of 2.5cm square. Normal duration of thrust of apical impulse is less than 1/3 of systole. Abnormalities of apical impulse Absent apical impulse Tapping apical impulse Hypodynamic apical impulse (felt with decrease thrust) Hyperdynamic apical impulse: Increase in amplitude without an increase in duration; >1/3 < 2/3 of systole and occupies more than one ICS Heaving apical impulse: Increase both in amplitude and duration: >2/3 of systole and occupies one ICS Diffuse apical impulse Double-Triple-Quadruple apical impulse

Behind the rib or sternum, Dextrocardia Papable S1: Mitral stenosis Acute MI, Pleural effusion, Pericardial effusion, Constrictive pericarditis, COPD LV volume overload: AR, MR, VSD, PDA LV pressure overload: AS, HTN, Coarctation of aorta Left ventricular aneyrysm HOCM

Parasternal Impulse Anterior movement of left parasternal area as felt by palm of hand in right ventricular enlargement and left atrial enlargement. Shocks: Palpable heart sound • Aortic area: A2 – Systemic HTN; Aortic ejection click – Congenital valvular aortic stenosis • Pulmonary area: P2 – Pulmonary HTN: Pulmonary ejection click – Pulmonary valvular stenosis • Apical: S1- MS; Opening snap- MS; S3-DCM; S4-HOCM Thrills: Palpable murmur – base of fingers Thrills Systole Carotid AS Aortic AS Pulmonary PS, ASD, VSD Loft lower parasternal VSD Apex MR, AS

Diastole Acute severe AR, Syphilitic AR PDA MS

Percussion Useful only is detecting aortic dilatation as in Aortic aneurysm and pulmonary dilatation as in pulmonary Hypertension Auscultation Mitral area – Apex; Tricuspid area – lower left sternal border; Aortic area – 2nd ICS left, pulmonary area – 2nd ICS right; Erb’s area – second aortic area, 3rd left ICS, Gibson’s area – 1st ICS left, PDA is best heard. Auscultation areas: Carotids, Inter and infrascapular areas, Axilla, Supra and infraclavicular areas

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Abnormalities of S1 Soft MR, TR, RV or LV dysfunction, TS, MS(calcified valve), Obesity, AR-acute, Prolong PR interval Splitting Reverse splitting Abnormalities of S2 Absent Old age due to calcified AS, Emphysema Splitting S2 Wide fixed Reverse splitting

Loud MS, TS, High output state, Short PR

Variable AF, Extrasystole, Complete heart block

RBBB with pulmonary HTN, Left ventricular pacing, Ectopic beats from LV Right ventricular pacing, Ectopic beat from RV

Soft A2: AS P2: PS

Loud A2: Systemic hyperperfusion, Aortic aneyrysm, atherosclerosis P2: Pulmonary HTN, Pulmonary artery dilation

Wide variable

Early A2: MR, VSD, Constrictive pericarditis Late P2:RBBB, Left ventricular ectpics, Left ventricular pacemaker

ASD, RVF, Massive PE Early P2: WPW Delayed A2: Hypertrophic caridiomyopathy, LBBB, Right ventricular pacemaker

S3 Physiological Children, Young adult, Athletes, Pregnancy

Pathological High output states, ASD, VSD, PDA, AR, MR, TR

S4: Hypertrophic cardiomyopathy, HTM, CAD Heart Murmurs Murmurs should be described in following ways: Area, Systolic/Diastolic, Timing (ESM, PSM, MDM, EDM), Intensity (grading), Pitch (low or high), best heard (bell or diaphragm – MDM is best heard will bel), conduction, posture (MDM of MS in left lateral position, EDM of AR in sitting and leaning forward), variation of murmur with dynamic auscultation. Levine and Freeman’s grading of Murmurs Systolic Diastolic I: Very soft I: Very soft II: Soft II: Soft III: Moderate III: Loud IV: Loud with thrill IV: Loud with thrill V: Very loud with thrill (heard with stethoscope) VI: Very loud with thrill (Heard even with stethoscope slightly away from wall) Systolic murmur Early systolic VSD, Acute severe TR, Acute severe MR

Mid systolic AS, PS, HOCM

Late systolic MVP, TVP, Papillary muscle dysfunction

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Pansystolic MR, VSD, TR

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Diastolic murmur Early AR, PR

Mid MS, TS

Late MS, TS, Complete heart block

Uncommon mid diastolic murmurs Carey-coomb’s murmur: Rheumatic valvulitis Austin flint murmur: Chronic AR Ritan’s murmur: Complete heart block

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Abdomen

General Examination • Nutritional status, Anaemia, Finger Clubbing, Leukonychia (Hypoalbuminaemia), Koilonychia (Iron deficiency). • Lymphadenopathy: Virchow’s node – Left supraclavicular node palpable in GI malignancy and in pelvic malignancy (Troisier’s sign) • Scratch marks of puritus, Kayser Fleisher ring – wilson’s disease • Tylosis of plam in carcinoma of oesophagus • Signs of liver failure o Alopecia o Fetor hepaticus – Sweetish, slightly fecal smell due to methyl mercaptan derieved from methionine in hepatocellular failure o Jaundice, parotid swelling, gynaecomastia o Spider naevi: Central arteriole with radiating vessels due to increase circulating estrogen – seen in SVC territory in liver failure and pregnancy o Palmar erythema, Dupuytren’s contracture, Asterexis, Xanthelasma. Inspection Shape • Generalized: Fat, fluid, flatus, faeces or fetus • Localized: Symmetric and centered around umbilicus – small bowel obstruction; Asymmetrical – liver or spleen or ovary • Scaphoid or shrunken: Advance starvation or malignancy Umbilicus • Normal: slightly retracted and inverted. Everted –Unblical hernia. Slit – Vertical in pelvic or ovarian tumor – Horizontal in ascities. Movements • Rise in inspiration and fall in expiration. In peritonitis abdomen is still. Visible pulsation • Seen in aortic aneurysm in thin patient Visible gastric peristalsis (VGP) or intestinal peristalsis (VIP) • VGP: Wave progressing from left hypochondrium and epigastric towards right lumbar region – Gastric outlet obstruction. • VIP: Step ladder form of peristaltic wave in umbilical region – small bowel obstruction. Skin • • •

Striae atrophica or gravidarum: White or pink linear marks seen by gross stretching Purple striae: Seen in cushing’s syndrome Prominent superficial vein: o Caput medusa: Distended vein around umbilicus in portal hypertension

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• • •

o SVC obstruction: Blood flow in vein is caudally above umbilicus. o IVC obstruction: In the area below umbilicus if flow is away from umbilicus – Portal hypertension, if it is towards umbilicus – IVC obstruction. Veins should be examined in standing position. Linea nigra: Pigment below umbilicus seen after pregnancy Cullen’s sign: Bluish discoloration of periumbilical region in hemorrhagic pancreatitis Grey Turner’s sign: Bluish discoloration in flank in hemorrhagic pancreatitis.

Measurement • Abdominal girth is measured at the level of umbilicus. • Distance between lower end of xiphisternum to xymphysis pubis – usually umbilicus is in midway. Umbilicus is displaced downwards in cirrhosis with ascities and upward in ovarian or pelvic tumors. • Spinoumbilical line: Line between anterior superior iliac spine and umbilicus is equal on both sides. Shift of umbilicus to one side indicates tumors originating from other side. Palpation • Superficial and deep palpation followed by palpation of organ. Liver •

• •

Hand flat on abdomen with fingers pointing upward, lateral to rectus and so that finger tips are parallel to expected edge of liver. Movement inwards and upwards and keep steady when patient takes deep breath through mouth. Wait for one full phase of respiration and continue workup laterally. Second method: Right hand below and parallel to costal margin. Palpate liver border against radial border of index finger. Findings on palpation o Soft, smooth, tender liver: Congestive liver failure, Acute viral hepatitis o Firm and regular: Obstructive jaundice, cirrhosis, chronic congestive cardiac failure o Nodular: Advanced secondary carcinoma, Hepatoma o Pulsatile: Systolic pulsation – TR; Diastolic pulsation – TS

Gall bladder • Palpable over lateral edge of rectus abdominis near tip of 9th costal cartilage on right – Ca head of pancreas, Mucocele, Ca GB. • Murphy’s sign: GB palpated during deep inspiration, at the height of inspiration the breath is arrested with gasp as the mass is felt – acute cholecystitis. Spleen • Spleen is palpable only when it is enlarged 2-3 times towards right iliac fossa. • Palpate from right iliac fossa to left hypochondrium, wait for one full respiration. • At the height of inspiration release the pressure on the examining hand so that the finger tip slips over the lower pole of spleen, confirming its presence and surface characterstics. • Move examining hand upward till rib margin if spleen is not palpable. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• • •

If still not palpable, position the patient in the right lateral position with the left hip and knee flexed then place other hand posteriorly to support the lower rib cage and repeat the examination. Alternatively examine the patient from left side curling the fingers of left hand beneath the costal margin as patient breaths deeply. Middleton’s maneuver: Examiner stands on the left side of the patient facing the foot of the bed. The hooked fingers of left hand are placed under the costal margin and with right hand pressure is exerted over the poster lateral aspect of the lower thorax. The patient is then asked to take a deep breath and spleen is felt at the end of deep inspiration.

Kidneys • Use bimanual technique placing one hand posteriorly below rib cage and the other over upper quadrant. Push two hands together firmly to feel lower pole as the patient breathes in deeply. Difference between Left Kidney and Spleen Features Left Kidney Location Posterior L1 region Edge Round Notch Absent Insinuation of fingers between Fingers can be costal margin and the organ insinuated Band of colonic resonance Present Enlargement Towards lumbar region Movement with respiration Bimanual palpation Ballotability Loin fullness and dullness

Restricted Palpable Ballotable Present

Spleen Anterior 9-11th rib Sharp Present Fingers cannot be insinuated Absent Towards right iliac fossa (Since left colic flexure and phrenicocolic ligament prevent the direct onward elargement) Moves freely on inspiration Non palpable Not ballotable Absent

Urinary bladder Palpated in suprapubic region Examination of groin, para aortic nodes and vessels • Examine groin for hernia • Palpate aorta and common iliac vessels • Para aortic nodes are palpable along umbilical region and epigastrium along the let border of aorta when considerably enlarged. Tenderness • Rebound tenderness: Inflammation of peritoneum • Shifting tenderness: Mesentric adenitis • Referred or crossed tenderness: Pressure applied over descending colon causes pain over right iliac fossa – Rovsing’s sign Percussion DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Liver • • • •

In normal liver upper border is in 5th ICS. Normal dullness over upper part of liver is reduced in: Severe emphysema, Large right pneumothorax, Gas or air in peritoneal cavity. Dull percussion below costal margin is in hepatomegaly. Liver span: Normally 12-15 cm extending from 5th rib (or below nipple) to palpable border or right costal margin

Spleen • Nixon’s method: The patient is placed on right side so the spleen lies above the colon and stomach. Percussion begins at the lower level of pulmonary resonance in the posterior axillary line and proceeds diagonally along the perpendicular line toward the lower mid anterior costal margin. The upper border of dullness is normally 6-8 cm above the costal margin. Dullness greater than 8 cm in an adult is presumed to indicate splenic enlargement. • Castell’s method: With supine, percussion in the lowest intercostal space in the anterior axillary (8th or 9th) produces a resonant note on full inspiration suggests splenomegaly. Bladder • Superior and lateral borders can be defined from the adjacent bowel. Fluid in abdomen • Shifting dullness: About 1000 ml of fluid should be present to elicit this sign • Fluid thrill: This is felt when there is large amount of fluid – more than 2000 ml. • Puddle’s sign: Can detect as little as 120 ml fluid. Patient is to lie in the prone position for 5 minutes then goes to arm knee position. Percussion around umbilicus gives dull note • USG can detect as little as 30 ml of fluid. Auscultation • Succssion splash: Pyloric stenosis, advance intestinal obstruction, Paralytic ileus, normal stomach within 2 hours of meal. • Bruit: o AAA: Bruit can be heard left of the umbilicus o Renal artery stenosis: Bruit over mid abdomen o Bruit over common iliac artery can be heard in stenosis or aneurysm o Bruit over liver may be heard in: Hemangioma, Hepatocellular carcinoma, acute alcoholic hepatitis. Hepatic artery aneurysm o Bruit can also be heard in coeliac artery stenosis and carcinoma of pancreas Venous hum: It is heard between xiphisternum and umbilicus due to turbulence of blood flow in welldeveloped collaterals as a result of portal hypertension (Cruveihier-Baugaren Syndrome). It signifies congenital patent umbilical vein draining into portal vein.

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Approach to Coma

State of Consciousness Auditory, visual and noxious stimuli of progressively increasing intensity should be applied to the patient. Respiration Cheyne Stokes Breathing • Rate of respiration will be around 30 per minutes. • Waxing and waning respiration. Waning is followed by apnoea for about 15 seconds. • Due to bilateral damage anywhere between forebrain and upper pons. Prolong circulation time due to cardiac failure also produces Cheyne strokes breathing. Central Neurogenic Hyperventilation • Rapid breathing of 40-70 breaths per minutes. PaO2 > 70-80mmHg and PCO2 > 40mmHg • Lesion of low midbrain ventral to aqueduct of Sylvius and upper pons ventral to fourth ventricle. Apneustic Breathing • Prolong inspiratory gasp with a pause at full inspiration. • Lesion of dorsolateral lower half of pons. Cluster Breathing • Periodic respiration that are irregular in frequency and amplitude, with variable pauses between clusters of breath. Ataxic Breathing • This is irregular rate and rhythm and is usually due to medullary lesions. • Ataxic breathing and bilateral VI nerve lesions may be a warning sign of brainstem compression from an expanding lesion in posterior fossa. Pupil Size and Reactivity Thalamic Lesion • Small and reactive pupil. Also noted in many toxic metabolic conditions resulting in coma. Hypothalamic Lesion • Result’s in Horner’s syndrome (Ipsilateral Ptosis, Miosis, Anhidrosis and Exophthalmos) • Lesion anywhere in sympathetic pathway causes Horner’s syndrome. Midbrain Lesion Dorsal Tectal Lesion • Interrupt the pupillary light reflex, resulting in mid position eyes, which are fixed to light but react to near. Ciliospinal reflex (Dilation of Ipsilateral pupil in response to pain applied to neck fact and upper trunk. Right sided pupil size increases 1-2mm from baseline if right sided pain is applied) is preserved. Nuclear Midbrain Lesion DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• Affects both sympathetic and parasympathetic pathway resulting in fixed, irregular mid position pupils which may be unequal. Lesion of III nerve • Lesion of III nerve in brain stem of after the nerve exits the brainstem cause wide pupillary dilation unresponsive to light. Pontine Lesion • Interrupts sympathetic pathway to cause small pupils (pinpoint pupil) which remains reactive. Lesion above Thalamus and below Pons • Should leave pupillary function intact, except for Horner’s syndrome in medullary or cervical spinal cord lesion. Ocular Motility Preservation of ocular motility implied that large portion of brainstem from oculomotor nucleus in midbrain to the vestibular nuclei at the Ponto medullary junction in intact. Evaluation of ocular movement consists of three main elements. Abnormalities of resting position including eye deviation. Spontaneous eye movement • Purposeful appearing eye movements occur in locked in syndrome, catatonia, pseudo coma and persistent vegetative state. • Rowing eye movement indicates intact brainstem and coma due to metabolic or toxic cause or bilateral lesion above brainstem. • Nystagmus is due to irritative or epileptogenic supratentorial focus. • Spontaneous conjugate vertical eye movements like ocular bobbing which is characterized by rapid downward jerk of both eyes followed by a slow return to the mid position. The center of lesion is Pons • Occulopalatal Nystagmus occurs to damage in lower brainstem involving Gullain Mollaret triangle, which extends between the cerebellar dentate nucleus, red nucleus and inferior olive. Reflex Ocular Movements Oculocehpalic reflex (Doll’s eye movement) • As head rotates to right eye moves to left if the test is positive. Cold Caloric Testing • Head is tilted back 60 degree from the horizontal plane. • 10 ml of ice cold water is slowly injected into ear canal. • There is a slow conjugate movement of eye towards stimulated ear which is corrected with Nystagmus fast phase towards the opposite ears. • Warm water irrigation produces reversal of flow. COWS (Cold water opposite, Warm water same side) • Normal response indicate intact brainstem. • Absent response indicate brainstem involvement. • Abnormal dysconjugate response occur with cranial nerve palsies, internuclear ophthalmoplegia or restrictive eye disease. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Motor System Posture • Head and eye deviation to one side and contralateral hemiparesis indicate supratentorial lesion, while ipsilateral hemiparesis indicates brainstem lesion. • Decerebrate posturing is bilateral extensor posture, with extension of lower extremities and adduction and internal rotation of shoulders and extension at elbows and wrist. This is due to bilateral mid brain or pontine lesion. Less commonly deep metabolic encephalopathy or bilateral supratentorial lesion involving the motor pathways may produce similar pattern. • Decorticate posturing is bilateral flexion at the elbows and wrists with shoulder adduction and extension of the lower extremities. Usually lesion is above the brainstem. • Unilateral dcerebrate or decorticate posture may be due to lesion anywhere in the motor system from cortex to brainstem. Adventitious Movements • Tonic clonic or other stereotyped movement indicates seizure. • Myoclonic jerking, nonrhythmic jerking movements in single or multiple muscle groups is seen with anoxic encephalopathy or other metabolic comas such as hepatic encephalopathy. • Rhythmic myoclonus which must be differentiated from epliptic movements is usually a sign of brain stem injury. • Tetany occurs with hypocalcaemia. • Cerebellar fits, resulting from intermittent tonsillar herniation are characterized by a detoriation of level of arousal, opisthotonos, respiratory rate slowing and irregularity and pupillary dilation

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Neurological Examination Examination of higher mental function Consciousness State of awareness of self or environment. Confusion Lack of clarity and coherence of thought, perception, understanding or action. First feature of cognitive impairment. Coma State of unconsciousness in which patient does not respond to any external or internal stimuli. Stupor or Semi-consciousness State of disturbed consciousness from which only vigorous external stimuli can produce arousal. Coma Vigil (Vegetative State) Patient is comatose but eyelids are open giving appearance of being awake. Patient may perform random limb and head movement but there is complete inability to respond to command or to communicate. Akinetic mutism Partial or fully awake patient who is immobile and silent. This state may be seen in hydrocephalus, mass in region of third ventricle or large bilateral hemispherical lesion. Abulia Mild form of Akinetic mutism. Patient is hypokinetic but is able to communicate. This is seen in lesion in the periaqueductal region, lower diencephalon. Locked in Syndrome (Pseudo Coma) Patient is awake and alert but non communicable with intact lid movement, eye movement in vertical plane, quadriplegia and involvement of lower cranial nerve. The lesion is in ventral pons or bilateral medulla with intact tegmentum (RAS). Catatonia Patient appears awake and blink spontaneously. There is waxy flexibility (Maintains the posture implemented by examiner). This is seen in schizophrenia. Delirium Acute confusion state characterized by period of agitation, heightened mental activity, increase wakefulness, hallucinations, motor hyperactivity and autonomic stimulation. There is impaired attention.

Dementia DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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It is a syndrome of acquired global or multifocal impairment of cognitive function involving decline in intellect, memory or personality in the presence of normal consciousness. Orientation Time, Place, Person and Self Handedness Dominant side is tested by asking patient to kick ball or to use his eye to see through a small hole. On asking patient to fold arm across chest, dominant hand is placed anteriorly. There is an anatomic difference between the sizes of dominant and non-dominant cerebral hemisphere. Planum temporale which is adjacent to the auditory center of Helschl’s transverse gyrus is larger in the left hemisphere in the right handed individual. General Intelligence • Abstract thinking o Patient is asked to explain the meaning of common proverb. • Reasoning o Patient is asked to compare object or asked to differentiate between lie and mistake. • Judgment o Asked questions like what would you do on seeing house on fire. • Attention o Asked to subtract 7 from 100 down to zero. • Calculation o Patient is asked to solve simple numerical problem. • Memory o It is a power to retain and recall past experiences. Components of Memory • Reception • Registration • Retention • Recall Types of Memory Immediate or short term memory • It is a memory for event of few seconds duration. • Patient is asked to spell “World” backward. • Impaired in acute confusion syndrome, Wernicke-Korsakoff syndrome. • Recent memory • Recall of information presented within minutes, hours or days. • Patient is asked to remember three unrelated common objects told to him few minutes ago. • Long term or secondary or remote memory • Memory for past events. • Tested by asking dates of some of public events DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Perception Delusion These are false beliefs which continue to be held despite evidence to the contrary. Hallucination These are false impressions referred to the organs of special senses in the absence of a stimulus. Illusion These are misinterpretations of stimuli. Obsession These are recurrent and persistent thoughts which intrudes into the patient’s mind despite best effort to get rid of them. Visuospatial Function Ask the patient to copy a drawing of five pointed star or three dimensional box. Constructional apraxia or visuospatial agnosia results in difficulty in drawing the lines. Apraxia It is a defect in the ability to carry out known acts in the absence of motor weakness, sensory loss or ataxia. Agnosia Failure to recognize known objects in the presence of intact sensory, visual and auditory pathway. Sleep Non REM has four stages and lasts about 90 minutes and progressed to REM sleep. Most of the dreaming occurs in this stage. Speech and Language Aphasia • Broca’s aphasia or expressive aphasia or motor aphasia • Poorly articulated and non-fluent speech with reduced number of words with errors of grammar and syntax. Wernicke’s aphasia or receptive aphasia or sensory aphasia • Speech is fluent but may contain jargon. • Conduction aphasia • Patient is unable to repeat words or phrase spoken by examiner. The lesion is in perisylvian area with damage to the fibers or arcuate fasciculus. • Transcortical aphasia • Broca’s or Wernicke’s type aphasia with normal repetition. • Global aphasia • Broca’s and Wernicke’s type aphasia Dysarthria • Cerebellar Dysarthria • Patient speaks slowly and deliberately, syllable by syllable. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• • • • • • • •

Pseudo-bulbar (spastic) Dysarthria Individual syllabus are slurred and the precision of consonant pronunciation is lost. Bulbar Dysarthria Nonspecific slurring of speech. Dysphagia and nasal regurgitation are present. Rigid Dysarthria Low volume monotonous speech. Extrapyramidal involvement – Parkinsonism. Cortical Dysarthria Irregular hesitancy in word production associated with difficulties I abstract, volitional movements of lips and tongue.

Examination of Cranial Nerves Olfactory - I The only sensory nerve with no thalamic connection. • Loss of smell – Anosmia o Nasal disease, Head injury, Tumors or anterior cranial fossa, Chronic basal meningitis. Kallman’s syndrome, Tabes dorsalis, Internal hydrocephalus, Aging, Alzheimer’s disease, Parkinson’s, Huntington’s chorea, Down’s syndrome. • Increase olfactory acquity – Hypersomia o Migraine, Addison’s, Hyperemesis gravidarum, Strychnine poisoning • Perversion of smell – Parosmia o Severe nasal infection, Phenytoin, Psychological • Foul smell – Cacosmia o Upper respiratory tract infection or atrophic rhinitis • Olfactory hallucinations o Epilepsy arising from uncinated gyrus of temporal lobe, psychosis. Optic nerve – II • Visual Acuity o Snellen’s chart is used. o Pin hole test: If the patient is able to see through pin hole then patient has refractive error. • Visual Field o Normally visual field is 1000 temporally, 600 nasally, 600 superiorly and 750 inferiorly. • Color Vision o Ishihara Chart • Pupillary Reflex o Bright light is swung from one eye to the other alternatively. The eye with optic nerve lesion will show a positive consensual light reflex but will not show positive direct light reflex. o Affected pupil starts to dilate when direct light is thrown into that eye – Marcus Gunn’s Pupil • Fundus o Early papilloedema  Blurring of superior and inferior margin of disc  Disc hyperaemia and dilated capillaries  Spontaneous venous pulsation are absent DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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 Splinter hemorrhages at or just off the disc margin  Optic cup is preserved o Established papilloedema  Disc margin becomes indistinct and central cup is obliterated.  Disc surface is elevated above the retina.  Venous engorgement and peripapillary oedema  Flame shaped hemorrhages and cotton wool spots.  Radiating folds around macula o Chronic paiilloedema  Central cup remains obliterated.  Hemorrhage and exudates gradually resolve. o Atrophic papilloedema  Retinal vessels are attenuated with perivascular sheathing.  Dirty white appearance of optic disc due to reactive gliosis. Oculomotor – III, Trochlear – IV and Abducent – VI Ptosis • Partial o Occurs with lesion of the cervical sympathetic pathway (Horner’s syndrome) due to weakness of tarsal muscle innervated by cervical sympathetic nerves. The upper eyelids can however be raised voluntarily. • Complete o The patient is not able to voluntarily open the affected eye. This is due to paralysis of levator palpabrae superioris innervated by III. Size of Pupils • Normal size of pupil is 3-5mm. Pupil less than 3 mm is called mitotic and > 5mm is called mydriatic. Pin point pupil is said to be present when pupillary size is less than or equal to 1 mm. • Miosis o Old age, Horner’s syndrome, Drugs or toxins (Neostigmine, Morphine, OP poisioning), Pontine hemorrhage. • Mydriasis o Infancy, Lesion of III (Midbrain), Drugs (Atropine, Pethedine), Optic atrophy. Pupillary reflexes • Light reflex o Light reflex is carried by optic tracts to Edinger Westphal nucleus bilaterally and then through ciliary ganglion to sphincter pupillae by the ciliary nerves. • Direct light reflex o Patient is asked to look at a distance to avoid accommodation reflex. When light is projected into eyes the pupil constricts. • Consensual reflex o Reflex is elecitated by placing partition between two eyes. When light is projected into one eye other eye respond by constricting. • Reaction to accommodation

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•

o Afferent stimulus goes to optic nerve then to occipital lobe, fibers pass to the frontal lobe and from here corticobulbar fibers go to third nerve nucleus. o The reflex comprises of adduction (convergence) of eyes and pupillary constriction when patient looks at near object. Agryl Robertson pupil is absent accommodation reflex and preserved light reflex – Syphilis, DM, Alcoholic polyneuropathy.

Ocular Movements Tested by holding object 60 cm away from eye of the patient. • Diplopia o Two types of diplopia. Uniocular and binocular. In binocular diplopia there is always true and false image formation. True image is near to eye and clear while false image is farther from eye and unclear. Red glass test is done to detect affected eye in patient with diplopia. A red glass is placed in front of affected eye visualizes false image as red. • Squint o Abnormality of ocular movement in which visual axis do not meet at the point of fixation. • Upper motor Neuron (Supranuclear) Lesion o Lesion of supranucleus causes conjugate gaze paralysis. • Lesion of PPRF – Lateral conjugate gaze paralysis • Lesion of midbrain at the level of superior colliculus – Upward gaze paralysis • Lesion of midbrain at the level of inferior colliculus – Downward gaze paralysis • Fronto-mesencephalic pontine pathway o Contraleteral Brodmann’s area -> Corona radiate -> Internal capsule -> Cerebral peduncle -> Decussates at the level of pons -> Descends to synapse contralateral pontine paramedian reticular formation (PPRF). • Parital and temporo mesencephalic pontine pathway o Paritral lobe -> Temporal lobe -> Pons -> Medial longitudinal fasiculus about the level of VI nucleus. • Internuclear lesion o Lesion is in medial longitudinal fasiculus. o Characterised by failure of adduction of eye on the side of leion of MLF and mild weakness of abduction with Nystagmus on the contralateral side. • Nystagmus o Pendular Nystagmus o Rapid horizontal oscillations to either side of the midline of equal amplitude seen on forward gaze. Causes: Visual defect in infancy, chorioretinitis. o Jerky Nystagmus o Ocular oscillation of unequal amplitude with slow drift in one direction and fast correcting movement in the other direction. Fast phase determining the direction of Nystagmus. Horizontal Nystagmus is due to lesion of vestibular nerve, medial longitudinal bundle or cerebellum. Vertical Nystagmus is due to condition involving brainstem. Rotatory Nystagmus is seen in labyrinthine disorder.  Grade I: Fast phase to left looking towards left only.  Grade II: Fast phase to left looking straight ahead. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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

Grade III: Fast phase to left looking towards right.

Trigeminal Nerve – V Sensory system • Pain, temperature and light touch are examined • Opthalmic division o Upper part of the side of nose • Maxillary division o Malar region and lip. • Mandibular division o Chin and anterior part of tongue. Motor system • Masseter and Temporal Muscle are palpated while patient clenches his jaws. • Lateral Pterygoids weakness causes jaw to deviate paralyzed side on opening mouth. Reflexes • Corneal reflex o Afferent is trigeminal nerve and efferent is facial nerve. Eyelid blinks when cornea is touched. • Jaw jerk o Patient is asked to open mouth slightly. The forefinger placed below lower lip is tapped with percussion hammer. There is slightly palpable upward jerk. It is exaggerated in pseudobulbar palsy. • Glabellar reflex o Afferent is trigeminal nerve and afferent is facial nerve. Percussion of supraorbital ridge results in bilateral contraction of the orbicularis oculi muscle. Facial Nerve – VII Motor • All facial muscles are innervated. Upper part of the face has bilateral innervation while lower part has unilateral innervation. So in UMN lesion upper part of face of affected side is spared. Sensory • Anterior two third portion of each half of the tongue is examined. • Saliva is wiped after protruding tongue. Tongue must be protruded during entire test. • Sugar, salt, citric acid and quinine is tested for sweet, salty, sour and bitter. • Patient is asked to identify pointing the specific taste written in the card. Secretory function •

•

Lacrimation o Schirmer’s test: Blotting paper is placed under the lower eyelid and removed after 5 minutes. Normally at least 10 mm of the blotting paper will be dampened by the evoked tear secretion. Nasolacrimal reflex

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Reflex secretion of tears by stimulation of nasal mucosa by irritating substance such as dilute solution of ammonia or formaldehyde. Afferent is trigeminal nerve and efferent is greater superficial petrosal nerve which is a branch of facial nerve. Salivation o Highly flavored substance is placed in tongue and patient is asked to elevate copious, a copious supply of saliva is seen to flow from the submandibular duct. Reflexes o Corneal reflex o Stapedial reflex Afferent is vestibulochochlear nerve and efferent is facial nerve. When the stapes is stimulated by loud noise, noamally the reflex contraction of stapedius leads to reduction in transmission of the sound. Patient may complain of hyperacusis for low tones. o

• • •

Vestibulocochlear Nerve – VIII Auditory function by use of the human voice • Normal conversation voice should be heard at 20 feet and whispering voice should be heard at 10 feet. • Non test ear should be occluded. Examiner should use unfamiliar words. Watch test • Quartz watch should be avoided. Tunning fork test A 512 Hz tuning fork is used. Rinne’s Test • Air conduction more than bone conduction = Positive • Positive: Normal ear, Sensorineural deafness • Negative: Conductive deafness Weber’s test • No lateralization – Normal ears • Lateralization to normal ear – Sensorineural deafness on opposite side • Lateralization to affected ear – Conductive deafness on the same side Absolute bond conduction test (Schwabach test) • Examiner should have normal auditory function. • Bone conduction of examiner is compared with patients. • ABC equal – Normal • ABC increased for patient – Conductive deafness • ABC decreased for patient – Sensorineuronal deafness Audiometric test • Test of vestibular function Fistula sign • Increasing pressure over external acoustic meatus by otoscope or repeatedly pressing tragus of the ear against auditory meatus proguces nystamus. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Oculocephalic reflex (Doll’s eye movement) • Normal response for the patient’s eye to deviate to the left as the head is turned to the right. It is a definite sign of normal midbrain function. Its absence suggests brain death. Positional vertigo • Vertigo is induced by certain head postures or by sudden change in the head position. Caloric test • Head is elevated to 30 degree to bring semicircular canal into the vertical plane. • Patient is instructed to fix upon a point in central gaze. • External ear canal is irrigated with water at 300 C and then 440 C for 30-40 seconds each. • COWS: Nystygmus -> Cold water Opposite side, Warm water Same side -> Normal response Glosopharyngeal – IX and Vagus – X • General sensation and taste over posterior 1/3 of tongue. • Palatal reflex: Elevation of soft palate on saying ah. • Gag reflex: Contraction of pharynx in stimulating pharynx. Accessory Nerve – XI • Testing of sternocleidomastoid muscle by turning face against resistance. • Trapezius muscle testing by shrugging shoulder. Hypoglossal Nerve – XII • Patient is asked to move tongue. Spinomotor System Nutrition (Bulk of muscle) • Muscle wasting is a sign of lower motor neuron lesion. • Both sides should be compared. o Circumference of limbs is measured at the following levels o Upper limb: 10 cm above and below olecranon o Lower limb: 18 cm above superior border of patella and 10 cm below tibial tuberosity. Tone Degree of tension of muscle at rest. Tone can be assessed by inspection, palpation of muscle group and passive movement of joint. In unconscious patient raising an arm in turn and allowing it to fall back. • Hypertonia o There is a resistance felt on the passive movements of the joints either in form of spasticity or rigidity. • Spasticity o Hypertonia of either agonist of antagonist group of muscle. Hypertonia of antigravity muscle group produces clasp knife rigidity. In hemiplegia tone of flexor group of muscle exceeds extensor. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• • •

•

•

•

•

Rigidity o Hypertonia is in both agonist and antagonist group of muscle. Plastic of lead pipe rigidity o Uniform resistance offered to passive movement. E.g. Parkinsonism, Basal ganglia neoplasm. Cog Wheel Rigidity o Resistance offered to passive movement interrupted by alternate contractions of agonist and antagonist muscle due to presence of associated tremor. E.g. Parkinsonism, CO poisioning Hypotonia o On inspection the muscle group is lax and assume a pendulous shape, on palpation the muscle group is flabby to feel and there is diminished resistance to passive movement of joints. Clonus o Sudden stretching of hypertonic muscle produces reflex contraction. Ankle clonus is demonstrated by dorsiflexing the foot after the hip. Patellar clonus by sharply moving patella downward. Sustained clonus is a sign of pyramidal tract lesion. Myotonia o This is a state in which muscle contraction continues beyond the period of time. When the patient is asked to smile and then relax his facial muscle, a delay in relaxation of the muscle is noted and the smile remains fixed on the face for longer. Power o Grade 5 – Normal power o Grade 4 - Movement against resistance o Grade 3 – Movement against gravity o Grade 2 – Gravity eliminated movement o Grade 1 – Flicker of contraction o Grade 0 – No movement

Coordination • Finger nose test o Patient is asked to keep limb outstretched and touch tip of his nose with forefinger. • Finger-finger nose test o Patient is asked to touch examiner’s tip of forefinger and then his own nose. • Tapping a circle test o A circle 1 cm diameter is drawn and patient is given a pencil and asked to tap out a series of dots all within the circle. • Dysdiadochokinesis o Failure to efficiently perform rapidly alternating movements. • The heel knee test o Patient is asked to place heel of one foot over the knee of the other foot and then to move the heel down over tibia. • Foot pat test

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PATAN ACADEMY OF HEALTH SCIENCES

o

The patient is asked to pat the ground with the heels of the both feet alternatively in the siting position.

