Clinical Scenarios in ICU

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title: Clinical Scenarios in Intensive Careauthor: Patey, Rona E.

publisher: Greenwich Medical Media Limitedisbn10 | asin: 1900151650

print isbn13: 9781900151658ebook isbn13: 9780511043116

language: Englishsubject Critical care medicine, Critical care medicine--methods--

problems.publication date: 1998

lcc: RC86P297 1998ebddc: 616.028076

subject: Critical care medicine, Critical care medicine--methods--problems.

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Clinical Scenarios in Intensive Care

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Greenwich Medical Media 1998

Greenwich Medical Media Ltd219 The Linen Hall162-168 Regent StreetLondonW1R 5TB

ISBN: 1 900 151 650

First Published 1998

Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permittedunder the UK Copyright Designs and Patents Act, 1988, this publication may not be reproduced, stored, ortransmitted, in any form or by any means, without the prior permission in writing of the publishers, or in thecase of reprographic reproduction only in accordance with the terms of the licences issued by the CopyrightLicensing Agency in the UK, or in accordance with the terms of the licences issued by the appropriateReproduction Rights Organization outside the UK. Enquiries concerning reproduction outside the terms statedhere should be sent to the publishers at the London address printed above.

The publishers make no representation, express or implied, with regard to the accuracy of the informationcontained in this book and cannot accept any legal responsibility or liability for any errors or omissions thatmay be made.

A catalogue record for this book is available from the British Library.

Distributed worldwide byOxford University Press

Designed and Produced byDiane Parker, Saldatore Limited

Printed in Great Britain byAshford Colour Press

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Clinical Scenarios in Intensive Care

byRona E. Patey MbChB, FRCA, FRCSNigel R. Webster BSc, MB ChB, PhD,

FRCA, FRCP

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Preface

This book gathers together clinical problems, many of which are common and often found on the generalintensive care unit. Although there are many tomes both large and small which detail the process of intensivecare and the knowledge base on which to place such practice, there are few books which set about the task in aproblem orientated manner. This book offers only a framework on which to base the practice of intensive care.The reader is encouraged to fill in the missing information and suggestions for further reading are given at theend of each case. These suggestions are not exhaustive, but have been included as they supplement informationreadily found in many intensive care textbooks.

The book is aimed at both students and teachers. We would anticipate that the book would be used during thestructured teaching sessions on intensive care for trainees. However it may also provide a useful framework fordiscussion by other staff who work on the intensive unit. Hopefully, it will provide a basis for discussion of thecommon problems and act as a forum to raise questions. Patients do not always survive treatment and outcomemay well be different in your unit!

R.E.P.R.R.W.1997

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Acknowledgements

We acknowledge the considerable support given to us by all members of the department at Aberdeen RoyalHospitals NHS Trust, and in particular those who have contributed cases to this text: Brian Cuthbertson, W.A.Hunter, Colin Reid, Andrew Ronald and S.A. Stott.

We also wish to thank Dr J.C. Patel for assistance with the ECG tracings and Prof J. Weir and Dr Olive Robbfor assistance with the radiological illustrations.

RONA E. PATEYNIGEL R. WEBSTER

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Contents

Case 1Asthma 1

Case 2Community Aquired Pneumonia 7

Case 3Cardiac Arrest 13

Case 4Aquired Immune Deficiency Syndrome 19

Case 5Acute Myocardial Infarction 25

Case 6Meningitis 31

Case 7Redo Cardiac Surgery 35

Case 8Pre-Eclampsia 41

Case 9Acute Respiratory Distress in a Child 47

Case 10Hypothermia 51

Case 11Coma 57

Case 12Acute Head Injury 63

Case 13Diabetes Mellitus 67

Case 14Acute Respiratory Distress Syndrome 73

Case 15Tetanus 77

Case 16Acute Renal Failure 81

Case 17Guillan-Barr Syndrome 85

Case 18Road Traffic Accident 89

Case 19Acute Pancreatitis 95


Case 20Trans Urethral Resection of Prostate 99

Case 21Post Operative Septicaemia 103

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List of Abbreviations

aHCO3 Bicarbonate

APTT Activated partial thromboplastin time

BE Base excess

CI Cardiac Index

CO Cardiac output

CVP Central venous pressure

ECG Electrocardiograph

ESR Erythrocyte sedimentation rate

FDP Fibrin degradation products

FIO2 Fractional inspired oxygen tension

gGT g Glutamyl transferase

GTN Glyceryl trinitrate

LDH Lactate dehydrogenase

MAP Mean arterial pressure

MPAP Mean pulmonary artery pressure

MCH Mean cell haemoglobin

PaO2 Partial pressure of arterial oxygen

PAOP Pulmonary artery occlusion pressure

PT Prothrombin time

SaO2/SvO2Haemoglobin oxygen saturation - arterial andmixed venous

sHCO3 Standard bicarbonate

SpO2 Haemoglobin oxygen saturation - pulse

SVR Systemic vascular resistance

TT Thrombin time

WCC White cell count

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Case 1

A 19 year old woman was admitted to the respiratory unit with a suspected exacerbation of long-standingasthma, presumably due to an acute infection. She had required admission to hospital on three previousoccasions. Her medication presently consisted of regular b-agonist and steroid inhalers, but no theophyllinederivatives. She had received short courses of oral steroids during previous severe exacerbations. On thisoccasion she gave a three day history of increasing wheeze, a cough with little sputum, i.e., she had beenunable to sleep well and was very tired. She had been using her inhalers increasingly frequently, and said shefelt that this was the most severe attack she had suffered.

