Data Interpretation in Critical Care Medicine [5 ed.] 9780750652735, 075065273X

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DATA INTERPRETATION in Critical Care Medicine B . Venkatesh T. J. Morgan C. J. Joyce S.C. Townsend

Data Interpretation in Critical Care

Medidne B. Venkatesh

.

MBBS MD(Int. Med), FFARCSI, FRCA, MD(UK), FJFICM

Assoriate Professor and Staff Spedalist in Intensive Care Royal Brisbane Hospital University of Queensland Australia

T. J. Morgan

MBBS, FANZCA, FJFICM

Deputy Oirector and Senior Lecturer in Intensive Care Mater Misericordiae Hospital, University of Queensland

Australia

C. 3 . Joyce

.

MB, chB FANZCA, FJFICM, PhD

Associate Professor and Senior Staff Specialist in Intensive Care Princess Alexandra Hospital, University of Queensland Australia

S. C. Townsend

MBBS, FANZCA, FJFICM

Staff Specialist in Intensive Care Royal Melbourne Hospital Victoria, Australia

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Contents

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U t T I H WOR T H N E M A N N

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Science I imited All right s reserved .

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« In ul Hala Vtnkatidi , I | Morgan, C. J . Jeiycc and S. C . Townsend In iilelillllrel 4 « «uthon < if this work has been asserted by them in tam " illi lin- < opinght , Designs and Patents Act 1988 .

Preface vii 1 Blood gases 1

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rcproduccd, stored in a rctricv il system , or by any incans, clcctronic, nicchanical , . IIIIK i n ntltcrwtM , » 11 limit cithcr the prior permission of i•• • I li i Manager . Pcrmissions Office , Hlscvicr Science IIH || I ' I|||II i l *i i nu ii lid Ih, i ni 11 i m i l , ftJS Wiiliini Street , Third Floor, Philadelphia PA l "|i i i i I S A i i n 4 II I II I permitling rcstrictcd copying in the United kingdom IMIIIII I » il » i opyrighl I icenting Agency , 90 Tottcnhain Oiurt tip h 44.1 i «i i NI hn|nii iil linn |iiihlii ,IIIIHI inav IH'

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Cardiovascular 37 Questions 37 Answers 52 Respiratory mechanics, ventilation and oxygenation Questions

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I ilnary ot ( IIngres Cataloging in Publication Data A julng ri otd hir this hook is available from the Library of Congress

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Note Medical knimicdgc is constantly changing. As new information becomes available , hange, in treatment, proccdures, equipmcnt and the usc of drugs becotne necessary The authors and the publishers have taken care to ensurc tliat tlie inlormation given in this text is accurate and up to date. Howevcr, rra lrr are trongly advised to confirm that the information , espccially with re gard to drug usage, complics with the latest legislation and standards of

Answers Neurocritical care Questions 77 Answers 82 Microbiotogy 85

practice

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Coagulation abnormalities Questions 100 Answers 105

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Haematology

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Answers 12 Biochemistry 18

121 121

Answers 125 10 Radiology 128 Questions 128 Answers 133 Glossary 135

Index

137

iH étM* IA V

Preface

The assessment of the ICU patient requires not only the powers of observation fundamental to the clinical examination of any patient, but also a thorough understanding of the information provided by 'numbers' generated from equipment and laboratory tests. In no other medicat specialty is the correct interpretation of monitoring and laboratory data more important than in critical care medicine. This is reflected in the increasing emphasis on data interpretation in the qualifying examinations in intensive care. However, although a number of definitive texts on intensive care exist, few focus specifically on data interpretation in critical illness.

Accordingly, the ten chapters of this book are based around data sets that cover important systems. The format consists of brief clinical scenarios accompanied by a set of clinical, laboratory or radiological data, followed by a series of questions. The answers are provided at the end of each chapter with explanations. The pocket- book format makes it portable for access during 'breaks'. Whilst the data covered is not exhaustive, it rehearses the candidate in 'pattern recognition', an important element of training. Although the book is designed primarily for candidates preparing for the Australian Fellowship Examination in Intensive Care ( FJFICM), it should be a useful resource for trainers and trainees in the specialty the world over.