Involuntary movements • Chorea o Semi purposive, irregular, non-repetitive and brief jerky movements. Due to involvement of Caudate Nucleus. • Athetosis o This is a slow writing movement, best seen at wrist, fingers and ankles. The fingers writhe, the wrists flex the forearm and arm rotate inwards, adduct and then rotate outwards in abduction. The foot is inverted. The movements are absent during sleep, minimally altered by eye closure, increased by voluntary movement and interfering with it. Due to involvement of Putamen. • Hemiballismus o Involve proximal joint of one arm resulting in wild, rapid, flinging movement of wide radius occurring constantly, interspersed with short periods of freedom. Due to involvement of Subthalamic Nucleus. • Dystonias o Involuntary sustained muscle contraction. Due to involvement of Putamen. • Tremors o Rest tremors  Tremor occurs when limb is at rest. Parkinson’s disease, Extrapyramidal disease o Postural tremors  Tremor occurs when limb maintains a posture like holding the arms and hands outstretche. Thyrotoxicosis, Anxiety, Alcohol, Caffeine, Structural brain disease o Intentional tremor  Tremor occurs when the limb approaches its target. Lesion of cerebellum and its connections: Multiple sclerosis, vascular disease. Abnormalities of gait • Circumduction gait o In patient with hemiplegia. • Spastic gait o Bipyramidal lesion involving both the lower limb. • High stepping gait o Seen in patient with foot drop. • High stepping and stamping gait o Seen in patient with posterior column lesion. There is high stepping with forceful landing of the foot. • Ataxic gait o Seen in cerebellar lesion • Shuffling gait o Seen in patient with lesions in extrapyramidial system. Patient makes a series of small, flat footed shuffles. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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•

Waddling gait o Seen in patient with proximal muscle weakness. Patient walks on broad base with an exaggerated lumbar lordosis.

Reflexes The components of reflex arc are; sensory receptor, afferent pathway, centre, efferent pathway, efferent organ. Deep tendon reflexes are monosynaptic reflexes and the superficial and visceral reflexes are polysynaptic reflexes. • Abdominal reflexes o Reflexes are retained till late in motor neuron disease and lost early in multiple sclerosis. In hemiplegia there is unilateral loss of abdominal reflex. • Plantar reflex o Classical method: Stroking lateral aspect of sole of foot. o Gorden reflex: Calf muscle are squeezed o Oppenheim reflex: Firm stroke with the finger and thumb is applied don either side of the anterior border of tibia, greater pressure being applied to the medial side. o Chaddock reflex: Stroke is applied down the lateral malleolus. o Minimal pyramidal lesion: Applying stimulus on the dorsolateral aspect of foot. o Medial stimulation: Assessing the density of lesion. o Extensor plantar response  This response is seen in lesion of corticospinal tract. There is dorsiflexion of great toe with extension and fanning of other toes.  Equivocal • Planter response is said to be equivocal in following situations o There is a rapid but brief extension of toes at first which is followed by flexion or predominant flexion followed by extension. o There is only extension of great toe or extension of great toe with flexion of small toes. o There is no response to planter stimulation particularly if there is paralysis of dorsiflexors. o There may be flexion of knee and hip with no movements of toes.  Minimal plantar response • On eliciting the plantar reflex, no movement of the toes may be seen. The presence of positive plantar response can then be assessed by feeling for the contraction of tensor fascia lata and adductors of thigh. o Pseudo Babinski sign  False Babinski sign may occur in absence of pyramidal tract lesion in following conditions.  Sensitive individual  As a response of plantar hyperesthesia.  In athetosis or chorea where big toe may extend as a response of dystonic posturing.  If short flexors of toes are paralysed due to LMN lesion.  Infancy  Deep sleep DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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      

Deep anaesthesia Narcotic overdose Alcohol intoxication Coma secondary to metabolic disturbances Post traumatic states Post ictal states Cheyne stokes respiration

Differentiation between Babinski and Pseudo Babinski Sign Traits Hamstring contraction Pressure on the base of great toe while eliciting the plantar reflex

Babinski

Pseudo Babinski

Felt Does not inhibit the extensor plantar response

Not felt Inhibits extensor plantar response

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Emergency Structure and Operation Contents Emergency Infrastructure ................................................................................................................................ 26 Resuscitation Bay and Team Dynamics ........................................................................................................... 27 Resuscitation Team ...................................................................................................................................... 28 Close loop communicaitons ......................................................................................................................... 28 Triage ............................................................................................................................................................... 29 Occupational Exposure and Universal Precaution........................................................................................... 30 Hepatitis B Exposure .................................................................................................................................... 30 HIV Exposure ................................................................................................................................................ 30 Universal precaution .................................................................................................................................... 31 Tetanus Prophylaxis ......................................................................................................................................... 32

PATAN ACADEMY OF HEALTH SCIENCES

Emergency Infrastructure

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PATAN ACADEMY OF HEALTH SCIENCES

Resuscitation Bay and Team Dynamics

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PATAN ACADEMY OF HEALTH SCIENCES

Resuscitation Team

Close loop communicaitons

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PATAN ACADEMY OF HEALTH SCIENCES

Triage Patient arriving at Airway Assessment Signs of airway obstruction • •

Ye

No further assessment, handover the patient immediately to RED

Ye

No further assessment, handover the patient immediately to RED

Ye

No further assessment, handover the patient immediately to RED

Ye

Handover the patient immediately

Cannot speak Stridor or gurgling sound

No Breathing Respiratory rate > 30

No Circulation SBP < 90 mmHg CRT > 2 sec

Mental Status

Cannot follow simple command

No CAN PATIENT WALK (Provided there is no injury to limb)? OR No potential life threatening condition • Penetrating Injury • High velocity collision

No

RED

Transfer to Yellow Yellow

Ye Transfer to

Green Classification of Triage Category according to Symptoms RED YELLOW Unconscious Stable vitals with Ongoing seizure • Abdominal injury Sudden onset retrosternal chest • Fall from height pain • In moderate to severe Respiratory Distress pain Actively Bleeding • Palpitation

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

GREEN Stable vitals with • Walking wounded • Weakness of limbs • Fever • Cough

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PATAN ACADEMY OF HEALTH SCIENCES

Occupational Exposure and Universal Precaution Hepatitis B Exposure Vaccination and antibody status of exposed workers

Source is HBsAg positive

Source is HBsAg negative

Source is unknown or not available for testing

Unvaccinated/Nonimm une

HBIG and HB vaccine

HB vaccine

HB vaccine

Non responder

No treatment

No treatment

No treatment

Known non responder

HBIG and Re Vaccination

No treatment

If known high risk source treat as HBsAg positive

Antibody response unknown

Test for antibody If inadequate HBIG and HB vaccine If adequate - no treatment

No treatment

Test for antibody If inadequate HBIG and HB vaccine If adequate - no treatment

Previously vaccinated

HIV Exposure Recommendation for HIV PEP for percutaneous injuries Exposure type

HIV positive - HIV positive Asymptomatic Symptomatic

Known source but HIV status cannot be determined

Unknown source HIV Negative

Less severe

2 Drug PEP

3 Drug PEP

No drug but consider 2 drug PEP for source with risk factor

No drug but consider 2 drug PEP for source with risk factor

No PEP

More Severe

3 drugy PEP

3 drugy PEP

No drug but consider 2 drug PEP for source with risk factor

No drug but consider 2 drug PEP for source with risk factor

No PEP

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PATAN ACADEMY OF HEALTH SCIENCES

Recommendation for HIV PEP for mucous membrane and non intact skin exposure Exposure type

HIV positive Asymptomatic

HIV positive Symptomatic

Known source but HIV status cannot be determined

Unknown source

HIV Negative

Less severe

2 Drug PEP

2 Drug PEP

No drug but consider 2 drug PEP for source with risk factor

No drug but consider 2 drug PEP for source with risk factor

No PEP

More Severe

2 drugy PEP

3 drugy PEP

No drug but consider 2 drug PEP for source with risk factor

No drug but consider 2 drug PEP for source with risk factor

No PEP

Basic Two Drug Regimen Zidovudine 300 mg BD or 200 mg TDS + Lamivudin 150 mg BD Expanded Three Drug Regimen Basic Two drug regimen plus Lopinavir/Ritonavir combination 400/100 mg BD

Universal precaution • • • • • •

Hand washing Gloves Mask and shields Gowns Disposals Environmental and work practice condition

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Tetanus Prophylaxis

1. A clean wound a. If previously receceived vaccine within 10 years i. Vaccine not needed b. If not received vaccine within 10 years i. Vaccine needed c. If vaccine status unknown i. Vaccine needed 2. Contaminated wound a. Primary tetanus prophylaxis not known – needs TIG b. Primary tetanus prophylaxis more than 5 years – Vaccine needed c. Primary tetanus prophylaxis less than 5 years – Vaccine not needed

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Resuscitation Contents Adult Basic Life Support ................................................................................................................................... 34 Pediatric Basic Life Support ............................................................................................................................. 35 Advance Cardiac Life Support (Pulse less VT/VF) ............................................................................................ 36 Advance Cardiac Life Support (Asystole/PEA) ................................................................................................. 37 Pediatric Advance Life Support ........................................................................................................................ 38 Primary Trauma Care ....................................................................................................................................... 39 2015 ACLS Updates .......................................................................................................................................... 42 Anaphylaxis ...................................................................................................................................................... 44 Sign and symptoms ...................................................................................................................................... 44 Pathophysiology of Anaphylaxis .................................................................................................................. 44 Treatment of Anaphylaxis ............................................................................................................................ 45 Disposition of Patients with Anaphylaxis..................................................................................................... 46 Acid Base Disorder ........................................................................................................................................... 47 Basic Interpretation ..................................................................................................................................... 47 Advance Interpretation................................................................................................................................ 47 Primary pH Changes and Compensation ................................................................................................. 47 Acute Respiratory Acidosis (acute hypoventilation)................................................................................ 47 Chronic Respiratory Acidosis (ie. chronic hypoventilation) ..................................................................... 47 Acute Respiratory Alkalosis (ie. acute hyperventilation)......................................................................... 48 Chronic Respiratory Alkalosis (chronic hyperventilation) ....................................................................... 48 Metabolic Acidosis (ie. acute and chronic) .............................................................................................. 49 Metabolic Alkalosis (ie. acute and chronic) ............................................................................................. 50 Approach to Acid-Base Disorders ............................................................................................................ 52 Sepsis................................................................................................................................................................ 55 Definitions .................................................................................................................................................... 55 3 hour Bundle............................................................................................................................................... 55 6 hour Bundle............................................................................................................................................... 55 Documentation ............................................................................................................................................ 55 Antiboitics ........................................................................................................................................................ 56 Renal Dosing ................................................................................................................................................ 56 Bactericidal vs. Bacteriostatic antibiotics .................................................................................................... 56 Penicillins ..................................................................................................................................................... 56 Cephalosporins ............................................................................................................................................ 58 Aminoglycosides .......................................................................................................................................... 59 Fluoroquinolones ......................................................................................................................................... 60 Tetracyclines ................................................................................................................................................ 62

PATAN ACADEMY OF HEALTH SCIENCES

Sulfa drugs.................................................................................................................................................... 62 Nitrofurantoin .............................................................................................................................................. 63 Carbapenems ............................................................................................................................................... 63 Vancomycin .................................................................................................................................................. 64 Linezolid ....................................................................................................................................................... 64 Inotropes .......................................................................................................................................................... 65 Definitions .................................................................................................................................................... 65 Adrenergic Receptors .................................................................................................................................. 65 Commonly-Used Inotropes .......................................................................................................................... 65 Details .......................................................................................................................................................... 66

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Adult Basic Life Support Check for danger

Check responsiveness

Shout for help

Open airway

Not breathing normally?

30 chest compression

2 rescue breath 30 compressions

Attach to AED as soon as available

Continue CPR until qualified personnel arrives or signs of life returns

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Pediatric Basic Life Support Stimulate and check responsiveness

Open Airway Head tilt chin lift (jaw thrust)

Check Breathing Look, Listen and Feel

If breathing Recovery position

Yes Breathe Deliver 2 effective breaths

If no chest rise Reposition airway Reattempt breaths

Assess for the sign of circulation (Movement ± pulse) Do not delay > 10 seconds

If no success Treat as for airway obstruction

No Chest compression 30 compression 2 ventilation Rate of about 100 compressions/minute Continue Resuscitation

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Advance Cardiac Life Support (Pulse less VT/VF) First Impression: Sick or not sick? Primary survey Unresponsive Open airway, give 2 breaths Give oxygen when available If no pulse, 30 compression 2 breath Attach to AED/Monitor/Defibrilato r

Asystole PEA

Assess ECG rhythm. Shockable? (Pulseless VT/VF) Yes No

Shock (Defibrillation) x 1 Resume CPR 5 cycles (about 2 minutes) without interrupting. During CPR give vasopressor Epinephrine 1mg every 3-5minutes Or Vassopresin 40IU in place of first or second Epinephrine

No

Assess ECG rhythm Shockable? Yes

Reassess/Monitor

• Airway • Oxygenation/ventilation • Paddle/Pad Position/ Contact • Effectiveness of CPR • No Oxygen flow over patient during shock

Attempt/verify • Advance airway position • Vascular access

Monitor and treat • Glucose • Electrolyte • Temperature

Shock (Defibrillation) x 1 Resume CPR 5 cycles (about 2 minutes) without interrupting. During CPR give consider antiarrythmic Amidarone 300mg IV/IO consider repeat dose of 150mg x 1 in 5 minutes or Lidocaine 1-1.5mg/kg IV/Io initial dose (if Amidarone is not available) Then0.5-0.75mg/kg PRN every 5-10 min Maximum cumulative dose 3mg/kg Consider Magnesium 2gm IV/IO for torsades de pointes Consider reversal cause of arrest

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

Defibrillation • • • •

Monophasic: 360J all shocks AED: Per manufacturer Biphasic: Per manual Biphasic unknown: 200J initially, then same or higher as first shock

Reversible cause • Identify and treat causes o Hypoxemia o Hypovolemia o Hypothermia o Hyeper/Hypokalaemi a and metabolic disorders o Tamponade o Tension pneumothorax o Toxins/poisons/drugs o Thromboembolism

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PATAN ACADEMY OF HEALTH SCIENCES

Advance Cardiac Life Support (Asystole/PEA) First Impression: Sick or not sick? Primary survey Unresponsive Open airway, give 2 breaths Give oxygen when available If no pulse, 30 compression 2 breath Attach to AED/Monitor/ Defibrillator

Assess ECG rhythm. Shockable? No Yes Resume CPR 5 cycles (about 2 minutes) without interrupting. During CPR give vasopressor Epinephrine 1mg every 3-5minutes Or Vassopresin 40IU in place of first or second Epinephrine

Treat as pulse less VT/VF Reassess/Monitor

• Airway • Oxygenation/ventilation • Paddle/Pad Position/ Contact • Effectiveness of CPR • No Oxygen flow over patient during shock

Yes

Assess ECG rhythm Shockable? No Resume CPR 5 cycles (about 2 minutes)

Defibrillation • • • •

Monophasic: 360J all shocks AED: Per manufacturer Biphasic: Per manual Biphasic unknown: 200J initially, then same or higher as first shock

Reversible cause • Identify and treat causes o Hypoxemia o Hypovolemia o Hypothermia o Hyeper/Hypokalaemi a and metabolic disorders o Tamponade o Tension pneumothorax o Toxins/poisons/drugs o Thromboembolism

Attempt/verify • Advance airway position • Vascular access

Monitor and treat • Glucose • Electrolyte • Temperature

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Pediatric Advance Life Support BLS Algorithm: Assess and support ABCs as needed Provide oxygen Attach monitor/defibrillator Assess rhythm (ECG) Not Shockable

Shockable

Asystole/PEA

VT/VF Give 1 shock • Manual: 2 J/Kg • AED > 1 year of age Use pediatric system if available for 1-8 years Resume CPR immediately

Resume CPR immediately Give Epinephrine IV/IO 0.01mg/kg (1:10 000: 0.1ml/kg) Endotracheal tube: 0.1mg/kg (1:10 00: 0.1ml/kg) Repeat every 3-5 minutes

Give 5 cycle of CPR Check rhythm Shockable rhythm?

No

Shockable

Is asystole go to box no 3 If electrical activity Check pulse

Continue CPR while defibrillator is charging Give 1 shock • Manual: 2 J/Kg • AED > 1 year of age immediately Give Epinephrine IV/IO 0.01mg/kg (1:10 000: 0.1ml/kg) Tracheal tube: 0.1mg/kg (1:10 00: 0.1ml/kg) Repeat every 3-5 minutes

If no pulse go to Asystole/PEA

No

Check rhythm Shockable rhythm? Shockable Go to VT/VF

If pulse present begin post resuscitation care

Give 5 cycle of CPR Check rhythm Shockable rhythm?

Give 5 cycle of CPR

No

Shockable Continue CPR while defibrillator is charging Give 1 shock • Manual: 2 J/Kg • AED > 1 year of age Resume CPR immediately Consider Antiarrhythmic Amidarone: 5mg/kg bolus IV/IO or lidocaine: 1mg/kg bolus IV/IO/TT or Magnesium 25 to 50 mg/kg IV/IO for torsades de pointes of hypomagnesemia (maximum 2g) After 5 cycle of CPR go to box 1

Box 1 • Push hard and fast (100/min) • Ensure full chest recoil • Minimize interruption in chest compression • One cycle of CPR: 15 compressions then 2 breaths • 5 cycle = 1 to 2 minutes • Avoid hyperventilation • Secure airway and confirm placement • After an advance airway is placed rescuers no longer delivers cycles of CPR. Give continuous chest compression without pause for breaths. Give 8 to 10 breathes per minute. • Check rhythm every 2 minutes • Rotate compression every 2 minutes with rhythm check • Identify and treat causes o Hypoxemia, Hypovolemia o Hypothermia o Hyeper/Hypokalaemia and metabolic disorders o Tamponade o Tension pneumothorax o Toxins/poisons/drugs o Thromboembolism

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Primary Trauma Care

The following patient should go full trauma assessment History: • Fall >3 meters • Motor vehicles accident with net speed > 30km/hr • Thrown from vehicle/trapped in vehicle • Death of a person in accident • Pedestrian vs. car/cyclist vs car/unrestrained occupant Examination • Airway or respiratory distress • BP>100mmHg • GCs1 area injured • Penetrating injury The assessment of trauma patient includes 1. Primary survey A: Airway B: Breathing C: Circulation D: Disability E: Exposure 2. Secondary survey Head examination • Scalp and ocular abnormalities • External ear and tympanic membrane • Periorbital soft tissue injuries Neck examination • Penetrating wounds • Subcutaneous emphysema • Tracheal deviation • Neck vein appearance Neurological examination • Glasgow coma scale • Spinal cord motor activity • Sensation and reflex DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Chest examination • Clavicles and all ribs • Breathe sounds and heart tones • ECG monitoring (if needed) Abdominal examination • Penetrating wound of abdomen requiring surgical exploration • Blunt trauma – a nasogastric tube is inserted (not in the presence of facial trauma) • Rectal examination • Insert urinary catheter Pelvis and limbs • Fractures • Peripheral pulses • Cuts, bruises and other minor injuries X rays (if possible) • Chest x ray • Cervical spine lateral view • Pelvis and long bone x ray

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PATAN ACADEMY OF HEALTH SCIENCES Trauma patient C spine protection

Airway assessment Talk to patient Signs of airway obstruction may include • Snoring or gurgling • Stridor or abnormal breath sounds • Agitation • Using accessory muscle of ventilation/Paradoxical chest movements • Cyanosis

Airway not clear Reassess

Airway clear

Oxygen/Chin lift/Jaw thrust Suction Guedel airway/nasopharyngeal airway Intubation (if needed)

Breathing assessment Look: cyanosis, chest movement, penetrating injury, use of accessory muscle Feel: Tracheal shift, broken ribs, subcutaneous emphysema, percussion Listen: Pneumothorax, detection of abnormal sounds in the chest

Breathing not clear Reassess

Oxygen Decompression and drainage of tension pneumothorax Closure of open chest injury Artificial ventilation

Breathing clear

Circulation assessment Shock: Hypotension, tachycardia, tachypnoea, pallor, cool extremities, decreased capillary refill

Circulation not clear Stop haermorrhage Establish IV line with 2 large bore canula Administer IV fluid

Circulation clear

Disability A: Awake, V: Verbal response, P: Painful response, U: Unresponsiveness

Exposure

Secondary survey

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2015 ACLS Updates • • • • • • • • • • • • • • •

If available, ECMO/ECPR should be considered for selected reversible causes of CA No vasopressin- no benefit and difficult to use Early epinephrine recommended Use of ultrasound to confirm ROSC and confirm ETT placement Use max 02 during CPR and titrate down after ROSC Low EtCo2 after 20 mins efforts = low likelihood of survival No routine lidocaine after ROSC (but may continue if started for VF/VT) PCI if: stemi, hemo/elec unstable if lesion suspected Post-arrest temp targeted to 32-36 with emphasis on avoiding fever Emphasis on CCR (cardiocerebral resus) vs CPR - uninterrupted compressions Emphasis on CAB vs ABC in ACLS - chest RECOIL is most important for improving flow/perf Delay airway for improved survival! (CAB) EXCEPT IN PEDS Although 30:2 comp:breath interval remains, Seattle hosp survival is highest in world and EHS uses uninterrupted CPR with breaths Q10 compressions spaced btw AVOID PULSE CHECKS! - use etco2 as a measure of ROSC!!! ONLY STOP CPR TO SHOCK (even then, shocking with gloves has been ok’d)

SPECIFIC ISSUES: Role of capnography: MANDATED. • Goal 12-15 during CPR (below 10= suboptimal) • Rise to 35-40 may indicate ROSC • DO NOT TERMINATE until 35-40 maintained (not just spike) Role of mechanical compression devices (autopulse or LUCAS) • So far no hard evidence of survival/neuro benefit • But this maybe due to a) comparison to very HQ CPR, b) unfamiliarity=lag to impliment’n Role of antiarrhythmics in CA • No med has shown long term survival benefit in CA • Amiodarone has shown improved ROSC but overall equal death to lidocaine • Ongoing trial comparing amio vs lido vs placebo - ALPS trial, out 2016 Role of dual shock therapy (?!) • 1989 study shows no benefit but recent jobs case series showed benefit • Expert recommendation to try if refractory VF an no other options Role of vasopressors in CA • No vasopressor has ever shown LT survival benefit in CA • Epinephrine improves rates of ROSC • Factors that may improve survival in subgroups: o Early Epinephrine (first minutes) o Consider avoiding in VF (likely due to MI - more vasoconstric) o Definite use in PEA o Not using too much… maybe titrate to etco2 drop (tho no evidence) DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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PATAN ACADEMY OF HEALTH SCIENCES

NOvel approach to assessmt of PEA: see Littman paper (2014) - SEE BELOW • Ensure NOT TO INTERRUPT QUALITY CPR for US When to call your code off? • If unwitnessed, initial rhythm unshockable, and no prehosp ROSC - rare survival • EtCO2 3-4 doses of IM Epi should be considered for IV Epi Steroids 1. Solumedrol 40-125mg (1mg/kg in peds) IV 2. HC 500mg (5mg/kg in peds) IV 3. Either of these can be followed by Prednisone 50mg (1mg/kg) PO qd x 3 days. +/- H1-antihistamines 1. The evidence for this is not strong, but it is a reasonable option 2. Diphenhydramine 50mg (1mg/kg in peds) IV DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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+/- Glucagon 1. This can be considered for patients on beta-blockers (who may be resistant to Epinephrine), or for patients who are refractory to the treatments above 2. Glucagon works independently of beta receptors--and has inotropic, chronotropic, and smoothmuscle relaxing effects 3. An initial dose of 1-5mg in adults (20-30ug/kg--to a maximum of 1mg in children) over 1-5 minutes is recommended. 4. This can be repeated and/or followed by an infusion of 5-10mg/hour (in adults) +/- Mg (only if asthma-related) 1. MgSO4 2-4g (50mg/kg) IV over 20 mins IV Epinephrine 1) Use the 1:10,000 concentration for IV dosing. 2) The dose is 0.01mg/kg (in peds) or 0.1mg (in adults) IV given over 10 mins. a) With 1:10,000 Epi, 0.1mg = 1mL 3) The adult dose (ie. 1mL) can be prepared as follows: a) Draw up 1mL of 1:10,000 Epi (ie. the Epi in the crash cart) b) Dilute this with 9mL of NS (to a total volume of 10mL) c) Inject this 10mL volume over 10mins

Disposition of Patients with Anaphylaxis 1) Patients with mild-to-moderate symptoms who respond completely to treatment can be discharged home after 2-6 hours of observation. a) It is reasonable to give them a 3-day course of Prednisone to take home 2) Patients with severe attacks that respond promptly to treatment may warrant observation for up to 24 hours. 3) Practically-speaking, however, these patients may be candidates for discharge home after 6-12 housr if they: a. Did not have a life-threatening presentation b. Responded completely to treatment c. Are young and healthy d. Live close to the hospital e. Are being discharged home with family 4) Patients with life-threatening attacks warrant admission until at least 24 hours after full recovery.

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Acid Base Disorder Normal Values • • • •

pH = 7.40 PCO2 = 40 mmHg HCO3 = 24mmol/ Anion gap o If using Na - Cl - HC03, the normal AG is 12mmol/L. o If using Na + K - Cl - HC03, the normal value AG is 16mmol/L

Basic Interpretation Disorder Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis

pH    

PCO2 N or  N or   

HCO3   N or  N or 

Advance Interpretation Primary pH Changes and Compensation Overview • Compensation is almost never "complete." That is to say, it almost never corrects the pH back to 7.40. • "Overcompensation" essentially does not occur. o The only exception is transient overcompensation that can occur during rapid shifts in pH, PCO2, and HCO3. o these rapid shifts can be quite common in sick patients--which can make ABGs in the Emergency and ICU somewhat confusing Acute Respiratory Acidosis (acute hypoventilation) Etiologies of acute respiratory acidosis include: • Acute CNS depression (eg. opioids, BZPs) • Acute respiratory failure (eg. COPD, muscular weakness, GBS, myasthenia, botulism) • Acute airway obstruction During acute hypercarbia, every increase of 10mmHg in the PCO2 causes a drop of 0.08 in the pH. • However, this pH change is only temporary--until renal compensation starts Renal compensation for acute respiratory acidosis is as follows: • Every increase of 10mmHg in the PCO2 causes an increase of 1mmol/L in the HCO3. • This usually starts in 6-12 hours. Chronic Respiratory Acidosis (ie. chronic hypoventilation) Etiologies of chronic respiratory acidosis include: DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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PATAN ACADEMY OF HEALTH SCIENCES

• •

Chronic respiratory failure (eg. COPD) Obesity hypoventilation syndrome

Renal compensation for chronic respiratory acidosis is as follows: • Every increase of 10mmHg in the PCO2 causes an increase of 4mmol/L in the HCO3. • This is usually maximal within several days. • The maximal HCO3 is ~45mmol/L. o Additional CO2 retention after this point causes serum acidosis Acute Respiratory Alkalosis (ie. acute hyperventilation) Some etiologies of acute respiratory alkalosis include: • Fear, anxiety, pain • ASA toxicity • Sepsis • Large PE • Stimulants • Drug withdrawal Acute respiratory alkalosis is much more common than chronic respiratory alkalosis--since most precipitants of hyperventilation are either: • Short-lived (eg. anxiety, fear, pain) • Rapidly-fatal unless fixed (eg. ASA toxicity, sepsis, large PE) During acute hypocarbia, every drop of 10mmHg in the PCO2 causes increase of 0.08 in the pH. However, this pH change is only temporary--until renal compensation starts Renal compensation for acute respiratory alkalosis is as follows: • Every drop of 10mmHg in the PCO2 causes a drop of 2mmol/L in the HCO3 • This usually starts in 36-48 hours. Chronic Respiratory Alkalosis (chronic hyperventilation) Etiologies of chronic respiratory alkalosis include: • CNS pathology (eg. brain tumor) • Chronic liver disease • Hyperthyroidism • Pregnancy Renal compensation for respiratory alkalosis is as follows: • Every drop of 10mmHg in the PCO2 causes a drop of 2-5mmol/L in the HCO3. • This is usually maximal by two weeks. • The minimum HCO3 in this setting is ~12mmol/L. • Chronic respiratory alkalosis is the only acid-base abnormality where the body can potentially approach full compensation (ie. get close to 7.40).