On examination she was very distressed, unable to complete a sentence without pausing for breath and wasusing accessory muscles of respiration. She complained of thirst, had a dry mouth and looked centrallycyanosed. Her pharynx was red and inflamed and on auscultation her chest was quiet with little wheeze. Bloodpressure was measured at 100/80 mmHg, pulse 125 beats/minute, temperature 38 C, respiratory rate 36breaths/minute and she was noted to have pulsus paradoxus of 20 mmHg. Humidified high-flow oxygentherapy was commenced and hydrocortisone and a loading dose of aminophylline (5mg/kg) givenintravenously. Her peak flow was 70 1/minute and FEV1 600ml.




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Initial results are recorded below.

Table 1.1On admission One hour after admission

FIO2 0.210.6

PaO2 5.6 kPa9.0 kPa

PaCO2 6.9 kPa8.6 kPa

SpO2 68%82%

Haemoglobin 156g/lWCC 15.3 x 109/lPlatelets 468 x 109/lChest X-ray clear with significant hyperinflationECG sinus tachycardia - 125 beats/minute

This patient's asthma might be described as status asthmaticus. That is, either very severe asthma at its onset orasthma that is continuing to deteriorate despite standard therapy.

Discuss the pathophysiology of a severe asthma episode.

How does this lead to the production of the signs and symptoms in the history above?

What are the indications that this episode was severe?

History and examination will frequently confirm the diagnosis of asthma, however what are the differentialdiagnoses or complicating conditions which must be considered in patients at different ages




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who present with acute airflow limitation?

How should these be excluded?

What pharmacological agents are used in the management of severe asthma, what are the side effects of thesetherapies and how can they be minimised?

The decision to intubate and ventilate an asthmatic patient can be difficult. How can one initially assess theseverity of an asthma attack and should the patients progress be monitored thereafter if ventilation is notimmediately required?

An assessment from the medical staff in the Intensive Care Unit (ICU) was requested. She was becomingincreasingly exhausted and urgent transfer was arranged to the ICU. On arrival an arterial cannula was insertedand 1200ml of intravenous fluid infused. Following pre-oxygenation anaesthesia was induced with ketamineand fentanyl. Suxamethonium provided rapid muscle relaxation, facilitating tracheal intubation followed bypositive pressure ventilation. Inflation pressures after intubation were measured at 56 cmH2O but reduced to 32cmH2O over the next two hours with alteration of ventilatory parameters, nebulised b-agonists and anintravenous aminophylline infusion (0.5 mg/kg/hour). Sedation was maintained with propofol and alfentanilinfusions. In an attempt to minimise ventilation inflation pressure, neuromuscular blockade was continuedinitially.

Intravenous antibiotic therapy was commenced to cover a community-acquired respiratory tract infection,hydrocortisone continued intravenously three times daily and an antimuscarinic agent nebulised in addition tothe bronchodilator therapy already underway.

Two hours after intubation and ventilation, PaO2 was 17kPa with FIO2 0.5. She was normocapnic with tidalvolumes between 700 and 900ml and a respiratory rate of 12 breaths/minute. Invasive monitoring of centralvenous pressure was commenced and was initially measured at zero. Seven




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litres of intravenous fluid were infused in the first 24 hours to correct dehydration and maintain circulatorystatus. Her central venous pressure rose to 5 cmH2O during this period. Blood, sputum and throat swabs weresent for bacteriological examination.

Why use ketamine for induction of anaesthesia in this patient?

Would you consider a ketamine infusion for sedation in this patient?

What would you consider to be an appropriate choice of antibiotics initially?

The aims of mechanical ventilation in asthmatic patients are to adequately oxygenate and ventilate whilstminimising peak airway pressures and intrinsic positive end expiratory pressure. Discuss the problemsachieving these and the ventilatory manoeuvres one might employ.

How can intrinsic positive end expiratory pressure be measured?

During the first 48 hours in ICU her management was unchanged. Neuromuscular blockade was thendiscontinued with no increase in inflation pressure. She began to produce thick mucous plugs with chestphysiotherapy although bacteriological results were negative.

This improvement continued and she was weaned from ventilation on the fourth day of ICU care.Aminophylline infusion was discontinued and steroid therapy was decreased. She was discharged to therespiratory unit the following morning and left hospital three days later.

When is it appropriate to discharge such a patient from the ICU? Regular peak flow measurements areimportant - why?




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Further Reading

Bone R.C., Burch S.G., Management of Status Asthmaticus. Annals of Allergy 1991; 67: 461-9.