We would like to thank our trainees, senior registrars and fellows in intensive care for keeping our minds ticking with their discussions, without which the stimulus for this book would not have arisen. Finally we would like to thank the staff of Elsevier Science for their assistance in the production of this book

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B Venkatesh T J Morgan C J Joyce S C Townsend 2002

vii

Blood gases

Question 1.1 You are called to the emergency department to review the blood gases of an obese 55year-old hypertensive male who complains of daytime somnolence. He has the following .11 terial blood gas results: Barometric pressure

760

rio 2

0.21

Hb

190

pH

7.33

POz

40

mmHg

PC02

64

mm Hg

HCO~-

33.3

mmoVL

Standard base excess

+5.4

mmol/l

mm Hg

g/l

A Describe the acid-base status. B Calculate and interpret the A- a gradient. C What is the likely diagnosis?

c ~ ol)4~

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y~~

Question 1.2

Question 1.3

You are called by a surgical resident mcdic.1l officer (l

5

Question 1.4

Question 1.5

A 20-year-old woman is involved in a motor vehicle accident. She is 32 weeks pregnant and has rib fractures, for which she has received analgesia. She is not shocked and her abdomen is non-tender. Her arterial blood gases and electrolytes are as follows:

A 45-year-old alcoholic woman treated with flucloxacillin for multiple staphylococcal lung abscesses has been improving, despite continuing pyrexia and muscle aches requiring regular oral paracetamol. After 3 weeks, while still in hospital, she becomes unwell again. Blood gas and biochemical data are as follows:

Barometric pressure

760 mmHg

Fi0 2

0.5

pH

7.32

PC0 2

24 mmHg

P02

150 mmHg

HC03"

9.5 mmol/L

PCOZ

42 mmHg

HC0 1

21.3 mmol/L

Sodium

135 mmol/l

(135-145}

Standard base excess

-5.8 mmol/L

8 mmoljkg

(111pcm.11w11

B A-a gradient = 33 mmHg. This is above the normal upper l11111t when brc.\thing air, even in elderly patients. Therefore the hypoxia is not purely due to hypoventilation - increased V /Q mismatch and/or shunt must also be operating. C Obstructive sleep apnoea.

Question 1.2: Answers A She has a severe primary metabolic alkalosis with appropriate respiratory compensation.

B A-a gradient = 20 mmHg. This is just above normal for an elderly person breathing air, suggesting that most of the hypoxaemia is due to hypoventilation.

C Correcting hypokalaemia, ceasing inciting agents such as diuretics, infusing saline, and possibly by administering parenteral acetazolamide.

0 \1 .~2 "1.·1.·1's' prq.1,11 t11l' 1IH normal l~tC0 2 is 30 mmHg with compensatory 11( 0~ r1.·d11u1on "ih{ now ii.ls .Kutl: C02 retention due to pain and narcotics, B" i11g tht· appc.1ra11cc of .111 uncompensated metabolic acidosis. However, this 11111'1 be 1ntcrpre1cd in the light of the normal changes of pregnancy. ltmcd A-a gradient of 158 mmHg, suggesting shunt and/or V/Q mismatch. l'otcntial causes include further loss ofFRC due to chest wall injury (already 1nl11ccd by 500 mL in the third trimester), pulmonary contusions, pncumothorax.

Question 1.5: Answers J\ \cvcre compensated metabolic acidosis with markedly raised anion gap (26 mEq/L). II Pyroglutamic acidosis.

l'.lracetamol and flucloxacillin administration in the setting of sepsis and renal .11\d hepatic dysfunction.

Question 1.3: Answers A A-a gradient has improved from 239 to 150 mmHg, indicating lessening V/Q mismatch and/or shunt.

B At 0700 h there was a primary acute respiratory alkalosis. At 1000 h this had changed to a dual acid-base disorder. There is now a respiratory alkalosis plus a metabolic acidosis with a raised anion gap (20 mEq/L). C Yes. There is improving oxygenation and a lessening of the primary component

of the respiratory alkalosis (but now there is a new clement of respirarory compensation for a high anion gap metabolic acidosis).