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Metabolic Acidosis (ie. acute and chronic) Overview • Respiratory compensation for metabolic acidosis begins immediately--and is maximal by 12-24 hours. • The minimum PCO2 in this setting is ~5mmHg (in extremely ill patients) • "Winter’s Rule" is used for primary metabolic acidosis. o Winter's Rule calculates the expected PCO2 for a primary metabolic acidosis. - Expected PCO2 = 1.5(HCO3) + 8 (+/-2) o Winter's Rule works for both primary AG and non-AG metabolic acidosis. • It does not work for metabolic alkalosis Increased anion gap metabolic acidosis • An increased anion gap suggests the presence of an acid that is either: o Not normally present in the body (eg. formic acid in methanol overdose) o Normally present in the body in only small quantities--but now present in large quantities (eg. lactic acidosis) • Specific etiologies of increased-AG metabolic acidosis include "MUDPILES CT": o Methanol (ie. formic acid) o Uremia (ie. phosphoric acid, sulfuric acid, ammonium) o DKA, alcoholic ketoacidosis, starvation ketoacidosis (ie. ketoacids) o Paraldehyde (ie. acetic and chloracetic acid) • This is an older medication that was previously used for sedation and seizure control o Phenformin/Metfomin (ie. lactic acid) • Phenformin was an older biguanide that has since been replaced by Metformin • Both agents can cause lactic acidosis in patients with renal failure o Iron overdose, INH overdose (ie. lactic acid) o Lactate (ie. lactic acid) o Ethylene glycol (ie. glycolic and oxalic acids) o Salicylates (ie. salicylclic, lactic, and ketoacids) o Cyanide, carbon monxoide (ie. lactic acid) o Toluene--from glue or solvent-sniffing • An increased AG essentially always indicates the presence of a metabolic acidosis (irrespective of any other acid-base disorders that may be present). Low/normal anion gap metabolic acidosis • This is caused by an imbalance of H+ and HCO3- in the body. • Specifically, it can be caused by: o Increased retention of H+ o Increased excretion of HCO3• Specific etiologies of a low/normal AG metabolic acidosis include "H-USEDCARP": o Hyperalimentation o Ureterosigmoid conduit o Small bowel fistula DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• •

o Extra chloride (ie. hyperchloremia) o Diarrhea o Cabonic anhydrase inhibitors (eg. acetazolamide) o Adrenal insufficiency o Renal tubular acidosis (all types) o Pancreatic fistula What these etiologies all have in common is that they cause either H+ retention or HCO3 excretion. In the Emerg and ICU, the most common cause of a low/normal AG metabolic acidosis is hyperchloremic acidosis. o This is usually caused by aggressive resuscitation with normal saline. o It is characterized on bloodwork by: - Decreased HCO3 - Normal or elevated Cl- Variable Na+ o The exact mechanism is controversial.

Co-existing metabolic acidosis and alkalosis • An "increased-AG metabolic acidosis" and a "metabolic alkalosis" can co-exist. o An anion gap is caused by acids which are not normally present. • These acids are not eliminated by an increased HCO3 • For example, a patient with sepsis and vomiting can have an increased-AG metabolic acidosis (from lactic acid), while simultaneously having a metabolic alkalosis (because of HCl loss from vomiting) • In contrast, a "non-AG-metabolic acidosis" (caused by relative loss of HCO3) usually cannot co-exist with a metabolic alkalosis (caused by relative retention of HCO3). • One cancels out the other The Delta Gap • The Delta Gap is a corollary of the following two principles: o With an isolated "elevated-AG metabolic acidosis", the rise in AG is approximately the same as the fall in HCO3. o With an isolated "non-AG metabolic acidosis", the rise in Cl is approximately the same as the fall in HCO3. • The Delta Gap = (AG - 12mmol/L) - (24mmol/L - HCO3) o A normal delta gap is -6mmol/L to 6mmol/L o A delta gap >6 suggests a metabolic alkalosis o A delta gap 95% of cases) are: o Diuretics o Vomiting

Classification of metabolic alkalosis • Metabolic alkalosis can be classified as either: o Chloride-responsive (more common) o Chloride-resistant (less common) Chloride-responsive metabolic alkalosis • This is caused by either: o Gaining HCO3 (or a HCO3 equivalent). • -If HCO3- is gained, Cl- must be excreted to keep the body electrically neutral o Losing chloride. • -If Cl- is lost, HCO3- must be retained to keep the body electrically neutral • Patients with a chloride-responsive metabolic alkalosis usually have a: o Low serum Cl o Low urinary Cl (ie. 20mmol/L) o Massive PRBC transfusion DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• • • • • • • •

The citrate in PRBCs is metabolized to HCO3 Treatment of chloride-responsive metabolic alkalosis involves: o Volume replacement with normal saline. This replaces both chloride and volume Once Cl- levels are repleted, this allows the body to excrete HCO3Excretion of HCO3- corrects the metabolic alkalosis o Adjunctive treatments for very severe alkalosis can potentially include: Acetazolamide Dialysis Intravenous HCl (rarely used)

Chloride-resistant metabolic alkalosis • This is caused by excessive aldosterone activity. o Excessive aldosterone activity causes hypokalemia. o The drop in serum K+ leads to compensatory K+ retention by the kidney. • -This, in turn, leads to H+ excretion by the kidney (via the H+/K+ antitransporter) • These patients typically have a urinary Cl >20mmol/L. • Specific etiologies of chloride-resistant metabolic alkalosis include: o Primary hyperaldosterinism (aka “Conn’s syndrome”) o Secondary hyperaldosterinism o Primary hyper-reninism o Black licorice (ie. real licorice--not the candy; acts like aldosterone) o Congenital adrenal hyperplasia o Excessive ACTH • Severe hypercalcemia, hypomagnesemia, or hypokalemia • Chloride-resistant metabolic alkalosis does not respond to normal saline. • Instead, treatment involves: o Fixing the underlying etiology o Correcting any electrolyte abnormalities o +/- Spironolactone (an aldosterone antagonist) Approach to Acid-Base Disorders Overview • First question -- Is this a primary acidosis or alkalosis (ie. which side of 7.40)? o Remember that the body almost never fully compensates for a primary acid-base disorder • Second question -- Is this a primary respiratory or metabolic abnormality? o What is causing the primary abnormality--the CO2 or the HCO3? • Third question -- Is the primary abnormality appropriately compensated? o Use the rules above to calculate appropriate compensation for the primary abnormality. o If the primary abnormality is metabolic acidosis, start by checking the anion gap o If the primary abnormality is anything else, check the anion gap last

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•

o If the primary abnormality is not appropriately compensated, this suggests multiple acidbase disorders. Fourth question -- If a metabolic acidosis is present, is it isolated? o This question can be answered in two ways... o #1 -- By understanding that:  With an isolated AG-metabolic acidosis, the rise in AG is about the same as the fall in HCO3  With an isolated non-AG metabolic acidosis, the rise in Cl is about the same as the fall in HCO3 o #2 -- By uing the Delta gap  The Delta Gap = (AG - 12mmol/L) - (24mmol/L - HCO3)  A normal delta gap is -6mmol/L to 6mmol/L  A delta gap > 6 suggests a metabolic alkalosis  A delta gap < -6 suggests a non-AG metabolic acidosis

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Sample question A 45-year-old lady presents to hospital in DKA. She has been vomiting for several days. She looks unwell. Her bloodwork is below. What acid-base disorder(s) is/are present? a. ABG 7.46 / 41 / 77 / 30 b. Lytes Na 139 / K 3.3 / Cl 86 / HCO3 30 1) Determine the primary acid-base abnormality. Metabolic alkalosis (ie. the pH is >7.40; this is being caused by the increased HCO3) 2) Determine the primary abnormality is appropriately compensated. a. Using the Marino compensation rule for primary metabolic alkalosis: -Expected PCO2 = 0.7(HCO3) + 21 = 42 b. Since the expected PCO2 is very close to the actual PCO2 (ie. 41), respiratory compensation for the metabolic alkalosis is appropriate. 3) Check the anion gap. a. The AG is 23. b. Since an elevated AG is present, the patient must also have a metabolic acidosis. c. Therefore, at least two acid-base disorders are present (ie. metabolic alkalosis and increased-AG metabolic acidosis) 4) Since a metabolic acidosis is present, check if it is isolated? a. With an isolated AG metabolic acidosis, the rise in the AG should be about the same as the drop in HCO3. -In our patient, this is definitely not the case -The rise in AG is 11 -Instead of a drop in HCO3, she actually has a rise in HCO3 of 6 -This extra HCO3 confirms that a metabolic alkalosis is also present b. This can be also be done using the Delta Gap = (AG - 12mmol/L) - (24mmol/L - HCO3) = (23-12) - (24-30) = 11 - (-6) = 17 A delta gap >6 confirms the presence of a metabolic alkalosis 5) As discussed above, an increased-AG metabolic acidosis and a metabolic alkalosis can co-exist. -They do not cancel each other out 6) In conclusion, therefore, this patient has a double acid-base disorder: a. Metabolic alkalosis -- Secondary to vomiting b. Metabolic acidosis -- Lactic acid from hypovolemia/hypoperfusion; ketoacids from DKA

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Sepsis Definitions • • • • •

Sepsis is defined as the presence (probable or documented) of infection together with systemic manifestations of infection. Severe sepsis is defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion Sepsis-induced hypotension is defined as a systolic blood pressure (SBP) < 90mm Hg or mean arterial pressure (MAP) < 70mm Hg or a SBP decrease > 40mm Hg or less than two standard deviations below normal for age in the absence of other causes of hypotension. Septic shock is defined as sepsis-induced hypotension persisting despite adequate fluid resuscitation. Sepsis-induced tissue hypoperfusion is defined as infection-induced hypotension, elevated lactate, or oliguria (Urine output < 0.5 ml/kg/hour)

3 hour Bundle TO BE COMPLETED WITHIN 3 HOURS OF TIME OF PRESENTATION 1. Measure lactate level 2. Obtain blood cultures prior to administration of antibiotics 3. Administer broad spectrum antibiotics 4. Administer 30ml/kg crystalloid for hypotension or lactate ≥4mmol/L

6 hour Bundle TO BE COMPLETED WITHIN 6 HOURS OF TIME OF PRESENTATION 1. Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65mmHg 2. In the event of persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion 3. Re-measure lactate if initial lactate elevated.

Documentation DOCUMENT REASSESSMENT OF VOLUME STATUS AND TISSUE PERFUSION WITH: 1. Either repeat focused exam (after initial fluid resuscitation) by licensed independent practitioner including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings. 2. OR TWO OF THE FOLLOWING: a) Measure CVP b) Measure ScvO2 c) Bedside cardiovascular ultrasound d) Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge

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Antiboitics Renal Dosing 1. In patients with renal failure (even if severe), the first dose of antibiotics should not be renally-dosed. a. This is especially important if the patient is very sick b. Renal-dosing for subsequent doses can be worked out on the ward 2. The following antimicrobials do not require renal-dosing: a. Cloxacillin b. Ceftriaxone c. Cefixime d. Erythromycin and Azithromycin (ie. Clarithromycin does) e. Moxifloxacin f. Doxycycline g. Clindamycin h. Metronidazole

Bactericidal vs. Bacteriostatic antibiotics 1. Bactericidal antibiotics include: a. Beta-lactams (eg. penicillins, cephalosporins, carbapenems) b. Fluoroquinolones c. Aminoglycosides d. Vancomycin (slowly bactericidal) e. Metronidazole 2. Bacteriostatic antibiotics include: a. Macrolides b. Clindamycin c. Linezolid d. Tetracyclines 3. The clinical significance of bactericidal over bacteriostatic antibiotics remains controversial. 4. Nontheless, as of 2014, bactericidal agents are indicated for most serious infections (eg. bacteremia, endocarditis, meningitis)

Penicillins Overview 1. The penicillins include: a. Natural b. Beta-lactamase-resistant (ie. anti-staphylococcal) c. Aminopenicillins (ie. extended-spectrum) d. Anti-pseudomonal e. Associated with beta-lactamase inhibitors 2. The penicillins are beta-lactam antibiotics. a. They are bactericidal

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Natural penicillins 1. These include: a. Pen G (parenteral) b. Pen V or VK (oral) c. Benzathine penicillin 2. These agents are generally: a. Active against: i) Many Strep species ii) Oral anaerobes (eg. peptostreptococcus, +/- Bacteroides) iii) Many GPBs (eg. Anthrax, Clostridium, Listeria, +/- Enterococcus) b. Not active against: i) Beta-lactamase organisms c. Staph species Beta-lactamase-resistant (aka penicillinase-resistant) penicillins 1. These include:

a. Cloxacillin b. Methicillin

2. These agents are generally: a. Active against:

i) Strep species ii) Staph aureus (ie. MSSA, not MRSA) b. Not active against: i) MRSA ii) Most strains of coagulase-negative staph (ie. usually only sensitive to Vancomycin) iii) Enterococcus iv) Gram-negatives v) Anaerobes

For non-Staph/Strep infections, the other penicillins are preferred. Aminopenicillins (ie. extended-spectrum)

1. These include:

a. Ampicillin b. Amoxicillin

2. These agents offer some GP and GN coverage: a. Strep species

b. c. d. e. f. g.

+/- Enterococcus fecalis (but not E. fecium) E. coli H. flu Salmonella Listeria Proteus

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3. The mnemonic is “SHEPS” (Salmonella, H. flu, E. coli, Proteus, Shigella) Anti-pseudomonal penicillins Pipercillin 1. This covers a. Strep species (but not as well as some of the other penicillins) b. E. fecalis (not E. fecium) c. Some anaerobes d. Pseudomonas e. Many Enterobacteraciae (eg. E. coli, Klebsiell) 2. Pipercillin is commonly combined with Tazobactam (see below), to provide even broader coverage. a. Ticarcillin b. Carbenicillin Pencillins associated with beta-lactamase inhibitors Pip-Tazo (ie. Pipercillin-Tazobactam) 1. Pipercillin is the antibiotic; Tazobactam is the beta-lactamase inhibitor 2. Pip-Tazo is a "big gun" antibiotic. 3. It covers a broad ranges of GP's, GN's (including Pseudomonas), and anerobes. 4. Pip-Tazo does not cover atypicals (ie. Mycoplasma pneumoniae, Legionella, Chlamydophlia pneumoniae). 5. As such, additional antibiotic coverage is needed for patients with community-acquired pneumonia (eg. macrolide, fluoroquinone, doxycycline) 6. Clavullin (ie. Amoxil-Clavullinic acid) 7. Tic-Clav (ie. Ticarcillin-Clavullinic acid)

Cephalosporins The cephalosporins are beta-lactam antibiotics. The first three generations of cephalosporins do not cover: a. Anerobes b. Enterococcus In general: a. First-generation cephalosporins cover more GP's, but some GN's c. Second-generation cephalosporins cover some GP's and some GN's b. Third-generation cephalosporins cover more GN's, but some GP's The mnemonic for gram-negative coverage of the cephalosporins is as follows: a. 1st-generation -- PEK (Proteus, E. coli, Kleb) b. 2nd-generation -- H-PEK (Hemophilus, Proteus, E. coli, Kleb) c. 3rd-generation -- HEN-PEK (Hemophilus, Enterobacteriaceae, Neisseria, Proteus, E. coli, Kleb) 1st-generation cephalosporins a. These include Cefazolin and Cephalexin DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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b. GP coverage includes Strep species, MSSA c. GN coverage includes PEK 2nd-generation cephalosporins a. These include Cefuroxime and Cefoxitin b. GP coverage includes Strep species, MSSA c. GN coverage includes H-PEK, Moraxella 3rd-generation cephalosporins a. The IV agents include Cefotaxime, Ceftriaxone, Ceftazidime b. The PO agents include Cefixime c. GP coverage includes Strep, +/- MSSA (if high-dose given) d. GN coverage includes HEN-PEK, most GN's, and Ceftazidime covers Pseudomonas -While Ceftazidime cover Pseudomonas, it has worse GP coverage than the other 3rd-gens Be aware that there are three different dosing regimens for Ceftriaxone: a. For uncomplicated pneumonia -- 1g IV q24h b. For suspected bacteremia or endocarditis -- 2g IV q24h c. For suspected meningitis -- 2g IV q12h As mentioned, Ceftriaxone does not require renal dosing.

Aminoglycosides These include: a. Amikacin b. Streptomycin c. Gentamicin d. Tobramycin Lung penetration of the aminoglycosides is poor. -As such, these agents should not be used for pneumonia The aminoglycosides have broad GN coverage--including Pseudomonas (especially Tobramycin) GP coverage is poor to non-existent. Extended-dosing of Gentamicin and Tobramycin (ie. 7mg/kg q24-48h) has replaced conventional dosing (ie. 2mg/kg q8h) for most indications. The aminoglycosides are commonly avoided because of fears of causing renal failure. a. While this is a significant concern with prolonged use, it is extremely rare with one-time use b. As such, for patients with severe sepsis of unclear etiology, consider giving a one-time dose of Gentamicin or Tobramycin to provide broad gram-negative coverage for 24-48 hours DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Fluoroquinolones These include: a. Ciprofloxacin b. Levofloxacin c. Moxifloxacin Fluoroquinolones (like macrolides) can prolong the QTc. The fluoroquinolones cover: a. Most GN's b. Atypicals c. Some GP's (ie. Levo and Moxi only) d. Some anerobes (ie. Moxi only) Ciprofloxacin a. This has good gram-negative coverage (including N. gonorrhea, H. influenzae, and Pseudomonas) -Pseudomonal coverage with the other fluoroquinolones is less reliable b. Ciprofloxacin does not cover any anerobes. Levofloxacin a. This has better gram-positive coverage than Cipro (ie. mainly Strep species) b. It covers most GNs, but its coverage of Pseudomonas is unreliable c. It also does not cover any anerobes Moxifloxacin a. This has quite broad-spectrum coverage, including: -Strep and Staph species -Most GNs, but not Pseudomonas -Anerobes b. Be aware that Moxifloxacin does not penetrate into the urinary system. -As such, it should not be used for urinary infections Macrolides These include: a. Erythromycin b. Clarithromycin c. Azithromycin These agents are bacteriostatic, not bactericidal. Macrolides (like fluoroquinolones) can prolong the QTc.

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The macrolides all have grossly similar coverage, including: a. Strep species b. H. influenzae (Azithro ≥ Biaxin > Erythro) c. Most atypicals Erythromycin a. This is active against: -Strep species -Atypicals -Chlamydia and Neisseria b. It has poor activity against H. influenzae. c. It is not commonly used--because of its significant GI side-effects (eg. nausea). Clarithromycin a. This is active against: -Strep species (including S. pneumo) -Atypicals -Moraxella -H. influenzae (more than Erythro, less than Azithro) b. It has fewer GI side effects than Erythromycin. Azithromycin This is active against: -Strep species -Atypicals -H. influenzae Azithromycin has a long half-life. -As such, a 3-5 day course is adequate for most indications Azithromycin has fewer GI side-effects than the earlier macrolides. Metronidazole (aka Flagyl) Metronidazole covers: a. Most anaerobes (especially gram-negative) b. Parasites (eg. Giardia, Entamoeba) Metronidazole's anerobe coverage is likely superior to Clindamycin's. Side-effects of Metronidazole include: -Nausea -Metallic taste -Neuropathy -Possible reaction with ethanol Clindamycin Clindamycin covers: a. Strep species (moderate coverage) DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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b. MSSA (good coverage) c. Community-acquired MRSA (although resistance rates are now quite high) d. Anerobes Clindamycin does not cover: a. GN's b. Enterococcus Clindamycin is bacteriostatic. It is probably the #1 cause of antibiotic-induced C. difficile.

Tetracyclines These include: a. Tetracycline b. Doxycycline c. Minocycline d. Tigecycline The tetracyclines are bacteriostatic. The tetracyclines cover several unusual organisms, including: a. Rickettsia b. Chlamydia c. Mycoplasma d. Vibrio cholera e. Brucella f. Borreila burgdorferii (ie. Lyme disease) Doxycycline is commonly used in the ED. a. GP coverage includes Strep pneumoniae, and some other GP's b. Doxycycline is somewhat unpredictable against Staph species, but covers some strains of communityacquired MRSA (but not hospital-acquired MRSA) c. Doxycycline reliably covers atypicals d. It does not cover anerobes

Sulfa drugs The most common sulfa drug in clinical use is TMP/SMX (aka Septra, Bactrim). Septra has broad-spectrum coverage, including: a. Streptococcus and Staphylococcus species (including community-acquired MRSA, but not hospitalacquired MRSA) b. H. influenza DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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c. Listeria d. Many Enterobacteraciae (eg. E. coli, Klebsiella, etc.) e. Stenotrophomonas f. PJP Septra does not cover Enterococcus. Septra is contraindicated in renal failure.

Nitrofurantoin NF is concentrated in the bladder. a. As such, it is only indicated for lower urinary tract (ie. bladder) infections. b. It should not be used for any upper urinary tract infections, pyelonephritis, or urosepsis NF is contraindicated in renal insufficiency.For bladder infections, NF is effective against: a. S. aureus b. Enterococcus c. E. coli d. Some strains of Klebsiella

Carbapenems The carbapenems include: a. Imipenem b. Meropenem c. Ertapenem Like Pip-Tazo, the carbapenems are "big gun" antibiotics. a. They cover a broad ranges of GP's, GN's (including Pseudomonas), and anerobes. b. Note that Ertapenem does not cover Pseudomonas. Carbapenems do not cover: a. MRSA b. Coagulase-negative Staph c. Atypicals (ie. additional antibiotics are needed for community-acquired pneumonia) The carbapenems: a. May cover Enterococcus fecalis (not Ertapenem) b. Generally do not cover Enterococcus fecium Ertapenem is not commonly used in the ED. a. It has convenient once-daily dosing, but is very expensive (ie. $100/day as of 2012) c. Unlike Imipenem and Meropenem, it has no Pseudomonal coverage d. It also has no Enterococcus coverage

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Vancomycin Vancomycin covers: a. Nearly all gram-positive aerobes (including MRSA, coagulase-negative Staph, Strep, Enterococcus, Listeria, Bacillus) b. Many gram-positive anaerobes (eg. C. difficile, peptostreptococcus) In general, however, Vancomycin is not a great antibiotic. a. It is inferior to beta-lactam antibiotics for treating beta-lactam-sensitive organisms. -Therefore, if an organism is sensitive to both Vancomycin and beta-lactam antibiotics (eg. penicillins, cephalosporins, carbapenems), choose the beta-lactam. b. Vanco is sometimes described as being bacteriostatic, however it is slowly bactericidal in most cases. Vancomycin remains in wide clinical use because it is a first-line antibiotic for: a. MRSA b. Coagulase negative Staph c. Enterococcus (especially E. fecalis, +/- E. fecium) -Vancomycin obviously does not cover VRE (ie. Vancomycin-resistant enterococcus)

Linezolid 1) Linezolid is a bacteriostatic antibiotic. -It can be given PO or IV 2) It is effective against many GP's: a. MSSA b. MRSA c. Strep species (including Strep pneumo, Group A Strep) d. Enterococcus fecalis (including VRE), +/- E. fecium 3) It has no activity against gram-negatives. 4) Linezolid is typically used: a. As a second-line agent for MRSA (ie. if resistant to Vancomycin) b. As a first-line agent for VRE

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Inotropes Definitions 1. Inotropes increase cardiac contractility. 2. Chronotropes increase heart rate. 3. Inotropes can have positive chronotropic effects (eg. epinephrine, NE, Dop, Dob), negative chronotropic effects (eg. digoxin), or minimal chronotropic effects (eg. Milrinone) 4. Vasopressors cause contraction of blood vessels. 5. Vasopressors generally cause an increase in blood pressure 6. However, an increase in BP does not necessarily correlate with an increase in end-organ perfusion

Adrenergic Receptors There are several types of adrenergic receptors: Alpha-1 -- Activation of this post-synaptic receptor causes peripheral vasoconstriction. Alpha-2 -- Pre- and post-synaptic activation of this receptor causes a variety of effects which are difficult to characterize from an inotropic/vasopressor standpoint. 3. Beta-1 -- Activation of these receptors increase cardiac inotropy and chronotropy. 4. Beta-2 -- Activation of these receptors in the: a. Lung causes bronchodilation b. Peripheral blood vessels causes peripheral vasodilation 1. 2.

Commonly-Used Inotropes Summary The following agents can be characterized in terms of their inotropic, chronotropic, and vasoconstrictive/vasodilative properties as follows (ie. if a property is not listed, it is assumed to be zero) Epi (1-20ug/min) a. 4+ inotropy b. 4+ chronotropy c. 4+ vasoconstriction 2. NE (1-20ug/min) a. 2+ inotropy b. 1+ chronotropy c. 4+ vasoconstriction 3. Dopamine a. 1-4ug/kg/min b. 1+ inotropy c. 1+ chronotropy 1.

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d. 1+ vasodilation 4-20ug/kg/min e. 2+ inotropy f. 2-3+ chronotropy g. 2-3+ vasoconstriction (ie. increasing vasoconstriction with increasing dose) 4. Dobutamine (2-20ug/kg/min) a. 3-4+ inotropy b. 1-2+ chronotropy c. 2+ vasodilation 5. Milrinone (0.125-0.5ug/kg/min) a. 4+ inotropy b. No chronotropy (unlike Dobutamine) c. 3+ vasodilation (although the risk of hypotension is lowered by avoiding an initial bolus dose)

Details 1.

Epinephrine ("Epi") a. Epinephrine is an endogenous catecholamine synthesized in the adrenal medulla from the amino acids phenylalanine and tyrosine. b. Action: +++B1, ++B2, +++a1 c. Epi causes profound inotropy, chronotropy, and vasoconstriction. Its vasodilatory B2-activity is more than outweighed by its vasoconstrictive a1-activity d. Epinephrine can be a useful agent for undifferentiated hypotension, but can have several troublesome side-effects:  Hyperglycemia (even in non-diabetics) e. Metabolic acidosis (ie. often down to a serum HCO3 17–21meq/L; usually self-limited)

2.

Norepinephrine (“Levophed”, "Nor-Ad") a. Norepinephrine is also an endogenous catecholamine synthesized in the adrenal medulla from tyrosine. b. Action: ++B1, +B2, +++ a1 c. Like Epi, NE's vasodilatory B2-activity is more than outweighed by its vasoconstrictive a1 activity d. While NE has a significant inotropic component, it tends to cause less chronotropy than many other inotropes (eg. epi, +/- Dopamine, +/- Dobutamine) e. As such, it may be a useful agent in patients with undifferentiated hypotension who are tachycardic f. Over the past ten years, NE has become a favoured agent in septic shock.

3.

Dopamine ("Dop") a. Like Epi and Norepi, Dopamine is a physiological catecholamine. b. From an inotropic standpoint, Dopamine acts indirectly--promoting release of the body's own endogenous catecholamines

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c. d. e. f.

Dopamine is more difficult to characterize from an inotropic/pressor standpoint because: It primarily stimulates dopamine receptors It has differing hemodynamic effects at different infusion rates Dopamine can be run at: 1. 0.5-3 ug/kg/min (low dose) -- Predominantly affects the dopamine receptors; possible selective vasodilation in certain visceral circulation 2. 3-10 ug/kg/min (moderate dose) -- Moderate B1 and mild a1 activity 3. 10-20ug/kg/min (high dose) -- Steadily-increasing a1 activity g. Dopamine has prominent chronotropic activity--and can cause tachycardia +/tachyarrhymias. h. At moderate doses, Dopamine acts as a diuretic (via a carbonic-anhydrase-inhibitor mechanism). i. Although this effect was previously believed to improve renal function in ARF, this notion of "renal-dose Dopamine" has since been debunked j. Patients maintained on Dopamine infusions for several days can have pituitary inhibition (eg. inhibition of PRL, TSH, LH) 4.

Dobutamine (“Dobutrex”, "Dob") a. Dobutamine is a synthetic agent. b. Action: +++B1, +B2, +a1 c. It is typically given at a rate of 2.5 (low-dose) to 20 (high-dose) ug/kg/min. d. Dobutamine acts an inotrope, a moderate chronotrope, and a vasodilator. e. The chronotropic effect of Dobutamine (which is not seen with Milrinone) can be beneficial or detrimental depending on the clinical setting f. In addition to its cardiac effects, Dobutamine causes peripheral vasodilation--with up to 3350% of patients having a decrease in blood pressure when started on Dobutamine g. Therefore, while Dobutamine is a useful agent for cardiogenic shock (especially in bradycardic patients), it is generally not beneficial (or even harmful) for other forms of shock.

5.

Milrinone a. Milrinone is a phosphodiesterase inhibitor. b. It effects include: c. Increased inotropy without increased chronotropy d. Enhanced lusitropy (ie. cardiac relaxation during diastole) e. Pulmonary and systemic vasodilation f. Milrinone toxicity manifests as cardiac dysfunction. g. Milrinone is renally-cleared, and a lower-dose should be used in renal failure h. Clinically, Milrinone can be used is similar settings to Dobutamine--especially if additional chronotropy is not desireable. i. As such, Milrinone is a useful agent for cardiogenic shock (especially in tachycardic patients), but is generally not beneficial (or even potentially harmful) for other forms of shock

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Cardiac Emergencies Contents Myocardial Infraction....................................................................................................................................... 68 Signs and Symptoms .................................................................................................................................... 68 Electrocardiography ..................................................................................................................................... 68 Q wave based criteria .............................................................................................................................. 68 ECG finding prediciting Culprit Coronary Artery...................................................................................... 68 Cardiac Enzymes .......................................................................................................................................... 69 Management ................................................................................................................................................ 69 PCI ................................................................................................................................................................ 70 Arrhythmias ..................................................................................................................................................... 72 Types of tachyarrhythmia: ........................................................................................................................... 72 Types of Brady Arrhythmia .......................................................................................................................... 73 Investigations ............................................................................................................................................... 73 Management ................................................................................................................................................ 74 Cardiogenic Shock ............................................................................................................................................ 76 Causes of cardiogenic shock ........................................................................................................................ 76 Clinical features............................................................................................................................................ 76 Investigations ............................................................................................................................................... 76 Management ................................................................................................................................................ 76 Acute Pulmonary Oedema ............................................................................................................................... 78 Introduction ................................................................................................................................................. 78 Clinical features............................................................................................................................................ 78 Investigations ............................................................................................................................................... 78 Management ................................................................................................................................................ 78 Hypertensive Crisis........................................................................................................................................... 79

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Myocardial Infraction Signs and Symptoms Features

High Likelihood

History

Chest of left arm discomfort as chief complaint reproducing prior documented angina Previous history of CAD

Examination Transient MR, Hypotension, Diaphorresis, Pulmonary Oedema or Rales ECG New or presumable new, transient ST segment deviation (1 mm of greater) or T wave inversion in multiple precordial leads Cardiac Elevated cardiac troponin I or CPK Markers MB

Intermediate Likelihood Chest of left arm discomfort as chief complaint Age more than 70 years Male sex DM Extracardiac Vascular Disease

Low Likelihood

Probable ischemic symptoms in absence of any of the intermediate likelihood characterstics Recent cocain use Chest discomfort reproduced by palpation Fixed Q waves T wave flattening or ST depression 0.5 or 1.0 inversion 1mm waves Normal Normal

Electrocardiography Q wave based criteria Location Electrocardiography Anteroseptal QS deflection in V1, V2, V3 and possibly V4 Anterior Rs deflection in V1 and Q WAVES IN V2-V4 or decrease in amplitude of initial R waves in V1-V4 Anterolateral Q waves in V4-V6, I and avl Lateral Q waves in I and avl Inerior Q waves in II, III, avf Interolateral Q waves in II, III, avf, V5 and V6 True posterior Initial R waves in V1 and V2 ? 0.04 sec and R/S ≥1 Right Ventricular Q waves in II, III, avf, and ST elevation in right side V4 ECG finding prediciting Culprit Coronary Artery Culprit artery ECG Finding ECG findings fof inferior ST segment elevation MI Right Coronary ST segment elevation in lead III greater than lead II plus ST segment depression of > Artery 1 mm in lead I , avl or both Proximal right In addition to the findings immediately above ST segment elevation on V1, V4R or coronary artery both Left circumflex Absence of the above findings plus ST segment elevation in leads I, avl, V5, V6 and artery ST segment depression in leads V1, V2 and V3 DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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ECG findings for anterior ST segment dlevation MI ST segment elevation inleads V1, V3 and V3 plus any of the features below Proximal left ST segment elevation of more than 2.5mm in lead V1 or RBBB with Q wave or both anterior descending artery Proximal left ST segment depression of > 1 mm in lead II, III, avf anterior descending artery Distal let anterior ST segment depression of ≤ 1 mm or ST segment elevation in leads II, III and avf descending artery

Cardiac Enzymes Enzyme Onset Peak CPK MB 3-12 hours 18-24 hours Troponin I 3-12 hours 18-24 hours Send Na, K, Createnine (other investigations as relevant)

Duration 36-48 hours Up to 10 days

Management 1. 2. 3. 4. 5.