Guidelines for the management of asthma in adults: II - acute severe asthma. Statement by the British ThoracicSociety, Research Unit of the Royal College of Physicians of London, Kings Fund Centre, National AsthmaCampaign. British Medical Journal. 1990; 301: 797-800.

Hall J.B., Wood L.D.H., Management of the critically ill asthmatic patient. Medical Clinics of North America1990; 74: 779-95.

Hemming A., Mackenzie I., Finfer S. Response to ketamine in status asthmaticus resistant to maximal medicaltherapy. Thorax 1990; 49: 90-1.

Kay A.B. Pathology of mild, severe, and fatal asthma. Am J Respir, Critical Care Medicine. 1996; 154: 566-9.

Valman H.B., Bronchial Asthma. British Medical Journal 1993; 306: 1676-81.




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Case 2

A 60 year old previously fit man was admitted to a general medical ward for investigation of pyrexia ofunknown origin. He was slightly confused, and gave little history other than a recent generally non-productivecough and feeling generally unwell and thirsty. On examination his temperature was 39 C, he had a heart rateof 116 beats/minute and was sweaty. Examination of his chest revealed dullness to percussion and bronchialbreathing at the right apex with vesicular breath sounds and crepitations at the left base. The only abnormalityon abdominal examination was a slightly enlarged non-tender liver. His sputum was noted to be purulent andrusty coloured, and he had proteinuria. A chest X-ray revealed extensive consolidation in the right upper andleft lower lobes.

This man was diagnosed has having a community-acquired acute pneumonic process. How should this beinvestigated?

What initial antimicrobial therapy would you start if he had presented to your unit?

Explain the rationale leading to your choice.

Results from initial investigations performed in this unit are as follows:

Table 2.1

Haemoglobin145 g/l

Na+129 mmol/l

WCC10.1 x 109/l

K+4.2 mmol/l

Platelets486 x 109/l

HCO3-24 mmol/l

ESR50 mm/hr

Urea8.9 mmol/l

Creatinine110 micromol/l

Sputum gram staingram positive coccus

Generally deranged liver function tests.




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What is the likely diagnosis and what is the appropriate treatment?

Blood cultures were taken and blood sent for viral and atypical serology and pneumococcal antigen. He wascommenced on intravenous antibiotic treatment, maintenance fluid intravenously and oxygen by mask (61/minute).

Twenty four hours later there had been no improvement and an additional antibiotic was added to his therapy.Pneumococcal antigen was negative. He was reviewed by a respiratory physician who suggested he beinvestigated for systemic vasculitis.

Which vasculitic processes can affect the lung and which other organs might be involved?

Is this a typical presentation of a vasculitic process?

How would you investigate the patient?

During the next 24 hours his condition significantly deteriorated and was discussed with the medical staff fromthe ICU. At assessment he was confused, but answered simple questions, tachypnoeic (45 breaths/minute) andcentrally cyanosed, despite increasing his oxygen to 12 1/minute. Arterial blood was taken for gas estimationand showed PaO2 6kPa and PaCO2 3.4 kPa whilst he was breathing oxygen at 12 1/minute through a facemask. He was transferred to ICU to permit invasive monitoring and ventilatory support.

On what do you base the decision to ventilate such patients?




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On arrival at the ICU he was noted to be cold and clammy, responding only to pain, in atrial fibrillation (144beats/minute), tachypnoeic (48 breaths/minute), hypotensive (90/70 mmHg) and centrally cyanosed. A pulseoximeter could pick up no trace. While he was pre-oxygenated with a non rebreathing bag, a radial arterial linewas inserted and connected to permit continuous systemic pressure monitoring. Anaesthesia was then induced,and after neuromuscular blockade, his trachea was rapidly intubated and intermittent positive pressureventilation commenced with an FIO2 of 1.0. With the addition of 10 cmH2O of positive end expiratorypressure the FIO2 was reduced to 0.8. His core temperature was measured at 38.4 C.

The following blood results were obtained.

Table 2.2

PaO210.6 kPa

PaCO25.7 kPa

pH7.27

Base excess- 5.3

Haemoglobin135 g/l

WCC12 x 109/l


Haematocrit40%

Na+129 mmol/l

K+3.9 mmol/l

Urea7.2 mmol/l

Creatinine125 micromol/l

He remained unstable after ventilation, requiring infusion of fluid and then commencement of dopamine tomaintain systolic blood pressure above 100 mmHg. A pulmonary artery flotation catheter was inserted and afterinitial measurements and calculations, a noradrenaline infusion added to the dopamine infusion and he wasdigitalised.




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Table 2.3

Heart rateMAPCVP

135 beats/minute65 mmHg12 mmHg

PAOPMPAP

9 mmHg22 mmHg

CO2CISaO2SvO2

5.5 1/minute3.2 1/minute/m296%71%

What is your interpretation of these results? Can you calculate the vascular resistances, stroke work indices andoxygen delivery and extraction ratio.