D Salbutamol-induced lactic acidosis superimposed on improving bronchospasm.

ll llrine screen for organic acids.

Question 1.6: Answers A ( ~ompensated metabolic alkalosis, hyperlactaemia with normal anion gap.

-

U 1lypoalbuminaemia reduces the sensitivity of the anion gap to unmeasured 111ions. 1lyperlactaemia due to impaired metabolic conversion of lactate in the fluid used in renal replacement therapy (normal dialysate concentration 45 mmol/L). Jo 1h1s case, sufficient lactate has still been metabolized and replaced by HC03- to produce a metabolic alkalosis.

Question 1.7: Answers A !'he pH is normal in the setting of a severe respirarory alkalosis. Th.is is therefore 1 mixed acid-base disorder due to a combination of a respiratory alkalosis and metabolic acidosis. The anion gap is raised, at 20 mEq/L.

D l'his acid-base disorder in combination with hypoglycaemia is seen in such wnditions as salicylate poisoning (anion gcr l;J, King 1-W, hhch.ll' YR. Sh.ll'p JT The .tlvcol.tr- merial oxygen llndicnt m young and elderly men dunns aar •nd ""'gen breathing. Am Rev Re,pir n" 1968: 97.376 -38 I

The normal A-a gradienr ranges fi-om 7 mmHg in young adults to 14 mmllg in elderly adults breathing air, and fi-om 31 mmHg (young) to 56 mmHg (elderly) when breathing 100% oxygen.

Mmn I, loo~ V, Lepccq 11 l 1766-1767

PaC0i [HCQ 3-J relationships in simple acid-base disturbances. PaC0 2 values are in mmHg, (HC03-J in mmol/L.

M11rgan T). Venlcatel>h B, Hall ) Cl)''t~llood '"""S 1011 diAcrcncc determines metabolic acid- base change during in viu·o hc1111Khluuon Crit C.lrc Med 2002; 30: I 57- 160

1. Acute respirarory acidosis. Expected fl IC0 3- ] .. 24 + 0. 1 x (PaC02

N.rin> RC..., Gardner LB Simple aC1d-ba>c Med Clin North Am 1980; 65:321-346 -

6. Metabolic aJkalosis. Expected PaC0 2

40

t

+

otkcn>r.tdt (.., A PJradoxic,tl effect of bronchodil.ttnn. Chc>t 1997;

M11r1\>111 Tl, Hall JA Hypc1factacm13 without mdom - Jn imc,tigation u'ing an m ,;cro model. Crit Care RcsuM: I J54 -~59

1999~

NJrtoa Re..;, l:'.mmetr M Simple and mixed Jl'id b.1.,.- di"irdcr' : A pr.Ktical approach. Medicine 198 1; 59:161 - 187

\ nhtc'h B, Morgan TJ, Garrell r The uses nt' error· mea>unng the lacurc g..ip. l..lncct 2001; 3581806 \\

4. Chrome rcsp1rarol) alkalosis. Expected [IIC0 3- ] - 24 - 0.5 x (40 - PaC0 2 ) 1.5 x [HC03- ]

n,

M1.t111g R, Grogono AW. ScvcnnghaU> )W lluman l'J "irh rhabdomyol)'t' 111th and without .ic.11c rcn.il f.ulure. J Clio Endc>e and chok;rcn>l e-.tera."' b)' th)Tnid hormone' fnzymc 198I,26:1-7 Ounn ('J, Pm and bypcrthyroidhm l"' 59 -7'1

in

the int•·n,i1c care

111111 .