Aspirin 300 mg PO Clopidogrel 300 PO Enoxaparin 30 mg IV bolus or Heparin 60 U/kg (Maximum 4000 U) Morphine 2-5 mg IV every 5-15 minutes PRN pain Nitroglygerine 0.6 mg every 4 min x 3 PRN pain or IV start at 10 microgram/min titrate to 10% reduction of MAP in normotensive and 30% reduction of MAP if hypertensive a. Contraindications: Right ventricular ischaemia, Hypotension 6. Metoprolol 50 mg PO 12 hourly on first day or if significant HTN 5 mg over 2 mins iv every 5 mins up to 15 mg a. Contraindiation: Hypotension 7. Streptokinase a. Indication: Patient with STEMI if time to treatment is 180/100 mmhg 2. History of chronic severe poorly controlled HTN 3. History of prior stroke more than 3 month or known intracranial pathology not covered in contraindication 4. Current use of anticoagulants with known INR >2-3 5. Bleedign diasthesis

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6. 7. 8. 9. 10. 11. 12. 13.

Trauma in last 2 weeks Prolonged CPR (more than 10 mins) Major surgery < 3weeks Non compressible vascular puncture Recent internal bleeding 2-4 weeks Previously treated with STK Pregnancy Active peptic ulcer bleeding

PCI STEMI within 90 minutes Non STEMI within first 48 hours Indications 1. 2. 3. 4. 5. 6. 7. 8.

Recurrent angina or ischemia with or without CHF Elevated cardiac enzymes New or presumly new ST depression High risk findins in non invasive stress test Deperssed left ventricular function Hemodynamic instability Sustained let ventricular tachycardia PCI within last 6 month or previous CABG

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Chest pain suggestive of ACS

ECG

ECG changes suggestive of STEMI

No ECG Changes

Cardiac enzymes to be sent Positive

Emergency Management 1. ABCDE 2. Cardiac monitor 3. Oxygen 4. IV line 5. Aspirin 300mg 6. Nitrates (if not contraindicated) 7. Morphin 8. Metoclopramide/ Promethazine

CPK MB/Troponin Negative

Positive ECG or Cardiac Enzymes

If pain still persistent Rule out other causes Repeat ECG at 30 mins Repeat cardiac enzyme at 4 hours Negative

High Risk

Admission in Cardiac Unit

TIMI score 1. Age ≥ 65 2. Presence of at least three risk factor of coronary heart disease 3. Prior coronary stenosis of ≥ 50% 4. Presence of ST segment deviation on admission ECG 5. Elevated serum cardiac biomarkers 6. At least two angina episodes in prior 24 hours 7. Use of aspirin in prior seven days 0-1: low risk, 2-3: intermediate risk, 4-7 high risk Low or Intermediate risk

Yes

Chest pain even after primary management No

Discharge

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Arrhythmias

Tachyarrhythmia (HR > 120bpm) and bradyarrhythmias (HR < 60bpm) may present with significant symptoms and hemodynamic compromise.

Types of tachyarrhythmia: Tachyarrhythmia

Narrow complex Tachyarrhythmia QRS complex ≤ 3 small squares

Regular Rhythm 1. Sinus Tachycardia 2. Atrial flutter 3. PSVT

Irregular Rhythm Atrial Fibrillation

Broad complex Tachyarrhythmia QRS complex > 3 small squares

Regular Rhythm Ventricular Tachycardia

Irregular Rhythm AF, atrial flutter with BBB

Sinus Tachycardia: A sinus rate more than 100 per minute usually due to increase in sympathetic activity associated with exercise, emotion stress, fever and variety of other pathological conditions (Heart failure, thyrotoxycosis etc) Atrial Flutter: There is rapid atrial rate around 250-300/min. The ECG shows characteristics saw toothed flutter waves.

Atrial fibrillation: In this arrhythmia the atrial beat is 350 to 500 bpm and ventricular response at irregular intervals. ECG shows irregularly irregular rhythm.

Paroxysmal Supraventricular Tachycardia (PSVT): This rhythm is due to re-entry within the AV node or accessory pathway and produces regular tachycardia.

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Ventricular tachycardia: This is a grave arrhythmia usually associated with serious heart disease and may be degenerated into ventricular fibrillation (This produces rapid ineffective uncoordinated contraction of the ventricles)

Types of Brady Arrhythmia Sinus Bradycardia: Sinus rhythm less than 60 beats per minutes Heart Block: Pathological non conduction of atrial impulse to ventricle due to the block at AV node or HIS system. 1. First degree AV block: Delayed conduction through AV node. ECG shows prolong PR interval which is more than 0.20 seconds. 2. Second degree AV block a. Type I: There is gradual prolongation of PR interval till one P fails to conduct to the ventricle. b. Type II: There is sudden non conduction of an atrial impulse to the ventricle. 3. Third degree AV block: Complete absence of conduction of atrial impulse to the ventricle. ECG shows AV dissociation with escape junctional or ventricular rhythm. Clinical feature 1. Palpitations 2. Chest pain 3. Breathlessness 4. Collapse or hypotension 5. Embolic event like stroke

Investigations • • • •

ECG Chest X ray: Cardiomegaly, pulmonary oedema Electrolytes: Hypokalaemia, renal impairments Cardiac Enzymes

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Causes of Arrhythaemia 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Ischemic heart disease, Cardiomyopathies Valvular Heart Disease Hypertension, Heart failure Pericarditis Endocarditis Myocarditis Pneumonia Pulmonary embolus Trauma Electrolytes disturbance Acidosis Thyrotoxicosis Alcohol

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Management 1. 2. 3. 4. 5.

Secure ABC Give oxygen Secure peripheral venous line Put patient in cardiac monitor If hemodyamically unstable catheterize the patient

Arrhythmia

Broad Complex Tachycardia

Narrow Complex Tachycardia

Treat as VT unless otherwise proved

Supraventricular Tachycardia

Ventricular Tachycardia

Hemodyamically Unstable

Hemodyamically Stable

Unsynchronized DC shock 360 Joules

Chemical cardioversion Amiodarone Loading dose: 300mg iv over 60 minutes followed by 900mg iv over 23 hours  200 mg po tds for 1 week 200mg po bd for 1 week Maintenance dose: 200400mg od iv or po

Unstable patient Synchronized DC shock 200 Joules

Stable Patient

Regular Rhythm: PSVT •Vagotonic Maneuvers •Inj Adenosine 6mg iv9mg iv 12mg iv •Digoxin, Calcium channel blocker (should be avoided in AVRT: eg WPW syndrome*), Beta Blocker •If there is degeneration of the rhythm into a broad complex tachyarrhythmia and or hemodyamically compromise  electrical cardioversion

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Irregular Rhythm: AF, Atrial Flutter

>48 Hours •Ventricular Rate Control: Beta blocker, digoxin, CCB •Heparin (UFH) 5000 IU followed by infusion or LMWH •Sinus rhythm control with amiodarone later

< 48 Hours Anticoagulatio n at presentation with LMWH or UFH followed by chemical cardioversion with Amiodarone

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Bradycardia

Hemodyamically Unstable Cardiac Arrest, Asystole, SBP < 90mmHg, Severe Pulmonary Oedema, Evidence of Cerebral f

Hemodyamically Stable Admit to CCU

Immediate Management: •Atropine 1mg iv bolus; repeat if necessary upto maximum 3 mg •Isoprenaline 0.2mg iv if there is delay in pacing and the patient remains unstable. Set up an infusion (1mg in 100 ml NS starting at 1ml/min titrating to heart rate) •Start percutaneous cardiac pacing and send to cardiac centre

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Cardiogenic Shock Cardiogenic shock is a clinical condition of inadequate tissue (end-organ) perfusion due to cardiac dysfunction.

Causes of cardiogenic shock • • • • • • • •

Myocardial Infraction (MI) End stage cardiomyopathy Myocarditis Septic shock with severe myocardial depression Left ventricular outflow obstruction: Aortic stenosis, Hypertrophic obstructive cardiomyopathy Obstruction to left ventricular filling: Mitral stenosis Acute mitral regurgitation Myocardial contusion

Clinical features • • • • • •

Hypotension Tachycardia Olyguria Cool periphery Respiratory Distress Jugular venous distention

Investigations • • • •

ECG Cardiac Enzymes Complete blood count: Leukocytosis is common Sodium, Potassium, Creatinine

Management 1. 2. 3. 4. 5. 6. 7.

Secure ABC Give oxygen Secure peripheral venous line Send investigations Put patient in cardiac monitor Catheterize the patient Correct Reversible factor • Arrhythmias • Electrolyte and acid base disturbances • Ventilation abnormalities: Intubate if necessary 8. Aim to improve hemodynamic status achieving SBP≥ 90mmhg IV fluid (with caution), Inotropic support ± diuretics

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Cardiogenic shock

Hypotensive

Dopamine (Upto 20µgm/kg/min) Noradernaline (Upto 20µgm/kg/min) Diuretics according to clinical condition

Non Hypotensive

Dobutamine (Upto 20µgm/kg/min) Noradernaline (Upto 20µgm/kg/min) Diuretics (Frusemide)

Vasopressors are indicated for a decrease of >30 mmhg from baseline systolic blood pressure, or a mean arterial pressure 150/100 mmhg nitroglycerine 0.2-0.4/kg/min and IV Furosemide If BP is low start Dopamine Inform ICU

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Hypertensive Crisis Blood pressure ≥220/120 mmHg

Without end organ damage

Hypertensive Urgency

For proven hypertensive Urgency maintain BP 600ml per 24 hours or >300ml over 4 hours Yes

No

Initial management

• ABC • IV open with NS or RL (may need fluid resuscitation or blood transfusion) • Oxygen • Blood for investigation (complete blood count, hematocrite, blood group, coagulopathy) • Chest x ray • Catheterization (if needed) • Place the patient in recovery position with bleeding lung down • Nebulisation if needed • Urine output monitoring

Hemodynamically stable No

Yes CBC and CXR

Referral for further urgent management

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Discharge on oral antibiotics if indicated

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Acute Exacerbation of Chronic Pulmonary Obstrutive Disase Diagnosis nomenclature Primary Diagnosis

Standard of diagnosis

Present condition

mMRC grading

Presence of right heart failure COPD (GOLD grading ) Stable Grade 0 to 4 Corpulmonale or AE or no signs of (Clinical) RHF e.g 1: COPD (Clinical), AE, mMRC grade 2, with no signs of RHF + other underlying conditions e.g 2: COPD (Gold II), AE, mMRC grade 2, with cor pulmonale + other underlying conditions

Diagnosis, Initial Assessment and Investigations Acute change in the following symptom that is beyond day to day variation. • Dyspnea • Cough • Sputum production Signs of severity • Use of accessory respiratory muscle • Paradoxical chest wall movement • Worsening or new onset of central cyanosis • Development of peripheral oedema • Hemodynamic instability • Detoriation of mental status mMRC grading of Shortness of breath • Grade 0: Get breathless with strenuous exercise. • Grade 1: Short of breath when hurrying on the level or walking up a slight hill. • Grade 2: Walks slower than people of same age on level ground. • Grade 3: Stops after walking 100 meters • Grade 4: Breathless on dressing or undressing Investigations • For all patient: Chest X ray and ECG • For selected patient if indicated (after evaluation): Complete Blood Count, Na, K, Creatinine, RBS, Urine Routine

Management Management of Severe but not life threatening exacerbations • Assessment: ABC, severity of symptoms, blood gas and chest radiograph • Supplement oxygen: o Should be titrated to improve patient hypoxaemia with target of saturation of 88-92% o Arterial blood gas should be checked after 60 minutes to ensure satisfactory oxygenation without CO2 retention. • Bronchodilators: SABA+SAAC (Use spacers preferably or nebulizers) DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• •

•

•

•

Corticosteroid: Predinisolone 30-40 mg orally or IV hydrocortisone if patient is unable to swallow Antibiotics: o To be started only for moderately to severely ill patient with increase in cough and sputum purulence o Choice of antibiotics: Aminopenicillin with or without clavulanic acid, Macrolids o Rout of antibiotics: Orally unless patient very sick or cannot take orally Noninvasive mechanical ventilation (Please see procedure section for ED-NIV operation): To be started if at least one of the following is present o Respiratory Acidosis: (arterial pH ≤ 7.35 and/or PaCO2 ≥ 45mm Hg) o Severe dyspnea with clinical sign suggestive of respiratory muscle fatigue, increase work of breathing or both, such as use of use of respiratory accessory muscle, paradoxical motion of the abdomen, or retraction of the intercostal space. o Invasive mechanical ventilation (Please see procedure section for ED-Ventilator operation) o Unable to tolerate NIV or NIV failure o Respiratory or cardiac arrest o Respiratory pause or loss of consciousness or gasping for air o Diminished consciousness, psychomotor agitation, inadequately controlled by sedation o Massive aspiration o Persistent inability to remove respiratory secretions o Heart rate < 50 per minute with loss of alertness o Severe hemodynamic instability without response to fluid and vasoactive drugs o Severe ventricular arrhythmia o Life threatening hypoxaemia in patient unable to tolerate NIV At all time o Monitor fluid balance o Consider subcutaneous heparin or LMWH (If needed) o Identify associated conditions (Heart failure, arrhythmia) o Closely monitor condition of patient.

Disposition Discharge criteria • Able to use long acting bronchodilators with inhaled corticosteroids • Inhaled SABA is required no frequently than 4 hours • Patient if previously ambulatory, is able to walk across the room • Patient is able to eat and sleep without frequent awakening by dyspnea • Patient has been clinically stable for 12 to 24 hours • Arterial blood gas have been stable for 12 to 24 hours • Patient fully understands correct use of medications • Follow up and home care management have been completed • Patient and family are confident that patient can be managed successfully at home On discharge • Medication to be adjusted as per guidelines of management of Stable COPD DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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• •

Follow up to be arranged in 4 to 6 weeks if stable Echocardiogram and PFT to be planned on follow up

Hospital admission criteria • Marked increase in intensity of symptom such as sudden development of resting dyspnea • Severe underlying COPD • Onset of new physical signs (Cyanosis, peripheral oedema) • Failure of exacerbation to respond to initial medical management • Presence of serious comorbidities (Heart failure, newly occurring arrhythmia) • Frequent exacerbations (More than 2 in a year) • Older age • Insufficient home support Indications of ICU admission • Severe dyspnea that responds to initial emergency therapy • Changes in mental status (confusion, lethargy, coma) • Persistent or worsening hypoxaemia (PaO2 < 40 mmHg) and/or severe/worsening respiratory acidosis (pH < 7.25) despite supplemental oxygen and noninvasive ventilation. • Need for invasive mechanical ventilation • Hemodynamic instability – need for vasopressor

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Exacerbation

Mild

Moderate or severe

Only 1 of 3 cardinal symptoms

At least 2 of 3 cardinal symptoms

Increase Dyspnea Increase sputum volume Increase sputum purulence

Increase Dyspnea Increase sputum volume Increase sputum purulence

Azithromycin Cephalosporin Doxycycline Trimethroprim/Sulfamethoxazole

Risk factors Uncomplicated COPD No risk factors

If recent (< 3 months) antibiotic exposure, use alternative class

• • • •

Age > 65 years FEV1 < 50% ≥ 3 exacerbations/ year Cardiac cause

Complicated COPD 1 or more risk factors

Is there risk for Pseudomonas?

Discharge on Oral Amoxycilline if stable

Levofloxacin 750mg PO or IV once daily or Ceftriaxome IV or Cefotaxime IV

No

• Recent hospitalization (2 days' duration during the past 90 days) • Frequent administration of antibiotics (≥4 courses within the past year) • Severe COPD (FEV1 55% Investigations (Requirement to be decided by treating doctor) Chest X ray, ECG, HCT and Echocardiography

Follow up Date and day should be specified. Following areas to be explored on each follow up • Are you better? (in terms of SOB, work, sleep) • Is that change worthwhile to you? • Smoking status • Device technique

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Bronchial Asthma Introduction Bronchial asthma is a chronic inflammatory disorder of the airways associated with airway hyper responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.

Clinical features • • • • •

Shortness of breath Wheeze Cyanosis Chest tightness Signs of severity: Respiratory rate ≥ 25/min Heart rate ≥ 110/min, Inability to complete sentence in one breath • Life threatening signs: Silent chest Poor respiratory effort Arrhythmia, exhaustion Altered conscious level Asthma Onset Anytime Smoking ± Cough and Smoking Less common Dyspnoea and exertion Variable Nocturnal symptoms Common Airway obstruction Diurnal variation Response to CS Good

COPD Mid to late adult life ++ Common Progressive Uncommon Little variation 15-20%

Investigations • • • •

Chest X ray: Exclude pneumothorax and to diagnose any parenchymal infection ECG: Usually normal, in severe asthmatics, sign of right heart strain may be present Complete blood count: to assess the sign of infection Electrolytes: Potassium may be lowered by high dose of beta agonist

Management 1. 2. 3. 4. 5. 6.

Secure ABC Sit the patient upright in bed Oxygen: High flow > 10lts per minutes by mask Intravenous access Blood for investigations Nebulisation (Salbutamol 1ml + Ipratropium 1ml + Normal saline 1 ml) repeat 3 times

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7. Steroids: Hydrocortisone 200mg iv 8. Antibiotics should be given if there is evidence of infection Management of bronchial asthma 1st Hour Oxygen Administration if SpO2 is less than 90%, otherwise leave on air. Inhaled Salbutamol + Ipratropium one nebulisation every 15 minutes for one hour Oral prednisolone 40-60 mg (1-2mg/kg/day in children) In patients who can’t tolerate oral meds, give IV hydrocortisone 200mg 6 hourly 2nd Hour

Four more doses of inhaled salbutamol and ipratropium Terbutaline sc 0.3-0.5mg (0.01mg/kg for child) (only if not able to tolerate nebulizers or not responding to nebulizers) IV Aminophylline 6mg/kg over 20-30 mins as loading dose (not required if on deriphylline) and maintenance dose 0.4 to 0.7 mg/kg/hr (* to be used with caution)

IV Magnesium sulphate 2gm over 20 mins Patient with signs of severity or life threatening signs should be admitted, others can be discharged if they are stable. Discharge medication • Oral steroid 1-3 week • Inhaled corticosteroid at high dose 1000-1500µgm • Inhaled long acting beta agonist (salmetrol) • Oral theophyllines if required

Admission criteria • • • • • • • • •

Persistent respiratory distress Patient without subjective improvement Patients with continued wheeze and diminished air movement Recent and multiple ED visit Symptoms for more than 1 week Pneumothorax Pneumomediastinum Pneumonia Fatigue

Discharge criteria • •

Patient reports subjective improvement Clear lungs with good air movement

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Community Acquired Pneumonia Introduction Community-acquired pneumonia is defined as an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the community

Clinical Features • • • • • •

Cough with sputum production Fever with chills Shortness of breath Pleuritic chest pain Abnormal vital signs: Tachycardia, tachypnoea, hypoxia Pulmonary examination: dullness on percussion, increased vocal fremtius, crepitation, ronchi

Prognostic variables: CRB65 (A simplified version of CURB65) • Confusion (based upon a specific mental test or disorientation to person, place, or time) • Respiratory rate >30 breaths/minute •

Blood pressure (systolic 2

Admission (Consider critical care) Preferred Treatment Co amoxiclav 1.2gms IV three times a day plus Clarithromycin 500 mg IV two times a day for 5 days or unless afebrile for 24 hours If legionella is suspected add levofloxacin If oral administration not possible Benzyl penicillin 1.2 gms IV four times a day plus Clarithromycin 500mg IV two times a day Alternative Treatment Benzylpenicillline 1.2 gm IV four times a day plus Levofloxacin 500 mg IV two times a day or Ciprofloxacin 400mg IV two times a day Or Ceftriaxone 2gm IV once daily or Cefotaxime 1 gm IV three times daily plus Clarithromycin 500mg IV twice daily If Legionella is strongly suspected consider adding Levofloxacin

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Pneumothorax

Small pneumothorax: visible rim on chest x ray < 2 cm Large pneumothorax: visible rim on chest x ray > 2 cm

Causes • • • • •

Primary Spontaneous: Healthy subjects with no underlying lung disease. More common in young, smoking men aged 20-40 years. Secondary Spontaneous: Pleural rupture due to underlying lung disease. Infection: Cavitating pneumonia, TB Trauma: RTA Iatrogenic: After pleural biopsy or aspiration

Clinical features • • •

Sudden onset of breathlessness Chest pain: Dull, central, heavy Signs of significant pneumothorax (Tension pneumothorax) a. Trachea shift to opposite side b. Raised JVP c. Hypotension d. Tachycardia e. Shock

Investigation •

Chest X ray

Management 1. 2. 3. 4. 5. 6. 7.

Check ABC Keep in upright position Check oxygen saturation Give oxygen Secure intravenous access Aspiration Intercostal drain

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Management

Pneumothorax

Primary Breathlessness and/or rim of air > 2cm in CXR Yes

Secondary

No

Aspiration

Successful

Aspiration Not Successful

No

Not Successful

Successfu

Consider repeat Successful aspiration Not Successful

Admit for 24 hour observation

Breathlessness and age > 50 years and/or rim of air > 2cm in CXR Yes Intercostal drain Not Successful

Successful

Refer to thoracic surgeon

Successful

Intercostal drain Not Successful Refer to thoracic surgeon

Discharge

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AMS/HAPE/HACE The diagnosis of Altitude Sickness Document the altitude where problem started, document itinerary and rate of ascent, pre existing and co sxisting illness, past medical history, medication history etc. Diagnostic criteria for AMS (Acute Mountain Sickness) in a person who recently arrived at high altitude (2700 and more), the presence of headache and at least one of the following: nausea or vomiting, fatigue or weakness, dizziness and insomania. High altitude pulmonary edema (HAPE) is diagnosed if at least 2 of these symptoms and 2 of these signs are present. Symptoms: Cough, fatigue, shortness of breath at rest and tightness in the chest Signs: Crackles in the lung, cyanosis, tachycardia(>120), tachypnea (>20). Patient with HAPE may have no headache. High altitude cerebral edema (HACE): This is the end stage of AMS. Definition: Neurological deterioration in a person with AMS or HAPE, characterized by ataxia and or mental status changes. If possible on the tandem gait test. Severely ill people with altitude sickness may have both HAPE and HACE. Kep in mind other illness lile MI, PE, SAH, CVA, hyponatraemia, diabetes. Just because someone is brought from the mountains does not mean they have altitude sickens. Lab test: ECG, Oxygen saturation, Chest X ray, CBC, Urine, Electrolytes, Creatinine, Blood culture if febrile, malaria smear if relevant, sputum for AFB(in nepalies), stool test (if diarrhea) High altitude cerebral edema (HACE) Goal is to reduce brain volume and ICP and stop leak of blood brain barrier. Adequate oxygen to raise the saturation > 90% Dexamethasone 4-8mg initially (depending on severity), then 4 mg 6 hourly PO or IV Coma care i.e. airway protection, bladder drainage, IV fluids, assisted ventilation as indicated (Caution not to over hyperventilate. Since the respiratory alkalosis already present and the use of oxygen will markedly reduce cerebral blood flow, further hyperventilation could result in cerebral ischemia) Consider fursemide or osmotic diuretics in those critically ill High altitude pulmonary oedema (HAPE) Oxygen to get the saturation > 90% Bed rest Consider chest infection and use suitable antibiotics if gram stain or culture positive Nifedipine 20-30 mg extended release BID, watch BP Coma care if necessary Stool softner Salbutamol nebulizer In an anxious dyspneic patient with stable blood pressure consider morphine 2.5mg PRN. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Treatment of HAPE and HACE Very often the HAPE and HACE treatment may need to be combined. Chest X ray opacities clear up in a day or two in HAPE, unlike pneumonia. So, a repeat chest x ray to help establish diagnosis. Intubation in HAPE or HACE is seldom required unless there is a concomitant illness. Obviously if someone is comatose the hypotensive with HAPE/HACE, do not give nifedipine, lasix or morphine. Oxygen and steroids are the mainstay and plan for CT/MRI

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Abdominal Emergencies Contents Gastritis .......................................................................................................................................................... 100 Causes ........................................................................................................................................................ 100 Clinical features.......................................................................................................................................... 100 Investigations ............................................................................................................................................. 100 Management .............................................................................................................................................. 100 Admission criteria ...................................................................................................................................... 100 Discharge criteria ....................................................................................................................................... 100 Upper GI Bleeding .......................................................................................................................................... 101 Introduction ............................................................................................................................................... 101 Clinical features.......................................................................................................................................... 101 Causes ........................................................................................................................................................ 101 Severity criteria .......................................................................................................................................... 101 Investigations ............................................................................................................................................. 102 Management .............................................................................................................................................. 102 Pancreatitis .................................................................................................................................................... 104 Introduction ............................................................................................................................................... 104 Clinical features.......................................................................................................................................... 104 Causes ........................................................................................................................................................ 104 Ranson’s Severity Criteria .......................................................................................................................... 104 Investigations ............................................................................................................................................. 105 Management .............................................................................................................................................. 105 Admission criteria ...................................................................................................................................... 105 Discharge criteria ....................................................................................................................................... 105 Liver Failure .................................................................................................................................................... 106 Introduction ............................................................................................................................................... 106 Causes ........................................................................................................................................................ 106 Clinical features.......................................................................................................................................... 106 Investigations ............................................................................................................................................. 107 Management .............................................................................................................................................. 107 Acute cholecystitis ......................................................................................................................................... 108 Introduction ............................................................................................................................................... 108 Diagnostic Criteria ...................................................................................................................................... 108 Investigations ................................................................................................................................................. 108 Management .............................................................................................................................................. 108 Acute Appendicitis ......................................................................................................................................... 109 Introduction ............................................................................................................................................... 109

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Appendicitis is a painful swelling and infection of the appendix. ................................................................. 109 Clinical features.......................................................................................................................................... 109 Diagnostic criteria ...................................................................................................................................... 109 Investigations ............................................................................................................................................. 109 Management.................................................................................................................................................. 109 Intestinal Obstruction .................................................................................................................................... 110 Introduction ............................................................................................................................................... 110 Cause .............................................................................................................................................................. 110 Pediatric consideration .................................................................................................................................. 110 Clinical features.......................................................................................................................................... 110 Investigations: ............................................................................................................................................ 110 Management:............................................................................................................................................. 111 PERFORATED VISCUS ..................................................................................................................................... 112 Introduction ............................................................................................................................................... 112 Causes ........................................................................................................................................................ 112 Clinical features.......................................................................................................................................... 112 Investigations ............................................................................................................................................. 112 Management .............................................................................................................................................. 112 Acute Diarrhoea ............................................................................................................................................. 113 Introduction ............................................................................................................................................... 113 Causes ........................................................................................................................................................ 113 Clinical features.......................................................................................................................................... 113 Investigations ............................................................................................................................................. 113 Management .............................................................................................................................................. 113 Abdominal Trauma (Blunt/Penetrating) ........................................................................................................ 115 Introduction ............................................................................................................................................... 115 Clinical features.......................................................................................................................................... 115 Investigations ............................................................................................................................................. 115 Management .............................................................................................................................................. 115 Testicular Torsion ........................................................................................................................................... 116 Investigations ............................................................................................................................................. 116 Management .............................................................................................................................................. 116 Uretetic Colic.................................................................................................................................................. 117 DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Overview .................................................................................................................................................... 117 Pathophysiology of Renal Colic .................................................................................................................. 117 Presentation of Renal Colic ........................................................................................................................ 117 Stone Location in Renal Colic ..................................................................................................................... 118 Lab Studies in Renal Colic .......................................................................................................................... 118 Imaging Studies in Renal Colic ................................................................................................................... 118 Management of Renal Colic ....................................................................................................................... 119

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Gastritis Causes Acute gastritis Drugs: Aspirin, Steroids, NSAIDS Stress: Sepsis, burn, trauma Alcohol Chronic gastritis: H. pylori infection

Clinical features • • • • •

Dyspepsia Epigastric pain or discomfort Bloating, indigestion, heartburn Anorexia, nausea, vomiting Hematemesis, Malena, pallor

Investigations • • •

ECG to rule out ischemic heart disease Complete blood count (if signs of blood loss) Amylase (if persistent pain)

Management 1. Antacid gel 2. GI cocktails: 30ml of antacids plus 10-20 ml of viscous lidocaine 3. H2 antagonist

Admission criteria • •

Evidence of upper GI bleeding Uncontrolled pain or vomiting

Discharge criteria • •

Symptoms relieved Unremarkable physical examination

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Upper GI Bleeding Introduction Upper gastrointestinal bleeding (or haemorrhage) is that originating from the oesophagus, stomach and duodenum.

Clinical features • • • • •

Hematemesis: Bright red, dark clots, coffee ground Malena: Black sticky smelly stool Weakness/sweating and palpitation Postural dizziness and fainting Collapse or shock

Causes • • • • • • •

Peptic Ulcer Gastroduodenal erosion Oesophagitis Varices Mallory weiss tear Upper GI malignancy Vascular malformations

Severity criteria • • • • • •

Age > 60 years Shock (BP < 100mmHg systolic in patients < 60 years or < 120mmHg in patients > 60 years). Measure postural change in BP in patients who are not shocked and change in HR Inappropriate Bradycardia or HR > 120 per minute Chronic liver disease, other chronic disease (e.g cadiac, renal, respiratory) Bleeding diathesis Decreased conscious level

Rockall’s Score Clinical variable Age (years) Shock

Patients scored 0 < 60 years No Shock

Co morbidity

Nil

Diagnosis Stigmata of recent bleed

Mallory Weiss None or dark spot

1 60-79 HR > 100 SBP > 100

All other

2 >80 HR > 100 SBP 8 = high risk of death DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Investigations • • • • •

Complete blood count Blood grouping and cross matching Electrolytes and creatinine Amylase ECG

Management 1. General management a. Check ABC b. Check oxygen saturation c. Give oxygen d. Open intravenous line with (16-18 G canula both side) normal saline Classification of Hypovolaemic shock by blood loss in adult Class I Class II Class III Class IV Blood loss < 750 750-1500 1500-2000 >2000 volume (ml) Blood loss (% of 0-15 15-30 30-40 >40 circulating blood) Systolic BP No change Normal Reduced Very Reduced Diastolic BP No change Raised Reduced Very Reduced/ Unrecordable Pulse Slight 100-120 120(thready) >120 (very Tachycardia thready) Respiratory Rate Normal Normal Raised Raised (>20/mins) (>20/mins) Mental State Alert, thirsty Anxious or Anxious, Drowsy, aggressive aggressive or confused or drowsy unconscious Blood transfusion should be considered after loss of 30% of circulating volume e. f. g. h. i.