Do you agree with the choice of vasoactive drugs?

On what evidence is your choice of vasoactive drugs based? Assuming the results in the text represent the worstresults obtained, calculate the APACHE II score for this patient from the time he was assessed by the ICU staff.

Can you comment on the relevance of this score?

What is the difference between the APACHE II and APACHE III scoring systems.

What are they designed to be used for and how useful are they?




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His therapy was reviewed with the microbiologists and antibiotics changed. Thus far all microbial culture andautoantibody screens were negative, and the gram positive coccus reported on the initial sputum sample wasreported as Staphylococcus epidermidis of doubtful significance. Diffuse alveolar infiltrates were now apparentin addition to the lobar consolidation on his chest X-ray. A nasogastric tube was inserted and he began toreceive enteral nutrition.

His condition steadily improved from this point, allowing steady reduction in the cardiovascular and ventilatorysupport. On the fifth day of intensive care, his gas exchange and general condition were such that his sedationwas reduced. He was gradually weaned from ventilation over the next two days, extubated and then transferredback to the general medical ward.

Shortly after arrival in the medical ward he was noted to have profuse diarrhoea. Nasogastric feeding wasstopped, intravenous fluid replacement recommenced and stool was sent for culture. This grew Clostridiumdifficile and a further antibiotic was commenced.

Diarrhoea is a common problem in the critically ill patient and occurs in up to 50% of those who are enterallyfed.

Discuss the causes of diarrhoea in the ICU patient and how you would proceed in the patient who had nogrowth on stool culture.

Why has this patient developed diarrhoea and what is the appropriate treatment?

Convalescent titres showed a large rise in Chlamydia psitticai. On further questioning he admitted to recentlypurchasing a bird table and regularly feeding the local pigeons.




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Further Reading

Garrard C.S., A'Court C.D., The diagnosis of pneumonia in the critically ill. Chest 1995; 108: 17S-25S.

Rello J., Quinrana E., Ausing V., Net A., Prat S.G. A three year study of severe community acquiredpneumonia with emphasis on outcome. Chest 1993; 103: 232-5.

American Thoracic Society: Guidelines for the Initial Management of Adults with Community-acquiredPneumonia: Diagnosis, Assessment of severity and Initial antimicrobial therapy. American Review ofRespiratory Disease 1993; 148: 1418-26.

Tabagcahli S., Jumaa P. Diagnosis and management of Clostridium Difficile infection British Medical Journal1995; 310: 1375-80.

Levinson M., Bryce A. Enteral feeding, gastrci colonisation and diarrhoea in critically ill patients; is there arelationship Anaesthesia and Intensive Care 1993; 21: 85-8.

Ringel A.F., Jameson G.L, Foster E.S. Diarrhoea in the intensive care patient. Critical Care Clinics. 1995; 11:465-477.

Knaus W.A., Draper E.A., Wagner D.P., Zimmermann J.E., APACHE II: A severity of disease classificationsystem. Critical Care Medicine 1985; 13: 818-29.

Knaus W.A., Wagner D.P., Draper E.A, Zimmermann J.E., et al. The APACHE III prognostic scoring system.Risk prediction of hospital mortality for critically ill hospitalised adults. Chest 1991; 100: 1619-36.




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Case 3

A 27 year old woman was rushed to the resuscitation room of the local hospital by paramedic staff. On arrivalshe had a pulse rate of 170 beats/minute and her blood pressure was 85/40 mmHg. She was intubated andbreathing spontaneously. Her pupils were fixed and dilated. Her Glasgow Coma Score was recorded as three. Itwas reported that she had collapsed suddenly at work and was in ventricular fibrillation when the paramedicstaff arrived at the scene.

This woman has had a cardiorespiratory arrest. Is it possible to assess her likelihood of survival at this point?

What information would you seek to obtain in order to make an assessment?

Ventricular fibrillation is by far the commonest primary rhythm of cardiac arrest. Outline the protocol formanagement of this dysrhythmia and the rationale behind it.

Which other heart rhythms may be associated with cardiac arrest?

When she collapsed, the staff in her office telephoned for an ambulance and reported they could feel no pulse.She had just risen from her desk to make coffee at the time of the collapse. The paramedic team arrived at thescene seven minutes after receipt of the call. There had been no basic life support carried out prior to theirarrival, but the patient had been turned into the recovery position. Basic life support was commenced by oneparamedic as the other attached the woman to a semi-advisory defibrillator monitor. Ventricular fibrillation wasdiagnosed and, prompted by the defibrillator, two DC shocks at 200J were administered. After the second shocka pulse could be felt in the region of the carotid artery and the monitor




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showed a supraventricular tachycardia of 170 beats/minute.

Prior to transfer, her trachea was intubated and ventilation was assisted using a non rebreathing bag withsupplemental oxygen although she was making some respiratory effort. Arrival in the resuscitation room was 22minutes after the call for the emergency services had been made.

Chest compression is performed in an attempt to maintain some circulation in a patient who had sustained acardiac arrest. How is this manoeuvre optimally performed and how successful is it at maintaining organ bloodflow?