Cm n MU, Wolf RO, Taylor LL, Hendrix TR Ongin of plcur.tl th11d anwl.u.: 1n c"'PhJj!l'JI ruprurc Ann Intern Med 1972, 76.985-986 S1hcr>tc1n l·J, Chier JR, .\l.ttc"un BJ ct .ti fhc ctkc1' ofadministracion oflithmm Jmon g.ip Am J Kidney n" 1989, 13.377-381

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Solomon SM , Kirby 111· The rctccd111g 'Ylldromc J review. JPF.N

J Parcm

'·'It' and magnc\lum 'IUlfatc on thl'

F.mcral Nutr 1990; 1490-97

Va,ik.1r,1n SD, TJlh, GA, Hraund WI Secondary hypo.1drcn.11i>m prc>enang Mth hypcrc.1lc:.1cm1.1 . C:hn l:ndoninul (oth.1lamic- p11uiw-y-adre11.il disorder.. Crit C'.lfc d111l 11d111w.11•h\

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of lntr.1-Aortic Balloon Coumcrpul;.tticm. 1'31rficld:

Corp 1997, USI\

1, ,mrl Ci\111, l'Jl.llrn Ml,/\ l'11lomu1.111 .1tll·11 ..11lw1n11.1111111 in anac>rhc,ia .ind imcnsive care. Br Ill 'l·l!i 95

J Anae.ih

1998;

~h 1.-.w ,\\ hhm,11.111 •(lli l'hY ' " ' " Ill• 111 ••I I •n11) . AclJ Ananihe,iol Sand 1998. 42 594-595 Pallon Ml\, Abmnh l;A Pulmonary dysti1nwon in d1ro111c l11·cr d"casc . Hq>.1tnlogy 2000. 32:859 -865 Gol 1998, 13 28 · 31 Network TARJ)S Vc11tilat1on w11h lcmcr m!JI \'Oltunc\ a> comp.ired \\1th tr.td111onal tid.11 volume-' for .1rntc lung 111111" and 1hc JClllC rc\r1rJtory dl\trc'-!> syndrome N Engl J Med 2000, 342. 1301 1308 Kunn I Diffu51on Jnd ahcol.ir capillJt) pcrmeab Im Bunawnrth· Hcincmann, 1993, 198- 218

Nunn

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rc,p1rarory ph,·,1oloj;\ . Oxford

ed. Applied rcsriratory phymilogy. Odcml

Ruttcl'\•nnh-lkrncnunn, 1993; 36-60 Rcynokh KJ. P,1b~ma E, Moyle JT, Sykn MK, H.1hn CE The cffc,, nf d)'hcmogloh11" on pul-.c mimctt) l'.111 I Theoretical .1ppro.t,·h and l'J1t ll , bx1>cnmcnml rc>ults using Jn 111 vitro tc>t ,y,rem J Clin Monn 1993, 9:81 - 911 Robin I· D. McCJulcy Rr An .m.1lris of pil1ypnc-orthodcoxia 'yndromc including a "new" therapcuuc JpproJdl 1997 112:1449 1451

Smyrn1m N, Curle~ I· lndirc.:t c.tlonmcn; In. Rippe R20 rc-prc'l'lll' .111 dt'\ .ll l'd 11~111111,11 g.1p ,111d 111~1 nt' IIt p1' ~rnu· 11! os1111111t .1lly

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l'ln,11cd 11~111111.11 p,.1p

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84 DATA INTERPRETATION IN CRITICAL CARE MEDICINE

Microbiology

Question 5.5: Answer A The diflerenrial diagnosis of this presentation would include some of the causes of a pure motor neuropath) . l'hese include postoperatin~ Gu11lain Barre syndrome, m}asthenia gravis, porphyria and wound botulism Snake bite, nck par.1lysis, toxins and intcstations are unlikely 10 days into hosp1tahzarion. Guillain Barre srndrome 1s unlike!)' in the setting of fixed dilated pupib and a normal CSF protein, though pupillat)' abnormaJities can occur, and the C'S'P protem can be normal in the initial stages. Myasthenia grav1s "ould nor normally cause fixed dilated pupils and the hyporeflexia argues against it. In the absence of an} se11.tires, mental changes, electrolyte abnormalities and discoloration of urine, porphyria is unlikely. Rarely an acute stroke could prese111 with fbcc1d weakness of the arms and legs; however with normal mentation and imaging, that is unlikely. Wound botulism has been described, classically in the postoperative seuing, and appears to present 10 days after surgery. The feature~ mcludc lower motor neuron type weakness, normal sensation and pupillary involvement. Bulbar palsy is almost always present, with the four Ds: dysphonia, dysphagia, diplopia, dysarthria. There are three characteristic features: symmetric, descending flaccid paralysis with prominent bulbar palsies; in an atcbrile p.nient; with a clear sensorium.