Send blood for investigations Catheterization (if needed) NG tube (if needed) Peptic Ulcer bleeding: Inj Pantoprazole 80mg IV bolus followed by continuous infusion of 8 mg/hour Variceal bleeding: Octeotride - 100µgm IV bolus followed by a continuous infusion of 25-50 µgm/h

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Upper GI Bleeding

Rockall’s Score < 3

Rockall’s Score > 3

Discharge Hypovolaemia class I

Monitor Urine output: Aim for 30ml/hour Signs of overload: raised JVP, pulmonary oedema, peripheral oedema

Hypovolaemia > class I

Slow infusion of Normal saline

Normal saline 1lts in 20-30 minutes

Hypovolaemia class I

Reassess

Hypovolaemia > class I Normal saline 1lts in 20-30 minutes Hypovolaemia class I

Reassess

Hypovolaemia > class I Blood transfusion 1 unit/hour ± Dopamine support at 6-10µgm/kg/min

Yes

Blood available No

ICU/ Urgent Endoscopy

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Normal saline 1lts in 20-30 minutes hour ± Dopamine support at 6-10µgm/kg/min

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Pancreatitis Introduction Inflammation of the pancreas due to activation, interstitial liberation and digestion of the gland by its own enzymes.

Clinical features • • • • • •

Abdominal pain: Epigastric or generalized of rapid onset but may occur anywhere (including chest), dull, constant radiating to back or between the scapulae often relieved by leaning forward. Nausea, vomiting ± dehydration ± jaundice Peritonitis with epigastric tenderness localized rebound tenderness or generalized abdominal rigidity. Tachycardia and hypotension; shock/collapse and respiratory failure in severe cases Very rarely signs of bleeding in pancreatic bed; Grey turner’s sign (echymosis in flanks) or Cullen’s sign (peri umbilical bruising) Hypocalcaemia, tetany

Causes • •

Common • Gall stone, Alcohol Uncommon: • Iatrogenic (Post surgery) • Trauma • Infections • Viral: Mumps, Hepatitis A and B • Bacterial: Mycoplasm • Drugs: Thiazides, frusemides, NSAIDs etc • Hypertriglyceridaemia, Hypercalcaemia, Hypothermia • Pancreatic carcinoma

Ranson’s Severity Criteria At presentation Age > 55 years WBC > 16 x 109/L Glucose > 10mM (Non diabetic) LDH > 350 IU AST > 250u/L

During the first 48 hours Hematocrite fall > 10% Urea rise >10mM Serum Calcium < 2.0 mmol/L Base excess > 4 mmol/L PaO2 ,8kPa Serum Albumin ,32g/l Estimated fluid sequestration > 6 lts Score: 7=100%

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Investigations • • • • • • •

Lipase, complete blood count: Raised Hematocrite and Leukocytosis Electrolytes and creatinine: Creatinine may rise due to hypovolaemia Blood glucose: May be raised Liver function test: AST and bilirubin is often elevated especially in gallstone pancreatitis Calcium: Hypocalcaemia Chest X ray: May show elevated diaphragm, pleural effusion Abdominal X ray: May show dilated gas filled loop in region of pancreas

Management a. b. c. d. e. f.

Check ABC , oxygen saturation, bed side blood sugar IV open with normal saline (Sometimes may need resuscitation) Send blood for investigations Pain management: Pethidine/Procholrperazine Keep NPO, adequate hydration Antiboitics: Ceftriaxone 1gm IV to prevent secondary infection Pancreatitis

Ranson’s Score < 3

Conservative therapy

Ranson’s Score > 3

Aggressive IV hydration (250 ml hourly for first 48 hours if cardiac status permits) and antibiotic, enteral or total parental nutrition

May need critical

No

Improvement Yes

Continue antibiotics for 7-10 days, enteral or total parental nutrition

Admission criteria • •

Acute pancreatitis with significant pain, nausea and vomiting, Hemorrhagic or necrotizing pancreatitis

Discharge criteria • •

Mild acute pancreatitis without evidence of Biliary tract disease and able to tolerate oral fluids Chronic pancreatitis with minimal abdominal pain and able to tolerate oral fluids

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Liver Failure Introduction Acute: Acute liver failure is a potentially reversible severe liver injury with an onset of hepatic encephalopathy within 8 weeks or appearance of the first symptoms and in the absence of pre existing liver disease Acute on Chronic liver failure: Patient with chronic liver disease presenting with decompentation. Hepatic encephalopathy (HE) is altered brain function is due to metabolic abnormalities, which occur as a consequence of liver failure.

Causes Acute liver failure Acute on chronic liver failure • Drug induced: Paracetamol, Halothane, • Intercurrent infection: Spontaneous NSAIDs bacterial peritonitis, Pneumonia, Skin infection • Viral Hepatitis • Acute GI hemorrhage • Toxins: Mushrooms • Additional hepatotoxic insult • Malignancy: Malignant infiltration Alcoholic binge • Vascular: Ischemic injury, venoAcute viral hepatitis occlusive diesese Hepatotoxic drugs • Others: HELLP syndrome, autoimmune • Drugs: Sedatives/narcotics, Diuretics hepatitis • Metabolic derangement • Hypoglycemia • Electrolyte disturbances • Major surgery • Constipation

Clinical features 1. Encephalopathy Grade Clinical features 0 Minimal hepatic encephalopathy (previously known as sub clinical hepatic encephalopathy) Lack of detectable changes in personality or behavior Minimal changes in memory, concentration, intellectual function, and coordination Asterixis is absent 1 Drowsy but coherent, mood change Altered sleep pattern Asterixis can be detected 2 Drowsy, confused at times, inappropriate behavior. Obvious Asterixis 3 Very drowsy and stuparose but rousable; alternatively restless, screaming 4 Comatose, barely rousable DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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2. 3. 4. 5. 6. 7.

Metabolic disturbances: Hypoglycemia, Hypokalaemia, Hyponatraemia are common Cardiovascular abnormalities: Diastolic BP falls as disease progresses. Respiratory failure: Hypoxia common Renal failure: decrease urine output, indicates worse prognosis Bleeding problem: Due to derangement of clotting factors Infection

Investigations • • • • • •

Complete blood count: To see signs of infection Blood glucose: Hypoglycemia PT/INR: To see risk of bleeding and prognosis Liver function test: Albumin low in acute on chronic liver failure ECG/Chest x ray: To see infection Electrolytes and creatinine: Hypokalaemia, Hyponatraemia, Deranged renal function

Management 1. 2. 3. 4. 5. 6. 7. 8. 9.

Assess ABC Check bed side blood sugar IV access and hemodynamic support with colloid or blood, avoid fluid over load. Send Blood for investigations Prophylactic antibiotics: Inj Cefotaxime 1gm IV stat (Cefotaxime 2 gm iv if SBP) N-Acetylcysteine if paracetamol overdose Vitamin K 10mg IV, may need fresh frozen plasma or platelets transfusion If signs of raised ICP: 100 ml of 20% Inj Mannitol Lactulose 20ml by mouth or NG tube, or rectal enema – 300 ml in 700 ml of NS, to be retained for 30 minutes

Liver failure

Acute Follow Box 1

Box 1 Prophylactic antibiotics: Inj Cefotaxime 1gm IV stat.

Flowchart 26: Management of Liver failure

Vitamin K 10mg IV, may Specific Management need fresh frozen plasma *All patients should be admitted e.g. N-Acetylcysteine if or platelets transfusion

paracetamol overdose

If no improvement consider critical care

Acute on Chronic

Lactulose 10ml by mouth or NG tube

Encephalopathy Grade 0-1

Follow Box 1 If no improvement consider critical care

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

Encephalopathy Grade > 1

Follow Box 1 and consider critical care

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Acute cholecystitis Introduction Acute Cholecystitis is inflammation of gall bladder wall. Clinical features • Pain over right upper quadrant: sudden onset of severe pain • Vomiting • Fever, Tachycardia, sweating, jaundice • Murphy’s sign: RUQ tenderness and peritonism especially in inspiration Acalculous Cholecystitis is seen in elderly or patients with co existing disease or rauma and patients on total parental nutrition.

Diagnostic Criteria A

Local signs of inflammation 1. Murphy’s sign 2. RUQ mass/pain/tenderness B Systemic Signs of Inflammation 1. Fever 2. Elevated CRP 3. Elevated WBC count C Imaging finding characteristics of Cholecystitis Definitive diagnosis 1. Any one of A and one of B 2. C confirms diagnosis when acute Cholecystitis is suspected clinically Investigations • • •

Complete blood count: Increase WBC cout Amylase: May be elevated USG abdomen: Gall stone, Biliary sludge, thickening of gall bladder wall

Management 1. 2. 3. 4. 5. 6.

Assess ABC IV access and NPO Send Blood for investigations Pain management: NSAIDs Admission IV antibiotics: Inj Cefotaxime 1 gm IV stat + Inj Metronidazole 500mg IV stat

*All cases of cholecystitis should be admitted for parenteral antibiotics, analgesia, fluid replacement

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Acute Appendicitis Introduction Appendicitis is a painful swelling and infection of the appendix.

Clinical features • • • • •

Pain abdomen: Occurs suddenly, often causing a person to wake up at night, initially over upper abdomen then moves lower and to the right, gets worse in a matter of hours, aggravated by moving, taking deep breaths, coughing, or sneezing Other symptoms: Loss of appetite, nausea, vomiting, constipation or diarrhea, inability to pass gas, a low-grade. McBurney’s point tender: Junction between lateral 1/3 and 2/3 of spinoumbilical line at right Rovsing’s sign: Pressure on left aggravates pain on right side Rebound tenderness

Diagnostic criteria Alvarado score (MANTERALS) • M: Migration of pain to right iliac fossa (1) • A: Anorexia (1) • N: Nausea/vomiting (1) • T: Tenderness in right iliac fossa (2) • R: Rebound tenderness (1) • E: Elevated temperature (1) • L: Leukocytosis (2) • S: Shift to right (1)

Alvarado Score 8: Very probably appendicitis

Investigations • • •

Complete blood count: Leukocytosis Urine routine examination: To rule out urinary tract infection USG pelvis: Especially important in female to rule out other pelvic conditions

Management

1. NPO and IV assess 2. NSAID for pain management 3. Antibiotics: Inj Cefotaxime 1gm/Ciprofloxacin 200mg IV stat + Inj Metronidazole 500mg IV stat (if planned for surgery single dose prophylactic preferred) 4. Prepare for surgery

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Intestinal Obstruction Introduction Obstruction of normal flow of intestinal contents due to mechanical or nonmechanical causes. Cause • Small Bowel • Adhesion: Most common • Hernias • Neoplasm • Stricture: Inflammatory bowel disease • Ascaris • Large Bowel • Carcinoma • Volvulus • Diverticular disease • Inflammatory disease • Ischemic colitis Pediatric consideration • Intussusceptions: Most common in 3-12 months of age • Incarcerated inguinal hernia • Malrotation with volvulus: Can occur as early as 3-7 days, double bubble often seen in upright abdominal radiograph due to partial obstruction of duodenum resulting in air in stomach and in first part of duodenum • Pyloric stenosis: Onset usually 2-5 weeks of age

Clinical features • • • • • • • • • •

Pain abdomen: Intermittent early, constant with strangulation Vomiting: Bile stained emesis with proximal obstruction, feculent emesis with distal obstruction Obstipation Tachycardia, Hypotension with significant fluid loss Fever with strangulation or perforation Hyperactive or high pitched bowel sound Diffuse abdominal tenderness Pain out of proportion to findings suggests ischemic or gangrenous bowel Guarding and rebound tenderness Hernias: Inguinal, femoral

Investigations: • •

Chest X ray erect with both dome of diaphragm: To see gas under diaphragm indicating perforation Abdominal X ray erect: To see air fluid level

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• • • • • •

Abdominal X ray supine: To see maximum dilatation (normal small bowel < 3 cm in diameter). Dilatation of cecum > 13 cm indicates potential rupture Complete blood count: Leukocytosis Electrolytes and Creatinine Blood sugar Amylase Urine routine examination

Management: 1. 2. 3. 4. 5. 6. 7.

Secure ABC Normal saline resuscitation when significant volume depletion, strangulation or perforation NG tube suction Foley catheterization Analgesics as needed Antiboitics: Inj Ceftiraxone 1 gm IV stat + Inj Metronidazole 500mg IV stat Liaison with surgical team

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PERFORATED VISCUS Introduction It is a perforation of any segment of GI tract due to inflammation, ulceration, trauma or obstruction. Chemical peritonitis occurs as a result of spillage of gastric or intestinal contents into peritoneal cavity.

Causes • • • • • • • •

Peptic ulcer disease Appendicitis Enteric fever Inflammatory bowel disease Diverticular disease Colon carcinoma Foreign body ingestion Trauma

Clinical features • • • •

Sudden and severe abdominal pain Rigidity, Guarding, Rebound tenderness Absent bowel sound Tachycardia, Hypotension

Investigations • • • • •

Chest x ray erect: Gas under diaphragm (pneumoperitoneum). Complete blood count Electrolytes, Createnine, blood sugar, Amylase Urine routine examination ECG

Management a. b. c. d.

ABC Correct hypovolemia: rapid fluid resuscitation with 0.9% NS 1 L in adults and 20ml/kg in children NG tube, Catheterization Broad spectrum antibiotics: Inj Ceftriaxone 1 gm iv stat + Inj Metronidazole 500 mg iv stat

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Acute Diarrhoea Introduction Diarrhea reflects increased water content of the stool, whether due to impaired water absorption and/or active water secretion by the bowel. In severe infectious diarrhea, the number of stools may reach 20 or more per day, with defecation occurring every 20 or 30 minutes.

Causes Pathogen Virus Bacteria

Small bowel Roravirus Salmonella* Escherichia coli* Clostridium perfringens Staphylococcus aureus Aeromonas hydrophila Bacillus cereus Vibrio cholerae

Protozoa

Cryptosporidium* Cyclospora Giardia lamblia

Colon Cytomegalovirus Campylobacter* Shigella Clostridium difficile Yersinia Vibrio parahaemolyticus Enteroinvasive E. coli Plesiomonas shigelloides Klebsiella oxytoca(rare) Entamoeba histolytica

Clinical features • • • • •

Pulse rate > 90 Postural hypotension Supine hypotension and absence of palpable pulse Dry tongue , Sunken eyeballs, Skin pinch Signs of severity: • Disorientation, lethargic • Anuria • Hypotention, cold perphhery

Investigations • • •

Stool routine examination: Fecal leukocyte > 10/hpf is an indicator if invasive diarrhea requiring antibiotics Stool for hanging drop: For cholera Electrolytes and creatinine: In case of severe dehydration

Management 1. 2. 3. 4.

ABC, Check vitals, Check blood sugar IV lock and send blood for investigation if needed Catheterization (if in shock) ORS or IV fluid as per need

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Acute Diarrhoea

Dysentry: Mucoid, blood mixed

Watery Diarrhoea

Emperical Antibiotics: Ciprofloxacin 500mg twice a day for 3 days If resistant to ciprofloxacin or camphylobacter infection Azithromycin 500mg daily for 3 days

Cholera Rice watery stool, excessive volume loss with hanging drop positive

Not Suggestive of Cholera

Aggressive fluid management Doxycycline 300mg stat or Azithromycin 1gm stat

Hemodynamically unstable Hemodynamically stable IV fluid bolus at least 2 liters or NS or RL + Antiboitics (Ceftriaxone)

Reassess

Stable

Unstable

IV fluid: Maintenance 100/50/20 rule Or bolus if required

Fluids + Ionotropic support

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ORS as tolerated Discharge if improvement

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Abdominal Trauma (Blunt/Penetrating) Introduction • • • • • •

Injury results from a sudden increase of pressure to abdomen. Solid organ injury usually manifests itself as hemorrhage Hollow viscous injuries result in bleeding and peritonitis from contamination with bowel contents. Solid organ injury is more frequently than hollow viscous Spleen is the most frequently injured organ followed by liver, intestine, retroperitoneal structures and kidney In penetrating injury liver is most commonly injured followed by small bowel,stomach, colon, major vessel and less often the spleen

Clinical features • • • • • •

Pain abdomen Nausea and vomiting Labored respiration due to diaphragm irritation of upper abdominal injury Left shoulder pain with inspiration from diaphragmatic irritation due to bleeding Signs of peritonitis: Abdominal guarding, rebound tenderness In severe intra abdominal bleeding: Pallor and Shock

Investigations • • • • • • •

Hematocrite Blood grouping and cross matching Electrolytes and creatinine Urine Routine examination X ray abdomen erect (if patient is hemodynamically stable) USG abdomen (if unstable, doctor should accompany) Four quadrant aspiration

Management • • • • • • • • • • •

C spine stabilization if needed A: Check airway and give oxygen B: Examine chest C: Two large bore IV with crystalloid infusion Apply sterile dressing to open wound Prepare for blood transfusion if needed Foleys catheter if patient is in shock NG tube if there is features of peritonitis Tetanus toxoid in penetrating injury Inj Ceftriaxone + Inj Metronidazole if penetrating injury Pain management: Opioids analgesics

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Testicular Torsion Testicular torsion is a true urologic emergency and must be differentiated from other complaints of testicular pain because a delay in diagnosis and management can lead to loss of the testicle. Though testicular torsion can occur at any age, including the prenatal and perinatal periods, it most commonly occurs in adolescent males; it is the most frequent cause of testicle loss in that population History includes a sudden onset of severe unilateral scrotal pain. • Scrotal swelling • Nausea and vomiting • Fever (16%) • Urinary frequency (4%)

Investigations • •

Urinalysis Complete blood count: CBC can be normal or show an elevated WBC count in as many as 60% of patients who have torsion.

Management • • • • • • •

Early diagnosis and prompt urologic consultation is essential since time is critical in salvage of the testicle. Analgesic pain relief should be administered as testicular torsion is typically very painful. Attempt manual detorsion with pain relief as the guide for successful detorsion. The procedure is similar to the "opening of a book" when the physician is standing at the patient's feet. Surgical management Most torsions twist inward and toward the midline; thus, manual detorsion of the testicle involves twisting outward and laterally. The physician then rotates the right testicle outward 180° in a medial to lateral direction. Rotation of the testicle may need to be repeated 2-3 times for complete detorsion and to provide

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Uretetic Colic Overview 1. In the US, renal colic affects 5% of the population. a. The incidence is lower in non-industrialized countries. b. The male-to-female ratio is 3:1 c. Peak age of onset is 20-40 years. 2. Beware of a "first episode of renal colic" in a patient >60 years old (ie. consider AAA) a. Nephrolithiasis in children is rare. 3. Without preventative treatment, recurrence rates after the first kidney stone are: a. 15% by 1 year b. 35% by 5 years c. 50% by 10 years

Pathophysiology of Renal Colic 1.

2. 3. 4.

5. 6. 7.

Most renal calculi are formed in the kidney when the urine becomes supersaturated with a salt capable of forming crystals. a. These crystals are then flushed into the ureter Rates of spontaneous stone passage are determined by: a. Stone size (#1), Stone location The "classically-described" critical stone size is 4mm. According to this "classic" teaching: a. Stones 9mm have only a 5% rate of spontaneous passage. Since most stones are small, the overall spontaneous passage rate is 85%. Since 2010, however, larger and larger stones are being considered for trials of conservative management. Risk factors for renal colic include: a. Hypercalcemia b. Sarcoid c. Crohns d. Renal Tubual Acidosis (Type 1) e. Recurrent UTI

Presentation of Renal Colic The pain in renal colic is caused by: Ureteral obstruction and spasm +/- Associated infection a. There is no correlation between degree of pain and likelihood of obstruction. b. The "classic" renal colic patient presents: 4. Squirming with pain 5. Unable to lie or sit still 1. 2. 3.

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6.

Fever is not part of uncomplicated renal colic, and suggests infection.

Stone Location in Renal Colic 1.

2. 3. 4. 5. 6. 7.

There are five narrowings in the urinary tract where stones typically impact: a. Renal calyx b. Ureteropelvic junction (UPJ) c. Pelvic brim (where the ureters arch over the iliac vessels) d. Ureterovesical junction (UVJ) (ie. the narrowest part of the ureter) e. Bladder neck The location of pain may suggest the position of the impacted stone: Calyx or UPJ stones often present with flank pain (ie. distension of the renal capsule). Ureteral stones can cause abrupt, severe, colicky pain in the flank and lower abdomen UVJ stones can cause irritative voiding symptoms (eg. urinary frequency and dysuria) Bladder stones are usually asymptomatic Persistent bladder stones typically arose in the bladder--not in the kidney or ureter. They are different entities than kidney stones

Lab Studies in Renal Colic Urinary RBCs a. Most patients with renal colic have some degree of hematuria b. The degree of hematuria is not predictive of stone size or likelihood of passage. 2. Urinary WBCs a. Pyuria (ie. >5 WBC/hpf on a centrifuged specimen) is sensitive, but not specific, for associated infection 3. Serum Cr a. Even if unilateral, large obstructing stones can cause a temporary rise in creatinine. 1.

Imaging Studies in Renal Colic 1.

2.

3.

4. 5. 6.

Most authors recommend diagnostic imaging: a. For first-time stones b. If the diagnosis is unclear c. If suspected proximal infection (ie. to rule out an obstructing stone) KUB (kidney-ureter-bladder) X-ray a. Sensitivity is 6 mm or hydronephrosis (with obstructing stones) Advantages of U/S include the lack of radiation. CT scan Advantages of CT for renal colic include: a. Specificity and sensitivity both >95-100% b. Rapid study (4mm (although this is highly variable) e. Intractable pain f. Inability to tolerate oral fluids or medications DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Neurological Emergencies Contents Headache ....................................................................................................................................................... 120 Meningitis ...................................................................................................................................................... 121 Clinical features.......................................................................................................................................... 121 Investigations ............................................................................................................................................. 121 Management .............................................................................................................................................. 121 Seizure ............................................................................................................................................................ 122 Seizure Physiology...................................................................................................................................... 122 Status Epilepticus ....................................................................................................................................... 122 Pathophysiology of Status Epilepticus ....................................................................................................... 122 Management of an Actively-Seizing Patient .............................................................................................. 123 Empiric therapy for drug-induced seizures................................................................................................ 125 Cerebrovascular Accident (CVA) .................................................................................................................... 127 Introduction ............................................................................................................................................... 127 Clinical features.......................................................................................................................................... 127 Investigations ............................................................................................................................................. 127 Management .............................................................................................................................................. 127 Head Injury ..................................................................................................................................................... 128 Introduction ............................................................................................................................................... 128 Clinical feature ........................................................................................................................................... 128 Investigation............................................................................................................................................... 128 Management .............................................................................................................................................. 129 Referral Criteria.......................................................................................................................................... 129 Discharge Criteria ....................................................................................................................................... 129 Treatment of raised ICP ................................................................................................................................. 130

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Headache Headache Occurs more than 15 days per month for more than 3 months

Primary Those not associated with underlying pathology: Migraine, tension, cluster headache

Bilateral

Aspirin or Paracetamol

No

Unilateral

New onset headache or headache different form their usual headache Yes OR With danger signs*

Cluster Headache

With following features Duration: 4-72 hours Onset: Gradual Frequency: 1-2/month Restlessness during attack: 0% Ipsilateral autonomic feature: Occasionally

Yes Migraine

Chronic Headache

No

No Tension Headache

Yes

Secondary Those associated with underlying pathology: Infection, neoplastic, vascular or drug induced

Inj Sumatriptan 6mg subcutaneous is recommended Infection: Meningitis Brain Abscess

CVA Neoplastic

Refer to Section on CVA and Meningitis for

Management • Opoids analgesic should not be routinely use • Paracetamol 1gm PO for mild to moderate migraines • Aspirin 900mg or Ibuprofen 400mg PO for severe migraine • If not improving or if previous attacks have not been controlled by simple analgesics, oral triptans (Amlotriptan 12.5, Eletripran 40-80 mg or Riaztriptan 10 mg) are recommended • If not controlled add oral Naproxen 500mg • Oral Metoclopramide to decrease nausea and vomiting

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Yes Fever No Yes

Neurological Signs No Associated with drug: Present for 15 days or more per month increased on taking medicine:

Can be managed on OPD basis once acute pain decreases

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Meningitis Clinical features • • • • • • • •

Classical triad: Fever, Neck rigidity, and a change in mental status Headache Older adults (especially those with underlying conditions such as diabetes mellitus or cardiopulmonary disease) may present insidiously with lethargy or obtundation, no fever, and variable signs of meningeal inflammation Seizures, focal neurologic deficits Skin manifestations: Petechiae and palpable Purpura(N. meningitidis) Brudzinski's sign: Spontaneous flexion of the hips during attempted passive flexion of the neck The Kernig's sign: Inability or reluctance to allow full extension of the knee when the hip is flexed 90º. Accentuation of headache by horizontal rotation of the head at a frequency of two to three times per second

Investigations •

CSF analysis: LP should be done unless contraindicated Total WBC count Protein (gm/L) Glucose (mg/dl) Viral Meningitis 5-100 0.5-2.5 Normal Bacterial Meningitis > 1000 > 2.5 10-45 Tubercular Meningitis 100-1000 > 2.5 10 • Complete blood count, blood culture, electrolytes and creatinine, blood glucose • ECG and Chest X ray

Management 1. Secure ABC, oxygen, keep vein open with Normal saline, send blood for investigations 2. Check bedside blood sugar, Catheterization (if needed) 3. IV steroids: Dexamethasone 0.15-0.4 mg/kg every six hours for four days (must be started before or with Abs and main use is in pneumococcal and in non HIV) Recommendation for empirical therapy Age Common Bacterial Pathogen Antibiotics < 1 month Streptococcus agalactiae, Escherichia Ampicillin plus cefotaxime; OR coli, Listeria monocytogenes, ampicillin plus an Klebsiella species aminoglycoside 1-23 months Streptococcus pneumoniae, Neisseria Vancomycin plus a thirdmeningitidis, S. agalactiae, generation cephalosporin Haemophilus influenzae, E. coli 2-55 years N. meningitidis, S. pneumoniae Ceftriaxone 2gm iv stat >55 years S. pneumoniae, N. meningitidis, L. Certriaxone 2 gm iv stat plus monocytogenes, aerobic gramAmpicilline 1gm iv stat negative bacilli

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Seizure Seizure Physiology 1. The brain is constantly in a state of balance between inhibition (mediated mainly by GABA) and excitation (mediated mainly by glutamate). a. Even small shifts in this balance can have dramatic effects 2. GABA is a chemical which binds to the GABA-receptor in the brain. a. It is activation of the GABA-receptor that inhibits neurotransmission 3. Additional agonists of the GABA-receptor include: a. BZPs b. Barbiturates However, these agonists are not effective unless GABA is also present.

Status Epilepticus 1. Status epilepticus was classically defined as either: a. A seizure lasting >30mins b. Multiple seizures cumulatively lasting >30mins without a return to normal LOC 2. Numerous changes for this definition have been proposed (eg. decreasing the time period to 5-10 minutes), but none have been universally accepted. a. In practice, any seizure lasting >5mins should be treated as status epilepticus 3. Patients with a previously-normal mental status who have a generalized seizure should start to wake up within 30 minutes. a. Patients who do not do this may have "non-convulsive status epilepticus" (NCSE)--in which their body is no longer actively seizing, but their brain continues to seize b. These requires EEG to detect

Pathophysiology of Status Epilepticus 1. Prolonged seizures reliably damage the brain. 2. Simply controlling the visible seizures does not reduce brain injury or mortality. a. Brain injury in seizure results from exhaustion of ATP--leading to breakdown of cellular gradients. b. This is why paralytics (which stop the body from seizing, but do not stop the brain) are not effective in status epilepticus. In fact, they are potentially dangerous--as they can mask ongoing seizures. 3. The most common precipitants of status epilepticus in adults are: a. Stroke b. Drugs c. Ischemia d. Metabolic abnormalities (eg. hypoglycemia, hyponatremia) 4. he most common precipitants of status epilepticus in children are: a. Febrile seizure (#1) b. Epilepsy c. Medication change d. Congenital abnormalities DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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e. Metabolic abnormalities (eg. hypoglycemia, hyponatremia)

Management of an Actively-Seizing Patient Summary a. Supportive treatment b. Check glucose c. Check electrolytes (ie. Na, Ca, Mg) d. BZPs e. Phenytoin and/or Phenobarb f. Propofol (if available) g. Not generally paralytics (unless required for other indication) h. +/- Empiric therapy for drug-induced seizures (eg. INH, oral hypoglycemics, TCAs) i. +/- Empiric therapy for other reversible causes of seizure (eg. eclampsia, intracranial lesion) j. ICU admission and treatments Initial Management 1. Supportive treatment a. Remember that the vast majority of seizures in the ED resolve in 220 and diastolic BP > 120 mmHg Control seizure with benzodiazepines and Phenytoin Treat increased ICP and cerebral oedema (headache, vomiting, Cushings response: Hypertension, Bradycardia and altered respiratory pattern) with mannitol

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Head Injury Introduction Primary Head trauma • Concussion: Head trauma associated with transient loss of consciousness or amnesia with no evidence of intracranial pathology in CT • Contusion: Focal injuries to brain characterized by coup (beneath area of contact) or countercoup (area remote to contact) • Diffuse axonal injury: Microscopic injuries scattered throughout the brain in a patient in deep coma Secondary Head trauma • Epidural Hematoma: Classically transient loss of consciousness with lucid interval. Hematoma will appear convex in CT. • Subdural Hematoma: Bleeding into subdural space. Hematoma will appear concave in CT. • Intracerebral hemorrhage: Bleeding into brain parenchyma.

Clinical feature •

• • • • • • •

Evidence of head trauma • Scalp laceration, echymosis • Raccoon’s eye: bilateral echymosis of orbits • Battle’s sign: echymosis behind the ear at mastoid process • Hemotympanum • Cerebrospinal fluid rhinorrhoea or otorrhoea Evidence of increasing intracranial pressure Decreasing level of consciousness Falling Glasgow coma score Seizure Cushing’s response: Bradycardia, hypertension, and diminished respiratory rate Dilated pupil associated with decorticates or decerebrate posture A dilated pupil, fall in GCS of two points or signs of cushings response indicated intracranial bleed or swelling. These patients should be transferred only after resuscitation.

Investigation • • • • •

CBC Blood grouping Electrolytes and creatinine Blood sugar CT head • Indications for CT head • Recent intracranial lesion seen on CT • Persisting coma after initial resuscitation • Confusion which persists for > 4 hours • Progressive focal neurological signs • Seizure without full recovery

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• • •

Depressed skull fracture Definite or suspected penetrating injury CSF leak or other sign of base of skull fracture

Management • • • • • •

Cervical spine precaution ABC (secure airway if GCS < 8) Oxygen (high flow) IV access (avoid 5% dextrose) Catheterisation If raised ICP o Elevate head of bed 20-30 degree o Mannitol boluses IV

Referral Criteria • • • •

Mass lesion associated with head trauma Subarachnoid hemorrhage and diffuse axonal injury Ongoing symptoms, disorientation Penetrating head injury

Discharge Criteria • • •

Resolved symptoms Negative head CT Minor head trauma with no loss of consciousness or amnesia and normal neurological examination

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Treatment of raised ICP 1. Supportive measures a. Keep the head in a neutral position to promote venous drainage b. Loosen any constricting bands/collars around the neck c. Anxiolytics and antiemetics 2. Raise head of bed to 30 degrees. 3. Mannitol a. The initial dose of Mannitol is 0.5-1g/kg IV over 15 mins. b. 20% Mannitol contains 20g of Mannitol per 100mL c. For example, in a 50kg patient, 1g/kg corresponds to 50g--which equals 250mL of 20% Mannitol d. Onset-of-action is within minutes. e. Peak action is 1 hour f. Duration of action is 6-8 hours g. Following the initial dose, a common maintenance regimen (in adults) is 100-200mL of 20% Mannitol (ie. 20-40g) IV q6h. h. This is titrated to an osmolality 320mosm/L ii. Altered mental status (eg. confusion, lethargy, stupor, coma) iii. Hyponatremia iv. +/- Renal failure 4. Hypertonic saline (HS) a. Optimal dosing of HS in patients with increased ICP is controversial. b. In patients who are coning, give 150mL of 3% NS wide open. c. For patients with ongoing increased ICP, start an infusion of 3% HS at 30mL/hour--and then titrate to: i. An acceptable ICP ii. Na 3.5 > 5.5

40 20 Stop K infusion

When blood sugar is < 215mg/dl start 5% dextrose infusion

Insulin Blood glucose Insulin infusion (hourly) mg/dl (units/hour) < 70 Stop insulin 70-126 0.5-1 127-200 2 201-360 4 >360 7 Aim for blood glucose fall of 90mg/dl/hour Keep blood glucose at 180-240 for first 24 hours until the Ketoacidosis resolves, maintain with 5% dextrose infusion

If pH < 7.1 Bicarbonate should be added to 0.45% saline infused in 3 hours. Estimation of bicarbonate amount to be infused (mEq): (8 – HCO3 ) x kg ideal body weight x 0.5 If cerebral oedema use manitol.