What is the rationale of the use of adrenaline in cardiac arrest protocols?

Initial management in the resuscitation room was to control ventilation with the aid of neuromuscular blockadeand continue supplemental oxygen. Arrangements were made to transfer her to the ICU after a computerisedtomography (CT) scan of her head. While awaiting transfer to the CT room, adenosine was given in incrementsin an attempt to treat the supraventricular tachycardia without effect. Her CT scan was reported as normal.

On arrival at ICU she still had a supraventricular tachycardia of 165 beats/minute. Invasive systemic arterialpressure monitoring was established and revealed an elevated blood pressure at 220/120 mmHg. This wastreated with increments of a beta blocker and her rhythm returned to sinus at 86 beats/minute and bloodpressure settled at 110/80 mmHg.




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It is stated this patient had a supraventricular tachycardia following her cardiac arrest. How would thisconclusion be reached?

Discuss the management of supraventricular tachycardia in this case.

Were there other treatment options?

What is the mechanism of action of adenosine?

Would the use of verapamil have been appropriate in this young woman?

Her husband has arrived and is very concerned about his wife's condition. He wants to know when you will beable to tell him whether she will survive and what quality of survival she will make. How will you councilhim?

Initial investigations included full blood count, urea and electrolytes, cardiac enzymes, chest X-ray, twelve leadECG and echocardiography. The results of these were unremarkable other than an initial serum potassium of2.8 mmol/l. It was decided to maintain sedation and keep her ventilated for 48 hours.

What is the evidence that elective ventilation is worthwhile in these types of patients and how long should itcontinue?

Her past medical records revealed a three year history of investigation of palpitations for which no cause hadbeen found. She was currently being treated for hypertension with a calcium channel blocking agent.




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Estimation of cardiac enzymes was repeated during the period of sedation and ventilation but results remainedwithin normal limits, however her serum potassium levels were persistently low. Several grams of potassiumwere infused to bring the level within the normal range. This was investigated further and revealed a highurinary excretion of potassium.

On day three sedation was withdrawn and she rapidly recovered consciousness and returned to a generalmedical ward later that day. Further investigations included 24 hour Holter monitoring and extensiveinvestigation of potassium handling. A diagnosis of primary ventricular fibrillation was made and animplantable defibrillator was inserted.

What role do electrolyte abnormalities play in the genesis of cardiac arrhythmias?

What are the other causes of arrythmias in this age group?

What factors commonly precipitate arrhythmia in such susceptible individuals?

Had this patient suffered an acute myocardial infarction thrombolytic therapy may have been needed. Is thiscontraindicated after cardiopulmonary resuscitation?




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Reading

Ballew K.A., Cardiopulomonary Resuscitation. British Medical Journal 1997; 314: 1462-5.

Emergency cardiac care committee and subcommittee, American Heart Association. Guidelines forcardiopulmonary resuscitation and emergency cardiac care. Journal of the American Medical Association 1992;268: 2171-295.

Ganz L.I., Freidman P.L., Supraventricular Tachycardia. New England Journal of Medicine 1995; 332: 162-73.

Grubb N.R., Elton R.A., Fox K.A.A., In-hospital mortality after out-of-hospital cardiac arrest. Lancet 1995;346: 417-21.

Handley A.J., Basic life suport. British Journal of Anaesthesia 1997; 79: 151-58.

Kellerman A.L., Hackman B.B., Somes G. Predicting the outcome of unsuccessful pre-hospital cardiac lifesupport. Journal of the American Medical Association 1993; 270: 1433-6.

Marsden A.K., Ng G.A., Dalziel K., Cobbe S.M. When is it futile for ambulance personnel to initiatecardiopulmonary resuscitation. British Medical Journal 1995; 311: 49-52.

Murdock C.J., Davis M.J.E. Management of the patient resuscitated from sudden cardiac death. Current Topicsin Intensive Care, No 1; Chapter eight.. WB Saunders Company Ltd 1994.

Robertson C.E., Advanced life support guidelines. British Journal of Anaesthesia 1997; 79: 172-7.

Tunstall-Pedoe H., Bailey L., Chamberlain D.A., et al. Survey of 3765 cardiopulmonary resuscitations inBritish hospitals (the BRESUS study): methods and overall results. British Medical Journal 1992; 304: 1347-51.




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Case 4

A 33 year old man was admitted to the ICU from the Emergency Department receiving room late one evening.He had sustained a respiratory arrest in an ambulance en-route to hospital. He had been intubated by aparamedic and given intermittent positive pressure ventilation with supplemental oxygen and maintained aspontaneous cardiac output at all times.

An ambulance had been called by friends as they had become scared by his rapidly progressing breathlessnessover the preceding few days. Apparently he had complained of a dry cough for one month and night sweats andfever for two weeks.

On arrival at ICU he was already intubated and ventilated. He looked pale and clammy and was tachycardic(115 beats/minute). Peripheral arterial and central venous cannulae were inserted and baseline investigationswere performed.