Question 5.6: Answer A Lithium O\"erdose. The calculated anion gap is in fact -6. A Im\ or ,1 negative anion g-year-old man has lmrn holidJyinq in the Northern Territory of Australia during the wet ~eason. In the l,1\I ~t'\ hn111., hP dflv£'1op 111.11k1•il 11111M 111 l1•mll'111P!>S. Intubation and ventilation is required h f. lll~e of rapidly p111q11 \\IVt hy11ox 11•11111 1cspi1.1lory f,1ilure. Tracheal aspirate shows ti 1111 lll'!Jcll iw hJdlll.

A What will you dV 111 thle?

11.0 101 Yt•lll

lrrhl ti 11\ll1lollc tit

111py, helt11c 111lt11re

results are

86 DATA INTERPRETATION IN CRITICAL CARE MEDICINE

MICROBIOLOGY - QUESTIONS 87

Question 6.3

Question 6.5

A 42-year-old man has had a cough for 2 weeks. He now presents with fever and a mild left hemiparesis. CT scan of the head demonstrates a lesion in the right frontal lobe. A stereotactic biopsy is undertaken.

A55-year-old hepatitis (-positive woman with known chronic liver disease presents with neck stiffness and drowsiness.

Gram stain shows weakly Gram-positi,·e beaded branching fil aments which arc weakly acid fast.

CSF

A What is the likely causative organism?

B What antibiotic therapy should be used?

Question 6.4 A 26-year-old man presents with shortness of breath, confusion, feve r and hypotension . CXR shows lobar pneumonia. Sputum sample shows Gram-positive diplococci.

WBC

90 x 106/L (Oro ol p.11il'lll!> .111d .1 ti·l·quentlr lll'gat•H' Gram sr;iin. .\l'l' suitJhk •'f~ the most likely cause of the cerebral lesions, given the clinical features suggestive of AIDS. 8 There 1s a high probability rhar the patient has an underlying HIV infection.

C An important differential to consider is cerebral lymphoma, which may be confused with cerebral toxoplasmosis in the HIV p.uient.

D Recommended therapy is pyrimethamine (combined with folinic acid to reduce the incidence of pyrimethamine associated myclotoxicity) and either sulfadiazin~ or clindamycm. If HIV infection is confirmed, antiretroviral therapy is also indicated.

Further reading naum S Mycoplnm1n p1uumo11i1tcand arypi•al pneumonia. In. Mandell l'rindpb and pr.1n1n ofmfecuom di..ca'c'. New York: Chu«·hill ljvml('lonc, 2000, 2018-2026

Filice G N1x:ard1o'i' In 1994;696-698

l~clbacher

J, Dolin R, cd>. Pri11..:1pb .ind practice ofinlC.:uou' di..:.A.'4."~. Nr>A

K e1 al., cd>. l'rin"ple5 ofinrcrnal mcdmne, 13th edn. Ne\\ York , Mc ''mplcx mm. In: Mandell G, Bennett York: Churchill Linng:.tonc, 2000; ISM-1580

cm. Principles of imcrn.tl

I

prJ and 'trokc prewmion Ar.:11 l11u:rn .\ I< I 1999; 159.2524 -2528 GallJ.nJlm n Thmmbm umc . In l\c:utler I'. Lkhtm.in M . Coller B. Kipp> T, ed, , William' llcm.uolo!I)'. 1'c11 )url \kGr.m ·H11l, 19 Hcmarology. Nl"\\ York ~kt;r.m - H11J, 1995 1290-ll l Gr.ilni by his mother. There was a history of head injury and post-traumatic epilepsy.

A The likely diagnosis is paraquat poisoning. This is based on the follm,~ng: • Easy access to paraquat, given the patient's occup