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Hypokalaemia • •

At the level above 2.0mEq/L Total potassium deficit is 100-200mEq/L to every 1mEq.L reduction in serum potassium At level below 2.0mEq/L Deficient is much higher since a significant portion of exogenous potassium is entreated by kidneys. Total replacement dose required may be greater than estimated

Cause •

•

Renal • With hypertension: Hyperaldostronism, Cushing’s syndrome, corticosteroids • With normal or low blood pressure: Diuretics, renal tubular acidosis Gastrointestinal: Diarrhea, vomiting, bowel obstruction

Management 1. Increase dietary Potassium 2. Oral Potassium • Preferable to IV therapy whenever possible 3. IV potassium • For serious or severe weakness • Emergency situations rate up to 40mEq/hour (Peds 0.3mEq/kg/hr) • Less urgent situations 10-20mEq/hour • Use central line for concentration more than 40mEq/hour • Frequent monitoring of potassium levels when large amounts of potassium is infused

Admission criteria • • •

Requiring IV potassium Dysrrhythmias Serum potassium level < 2.5mEq/L

Discharge Criteria • •

Asymptomatic Able to replace deficiency with oral medicine

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Hyperkalaemia Cause •

• • •

Ineffective elimination • Renal insufficiency • Drugs: ACE inhibitors, NSAID • Addison’s disease Excessive release from cell Burn, tissue necrosis Excessive intake

Management • • •

ABC IV access Cardiac monitor

Hyperkalemia

> 7mEq/L

< 7mEq/L

Treatment No ECG Changes Asymptomatic

No Treatment

ECG Changes: Tall tented T waves Broad QRS Flat P waves Symptomatic Dysrrhythmia Generalised weakness

• 10ml of 10% Calcium gluconate iv over 10 minutes, can be repeated every 10-20 minutes until ECG normalizes • Salbutamol nebulisation (5-10mg) • 50ml 50% of dextrose with 10U plain insulin over 15-30 minutes • 250mg of frusemide over 1 hour (if not responding)

Admission Criteria Potassium level rising continuously

Discharge Criteria Potassium level < 6.0mEq

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Hyponatremia Diagnostic Algorithm for Hyponatremia 1. The following algorithm may be useful for determining the etiology of hyponatremia. 2. In hyponatremic patients, sequentially look at the following: a. Step #1 -- Serum osmolarity b. Step #2 -- Urinary sodium c. Step #3 -- Total body volume Step #1 -- Check serum osmolarity 1. Hyponatremia with decreased serum osmolarity. a. Proceed to Step #2 2. Hyponatremia with normal or increased serum osmolarity a. Etiologies include pseudohyponatremia due to increased: -Lipids (eg. hypertriglyceridemia) -Proteins (eg. multiple myeloma) -Glucose (eg. DKA) 3. The psueudohyponatremia due to increased lipids or protein is an actual lab error which falsely lowers the reading for serum sodium. 4. The decreased serum Na seen with hyperglycemia is often also referred to as "pseudohyponatremia," but this is a misnomer. a. The hyponatremia seen with hyperglycemia is real b. It is caused by interstitial water being dragged into the vasculature by the elevated glucose c. The term "pseudohyponatremia" refers to the fact that the sodium will return to baseline once the hyperglycemia has resolved Step #2 -- Check urinary sodium In patients with hyponatremia and decreased serum osmolarity: 1. High urinary Na concentration (ie. >20-40mmol/L). a. Proceed to Step #3 2. Low urinary Na concentration (ie. 1L/hr ii. Despite the dilute urine, this overwhelms the kidney’s ability to excrete free water-leading to hyponatremia Step #3-- Check total body volume In patients with hyponatremia, decreased serum osmolarity, and high urinary Na concentration: 1. Increased total body volume (ie. edema) suggests the following etiologies: a. CHF b. Nephrotic syndrome c. Ascites d. Surgical third-spacing DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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2. Normal total body volume suggests the following etiologies: a. SIADH b. Hypothyroidism c. Hypoaldosterinism d. Primary adrenal insufficiency e. Medications i. ACE-i or ARBs (decrease aldosterone) ii. Opioids (can cause ADH release) iii. Long-term Carbamazepine use (can cause SIADH) 3. Decreased total body volume suggests: a. Diarrhea b. Over-diuresis c. Cerebral salt wasting

Presentation of Hyponatremia 1. The clinical presentation of hyponatremia depends on both the rate and magnitude of the drop. a. In acute hyponatremia, symptoms can be seen when the Na drops to 40 mmol/L d. Urine osmolality >100 mosmol/L e. Large urinary volume is common, but is not one of the diagnostic criteria. 2. Potential distinguishing characteristics between SIADH and CSW include the following: a. Patients with SIADH are euvolemic and usually have a small volume of urine output b. Patients with CSW are hypovolemic and usually have an large volume of urine output

Treatment of CSW 1. Agressive volume repletion with normal saline. 2. +/- Salt tablets Prognosis of CSW 1. Resolution of CSW usually occurs within 3-4 weeks. 2. Long-term therapy is usually not necessary.

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Diabetes Insipidius

1. DI is caused by either: a. Lack of ADH secretion by the brain ("neurogenic DI") b. Lack of ADH effect on the kidney ("nephrogenic DI") 2. DI is characterized clinically by: a. Diuresis of large amounts of dilute urine b. Resultant hypernatremia and hyper-osmolarity 3. The diagnostic criteria for DI are as follows (although this varies with different sources): a. Serum Na >148 mmol/L b. Serum osmolality >290 mmol/L c. Urine output >400cc/hr x >2 hours d. Urine osmolarity 6-8L in a 24-hour period) b. These agents reduce urine output--which makes fluid replacement logistically easier. c. Vasopressin (ie. ADH) stimuates V1 and V2 receptors. i. V1-receptor stimulation causes vasoconstriction ii. V2-receptor stimulation causes anti-diuresis iii. Vasopression is administered as a continuous IV infusion of 0.01-0.03 U/min (to DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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desired effect) iv. Very low doses can be effective in DI d. Desmopressin ("DDAVP") is a synthetic ADH analogue. i. It only stimulates the V2 receptors--causing antidiuresis without vasoconstriction ii. Its anti-diuretic properties are up to 1,000X stronger than Vasopressin's iii. The dose of DDAVP for DI is 2ug IV q6-12h--titrated to urine output and serum sodium 5. Treatment for nephrogenic DI is complex, and warrants Nephrology consultation.

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Hypoglycaemia Management • • • •

• •

ABC IV access Send blood for investigation Administer dextrose • Adult 50ml of 50% dextrose IV • Children: 25% of dextrose 2ml/kg • Infant: 10% dextrose 2ml/kg Initiate continuous IV infusion of 5-10% of glucose solution Monitor blood sugar 4 hourly

Admission Criteria • •

Recurrent hypoglycemia Failure of neuroglycopenic symptoms (dizziness, confusion, seizure etc) to improve after 1 hour

Discharge Criteria •

Symptoms resolved after 24 hours and Tolerating orally

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Toxicology Contents General Management of Poisoning ............................................................................................................... 148 Toxidromes .................................................................................................................................................... 155 Primary Management of Posoining ............................................................................................................... 156 Tricyclic Antidepressant ................................................................................................................................. 156 Serotonin syndrome ...................................................................................................................................... 156 Clinical feature ........................................................................................................................................... 156 Management .............................................................................................................................................. 156 Anti psychotics ............................................................................................................................................... 156 Extrapyramidal symptoms ......................................................................................................................... 156 Management .............................................................................................................................................. 156 Benzodiazepam .............................................................................................................................................. 157 Clinical feature ........................................................................................................................................... 157 Management .............................................................................................................................................. 157 Paracetamol ................................................................................................................................................... 158 Diagnosis .................................................................................................................................................... 158 Treatment .................................................................................................................................................. 158 Beta Blocker ................................................................................................................................................... 159 Clinical Feature........................................................................................................................................... 159 Management .............................................................................................................................................. 159 Calcium Channel Blocker ............................................................................................................................... 159 Clinical Feature........................................................................................................................................... 159 Management .............................................................................................................................................. 159 Organophosphorous Poisioning (Insectisides) .............................................................................................. 160 Clinical features.......................................................................................................................................... 160 Management .............................................................................................................................................. 160 Zinc Phosphide (Rhodenticides)..................................................................................................................... 161 Clinical features.......................................................................................................................................... 161 Management .............................................................................................................................................. 161 Cypermethrime (Insecticides) ........................................................................................................................ 162 Clinical features.......................................................................................................................................... 162 Management .............................................................................................................................................. 162 Mushroom...................................................................................................................................................... 163 Clinical features:......................................................................................................................................... 163 Investigations ............................................................................................................................................. 163 Treatment .................................................................................................................................................. 163 Carbon Monoxide Toxicity ............................................................................................................................. 164

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General Management of Poisoning

Overview: One of the commonest causes of admission of young adults in the medical ward in Nepal The annual incidence of poisoning is increasing A great challenge to the ER attending physician esp. in our country Presentation to hospital with poisoning is usually an acute medical exacerbation of a chronic psychosocial disorder Apart from infections, self-poisoning is the common easily managed fully reversible conditions Kathmandu University Medical Journal (2006), Vol. 4, No. 1, Issue 13, 100-104 UpToDate Importance of Risk Assessment Approach:  Management of an individual patient requires more than just understanding of the agent ingested.  Intoxications run a discrete, dynamic and usually predictable clinical course. May require time-critical interventions  Attention to the principles of critical care ensures the survival of the vast majority of patients rather than complex maneuvers such as • Decontamination, Enhanced elimination, Antidotes  This approach emphasizes the fundamental importance of an early risk assessment in determining a rational approach to subsequent management

1. 2. 3. 4. 5. 6. 7. 8.

Steps of Risk Assessment Approach: Resuscitation Risk assessment Supportive care and monitoring Investigations Decontamination Enhanced elimination Antidotes Disposition

1. Resuscitation  Always manage from Airway Breathing Circulation o Intubation, O2, Establish IV, Cardiac monitor  Detect & correct o Seizure control  Always generalised when due to toxicologic causes  Benodiazepines first line Rx  Barbiturates 2nd line DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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o o o o

 Phenytoin is of no use. Correct hypoglycemia  Rx if BS< 70mg/dl ; 50ml of 25% dex(5ml/kg 10% in child) Correct Hypo/hyperthermia  Temp > 38.5 C prompts urgent intervention Consider coma cocktail  Thiamine, 50% Dex, Naloxone Emergency antidotes administration  Sometimes indicated in resuscitation phase  eg. Atropine in OP, Naloxone in opioid, NaHCO3 in TCA

2.   

Risk Assessment Start as soon as possible, only resuscitation is a greater priority It is a distinct quantitative cognitive step to predict the likely clinical course & potential complication Helps in the subsequent management steps o Supportive care, Screening, decontamination…  In the majority of cases it reassures the clinician that basic supportive care will be sufficient to ensure a good outcome I. Agents II. Doses III. Time since ingestion IV. Current clinical features and progress V. Patient factors ( Wt. & co-morbidities)  The agent, dose & time since ingestion should correlate with patient’s current clinical status. If not Risk assessment needs to be reviewed  When altered mental status prevents an accurate history – Tablet counts – Collateral history from family and friends – Correlation of clinical status with toxico-epidemiologic trends

Risk Assessment Clinical Features:  Neurological examination  Mental Status (GCS)  Pupil size  Muscle tone/movements  Reflexes/clonus  Focal signs  Bowel sounds DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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 Urinary retention  Skin  Pressure areas  Colour  Sweating  Bullae  Evidence of trauma 3. Supportive Care and Monitoring Good supportive care prevents complications • Hypoxic brain injury • Pulmonary aspiration-atelectasis • Pressure injuries – compartment syndromes – rhabdomyolysis • Urinary retention • Acute renal failure • Hyperthermia • Traumatic injuries secondary to agitated delirium • Airway Intubation • Breathing O2 , Ventilation • Circulation IV fluids, Inotropes , Control hypertension • Sedation Titrate IV benzodiazepines • Seizure control & prophylaxis Titrate IV benzodiazepines • Metabolic Ensure euglycaemia , Electrolytes • Renal function Adequate hydration, Haemodialysis • General Respiratory care, Bladder care, Pressure areas, Thrombo-embolism prophylaxis, Nutrition, Mobilisation Criteria for Admission in ICU include requirements for: a) Airway control/ Ventilation b) Prolonged or invasive hemodynamic monitoring / support c) Haemodialysis Criteria for admission in Emergency Observation Unit: a. Ongoing cardiac monitoring not required b. Adequate sedation achieved c. Clinical deterioration not anticipated

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4. Investigation:  Either as screening test or for specific purpose  Recommended screening test : o ECG (readily available, non invasive)  May identify potentially lethal cardiac conduction abnormalities eg. TCA o Serum Paracetamol level (universal analgesic;  send at the time of presentation ; If confirmed ingestion  after 4 hrs o Plasma Cholinesterase level ( most common in our context)  Not correlate well with the severity of poisoning.  A depression of 25% or more is strong evidence of excessive organophosphate absorption.

 Serum cholinesterase level did not correlate with the total dose of atropine Prognostic Value of Serum Cholinesterase in Organophosphate Poisoning Nouira S. et al, CHEST.1994;106(6):1811-1814. doi:10.1378/chest.106.6.1811  Monitoring serial levels can be used to determine a response to therapy  Indication for other investigation:  Used to answer specific questions  Drug levels may refine the risk assessment or identify specific intervention thresholds  Paracetamol  Digoxin  Valproic acid  Carbamazepine  Iron  Salicylate 5.         

Decontamination The objective is to decrease the absorbed dose Not a routine intervention Decisions regarding decontamination are always based on the risk assessment in that particular individual Human volunteer trials and retrospective studies suggest that decontamination helps some patients Benefit from GI decontamination is most likely when it can be performed within one hour of poison ingestion GI decontamination is most likely to benefit patients that: Present for care soon after ingestion Have ingested a poison and amount suspected to be toxic Are symptomatic on presentation

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 Do not have clinical factors (such as CNS depression) that make decontamination dangerous  Potential risks : o Pulmonary aspiration ; Hypoxia ; Laryngospasm; Hypothermia o GI complication  Bowel obstruction, perforation, MW tear o Water intoxication esp. in children o Distraction and diversion of staff &resources from resuscitation and supportive care priorities  Forms of GI Decontamination o Induced emesis • Ipecac: No role for Ipecac in management of overdoses in the ED setting o Gastric Lavage • The amount of toxin removed by gastric lavage is unreliable and negligible if performed after the first hour • Does not confer any clinical benefit when performed routinely on unselected patients • Despite huge spread use of multiple gastric lavages for OP pesticides poisoning across Asia, there is currently no high quality evidence to support its clinical effectiveness . [Systematic review of controlled clinical trails of Gastric Lavage in acute OP pesticides poisoning Li Y et at Clin toxicology (phila) 2009 Mar:47(3):179-92 ; ED , Peking Union Medical College Hospital, Chinese Medical Academy and Pekin Union Medical college,Beijing] o Activated Charcoal • Benefit must outweigh risk • Aspiration can cause severe lung injury • In Pediatric population in Australia, from natural poisons info data, pediatric deaths are due to 2 reasons: 1. Opiates 2. Activated charcoal aspiration • Oral Activated Charcoal is generally the preferred method of decontamination. • In the intubated patient AC may be given via oro- or nasogastric tube after tube placement is confirmed. o Whole bowl irrigation Potentially Useful  Iron overdose >60mg/kg  Slow-release KCl ingestion > 2,5 mmol/kg  Life threatening slow-release Verapamil / Diltiazem ingestion  Lead ingestion  Body packers PEGLEC 500 – 2000 ml/hr via NG (25cc/kg/hr peds) DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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4-6 hours duration 6. Enhanced Elimination  The objective is to move the agent away from the target organ o at a rate much greater than achieved by endogenous elimination o when other therapies cannot guarantee a good outcome  Indicated in specific poisonings  Relies on specific pharmacokinetic properties of the agent  Multiple dose activated charcoal for o Carbamazepine o Theophylline o Phenobarbitone o Quinine o Dapsone poisoning o Manipulation of urinary pH o Salicylate o Phenobarbitone  Haemodialysis o Toxic alcohols o Salicylate o Theophylline o Valproic acid o Carbamazepine o Metformin lactic acidosis o Potassium o Lithium o Amanita cyclopeptide mushroom 6. Antidotes Drugs with specific properties used to decrease or treat the effects of poisoning All have i. Specific indications and contraindications ii. Methods of administration iii. Monitoring requirements iv. Therapeutic endpoints v. Adverse effect profiles 7. Disposition • Patient must be admitted to an environment capable of providing

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 Adequate level of monitoring & supportive care •

•

Risk assessment determines: • Appropriate duration of observation • Time of likely maximal clinical effects • Duration of cardiac and respiratory monitoring • Duration of observation for seizures and / or CNS depression Allows early planning for appropriate medical and psychosocial disposition. ICU Admission Unstable patient Potentially lethal overdose Cardio toxic overdose Hospital Admission Moderately symptomatic patient with low fatality potential

A Need of Emergency Observation Unit.  Have been established in many ED of different countries  Ideally located adjacent to ER  To provide short term focused goal- oriented care.  EOU have been remarkably successful in:  Efficient treatment in suitable condition  Reducing total bed days  Increasing patient satisfaction  Reducing inappropriate discharge and lawsuit. Never Discharge with out Psychiatric counselling .

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Toxidromes Toxidrome Opoid

Representative Agent Morphine

Sympathomimetic

Cocaine

Most common findings CNS depression, miosis, respiratory depression

Psychomorot agitation, mydriasis, diaphoresis, tachycardia, hyperthermia Cholinergic Organophosphorous Muscarinic effects – Salivation, lacrimation, diaphrosis, nausea, vomiting, urinatin, defecatin, bronchorrhea Nicotinic effect – muscle fasciculation, weakness Anticholinergic Aropine Altered mental stats, mydriasis, dry flushed skin, urinary retention, decreaed bowel sound, hypethermia, dry mucous membrane Sedative Hyptonics Barbiturates, Depressed level of Benzodiazepines consciousness, slurred speech, ataxia

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Additional findings Intervention Hypothermia, bradycardia, death may be due to respiratory arrest or acute lung injury Seizure, rhabdomyolysis, MI, death may be due to seiqure, cardiac arrest, hyperthermia Bradycardia, miosis, seizures, respiratory failure, paralysis. Death may be fom respiratory arrest, bronchorrhoe or seizure

Ventilation or Naloxone

Seizure, dysrhythmias, rhabdomyolysis, death may be from hyperthermia and dysrhythmias

Physostigmine, sedation with benzodiazepines, cooline, supportive management

Stupor to coma, depressed rspirations, apnea, bradycardia

Ventilatory support

Cooling, sedatin – benzodiazepam, hydration

Airway protection and ventilation. Atropine, parlidoxime

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Primary Management of Posoining Tricyclic Antidepressant Properties of TCA Antihistamine Anticholinergic Norepihephrine post synaptic antagonist Serotonin Na channel block

Effect on overdose Sedation Altered mental status, dry Hypotension

Management Symptomatic Symptomatic Norepinephrine

Serotonin like syndrome Wide QRS

K channel block

Prolong QT

Cyproheptadine Sodium bicarbonate 1-2 meq/kg till pH is 5.5 to 7.55 Magnesium sulphate

Serotonin syndrome Clinical feature Altered mental status, increase muscle tone, hyperreflexia, hyperthermia, intermittend body tremor, death may be dur to hyperthermia

Management 1. Cooling 2. Sedation with benzodiazepam 3. Cyproheptadine a. 4-10 mg po stat b. If responding 4 mg 6 hourly for 48 hurs c. If not responding then repeat dose in 2 hour up to total 32 mg

Anti psychotics Extrapyramidal symptoms 1. Early onset reversible – hours to days a. Acute dystonia – hyperkinetic movemen disorder b. Akathsia – subject sensation of morot restlessness 2. Delayed onset reversible – days to week a. Parkinsonism and Neuroepileptic malignant syndrome (Tetrad: Fever, Muscle rigidity, Autonomic dysfunction, Altered mental status) 3. Irreversible – Months to years a. Tardive dyskinesia

Management 1. Withdrawal of drug 2. Intubation and paralysis with non depolarizing agent 3. Dantrolene 0.5-2.5mg/kg then 1mg/kg 6 hourly (should not be used with calcium) DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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Benzodiazepam Short acting Midazolam Alprazolam Intermediate acting Lorazepam Long acting Clonazepam Diazepam

Onset

Half life

Duration of action

1 minute 1 hour

2 hours 3 hours

3 hours 6 hours

5 minutes (IV)

Less than 12 hours

12 hours

1 hour 1 min (IV)

12 hour 12 hour

20-80 hour 20-50 hour

Clinical feature 1. 2. 3. 4.

Dizziness, confusion, ataxia, incoordination, coma Anterograde amnesia (Lorazepam, Midazolam) Respiratory depression, Hypotension Propylene glycol as diluent in parentral Diazepam and lorazepam causes severe metabolic acidosis, nephrotoxicity, hyperosmolar satate if more than 1 mg/kg/day

Management Flumazanil 0.2 mg iv upto 3 mg (Half life 1 hour)

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Paracetamol Time Clinical features

Stage I 24 hours Anorexia, Nausea, Vomiting, malaise

Stage II Day 2-3 Improvement

Lab

Hypokalaemia

Increase AST, BP, Bilirubin

Stage III Day 3-4 Anorexia, Nausea, Vomiting, Encephalopathy, Anuria, Jaundice Acidosis, Coagulopathy, Renal failure, Pancreatitis

Stage IV Day 5 Recovery or Death

Diagnosis Adult: More than 10 gm or 200mg/kg as single dose or over 24 hours More than 6 gm or 150mg/kg over 24 hours for 2 days Acetaminophen level should be sent at 4 hours Four hour acetaminophen level • 200 microgrm/ml with AST more than 1000 – Mortality 5%, Hepatotoxicity 30% • 300 microgram/ml with AST more than 1000 – Mortality 5%, Hepatotoxicity 90% • Less than 150 microgram/ml with AST more than 1000 – Mortality 0%, Hepatotoxicity 1%

Treatment N- Acetylcystiene 150mg/kg in 200 ml 5% dextrose over 60 minutes then 50mg/kg in 500 ml 5% dextrose over 4 hours then 100mg/kg in 1000 ml 5% dextrose over 16 hours Monitor for Anaphylactoid reaction

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Beta Blocker Clinical Feature • • •

Cardiac: Hypotension, Bradycardia, Asystole, Conduction delays, Decrease contractility CNS: Decrease mental status, coma, seizure PulmonaryL Bronchospasm

Management • • • •

GI Decontaminaiton: Activated choarcoal or Whole bowel irrigation Glucagon: 0.05-0.15mg/kg bous followed by 1-10mg/hour as maintenance Adernergic receptor agonist: Norepinephrine, Dopamine Hyperinsulinemia-Euglycaemia Therapy: Insulin 1unit/kg then 0.5unit/kg/hour with 50% 50 ml Dextrose bolus and maintenance with dextrose solution (Monitor Potassium) • Atropine for bradycardia • Calcium: 10% of 10ml Calcium Gluconate • Phosphodiesterase inhibitor • Sodium bicarconate: if wide QRS

Calcium Channel Blocker Clinical Feature • • •

Hypotension, Braducardia, Shock Cardiogenic and non cardiogenic pulmonary oedema Seizure, delirium

Management Management similar to beta blocker, lipid emulsion is also helpful

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Organophosphorous Poisioning (Insectisides) • • •

Garlic like odour Nuvan (Dichlorovos): Blue liquid in small glass bottle Metacid (Methyl parathion): White liquid in metal container

Clinical features • • •

Muscarinic (DUMBELLS): Defecation, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, salivation Nicotinic: Muscle weakness, Fasciculation, Tachcardia, Cramping of skeletal muscle, Hypertention, Hiaphoresis, Mydriasis CNS: Anxiety, restlessness, lethargy, confusion, coma, seizure, respiratory & CNS depression

Management 1. ABC 2. IV access: give 1-2 liters of IV fluids depending upon the amount of fluid loss 3. Decontamination: • Wash the skin and remove the contaminated clothes if poison is spilled in the skin or in patients with dermal exposure • Gastric lavage only after stabilizing (and incubating a comatose) patient who arrives within 1-2 hours of ingestion of poison. • Give activated charcoal (1gm/kg) at the end of gastric lavage and 8 hourly for 24 hours 4. Atropinization • Give atropine 3-5 ampoules (0.5 mg each ampoule) IV stat and every 5 minutes until the patient is fully atropinized (heart rate > 120bpm, dilated pupils, absence of wheeze in chest, systolic BP>90 mmHg and dry mouth and axillae). A uniform improvement in most of these parameters is essential, not in only one or two. • In children give atropine 0.01- 0.05mg/kg/dose as required not less than 0.1mg total dose (if total dose 120/min). Reduce atropine by 25% and give diazepam if severe agitation 5. Cholinesterase reactivators (Oximes): Parlidoxime 1gm 4-6 hourly (or 8mg/kg/hour). In children2550mg/kg over 5-10 minutes, not more than 4mg/kg/min 6. Diazepam if severe agitation or seizure

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Zinc Phosphide (Rhodenticides) Clinical features • • • •

Nausea, vomiting (Early symptoms) Tightness in chest, excitement, agitation, thirst, feeling of cold Later may develop shock, oliguria, coma and convulsion May develop: Pulmonary oedema, metabolic acidosis, hypocalcaemia, liver damage, bradycardia, ST and T wave changes and thrombocytopenia

Management • • • • • •

ABC Oxygen Gastric lavage within 30 minutes post ingestion Administration of activated charcoal mixed with water Admission for 48-72 hours to observe the development of delayed onset of pulmonary oedema Cardiac monitoring

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Cypermethrime (Insecticides)

Cypermethrin is a synthetic pyrethroid insecticide used to kill insects on cotton and lettuce, and to kill cockroaches, fleas, and termites in houses and other buildings.

Clinical features • • •

Type I hypersensitivity: Anaphylaxis or irritant action to the exposed mouth, lips, eyes or skin. Ingested in large doses it may produce neurotoxicity like, tremor, fasciculation, convulsion, coma and even respiratory failure It also causes increased salivation, upper gastrointestinal bleeding, and rarely renal failure.

Management • • • • • •

ABC Oxygen Secure IV line NG wash Charcoal through NG tube Supportive management

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Mushroom Amanita Phalloids appropriately called “death cap” accounts for the majority of cases.

Clinical features: • • •

•

•

Poisoning is characterized by a latent period of 6-12 hours after ingestion (range 6-48 h), during which the patient is asymptomatic. Some patients may present with GI symptoms earlier than 6 hours At the end of this latent period, a sudden and severe gastroenteritis like illness phase occurs • Abdominal pain • Vomiting, • Profuse watery diarrhea, • Electrolyte abnormalities • Circulatory collapse in young and elderly persons. This phase, which may last as long as 2-3 days, is followed by an apparent recovery phase • Characterized by an apparent clinical improvement • Asymptomatic rise in hepatic enzyme levels signifies the onset of hepatic necrosis The third phase of • Jaundice • Hypoglycemia • Coma • Multi organ and system failure followed by death

Investigations • • • •

CBC Blood sugar, electrolytes, createnine LFT: Liver enzymes usually raises after 36-72 hours PT/INR

Treatment • • • •

ABC Hydration Gastric lavage Decontamination with charcoal

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Carbon Monoxide Toxicity

Physiology 1. Hemoglobin a. Each molecule of hemoglobin contains four "heme groups"--each of which holds a molecule of iron. b. When the iron molecule is in its reduced state (ie. Fe2+), it can bind a molecule of oxygen. c. When the iron binds a molecule of oxygen, it is oxidized to its oxidized state (ie. Fe3+). d. When oxygen binds to any of the four heme groups, this promotes oxygen binding at the remaining three heme groups. i. As such, hemoglobin is usually either fully bound to oxygen ("oxyhemoglobinemia") or is bound to no oxygen ("deoxyhemoglobinemia") e. After an oxygen molecule leaves a heme group, the Fe3+ is reduced back to Fe2+ by the enzyme "NADH-MetHb reductase.” 2. Unfortunately, instead of oxygen, a heme group can also bind carbon monoxide--resulting in carboxyhemoglobinemia (COHb). a. When CO is bound to one of the heme groups, the other three heme groups hold onto their oxgyen molecule more tightly (ie. the Hb-dissociation curve is shifted to the left) 3. Pulse-oximetry a. Different molecules preferentially absorb different wavelengths of light. i. As such, the "absorption spectra" of a substance can be used to identify it b. The absorption spectra of oxyhemoglobin and deoxyhemoglobin are different. i. Therefore, the relative amounts of oxyhemoglobin vs. deoxyghemoglobin in a blood sample can be determined c. A regular pulse-oximeter uses only two wavelengths of light. i. It can only read Hb as either "oxygenated" or "deoxygenated" ii. Standard pulse-oximetry cannot differentiate between oxyhemoglobin and COHb iii. Therefore, with significant COHb, a standard pulse-oximeter typically reads 100% saturation 4. A "co-oximeter" is similar to a pulse-oximeter, but it uses >4 wavelengths of light--which allows distinction between: a. Oxyhemoglobin b. Deoxyhemoglobin c. COHb d. MetHb/SulfHb Carboxyhemogloblinemia (COHb) 1. Carbon monoxide (CO) is produced from incomplete combustion of hydrocarbons (HC). a. Complete HC combustion produces only CO2 and H20 2. CO is an odorless, colourless gas. a. It is typically only detectable in the environment using a CO detector 3. CO toxicity should be considered in any patient presenting with new-onset neurological symptoms (especially if other people/animals in the home/workplace are also affected). Etiologies of COHb DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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i. ii. iii. iv.