Arterial blood gas results on admission were:

Table 4.1

FIO20.6

SaO286%

PaO28.0 kPa

PaCO26.2 kPa

pH7.23

Further examination revealed lymphadenopathy of his neck, axillae and groins and he had evidence of an oralcandida infection. His temperature was 39.3 C. His friends revealed that the man was homosexual and hadspent some years in the United States of America. His partner had lost




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weight over the last five months and so the patient had had an HIV antibody test 3 months earlier, though hehad said that this had been negative.

He had no clinical chest signs when settled on the ventilator and the initial chest radiograph was clear.However, gas exchange remained poor (PaO2 10.6 kPa) despite FIO2 1.0 and 10 cmH2O positive endexpiratory pressure (PEEP).

What investigations would you perform on this patient and why?

What is your differential diagnosis, and what therapy would you start?

His gas exchange showed little improvement over the next few hours. Although there were fewtracheobronchial secretions broncho alveolar lavage (BAL) was performed and a specimen sent forexamination. His admission white cell count was 3.4 x 109/1 (15% lymphocytes). His Tcell subset CD4 countwas 180 x 106/1 and HIV antibody test was confirmed positive by antigen tests. BAL specimen confirmedPneumocystis carinii infection, presumed to be HIV related.

What is the Acquired Immune Deficiency Syndrome?

How does it usually present and how long is the incubation period?

Pneumocystis carinii with resulting acute respiratory failure is the commonest cause of ICU admission in HIVinfected individuals in North America. It would have been unusual for Pneumocystis carinii to occur had theCD4 count been greater than 250 x 106/1 cells/mm3. However other aetiologies must be considered.




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What in particular would you consider?

Lactate dehydrogenase is characteristically elevated in patients with this pathology, and the level will correlatewith the severity and the course of the infection. However this enzyme can be elevated in a number of otherpathologies.

Discuss the differential diagnosis of an elevated lactate dehydrogenase.

BAL is positive in greater than 80% of Pneumocystis carinii infections if the sample is appropriately examined.

How is a BAL performed, how should the patient be monitored and what are the complications of thetechnique?

Would a trans-bronchial biopsy have been appropriate in this patient?

High dose intravenous cotrimoxazole, intravenous steroid and nebulised pentamidine were commenced. Inaddition, he received intravenous diuretic therapy and nebulised bronchodilators to manage intermittentbronchospasm. Fluconazole was given as treatment for candida. He was now nursed in an isolation room.

His chest X-ray had deteriorated within hours of admission first showing only peri hilar shading, thenprogressing to diffuse bilateral gross alveolar shadowing (Fig. 4.1).

Three days after admission he still required significant respiratory support to maintain a PaO2 greater than 8.0kPa (FIO2 1.0, PEEP 15 cmH2O) with pressure controlled mode of ventilation. He was sedated andneuromuscular blockade continued to facilitate ventilation. All bacteriological investigations were reviewed asthere had been no improvement, however all other results were negative. In particular, there was no evidence oflegionella or mycobacteria. Serology and a sample of diarrhoea on day five




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were positive for cytomegalovirus.

Gancyclovir was commenced but as he developed a generalised erythematous rash, this was changed toFoscarnet.

By day 12 he was apyrexial, his gas exchange was much improved and he required less respiratory support.Despite no radiological improvement he was weaned from the ventilator at day 18. Two days later whendischarged to the infectious diseases unit he was commenced on anti-HIV therapy, acyclovir and oral septrin asPneumocystis carinii prophylaxis.

His chest X-ray had cleared by day 21. He received counselling for his HIV and AIDS diagnosis.

Fig. 4.1

What is the rationale for using isolation rooms in such patients?

What other precautions may be required for this patient?




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What are the other common measures taken on an ICU to prevent cross infection?

What is the evidence for their effectiveness?

What other manifestations of HIV infection are likely to present to the ICU?

Further Reading

De Palo V.A., Millstein B.H., Mayo P.H., Salzman S.H., Rosen M.J. Outcome of intensive care in patients withHIV infection. Chest 1995; 107: 506-10.

Gachot B., Clair B., Wolff M., Regnier B., Vachan F. Continuous positive airway pressure by face mask ormechanical ventilation in patients with human immunodeficiency virus infection and severe Pneumocystiscarinii Pneumonia. Intensive Care Medicine 1992; 18: 155-9.

Millar A., Hand C. AIDS and the lung. Hospital Update 1991; 17: 177-96.

Poznansky M. HIV positive patients first presenting with an AIDS defining illness. British Medical Journal1995; 311: 156-8.

Sattler F.R., Feinberg J. New developments in the treatment of Pneumocystis pneumonia. Chest 1992; 101:451-7.

Wachter R.M, Luce J.M, Hopewell P.C. Critical care of patients with AIDS. Journal of the American MedicalAssociation 1992; 267: 541-7.