Cigarette smoke City pollution Car exhaust Space-heaters

4. Fires a. Several materials release both CO and cyanide when they burn. b. Concomitant cyanide toxicity should be considered in fire victims with a lactate >10mmol/L Pathophysiology of COHb toxicity 1. CO binds to numerous substances much more strongly than oxygen--including: a. Hb b. Myoglobin (ie. heart tissue) c. Numerous tissues throughout the body d. Cytochrome aa3 (ie. an essential molecule in the electron transport chain and aerobic metabolism) 2. Hemoglobin's affinity for CO is 240X stronger than its affinity for oxygen. a. As such, once bound to Hb, CO will only dissociate off in the pulmonary capillaries (because of competitive binding by oxygen). b. This process is relatively slow on room air, but much faster when the patient is breathing 100% oxygen (see below). c. Fetal Hb binds CO more strongly than adult Hb. i. As such, fetal COHb levels are typically 10-15% higher than maternal levels 3. When CO binds to cardiac myoglobin, it can result in profound myocardial dysfunction. 4. Once dissolved in the plasma, CO can diffuse into numerous peripheral tissues. a. This is likely responsible for most clinical CO toxicity i. Tissue CO levels correlate far better with morbidity/mortality than hemoglobin-CO levels b. In general, prolonged exposure to low-to-moderate dose CO is much worse for a patient than brief exposure to high-dose CO. Symptoms of CO Toxicity 1. Non-specific CV and CNS symptoms predominate: a. CV (eg. angina, arrhythmias, myocardial depression) b. CNS (eg. amnesia, difficulty concentrating, dizziness, weakness, somnolence, seizures, coma) 2. Other potential complications of CO toxicity can include: a. Hypotension--caused by both myocardial depression and systemic vasodilation b. Rhabdomyolysis c. Non-cardiogenic pulmonary edema d. DIC e. ARF 3. The CNS sequelae of CO toxicity are not simply secondary to hypoxia. DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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a. CO is directly toxic to the basal ganglia and hippocampus 4. Delayed neurological sequelae (DNS) are seen in up to 40% of patients with significant CO exposure. a. The onset of these symptoms is anywhere from 3 to 240 days after recovery (although most occur within 20 days). i. The precise mechanism is unknown b. Symptoms can include: i. Headache and fatigue ii. Variable cognitive deficits iii. Personality changes iv. Movement disorders v. Focal neurologic deficits c. Mild DNS symptoms resolve in nearly all patients by 2 months i. Severe DNS symptoms resolve in 75% of patients by 1 year. d. The development of DNS correlates poorly with COHb levels. COHb Levels 1. For the reasons discussed above, COHb levels are generally a poor marker of CO toxicity. a. They do not correlate strongly with either morbidity nor mortality b. Nonetheless, they remain commonly cited in the literature--and are therefore discussed below 2. Normal COHb levels are: a. 0-3% in rural dwellers b. 3-5% in city dwellers c. 5-15% in smokers 3. The following "classical" COHb symptoms are frequently cited: a. 10-20% COHb-- Headache, malaise b. 30% -- Impaired judgment c. 40%-50% -- Confusion, decreased LOC, possible death d. 60% -- Seizures, cardiovascular collapse, probable death e. 80% -- Rapidly fatal Testing in Suspected CO Toxicity 1. EKG 2. Co-oximetry a. Not simple pulse-oximetry (which will read the sats as 100%) 3. Lactate 4. CK and Troponin 5. CXR Treatment of CO Toxicity 1. 100% O2 DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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a. All patients should be given 100% O2 by NRB or ETT. b. The half-life of COHb is: i. 4 hours on room air ii. 45-90 minutes on 100% O2 iii. 23 minutes on 3atm of hyperbaric oxygen 2. +/- Hyperbaric oxygen (HBO) a. Despite its widespread use, HBO is likely not an effective treatment for CO toxicity. b. If effective, it is only effective at reducing delayed neurological sequelae (see above) i. It is not a life-saving measure

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Common Problems Contents Alcohol Intoxication ....................................................................................................................................... 168 Alcohol Withdrawal ....................................................................................................................................... 170 Diagnosis Nomenclature ............................................................................................................................ 170 Diagnosis, Initial Assessment and Investigations ...................................................................................... 170 Investigations ............................................................................................................................................. 171 Management .............................................................................................................................................. 171 Criteria for Ambulatory Detoxification ...................................................................................................... 172 Disposition ................................................................................................................................................. 172 On follow up at Alcohol clinic .................................................................................................................... 172 Motivational Interview .............................................................................................................................. 173 If not improving.......................................................................................................................................... 173 Dyslipidemia ................................................................................................................................................... 174 Diagnosis Nomenclature ............................................................................................................................ 174 Diagnosis, Initial Assessment and Investigation ........................................................................................ 174 Investigations ............................................................................................................................................. 175 Management .............................................................................................................................................. 175 Antibiotics Protocol........................................................................................................................................ 179 Undifferentiated Fever in Adult Patients................................................................................................... 179 Upper Respiratory Tract Infections............................................................................................................ 179 Urinary tract infection................................................................................................................................ 180

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Alcohol Intoxication

It is important to remember that sick patients drink alcohol (to numb the pain) and people who drink alcohol frequently become ill. The diagnosis of alcohol intoxication is therefore a diagnosis of exclusion. Differential diagnosis: Head injury, other toxin, hypoglycemia, drug toxicity, extreme vertigo, psychosis, sepsis including meningitis, hepatic encephalopathy. THINGS THAT COMMONLY KILL THESE PATIENTS 1. 2. 3. 4.

Airway problems (respiratory depression, aspiration) Hypoglycaemia Associated injury/ illness or toxin Hypothermia

•

Patients who have drunk alcohol are difficult to assess, often aggressive or uncooperative, frequently unkempt or smell bad. They will test your medical skill, your compassion and your professionalism to the limit.

•

Emergency medicine involves treating substantial numbers of patitents with alcohol related illness and injury. Most ward based jobs do not. ED staff must accept the challenge of the special role.

Effects Alcohol produces effects to anesthetic agents. Blood level mg% 50-100

Impaired co-ordination

100-150

Difficulty with gait/balance

150-250

Lethargy, difficulty sitting

300

Coma

400

Respiratory depression

Peak alcohol levels occur usually 30-40 minutes after ingestion •

Rapid absorption from the stomach makes washouts of little value.

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• • • • • • •

Put them on a trolley with sides, have them in the recovery position at all times. If they need the toilet give them a bed pan or have them accompanied. Take a rectal temperature and commence warming measures of below 95 degrees F Site an IV line, push 50mls of 50% dextrose then start a dextrose drip 6 hourly Give 100mg of IV thiamine Ask for, or do yourself, hourly observations of GCS, pulse, temperature and respiratory rate. If the respiratory rate goes below 12 consider the intubation and ventilation may be required If the GCS if falling, or if the patient fails to regain consciousness after 6 hours then the diagnosis of alcohol toxicity is probably wrong and should be reviewed.

ROAD TEST Before discharge from ED you must be convinced that a patient who comes alone can travel home without further injury. He/she must therefore • •

Be able to walk steadily Be lucid

When you discharge the patient you should, if patient presented with severe intoxication 1. Assess the possibility that patient will develop delirium tremens. If this is already frank then admit the patient. Otherwise prescribe 10-20 mg Diazepam, four times per day orally for those who consider a 2. t risk. 3. Make a follow up arrangement in OPD for three days later where the possibility of chronic alcohol abuse can be dealt with. RESTRAINT Intoxicated patient frequently cause trouble. A calm and friendly approach is least likely to end in the patient becoming violent. It may be necessary to tie the patient. Tie all four limbs to a trolley with the patient prone (on his/her face) to prevent or biting. 2.5 mg haloperidol may be additionally required.

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Alcohol Withdrawal Diagnosis Nomenclature Diagnosis

CIWA Ar Score

Other Diagnosis

Alcohol Abuse/Uncomplicated Alcohol Withdrawal/ Withdrawal Seizure/Alcoholic Halllucination/DT

Score

HTN, DM etc

e.g: Alcohol Withdrawal Seizure, CIWA Ar 18 with Hypertension

Diagnosis, Initial Assessment and Investigations Alcohol abuse Alcohol abuse is pattern of alcohol use associated with one or more of the following: • Failure to fulfill role obligations (eg, at work, school or home) • Recurrent substance use in physically hazardous situations • Recurrent legal problems related to substance use • Continued use despite alcohol-related social or interpersonal problems Alcohol dependence Alcohol dependence is pattern of use associated with three or more of the following: • Tolerance • Withdrawal • Substance taken in larger quantity than intended • Persistent desire to cut down or control use • Time is spent obtaining, using, or recovering from the substance • Social, occupational, or recreational tasks are sacrificed • Use continues despite physical and psychological problems Withdrawal

Uncomplicated Alcohol Withdrawal • • • • • • •

Insomnia Tremulousness Mild anxiety Gastrointestinal upset; anorexia Headache Diaphoresis Palpitations

Withdrawal Seizure Withdrawal-associated seizures are generalized tonic-clonic convulsions that usually occur within 12 to 48 hours after the last drink, but may occur after only two hours of abstinence. The seizures occur predominantly in patients with a long history of chronic alcoholism.

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Alcoholic Hallucination and Delirium Tremens Features

Alcoholic Hallucination

Delirium Tremens

Onset

12-24 hours

24-48 hours

Resolves

24-48 hours

7 days

Clouding of consciousness

Present

Absent

Hallucination

Usually Visual

Auditory and Tactile

Vital signs

Normal

Tachycardia, hypertension, fever, agitation, and diaphoresis

Investigations • • •

Complete blood count, serum electrolytes, glucose, liver function and renal function tests, urinalysis Premenopausal women should have an HCG test. An EKG is suggested for patients over 50 years, or if there is a history of cardiac problems. A chest xray may be indicated for patients with chronic respiratory problems or respiratory symptoms.

Management Minor withdrawal

Diazepam 10 to 20 milligrams orally OR Chlordiazepoxide 50 to 100 milligrams orally OR Lorazepam 2 to 4 milligrams IV every 1 to 2 hours until CIWA-Ar scores are 15 or DTs should be hospitalized for more aggressive treatment and careful monitoring) Able to take oral medications Has a reliable family member or close contact who can stay with the patient throughout the detoxification period (usually three to five days) and monitor the patient for worsening symptoms. Able to commit to daily medical visits No unstable medical condition Not psychotic, suicidal, or significantly cognitively impaired Not pregnant No concurrent other substance abuse that may lead to withdrawal (ie, sedative withdrawal) No history of DTs or alcohol withdrawal seizures

Disposition • • • •

CIWA-Ar score 15 - Psychiatric referral for admission

On follow up at Alcohol clinic Assessment of at risk drinking • Greater than 14 drinks per week or four drinks per occasion for men • Greater than seven drinks per week or three drinks per occasion for women • Evaluation of stage of change (Need to document on each visit) o Precontemplation: Not thinking of quitting o Contemplation: Accepting need of quitting o Preparation: Makes plan to quit o Action: Acts on plan to quit o Maintenance: Quits DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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o

Relap: Starts again

Motivational Interview Four-session, brief-contact intervention based on MI involving comprehensive assessment of drinking and related behaviors and feedback Four Basic Skills of Motivational Interview (OARS) 1. Open ended Question: Questions that cannot be answered with limited response like “Yes”, “No” 2. Affirmations: Acknowledging positive behaviour and strength 3. Reflective listening: Paraphrasing comments by repeating back what they have said 4. Summary statements: Putting together what they have said Five principles of motivational interview (DEARS) - Sample questionnaire in appendix 1. Develop discrepancy: Creating the gap between where the person has been and where is he/she now. 2. Express Empathy: Listening to get their ideas and concerns. When people feel to be understood, they are more likely to open up to share experiences 3. Amplify Ambivalence: Ambivalence to change is normal. However it can be paralyzing and causes some people to stuck. By verbalising and recognising ambivalence you help people to acknowledge their ambivalence by discussing it with them and and exploring two different sides they are dealing with, which can help them work through it. 4. Roll with resistance: Forcing, threatening and imposing will not work. Resistance is a tell tale sign for interviewer to respond differently. Encourage people to come up with their own solution. 5. Support self efficacy: Person’s belief in understanding that change is possible is important motivator in making change. There is no right way. Specific plan for change may not work. People may come with different plan.

If not improving Referral for CBT or Anti craving therapy

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Dyslipidemia Diagnosis Nomenclature Diagnosis

ASCVD Risk Score ASCVD Risk = 8%

Statin or non statin Other Diagnosis therapy Dyslipidemia ( Not started DM, HTN, Metabolic LDL, HDL) For primary prevention Syndrome etc For secondary prevention e.g. Dyslipidemia ( LDL, HDL) with ASCVD Risk Score 8% on Statin therapy for primary prevention with Metabolic Syndrome

Diagnosis, Initial Assessment and Investigation • •

• •

•

Screening recommended for Age more than 20 years Identification of four statin benefit group 1. Individual with clinical ASCVD (Atherosclerotic cardiovascular disease) 2. Individual with primary elevations of LDL-C ≥ 190mg/L 3. Individuals 40 to 75 years of age with Diabetes with LDL-C 70-189mg/L 4. Individuals without clinical ASCVD or diabetes who are 40-75 years of age with LDL-C 70189mg/L and estimated 10 years ASCVD risk of 7.5% or higher ASCVD risk calculators are available online or application stores. Alternatively score sheet given in appendix can be used. Causes of secondary dyslipidemia to be evaluated o Diabetes o Hypothyroidism o Obstructive liver disease o Chronic renal failure o Drug that increases LDL-C, and decreases HDL-C (Progestins, anabolic steroids and corticosteroids) Evaluation for Metabolic Syndrome Risk Factor Defining Level Abdominal Obesity • Men • >102 cm (>40 in) • Women • >88 cm(>35 in) Triglycerides ≥ 150mg/dl HDL Cholesterol • Men • 400mg/dl RelativeTG>200mg/dl

LDL - 5-25% HDL- 15-35% TG- 20-50%

Gemfibrozil – 600mg BD Fenofibrate – 200mg

Absolute- Chronic liver disease, severe gout Relative – Diabetes, Hyperuricaemia, Peptic ulcer disease Absolute- Severe renal disease, Severe hepatic disease

LDL - 5-20% Dyspepsia (May increase in Gall stone patient with high Myopathy TG) HDL- 10-20% TG- 20-50% *Macrolid antibiotics, Anti fungal agent, Cytochrome P450 inhibitor (Niacin and Fibrates should be used with great caution) Dietary Advice • Emphasize intake of vegetables, fruits, and whole grains

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• • • •

Include low fat dairy products, poultry fish, legumes, non tropical vegetable oil and nuts Limit intake of sweet, sugar, beverages and red meat Reduce saturated fats and Trans fats Lower sodium intake, no more than 2400mg/day

Exercise • Moderate to severe intensity aerobic exercise • 3 to 4 session in a week • Each session lasting 40 minutes On follow up Indicators of anticipated therapeutic response and adherence to selected statin intensity • High intensity statin therapy reduces LDL-C approximately ≥ 50% from the untreated baseline • Moderate intensity statin therapy reduces LDL-C approximately 30 to < 50% from the untreated baseline Access medication and lifestyle adherence – Fasting lipid panel • If anticipated therapeutic response achieved then follow up in 3 to 12 month • If less than anticipate response o Access for intolerance and if present management of intolerance o If no intolerance • Exclude secondary cause and or • Reinforce adherence and or • Increase statin therapy and or • Addition of non-statin therapy • Follow up 4-12 week • Decreasing statin therapy can be considered when two consecutive values of LDL-C levels are below 40mg/dl

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Antibiotics Protocol Undifferentiated Fever in Adult Patients Documented fever of 38° or more for 3 or more days with no clear focus of infection on preliminary physical examination and laboratory tests. If patient is in shock or is septic, disregard this guideline. First choice •

For non diabetics and age below 50

•

Gatifloxacin 10 mg\kg\day, OD, for 7 days. Needs consultant’s co signature.

Second choice •

Azithromycin 20 mg\kg\day not exceeding 1 G OD for 7 days.

Third choice •

Ofloxacin or Levofloxacin 20 mg\kg\day for 7 days in 2 doses.

Upper Respiratory Tract Infections 1. Patients presenting with predominant nasal symptoms (nasal discharge, blockade/stuffiness, itching) with or without cough, throat discomfort, fever and myalgia and duration less than five days: No Antibiotics, review again in 3 days. 2. Patients presenting with predominant throat pain and fever WITHOUT nasal symptoms: Consider antibiotics only if throat examination reveals pharyngeal or tonsillar exudates 3. Patient with progressive or persistent nasopharyngeal symptoms as in '1' above and duration more than 5 days: consider Antibiotics (Azithromycin preferred to cover adult pertussis and atypical organisms as well) 4. Persistent fever and dry cough with no localizing signs: treat as 'undifferentiated febrile illness' (refer to 'fever' protocol) Choice of Antimicrobial 1. Cap Amoxicillin 500 mg thrice daily for 10 days 2. Tab Azithromycin 500 mg daily for 5 days (if penicillin allergic) (Applicable only in hemodynamic ally stable patients)

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Urinary tract infection Uncomplicated UTI (Otherwise well patients without major comorbidities who are not pregnant, not recently hospitalized, not catheterised and not thought to have any abnormal urinary tract anatomy and with normal renal function( GFR< 60ml/min) Acute cystitis  Absence of fever, flank pain or any other signs and symptoms of pyelonephritis  Able to take oral meds Choice of Antimicrobial Any one of the recommended antibiotics can be used: 1st choice Nitrofurantoin monohydrate 100mg tid for 5 days 2nd choice Trimethoprim sulfamethoxazole 160/800 mg bid for 3 days Acute pyelonephritis If hospitalization is required Flouroquiolones or Aminoglycosides should be used Choice of Antimicrobial • Ciprofloxacin 500 mg bid for 7 days OR • Levofloxacin 750 mg od for 5-7 days Pregnancy Choice of Antimicrobial 1st choice Nitrofurantoin 100 mg tid (avoid in 3rd trimester) 2nd choice Cephalexin 500 mg bid  All are category B drugs  Should be taken for 7 days  Amoxicillin is not recommended for empirical use however can be used if culture sensitivity is present.

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Environmental Injuries Contents Burn ................................................................................................................................................................ 181 Electrical injuries ............................................................................................................................................ 183 Rabies ............................................................................................................................................................. 184

PATAN ACADEMY OF HEALTH SCIENCES

Burn Introduction Burn may be flame, liquid, chemical or electric. Clinical features • First degree burn: • Involves epidermis only • There is local Erythema and pain only • Healing occurs in several days • Second degree burn: • Involves epidermis and dermis sparing portion of dermal appendages. • Here skin is erythematous, moist, often with blister and bullae. • Deep partial thickness burn may have blanched, white areas and thick wall blisters. Sensation is intact • Heals in 2-6 weeks • Third degree burn: • Destroys epidermis, dermis including dermal appendages • Appears white and leathery • Thrombosed blood vessels or skin charring may be visualized • Wounds are insensitive • Inhalation injury • Facial burns • Carbonaceous sputum • Pharyngeal congestion • Wheezing • Hoarseness of voice Investigations • Complete blood count • Electrolytes and creatinine • Blood glucose Management 1. ABC: Patient with upper airway injury needs early intubation 2. IV access 3. Oxygen 4. Catheterization 5. Adequate analgesia: Morphine 6. Burn assessment

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* In case of child, patient’s palm can be used to calculate % body surface area (e.g area of palm = 1%)

•

Fluid Management Parkland formula: 2-4ml of RL/NS x Body weight x % of body surface area burn. Half of the fluid in first 8 hours and next half in 16 hours

Admission Criteria • Partial thickness burn of non critical areas (eyes, ears, neck, hand feet or perineum) involving 1020% of body surface area in adult older than 10 years and younger than 50 years • Partial thickness burn of non critical areas involving 5-10% of body surface area in children younger than 10 years. • Second or third degree burn involving > 10% of body surface area in patient younger than 10 years and older than 50 years • Second or third degree burn involving > 20% of body surface area in any patients • Third degree burn involving > 5% of body surface area • Significant burn of face, hands, feet, genitalia, perineum or major joints Discharge criteria • Patient not meeting above criteria

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Electrical injuries Introduction Alternating current (AC): • Found in residential power supply • Can cause tetanic muscle contraction prolonging contact • More likely results in ventricular fibrillation Direct current (DC): • Tends to throw patient from the source • More likely to result in asystole Clinical features • Cardiac arrhythmias • Respiratory arrest due to brain injury • Altered mental status, Seizure, Coma • Compartment syndrome • Renal failure • Thermal burn • Other associated injuries due to falls Investigations • ECG, C spine x ray • Urine for myoglobinuria • Troponine I /CPK MB • Electrolytes, Creatinine, Management • ABC • Oxygen • Spinal Immobilization • IV fluids to maintain urine output of 1ml/kg/hour • Catheterization • Tetanus prophylaxis • Local wound care Admission criteria • Documented loss of consciousness • Arrhythmia, Myocardial infraction • Suspicion of deep tissue burn Discharge criteria • Minor, low voltage injury ( 10 days or laboratory confirmation of no rabies, ARV can be stopped Start ARV. If the animal survives > 10 days or laboratory confirmation of no rabies, ARV can be stopped

Not needed

Recommended

Rabies vaccination not needed for bite by Mouse, Monkey, cow, goat, horse etc

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Orthopedic Injuries Contents Principles of fracture management and dislocation ..................................................................................... 185 Spinal Injuries ................................................................................................................................................. 186 Overview of fracture management ............................................................................................................... 187 Shoulder Dislocation ...................................................................................................................................... 188

PATAN ACADEMY OF HEALTH SCIENCES

Principles of fracture management and dislocation Introduction Before definitive treatment of a fracture is undertaken, attention must be directed to first aid treatment, to the clinical assessment of the patient with special reference to the possibility of associated injuries or complications, and to resuscitation. Fracture type • Closed Fracture • Open Fracture Dislocation type • Complete dislocation • Subluxation: Partial dislocation Clinical features • Swelling, Deformity • Wound • Tenderness, Abnormal bony movement • Decreased or absent range of movement of joint • Distal neurological and vascular status should be accessed • Other associated injuries should also be assessed Investigation • X ray of the affected site (trauma series e.g. C spine lateral, pelvis anterior and chest x ray posterior anterior view is also needed in some cases) • Hb , Blood grouping and cross matching (as fracture femur and pelvis may cause blood loss > 2lts) Management • ABC • If open fracture: • Surgical toileting • Inj TT • Inj Cloxacilline 1 gm iv stat • Immobilization: fracture site including proximal and distal joints • If dislocated: requires urgent relocation Admission criteria • Open fracture Discharge criteria • After immobilization

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Spinal Injuries Introduction Most spinal cord injuries are produced in association with injury to the vertebral column. These can include any one or more of the following: • Fracture of one or more of the bony elements • Dislocation at one or more joints • Tearing of ligament(s) • Disruption and/or herniation of the intervertebral disc Clinical features • Pain • Weakness • Bowel and bladder dysfunction • Spinal Shock: • Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord function caudal to the level of the injury • Flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity. • There may also be Bradycardia and hypotension • These last several hours to several weeks • Absent bulbocavenous reflex and decrease anal tone • Loss of motor and sensory function loss below the lesion • SCIWORA — Spinal cord injury without radiographic abnormality (SCIWORA) is often defined as the presence of neurologic deficits in the absence of evidence of bony or ligamentous injury Investigations • X ray spine AP and Lateral Management • Stabilization of C spine • ABCDE • Stabilization of spine in hardboard • Per rectal examination • Secondary survey *Patient with spinal injury should not be discharged

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Overview of fracture management Fracture Phalynx Metacarpal

Management Strapping Ball bandage

Scaphoid

Scaphoid cast

Colles

Colles cast

Both bone forearm

Cast

Around elbow

Back slab

Shaft of humerus Proximal Humerus Clavicle

Collar cuff sling Strapping Figure of eight bandage

Pelvis Femur Patella

Strapping with hard board Traction Cylindrical cast

Around knee joint

Long leg cast

Leg

Long leg cast

Ankle

Boot cast

Foot

Boot cast

Toes

Strapping

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

Technique With adjacent finger Place a cotton or gauze ball in hand and bandage it in neutral position (slight extension of wrist and MCP joint and flexion of IP joint) alternatively volar slab Cast in neutral position extending from MCP joint of 2nd to 5th MCP joint and involving IP joint of Thumb to mid forearm Cast from MCP joint to mid Forearm with wrist in slight flexion and Ulnar deviation Extending from MCP joint to mid arm with elbow flexion Extending from MCP joint to mid arm with elbow flexion Collar cuff sling with free elbow Elbow arm strapping Bandage across both shoulder in a figure of 8

Extending from malleolus to upper 2/3rd of thigh Extending from MCP joint to upper 2/3rd of thing Extending from MCP joint to upper 2/3rd of thing Extending from MCP joint to upper upper third of leg Extending from MCP joint to upper upper third of leg Strapping with another toe

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Shoulder Dislocation

Overview 1) Shoulder dislocations occur most commonly in: a. Men aged 20-30 years b. Women aged 60-80 years 2) The pattern of shoulder dislocations is: a. Anterior (98%) b. Posterior ( 12hours • Primary diagnosis is consolidation/pneumonia or COPD • Patient is complaining of dryness/ discomfort or is experiencing nosebleeds or other symptoms of upper airway drying. For medication delivery, the following options are preferable: • MDI with spacer (with or without face mask). If the patient cannot tolerate being removed from CPAP, small volume nebulizer tee’d into the CPAP circuit should be considered, with the consideration that this may result in a vastly reduced deposition of the drug. Weaning of NIV The Patient should meet the following weaning criteria before weaning NIV: • Clinically stable • RR < 25 BPM • HR < 110 BPM • pH >7.35 • SpO2 > 92% on < 50% If the patient meets the above weaning criteria, a trial off NIV therapy on comparable FiO2 may be considered. Post NIV removal, assess and monitor the patient’s respiratory parameters. MO may consider ABG post discontinuation of CPAP to assess respiratory status. If the patient demonstrates clinical evidence of respiratory distress reinstitute NIV at previous settings and optimize NIV. Documentation Chart all procedures done, complications, changes and respiratory assessments on the xPAP flowsheet. Ventilation and patient status will be monitored at least Q3H while patient on NIV therapy. All measurable and set parameters will be recorded in the xPAP flowsheet with justification for parameter changes.

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Rapid Sequence Intubation Preparation Preparation includes assessing the patient's airway, developing an airway management plan, and assembling necessary equipment and medications. Airway assessment (LEMON) Look externally: Facial deformities Evaluate (3-3-2 rule): • 3: This assessment indicates the ease of access to the airway. A normal patient can open his mouth sufficiently to permit three of his own fingers to be placed between the incisors. Adequate mouth opening facilitates both insertion of the laryngoscope and obtaining a direct view of the glottis. • 3: This assessment provides an estimate of the volume of the submandibular space. A normal patient is able to place three of his fingers along the floor of the mandible between the mentum and the neck/mandible junction (near the hyoid bone). • 2: This assessment identifies the location of the larynx relative to the base of the tongue. A normal patient is able to place two fingers in the superior laryngeal notch (ie, the space between the superior notch of the thyroid cartilage and the neck/mandible junction, near the hyoid bone). If the larynx is too high in the neck, direct laryngoscopy is difficult or impossible because of the angles that have to be negotiated to permit visualization. Mallampati score: Class I and II are easy, III and IV are difficult Obstruction/Obesity: Airway obstruction with supraglottic mass Neck mobility Difficult bag and mask ventilation • • • • •

M: mask seal – , absence of facial hair, lack of interfering substances, such as excessive vomitus or bleeding, and the ability to apply pressure to the face with the mask. O: Obstruction/Obesity – Placing the bed at an angle with the head higher than the feet (ie, reverse Trendelenburg) may reduce impedance to airflow from abdominal weight. A: Age – In one study, age >55 years was a marker of difficult N: No teeth – Edentulousness creates difficulty with BMV. Teeth provide a framework against which the mask sits and support the cheeks, enhancing mask seal. S: Stiffness – “Stiffness” is used to connote resistance to ventilation that occurs in conditions that increase the required inspiratory pressure to ventilate the lungs and include asthma, chronic obstructive pulmonary disease (COPD), pulmonary edema, widespread infiltrates, and any other condition that decreases pulmonary compliance.

Preoxygenation Any patient who may require urgent tracheal intubation should immediately be given high flow oxygen at the highest possible concentration. Alternatively, 8 vital capacity breaths may be used in cooperative patients and will provide equivalent pre-oxygenation in less than one minute. Apneic oxygenation is continuing oxygen in high flow through nasal prong during intubtion.

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Pretreatment Pretreatment with Lidocain can blunt reflex and prevents elevation of ICP during intubation. If patient is very dyspneic and using bicarbonate as pretreatment might be helpful.

Paralysis and induction Inj Ketamine 1-2 mg/kg iv (In an average 100 mg) Inj Suxamethonium 2 mg/kg iv (In an average 100 mg)

Positioning and protection Sniffing positon and BURP (Behind Upward Right Posterior ) pressure to thyroid cartilage

Placement with proof Direct visualization ETCO2 Ultrasound confirmation

Double track sign in trachea

Post intubation procedure Positioning, taping etc.

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Emergency Cricothyroidotomy 1) The cricopharyngeal membrane is only 1cm tall vertically. 2) As such, the largest ETT that should be placed through it is a Size 6. -Remember that ETTs are sized according to their inner diameter (in mm) Predictors of a Difficult Cricothyroidotomy -- "FOR ITCH" a. Flexed neck b. Obese c. Radiation therapy d. Infection e. Tumor f. Coagulopathy g. Hematoma Procedure Equipment 1) Scalpel 2) Skins hooks x 3 3) Snaps x 2 4) Scissors 5) Tracheal (“Trousseau”) dilator or a Kelly 6) Size 6 cuffed ETT tube 7) Sutures or trach ties Technique (for right-handed physicans) 1) If there is time, prep the neck with Betadine. 2) Give sedation +/- paralysis if the patient is awake and/or moving. 3) If the patient is not in C-spine precautions, hyperextend the neck. 4) Stabilize the larynx with the left hand. 5) Make a 4cm vertical midline incision in the skin over the cricothyroid membrane--thereby exposing the membrane. 6) Place a skin hook on either side of the skin incision and have an assistant hold the field open. 7) Make a 1cm horizontal stabbing incision through the inferior cricothyroid membrane (to avoid the cricothyroid arteries). a. Only allow the tip of the scapel to enter the trachea b. Avoid perforating the posterior tracheal wall 8) Before removing the scalpel, insert a Kelly into the hole. 9) After the Kelly is in place, remove the scalpel and extend the horizontal cricothyroid membrane incision with scissors. 10) Place a tracheal hook on the superior side of the horizontal cricothyroid membrane incision and get an assistant to hold it upwards. 11) Leaving the Kelly in place, gently insert the Trousseau dilator into the hole. a. The Kelly will need to be gradually removed as the Trousseau dilator is inserted DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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b. If a Trousseau dilator is not available, use the Kelly to dilate the hole directly 12) Insert a Size 6 cuffed ETT tube into the hole. a. The Trousseau dilator (or Kelly) will need to gradually be removed as the ETT is inserted. b. Do not insert the ETT tube too deeply down the trachea (to avoid a right-mainstem intubation). 13) If possible (and oxygenation permits), confirm placement with a video device (eg. bronchoscopy) before bagging the patient. 14) Inflate the ETT cuff and confirm CO2 return. 15) If not already done, confirm placement with a video device. 16) Secure the tube with sutures or a trach tie. Complications of Cricothyroidotomy 1) The most common complications are: a. Bleeding b. Failed procedure c. Incorrect site of tube placement d. Prolonged procedure time 2) Long-term complications of cricothyroidotomy are rare. -The most common long-term complication is dysphonia or voice change

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Using ventilator in ED

Starting • Patient’s attendant need to know that we might not have control on all parameters with this ventilator for long period, so needs to be shifted as soon as possible. Ventilator preparation - Cross vent 3 (biomed) 1. Check the power cable, vent circuit, exhale volume sensor, oxygen tube connection. 2. Power on with switch button 3. You can setup with setup key at monitor (Usually this step is not needed as ventilator is already in functional mode). 4. Three knob at the bottom of ventilator: 1st PIP – set to 15 to 25 (usually 20). 2nd Knob (PEEP) – set to 5. 3rd knob (flow rate) - keep it to 60 L/min. 5. Touch Main then touch A/C mode 6. Touch Rate then change with up/down key to 14 to 16. 7. Touch TV and change with up/down key to 8-10ml/kg (450-550ml). 8. Attach the circuit of the ventilator to the ET tube. 9. If you want to change to SIMV/CPAP mode, touch SIMV/CPAP and repeat the same. 10. Make sure to sedate patient if you are using A/C mode. Medications for Rapid Sequence Intubation • Sedation and analgesia: Ketamine 1-2 mg/kg • Paralysis: Succniyl choline 2 mg/kg • Example: For 50 kg- 100 mg of Ketamine (2ml) and 100 mg of Sux (2ml) Connect to ventilator • Settings may change when connected to patient, so please see monitoring panel • For monitoring panel touch Alarm 1 and Alarm 2 in monitor • Fill up sick patient monitoring chart Muscle Relaxation: use Vecuronium as below • Loading: 0.05mg/kg i.v following 5 minutes of Succinylcholine administration (e.g: for 50kg 0.05 x 50=2.5mg) • Maintenance: 0.01-0.015 mg/kg i.v 20-45min post initial dose. (e.g: for 50kg 0.01 x 50 =0.5 mg) Sedation • Midazolam 1 mg per hour and additional 1 mg as per needed in between. • Caution: Hypotension Analgesia • Morphine 1 mg per hour • Caution: Hypotension, Respiratory depression Alternatively for sedation and analgesia • Ketamine 0.1-0.5 mg/min iv

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Capnography Normal Waveform CO2

A-B: Zero baseline – beginning of exhalation B-C: Rapid sharp rise – anatomical dead space gas replaced by more distal airway gass that contain more CO2 C-D: Alveolar plateau – containes mixed alveolar gases D: End Tidal CO2 – highest concentration of exhaled CO2 D-E: Rapid sharp downstorke – inhalation phase, frsh gas rapidly replaces CO2

Endotracheal tube in oesophagus

No CO2 measured. Only small short lived capnogram displayed.