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Case 5

A 60 year old man complained of sudden severe gripping chest pain while participating in a bowls match andthen collapsed on the green. An ambulance was called and he was transferred to the local hospital. On arrivalhe was noted to be distressed, pale, cold, clammy and breathless. He was able to report that he had recently hadincreasingly frequent chest discomfort, but had thought this was indigestion. He had smoked 30 cigarettes perday for over 30 years.

What is the differential diagnosis?

His pulse rate was 110 beats/minute, blood pressure 100/60 mmHg and his neck veins appeared full. High flowoxygen was administered through a face mask and blood taken for full blood count, urea and electrolytes,cardiac enzymes and arterial blood gases. A twelve lead ECG showed sinus tachycardia with ST elevation inleads V1-V3 (Fig. 5.1), and a chest X-ray was clear.

Fig. 5.1




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The working diagnosis was acute myocardial infarction and the patient was transferred to the coronary careunit. In the coronary care unit he received thrombolytic therapy.

What are the indications and contraindications for thrombolytic therapy?

Which agents can be used and is there an optimal time for their administration?

What are the hazards of this therapy?

What other measures have been described to limit myocardial cell death post-infarction?

Which blood estimations will help establish if a patient has suffered a myocardial infarction?

His condition improved and three days later he was transferred to the general medical ward. Twenty four hoursafter this he again complained of chest pain and became extremely dyspnoeic. His pulse rate was 125beats/minute and his blood pressure 80/60 mmHg. A twelve lead ECG revealed sinus tachycardia with evidenceof the recent infarct and generalised ischaemia. A chest X-ray was performed which revealed widespreadpulmonary oedema. Acute left ventricular failure with cardiogenic shock was diagnosed and he was transferredback to the coronary care unit.

Discuss the pathophysiology of left ventricular failure and cardiogenic shock.

Describe how these conditions can be treated.




Page 27

How should these treatments be assessed and monitored in the sick patient?

What are the hazards and complications of drug therapy in such patients?

In the coronary care unit high flow oxygen and a continuous intravenous infusion of an inotropic agent werecommenced and an intravenous bolus dose of loop diuretic given. One hour later his blood pressure remainedlow despite increasing rate of infusion of inotrope and only 30mls of urine had been passed after insertion of aurinary catheter.

How would you proceed?

What complications of myocardial infarction should you consider?

A pulmonary artery catheter was inserted with difficulty and the procedure was complicated by several shortepisodes of ventricular tachycardia (VT). A bolus dose of an anti-arrythmic agent was then given, but despitethis, there was a further episode of VT during which no peripheral pulses could be felt.

He reverted to sinus rhythm after defibrillation with 200J and his pulse and blood pressure returned as before.The pulmonary occlusion pressure was 22 mmHg and a prominent ''v" wave noted. One hour later, despiteincreased inotropic support, his blood pressure remained low, a pulse oximeter could not pick up a reading andhe had passed no further urine.

Which inotropic agents are you aware of and what is the mechanism of action of these agents?




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He was transferred to the ICU and after intravenous induction of anaesthesia, intubated and intermittent positivepressure ventilation commenced. His inotropic support was increased and a trans-oesophagealechocardiography performed which revealed severe mitral regurgitation resulting from a flail posterior valveleaflet. His left ventricular function was described as good and he was referred for emergency mitral valvereplacement.

Trans-oesophageal echocardiography is increasingly used in cardiology and cardiac surgery/anaesthesia. Whatadvantages does it have over conventional echocardiography?

In which circumstances is it particularly useful?

Two hours later he was transferred to theatre with a heart rate of 160 beats/minute, blood pressure 70/40 mmHgand pulmonary artery occlusion pressure of 23 mmHg. He was receiving significant inotropic support, but hadonly passed 50 mls of urine during the preceding 4 hours. During surgical preparation of the skin there was anepisode of ventricular fibrillation which rapidly reverted to sinus tachycardia with a 200J DC shock. Surgeryproceeded but during aortic cannulation he again became unstable with runs of ventricular and supraventriculartachycardia. This was rapidly followed by ventricular fibrillation and after a brief period of internal cardiacmassage cardiopulmonary bypass was rapidly instituted. The aorta was cross-clamped and cardioplegiaadministered, whereupon the heart was opened and a flail anterior valve leaflet resulting in severe mitralregurgitation was revealed. The papillary muscle had ruptured and the chordae and papillary muscle wereprolapsing into the left atrium. A mitral valve replacement was performed.

Initial attempts to wean from cardiopulmonary bypass were unsuccessful and an intra-aortic balloon pump wasinserted via the left femoral artery whereupon he was weaned from bypass with significant inotropic support.




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An intra-aortic balloon pump was inserted to provide support to the heart following cardiopulmonary bypass.

What other mechanical means have been described as a means of providing support to the failing heart?

What complications are associated with the use of such devices?

His blood pressure fell precipitously as the surgeon attempted to close the chest and so the chest was left openand he was transferred to the cardiac ICU. Shortly after that he became bradycardic and then asystolic.Cardiopulmonary resuscitation was commenced, the dressings removed and internal cardiac massagecommenced. There was no evidence of an acute tamponade. He failed to respond to fluids or further inotropesand further resuscitation was abandoned 30 minutes later.