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Endotracheal tube leak

If air leak around endotracheal tube cuff, alveolar (end tidal) CO2 gas is diluted. The alveolar plateau is blunted and it bends with the downstroke of the capnogram. Look for • •

A deflated or leaky endotracheal or tracheal tube cuff An artificial airway that is too small for patient.

Decerased muscle relaxan effect of breathing against ventilator

The cleft in the far right portionof the alveolar plateau indicates that the diaphragm is moving and is causing entrainment of fresh air. A cleft can occur in any part of the alveolar plateau when the patient attempts to breath against ventilator. Cleft in capnogram (may not be on every waveform) Humped waveform (indicating attempts at spontaneous breathing)

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PATAN ACADEMY OF HEALTH SCIENCES

Endotracheal tube kinked or airway obstructed

If exhaled CO2 gas is completely or partially obstructed, the slope of the ascending limb of the capnogram has litter or no alveolar plateau. Look for Partially kinked or occluded artifically airway Herniated endotracheal or tracheal tube cuff Bronchospasm, COPD Foreign body in upper airway Rebreathing CO2

If the patient is rebreathing previously exhaled CO2. ETCO2 values increase and the baseline elevated. The waveform does not return to zero at the end of inspiration. Look for Inadequate expiratory time Malfnctioning inspiratory valve Malfunction of circuit Insufficient inspiratory flow rate.

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PATAN ACADEMY OF HEALTH SCIENCES

Central Venous Line Place the patient in tendlenburg position. Proceed in 45 degree to skin surface. Internal jugular vein in 2-3 cm below skin, if vein not hit change direction or angle of needle.

Success rate increases and complication decreases with use of USG.

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Percutaneous Cardiac Pacing Pad placement

Pacing • Connect cable to electrode • Turn the output courrent dial as low as possible • Set the pacing rate between 80 and 90 beats per minute • Select pacer function • Turn it on • Gradually increase the current output to 5 to 10 mA at a time until capture is achieved. Assessment of successful pacing • Successful capture is usually characterized by a wde QRS complex and broad T wave. • Electrical capture is best judged by the presence of consistent ST segment and T wave after each generated facer spike.

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PATAN ACADEMY OF HEALTH SCIENCES

FAST

Consists of 4 views – Subxiphoid – Right Upper Quadrant – Left Upper Quadrant – Pouch of Douglas Right upper quadrant

Left upper quadrant

Pelvis

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

216

PATAN ACADEMY OF HEALTH SCIENCES

FOCUS (Focal cardiac ultrasound) Figure 1

Figure 1 Subxiphoid view Place the probe at subxiphoid area pointing towards left shoulder.

Figure 2

Figure 2 Parasternal short axis Place the probe at 3rd or 4th intercoastal space with marker pointed towards left shoulder Figure 3 Parasternal long axis Place the probe at 3rd or 4th intercoastal space with marker pointed towerds right shoulder Figure 4 Four chamber view Place the probe at apex with marker pointed towards left shoulder

Figure 3

Figure 4

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

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PATAN ACADEMY OF HEALTH SCIENCES

Chest tube insertion Review

Sengstaken Blackmore tube • •

• • • • • •

Insert the lubricated SB tube until the 50 cm mark is located just outside the nares or teeth. Confirm its position in stomach by flushing and aspirating the port with air while auscultating over the epigastrium Inflate the gastric bulb with 200 to 250 ml of air then pull back until resistance Apply traction and fix the tube Inflate oesophageal balloon to ta pressure of 25mmHg If bleeding continues increase the oesophageal balloon pressure in 5 mmHg increment until 45 mmHg If bleeding is controlled reduce oesophageal balloon pressure every 3 hourly until 25 mmHg Deflate oesophageal balloon for 5 minutes every 6 hourly to avoid oesophageal pressure necrosis

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Procedural Sedation

Level of sedation analgesia Minimal sedation (Anxiolysis) Responsiveness Normal response to verbal stimulation Airway Unaffected Spontaneous ventilation Cardiovascular function

Deep sedateion

Unaffected

Moderate sedation (Conscious sedation) Purposeful response to verbal or tactile stimulation No intervention required Adequate

Unaffected

Usually maintained

Usually maintained

Purposeful response after repeated or painful stimulation Intervention may be required May be inadequate

General Anaesthesia Unarousable even with painful stimulation Intervention often required Frequently inadequate May be impaired

Principle of procedural sedation and analgesia • Determine appropriate level of sedation desired • Have appropriate monitoring and rescue equipment • Administer analgesic before sedative • Titrate agents to desired level of sedation • Observe and monitor until recovery to baseline mental status Recommendation regarding fasting state in low risk patient Fasting state Urgency Risk of aspiration No oral intake < 3 h Any Low Any clear liquid < 3 h Urgent Higher Any clear liquid < 3 h Non urgent Higher Light snack < 3 h Urgent Higher Light snack < 3 h Non urgent Higher Meal < 3h Urgent Highest Meal < 3 h Non urgent Highest Sedation agent for adult procedural sedation and analgesia Medication Dose Route Onset Midazolam 0.05-1mg/kg IV 1-3min May repeat 0.05mg/kg every 2 min until necessary sedation Ketamine 1-2mg/kg IV 1-3min Propofol 1mg/kg followed by 0.5mg/kg IV 1-2min every 3 min if needed

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

Suggested sedation level No limitation No limitation Limit to moderate sedation Limit to brief deep sedation Limit to moderate sedation Limit to moderate sedation Limit to minimal sedation Duration 1h

Use Minimal or moderate sedation

10-20 min 5-10min

Dissociative sedation Moderate/ deep sedation

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PATAN ACADEMY OF HEALTH SCIENCES

Ketofol (Ketamin+ Propofol)

10mg/ml of both medication mixed in1:1 Given 1-3 ml every 2-3 min until desired sedation is achieved

IV

1-2 min

10-20 min

Moderate and deep sedation

Interscaleni Block Review

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Drug Preparation Formula Drug in ml/hour =(Drug dose required (mcg) x weight (kg) x 0.06)/(Drug in bag (mg)/Fluid in bag (ml) Calculaiton of drops Pediatric set: ml/hr = drops/min Adult set: (ml/hr)/3

Dopamine Dose: 5-20mcg/kg/min Each 5 ml contains 200 mg of Dopamine Add 5 ml Dopamine in 100 ml of NS Dose 5mcg/kg/min 10 mcg /kg/min 15 mcg /kg/min 20 mcg /kg/min

35 kg 5ml/hr 10ml/hr

40 kg 6 12

45 kg 7 13

50 kg 8 15

55 kg 8 16

60 kg 9 18

65 kg 9 19

70 kg 10 21

15ml/hr

18

20

22

24

27

29

31

20ml/hr

24

27

30

33

36

39

42

Noradrenaline Dose: 0.01-3mcg/kg/min Add 4ml = 4mg in 100 ml of NS Add 4ml /100 ml of NS Dose 0.03mcg/kg/min 0.1mcg/kg/min 0.5mcg/kg/min 1mcg /kg/min 2 mcg /kg/min 3mcg /kg/min

50 kg-60 kg 3ml/hr 8ml/hr 38ml/hr 75ml/hr 150ml/hr 300ml/hr

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE

70-80 kg 4ml/hr 12ml/hr 60ml/hr 120ml/hr 240ml/hr 500ml/hr

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Protocol for Management of Common Paediatric Problems Department of Pediatrics Patan Hospital 3rd edition; 2070 (2013)

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CONTENTS 1. WHEEZING ........................................................................................................................ 225 2. STRIDOR ............................................................................................................................ 227 3. BRONCHIAL ASTHMA .................................................................................................... 229 4. TRAUMA ............................................................................................................................ 230 5. STATUS EPILEPTICUS ..................................................................................................... 232 6. COMA.................................................................................................................................. 234 7. NEUROCYSTICERCOSIS ................................................................................................. 237 8. DRUG/ FLUID DELIVERY IN A SICK CHILD ............................................................... 239 9. INITIAL ASSESSMENT OF A SICK CHILD ................................................................... 241 10. BASIC LIFE SUPPORT (AHA guideline, 2013).............................................................. 242 11. BURNS .............................................................................................................................. 243 12. CHOKING .........................................................................................................................246 13. NUTRITION REQUIREMENTS FOR CHILDREN ........................................................ 247 14. IV FLUID RESCUSITATION IN DEHYDRATION ................................................. 249 15. URINARY TRACT INFECTION ..................................................................................... 252 16. NEPHROTIC SYNDROME.............................................................................................. 255 17. MANAGEMENT OF DIABETIC KETOACIDOSIS IN CHILDREN ............................ 258 18. SEPTIC SHOCK................................................................................................................ 261 19. RECOGNITION OF MENINGOCOCCAL DISEASE..................................................... 264 20. ORGANOPHOSPHATE (OP) POISONING .................................................................... 265 21. EYE INFECTIONS ........................................................................................................... 269 22. OTHERS ............................................................................................................................ 270 I. RULES OF THUMB FOR EXPECTED INCREASE IN WEIGHT.................................................................. 270

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II. RULES OF THUMB FOR EXPECTED INCREASE IN HEIGHT ................................................................. 270 III. RULES OF THUMB FOR EXPECTED INCREASE IN HEAD CIRCUMFERENCE ................................. 271 IV. PAEDIATRIC NORMAL VALUES FOR VITAL SIGHS ............................................................................ 271 V. NORMAL HEMOGLOBIN LEVELS.............................................................................................................. 271 VI. NORMAL BLOOD PRESSURE IN CHILDREN .......................................................................................... 272 VII. NORMAL HEART RATE IN CHILDREN .................................................................................................. 272 VIII. NORMAL RESPIRATORY RATE IN CHILDREN ................................................................................... 272 IX. APPROXIMATE AVERAGE HEIGHT AND WEIGHT FOR NORMAL CHILDREN ............................... 272 X. INTRAVENOUS FLUID REQUIREMENTS.................................................................................................. 273 XI. DAILY ELECTROLYTE REQUIREMENTS ................................................................................................ 273 XII. PLEURAL EFFUSIONS ............................................................................................................................... 273 XIII. ASCITIC FLUID .......................................................................................................................................... 273 XIV. PERICARDIAL EFFUSIONS...................................................................................................................... 274 XV. BLOOD CULTURE COLLECTION ............................................................................................................ 275 XVI. ASSESSMENT OF DEVELOPMENTAL MILESTONES ......................................................................... 276 XVII. GUIDELINES FOR PHOTOTHERAPY IN NEONATAL JAUNDICE .................................................... 280 XVIII. GUIDELINES FOR EXCHANGE4 TRANSFUSION IN NEONATAL JAUNDICE .............................. 281 XIX. NORMAL VALUES FOR THYROID FUCTION TESTS IN CHILDREN ............................................... 282 XX. INDICATIONS FOR PICU ADMISSSION .................................................................................................. 282

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1. WHEEZING First wheezing & severe respiratory distress • Start oxygen • Give salbutamol nebulization (< 2years: 0.2 -0.6 mg/kg/day divided q4-6 hourly, > 2years: 0.6-2.5 mg 4-8 hourly) • A trial of epinephrine nebulization can be given if bronchiolitis is suspected • No CXR or blood tests in ER • Pediatric resident will likely admit and decide if CXR and blood tests are needed • Avoid IV lines in children 50-60

5 years 5-10 mgIV (Can also be given PR: 2-5 years: 0.5 mg/kg, 6-11 years: 0.3 mg/kg, ≥ 0.2mg/kg) Emperic treatments: • For possible infection o Ceftriaxone (100 mg/kg IV, maximum single dose 2 g), Vancomycin (age specific dose), and Acyclovir (age specific dose) • For possible ingestion o Naloxone: (If opiate intoxication is suspected: miosis, repiratory dipression, hypotonia): 20 Kg or > 5 years: 2 mg IV, IM, SC or ET. Repeat as necessary, keeping in mind its short half life • For possible increased ICP o Mannitol: 0.5 to 1 gram/kg IV • For possible non-convulsive status o Lorazepam: 0.1 mg/kg IV (max single dose 5 mg) or o Diazepam: 6 months to 5 years: 0.2-0.5 mg IV, > 5 years 5-10 mg IV (Can also be given PR: 2-5 years: 0.5 mg/kg, 6-11 years: 0.3 mg/kg, ≥ 0.2mg/kg) If suspicion of seizures continue, treat as status epilepticus • For possible Wernicke encephalopathy o Thiamin: 100 mg IV (before starting glucose). Consider in adolescents for deficiencies secondary to alcoholism or eating disorders. • If ingestion of toxic substances is suspected, airway must be protected before GI decontamination • Monitor Glasgow Coma Scale and reassess frequently

236

7. NEUROCYSTICERCOSIS Differential diagnosis: • Brain abscess • Cerebral amebiasis • Central nervous system (CNS) tumors • CNS toxoplasmosis • Mycotic granulomas • Neurosarcoidosis • Tuberculosis of the CNS • Carotid disease and stroke General considerations: • Administer antiepleptic therapy to all patients with seizure • Always give steroids if antiparasitic treatment is admininstered • If cerebral edema is present, treat cerebral edema before administering antiparasitic treatment Treatment of parenchymal NCC • Antiepileptic therapy: Phenytoin or Carbamazepine (monotherapy is usually sufficient) o Administered to all patients with NCC who present with seizures or o If seizure is absent but multiple lesions are seen in the CT scan, specially degenerating lesions and those with surrounding inflammation o Continue for 6-12 months after radiographic resolution of active parasitic infection o If the patient has recurrence of seizure during trial off of antiepileptic treatment, long-term treatment should be re-instituted • Antiparasitic therapy: Consider in all patients with NCC and always use together with corticosteroids o Single lesion:  Albendazole: 15 mg/kg/day for 7 days  Prednisolone: 1 mg/kg/day for 5-10 days Or Dexamethasone 0.1 mg/kg/day for 5-10 days followed rapid taper

o Multiple lesion: 237

 Albendazole: 15 mg/kg/day in two divided doses for 10-15 days  Dexamethasone high dose **For subarachnoid disease, Albendazole should be given for 28 days**

• Anti-inflamatory therapy: Indications for corticosteroids o Along with antiparasitic therapy o Cysticercal encephalitis o Subarachnoid cystecercosis Things to do before initiating corticosteroids o Mantoux test (and other investigations as indicated) to rule out tuberculosis o If indicated, screen for strongyloidiasis o Ophthalmologic examination to rule out ocular cystecercosis

Indications for surgical intervention • Altered mental status or impaired herniation due to hydrocephalus secondary to NCC • Intraventricular cysts with hydrocephalus • Subarachnoid cysticercosis (giant cysticerci) • Ocular cysticercosis • Spinal cysticercosis Follow-up • CT scan o In 1-2 months and then after 6 months of diagnosis of parenchymal or subarachnoid cysticercosis. Once lesions have resolved, imaging is less useful.

238

o Before discontinuing antiepileptic drugs o New, worsening or persistent symptoms • Patients with VP shunts should be educated to seek prompt medical advice for symptoms of hydrocephalus

8. DRUG/ FLUID DELIVERY IN A SICK CHILD Intravenous access: If cannot be established within 90 seconds, go direct to intra-osseous access! • In children any IV access anywhere is effective if drugs are flushed through after administration. • Central venous access is the best route of administration; but should only be attempted by experienced personnel and is relatively contraindicated in trauma patients.

Intraosseous access: • After giving drugs, flush them through. Dilute strong alkalis and hypertonic solutions. Setting up intraosseous infusion Equipment: Alcohol or Betadine swabs: Intraosseous needle or 16-gauge cannula at least 1.5 cm in length 20 ml syringe with normal saline Infusion fluid

Procedure: Identify the infusion site. Avoid fractured bones, or limbs with proximal fractures. If possible avoid areas of infected burns or cellulitis. Proximal tibia: Anteromedial surface, 2-3 cm below the tibial tuberosity. Distal tibia: Proximal to the medial malleolus. Distal femur: Midline, 2-3 cm above the external condyles. • Prepare the skin and if necessary use local anesthetic. • Insert the needle through the skin, perpendicularly and slightly away from the growth plate

239

into the bone with a screwing motion. There is a feeling of ‘giveway’ as the marrow cavity is entered. Unscrew the trocar and confirm position by aspirating bone marrow or by flushing with 5-10 ml normal saline. • Secure the needle and splint the limb.

Fluids can be infused through an intraosseous needle as through a standard intravenous cannula. If rapid fluid replacement is required, infuse under pressure using a 50 ml syringe. Dilute strong alkalis and hypertonic solutions. After giving any drug- flush it through.

Contraindications: Ipsilateral fracture, ipsilateral vascular injury, osteogenesis imperfect, osteoporosis.

Complications: Failure to enter the bone marrow, extravasation or sub-periosteal infusion. Osteomyelitis is rare with short term use. Local infection, skin necrosis, pain, compartment syndrome; fat and bone marrow microemboli have all been reported.

Doses of pharmacologic agents in pediatric resuscitation Oxygen Glucose Epinephrine

Atropine Sodium bicarbonate

100% initial dose, wean as clinically indicated Newborns: 10% Dextrose 2ml/kg IV Children: 10% Dextrose 5 ml/kg IV 0.01 mg/kg IV/IO (0.1 mL/kg of the 1:10,000 solution). Repeat every 3-5 min as required 0.1 mg/kg endotracheal (ET) (0.1 mL/kg of the 1:1000 solution) 0.02 mg/kg IV or IO (minimum 0.1 mg, maximum single dose 0.4mg) 1meq/kg IV/IO initial dose over 1-2 minutes, then 0.5 mEq/kg subsequent doses every 10 minutes of arrest. Maximum 8 meq/kg/day

Endotracheal tube sizes Rough guide: Tube diameter = Diameter of child's little finger or nostril Internal diameter (mm) = (Age/4) + 4 in a child over one year

240

Length (cm) = (Age /2) + 12 for an oral tube Length (cm) = (Age/2) + 15 for a nasal tube

9. INITIAL ASSESSMENT OF A SICK CHILD Airway and Breathing: Obstruction? Work of breathing - grunting, nasal flaring, recession or in drawing Respiratory rate Auscultation Cyanosis? Circulation: Heart rate Pulse volume Capillary refill Skin temperature Disability: Posture and tone Pupils Mental status - the AVPU scale A - Alert V - Responds to verbal stimuli P - Responds to painful stimuli U - Unresponsive It should be possible to perform this assessment within the first minute. If the child is very sick, CALL FOR HELP. It is better to call for help early. You can then go on to: Initial management Initial formal observations: pulse, respiration, BP, temperature, O2 saturations, BM stix, weight Initial investigations Definitive management

241

10. BASIC LIFE SUPPORT (AHA GUIDELINE, 2013) Component

Recommendations Children

Recognition

Infants

Unresponsive No breathing or only gasping No pulse felt within 10 seconds

CPR sequence

Chest compressions, Airway, Breathing (CAB)

Compression rate

At least 100/min

Compression depth

At least 1/3 AP diameter

At least 1/3 AP diameter

About 2 inches (5 am)

About 1 ½ inches (4 cm)

Chest wall recoil

Allow complete recoil between compressions Attempt to limit interruptions to 10 years, 1000 ml/day Special milk': i n i t i a l feed for severely malnourished children >6 months 130 ml/kg/day (=99 kcals, 1.4 g. protein, /kg/day) divided as 3 hourly feeds

Ward Food Values Energy

Proteing

247

Kcals

G

Tea ( Sugar – free)

80 (40)

2

Haluwaa

264

5

Sugar – Free Porridge

249

11

Milk 120ml

80

4

Yoghurt 120ml (140g)

84

4

Lito : full 150 ml

209

6

105

3

Khichiri

359

11

Rice meal : full

807

19

Half

505

12

Quarter

296

8

Afternoon Snack : full

436

11

Half

286

8

Quarter

244

6

Special milk 100ml

76

1

Paustik Sanjiwani : 500ml

754

27

Half 75 ml

Sugar free

634

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14. IV FLUID RESCUSITATION IN DEHYDRATION

Laboratory investigations Serum sodium • Hyponatraemia (serum Na 150mEq/L) Serum potassium Both hypokalaemia or hyperkalaemia can occur in dehydration. If the child has oligurea or anuria, do not add potassium in the iv fluid until serum potassium is

249

determined. Serum bicarbonate (can be measured by capillary or venous blood gas) Serum bicarbonate 1/3 & Inc maintenance K oral/iv 3-4 meq/kg/day

If ECG abnormal or symptomatic ->K rapid correction to be given. If serum K+ 100,000 organisms infection likely < 10,000 unlikely, repeat culture. Boy- > 10,000 infection likely Girl- > 100,000 infection likely

Clean Void

252

Antibiotics •

Infants < 2 months: IV antibiotic ( 2months: Oral ofloxacin if not vomiting. IV amikacin or ceftriaxone if vomiting

•

If enterococcal UTI is suspected or proven: Add Ampicillin

Duration of antibiotics •

Infants 2 months and febrile or immunocompromised: If on iv antibiotics, continue IV antibiotics until afebrile. Change to oral antibiotics once afebrile and continue for a total duration of 10 days

•

> 2months and afebrile in immune competent children: Oral antibiotics for 5 days

Repeat urine culture: •

No need to repeat urine culture if the pathogen is susceptible to the antibiotic being used and the patient is responding as expected

•

Repeat urine culture after 48 hours of treatment if the pathogen is not susceptible to the antibiotic being used or if the patient is not responding to the treatment

Indications for hospitalization: • Age 3mg protein/ mg creatine in early morning spot urine sample • Hypoalbuminemia : Serum albumin < 3 g/dL Other associated features are • Edema and • Hyperlipidemia DEFINITIONS The following are terms commonly used for management of nephrotic syndrome. Remission: Urine protein/creatine 4 relapses in any 12-month period. Steroid dependent: Relapse during taper or within 2 weeks of discontinuation of steroid therapy. Steroid resistant: Inability to induce a remission with 4 weeks of daily steroid therapy. 255

Criteria for minimal change disease • Age older than 1 year and younger than 10 years of age • None of the following findings: hypertension, gross hematuria, and a marked elevation in serum creatinine • Normal complement levels • No extra-renal symptoms such as malar rash or purpura Kidney Disease Improving Global Outcomes (KDIGO) 2012 guidelines to manage children with steroid-sensitive nephrotic syndrome as follows: Initial therapy: • Prednisolone 60 mg/m2 or 2 mg/kg per day for four to six weeks (maximum dose of 60 mg/day) followed by, • Alternate-day prednisone of 40 mg/m2 or 1.5 mg/kg (maximum dose of 40 mg/day) and continued for two to five months with tapering of the dose. Infrequent relapses: • Prednisone 60 mg/m2 or 2 mg/kg per day (maximum dose of 60 mg/day) until the urine protein tests are negative or trace for three consecutive days, followed by • Alternate-day prednisone of 40 mg/m2 or 1.5 mg/kg (maximum dose of 40 mg/day) for at least four weeks. Frequent relapses or steroid-dependent disease: • Prednisone 60 mg/m2 or 2 mg/kg per day (maximum dose of 60 mg/day) until the urine protein tests are negative or trace for three consecutive days, followed by • Alternate-day prednisone for at least three months. • The dose of alternate-day prednisone should be the lowest dose needed to maintain remission without adverse side effects. In patients in whom alternate-day therapy is not effective in maintaining remission, the lowest possible dose of daily prednisone is given to maintain remission to minimize adverse side effects. Daily prednisone should be given to patients during episodes of upper respiratory tract infection and other infections that are associated with relapse. • Corticosteroid-sparing agents should be given to children with frequently relapsing or steroiddependent disease who develop steroid-related adverse effects. Data are insufficient to choose among the following agents. Drug selection is based on the reported efficacy, adverse effects, local availability, and cost. Corticosteroid sparing agents: • Cyclophosphamide (dose of 2 mg/kg per day for 8 to 12 weeks [maximum cumulative dose of 168 mg/kg]) or • Chlorambucil (dose of 0.1 to 0.2 mg/kg per day for 8 weeks [maximum cumulative dose 11.2 mg/kg]). • Levamisole (dose of 2.5 mg/kg on alternate days for at least 12 months). • Calcineurin inhibitors include cyclosporine (initial dose of 4 to 5 mg/kg per day given in two divided doses) or tacrolimus (initial dose of 0.1 mg/kg per day given in two divided doses

256

• Mycophenolate mofetil (initial dose of 1200 mg/m2 per day given in two divided doses for at least 12 months). • Rituximab (an anti-CD20 monoclonal) should be considered only in children who have failed combination therapy of prednisone and other corticosteroid-sparing agents and have serious adverse effects of therapy. Both mizoribine and azathioprine are NOT recommended in the management of children with NS) Steroid-Resistant Nephrotic Syndrome Management ● Kidney biopsy; ● Tailor therapeutic regimen according to kidney histology; and ● Provide optimal supportive therapy. Treatment for steroid-resistant nephritic syndrome: • Immunosuppressive o Alkylating agents o Calcineurin inhibitors (CNIs)– Cyclosporin and tacrolimus o Mycophenolate mofetil o Rituximab • Nonimmunologic antiproteinuric therapy o Angiotensin-converting enzyme inhibitors (ACE-Is) o Angiotensin receptor blockers (ARBs) Symptomatic treatment of nephrotic syndrome • Oedema o Salt restriction o Fluid restriction (Insensible loss + urine output)  Maybe helpful in stabilizing patient’s weight and  If serum sodium ≤ 130 mEq/L o Diuretics (Frusemide is the first choice) Particularly useful when fractional excretion of sodium (FeNa) >2% indication volume expansion o Frusemide with albumin  Anasarca with respiratory compromise due to ascites and/or pleaural effusion  Severe scrotal oedema  Peritonitis  Severe tissue breakdown • Hypercoagulability: Patients with severe hypoalbuminaemia (serum a albumin 6g/L are at high risk. o Mobilisation o Avoidance of haemoconcentration o Early treatment of hypovolaemia and sepsis Prophylactic anticoagulation is not indicated unless there is H/O thromboembolic phenomena • Infection: Prophylactic antimicrobials are not recommended. o High risk for development of Pneumococcal or E.Coli infection (Peritonitis, pneumonia, sepsis)

257

High risk for varicella infection- treat with Acyclovir if varicella infection develops while on steroid therapy **Pneumococcal and varicella vaccines are recommended** • Hyperlipidaemia: Statins are indicated for only those children who remain persistently nephrotic and have hyperlipidaemica • Hypertension: Children with persistent hypertension in nephrotic syndrome are more likely to develop chronic kidney disease. Therefore, antihypertensive of choice are o ACE inhibitors or o Angiotensin II receptor blockers (Discontinue these drugs if hyperkalaemia cannot be controlled or creatinine clearance is >30% of the baseline) • Other dietery measures: No clear role. Low fat diet can be suggested to prevent excessive weight gain. o

17. MANAGEMENT OF DIABETIC KETOACIDOSIS IN CHILDREN Diagnostic criteria for diabetic ketoacidosis (DKA) • Hyperglycemia, serum glucose of >200 mg/dL (11 mmol/L) AND • Metabolic acidosis, defined as a venous pH 7.30, serum bicarbonate >16 meq/L • No neurologic impairment • Estimated volume deficit less than 3 percent • Not vomiting These patients may be managed in an ambulatory setting under the supervision of an experienced medical team. However, hospitalization may appropriate for young children (eg, 40ml/kg isotonic fluid in one hour. Cardiovascular dysfunction: • Hypotension • Reliance on vasoactive drug administration to maintain a normal blood pressure Or, two of the following • Prolonged capillary refill, • Oliguria, • Metabolic acidosis, or • Elevated arterial lactate Rapid recognition of septic shock: Inadequate tissue perfusion in a seriously ill child • Fever • Tachycardia or bradycardia • Decreased peripheral pulses compared with central pulses • Mottled or cool extremities • “Flash” or >3 second capillary refill • Dry mucus membranes, sunken eyes, and decreased urine output • Tachypnea, bradypnea, or apnea • Hypotension • Altered mental status (irritability, anxiety, confusion, lethargy, somnolence, apnea) • Hypothermia (especially neonates) Signs of infection Suggestive laboratory findings • Lactic acidosis (>3.5 mmol/L) • Age-specific leukocytosis or leukopenia (table 1) 261

• Platelet count 2 times upper limit of normal for age

262

263

19. RECOGNITION OF MENINGOCOCCAL DISEASE Figure: Algorithm for the early management of meningococcal infection. (Copyright Pollard AJ, Nadel S, Habxbi P, Faust I, Maconochie I, Britto Levin M 1998. Department of paediatrics, Imperial College School of Medicine, Si Mary' Hospital london.) . Purpuric or petechial rash or signs of meningitis/septicaema Call consultant in A&E, paediatrics, anaesthetics or intensive care Shock ?

Tachycardia, cold peripheries, increased capillary refill time (> 4 s) decreased urine output,(12 yrs initial dose 1-2 mg; 12 yrs 1 - 2 g IV infusion over 30 min; 10yrs

RR 40 30 20 18 18

IX. APPROXIMATE AVERAGE HEIGHT AND WEIGHT FOR NORMAL CHILDREN Age 3 - 12mths 1 - 6yrs

Kg Age (months) + 9 2 Age (yrs) x 2 +8

7 - 12yrs

Age (yrs) x 7 - 5 2

Age At birth lyr 2-12yrs

Length/ Height (cm) 50cm 75cm Age(yrs) x 6+77

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X. INTRAVENOUS FLUID REQUIREMENTS Body weight First 10 kg Second 10 kg Subsequent kg

Fluid requirement per Fluid requirement per 100 ml/kg 4 ml/kg 50 ml/kg 2 ml/kg 20 ml/kg 1 rnl/kg

The standard fluid bolus in shock is 20 ml/kg. for children, and 10ml/kg for neonates Fever increases requirements by 12% for each degree Celsius rise.

XI. DAILY ELECTROLYTE REQUIREMENTS Sodium 2-3 mmol/kg/day Potassium 2-3 mmol/kg/day

XII. PLEURAL EFFUSIONS WBC PMN% Pr(fluid):Pr (Serum) LDH Glu PH Investigations to be sent

Transudate

Purulent

Empyema

Complicated

1000 50% 90% >0.5 >200 95% >0.5

55000 >95% >0.5