Further Reading

Weston C.F.M, Penny W.J, Julian D.G. Guidelines for the early management of patients with myocardialinfarction. British Medical Journal 1994; 308: 767-71.

McMurray J, Rankin A. Recent Advances. Cardiology - I: Treatment of myocardial infarction, unstable angina,and angina pectoris. British Medical Journal 1994; 309: 1343-9.

Anderson H.V., Willerson J.T. Current Concepts: Thrombolysis in Acute Myocardial Infarction. New EnglandJournal of Medicine 1993; 329: 703-9.

Calif R.M., Bengston J.R. Cardiogenic Shock. New England Journal of Medicine 1994; 330: 1724-30.

Skarvan K. Perioperative left ventricular failure: the rationale for use of vasoactive drugs. In Vasoactive Drugsed. Skarvan K. Bailliere's Clinical Anaesthesiology 1994; 8: 215-42.




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Beique F, Joffe D, Kleiman S. An introduction to transoesophageal echocardiography. Part I. Basic Principles.Canadian Journal of Anaesthesia 1996; 43: 252-77.

Oxorn D, Edelist G, Stafford Smith M. An introduction to transoesophageal echocardiography. Part II. ClinicalApplications. Canadian Journal of Anaesthesia 1996; 43: 278-94.

Barnard M.J, Linter S.P.K. Acute circulatory support. British Medical Journal 1993; 307: 35-41.




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Case 6

A previously well 18 year old male was admitted as a medical emergency with a two day history of fever andsix hour history of severe "bursting" headache and photophobia. When seen at home by his general practitionerhe displayed cervical rigidity and a positive Kernig's sign. The general practitioner administered 2.4g of benzylpenicillin intravenously and transferred him by ambulance to the nearest hospital some 45 miles away.

During ambulance transfer his conscious level deteriorated and on arrival at hospital his Glasgow Coma Scorewas 11 (E3, M5, V3). He was pyrexial (axillary temperature 38.8 C), his systolic blood pressure was 100mmHg and had a heart rate of 115 beats/minute. His oxygen saturation was measured by pulse oximetry at 94%and so 6 1/minute of oxygen was commenced by face mask. Blood was sent for routine haematology,biochemistry and blood culture. There was no evidence of papilloedema.

What is your working diagnosis at this stage and what other investigations should be performed?

Is a lumbar puncture mandatory?

An urgent CT scan of his head was performed which revealed no abnormality. However, during the procedurehe further deteriorated and had a grand mal convulsion which resolved with bolus intravenous benzodiazepinetreatment. Neuromuscular blockade was established to permit protection of his airway by tracheal intubationand he was transferred to the ICU.

On arrival in the ICU, invasive monitoring was established and a lumbar puncture performed. The CSF wasturbid and under pressure (not measured). CSF glucose was 1.8 mmol/l (serum glucose 7.8 mmol/l) and protein




Page 32

was 3 g/l. The cell count was 300, predominately polymorphonuclear leukocytes and a film revealed gramnegative intracellular diplococci.

Comment on these results. What is your initial management plan now?

What are the usual organisms causing meningitis in neonates, children and adults? Resistance to some of thecommonly used antibiotics is now regularly found with some organisms.

What are the appropriate antibiotics to use in these three age groups initially?

What is the place of steroids in management?

The diagnosis was confirmed as meningococcus. He had a neutrophilia (16 x 109/1) Blood cultures were allnegative. Sedation was maintained with propofol, benzodiazepine and opioid infusions. His respiratory functionwas good and he was ventilated with an F1O2 of 0.35 to maintain a PaCO2 of 3.8 kPa. Enteral feeding wascommenced after insertion of an orogastric tube. He remained cardiovascularly stable and developed no rashindicative of meningococcal septicaemia. There were no further convulsive episodes.

Would you alter treatment if there were further seizures?

Would you advocate any further monitoring or treatment aimed at the central nervous system?

His pyrexia subsided and his white cell count fell to normal within 24 hours. Sedation and full ventilation withcontrol of PaCO2 was continued




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until 48 hours after ICU admission. His sedation was reduced and he quickly weaned from assisted ventilationand was extubated on day three, after it was evident he had no obvious neurological impairment.

His antibiotic treatment continued on discharge to the infectious diseases unit. His family, friends and workcolleagues received rifampicin as prophylaxis.

Further Reading

Strang J, Pugh E. Meningococcal infections: Reducing the fatality rate by giving penicillin before admission tohospital. British Medical Journal 1992; 305; 141-3.

Begg N. Reducing mortality from meningococcal disease. British Medical Journal 1992; 305; 133.

Kristiansen. Secondary prevention of meningococcal disease. British Medical Journal 1996; 312; 591-2.

Schaad U.B., Kaplan S.L., McCracken G.H. Steroid treatment for bacterial meningitis. Clinics in InfectiousDiseases 1995; 20: 685-90.

Kennedy N.J., Duncan A.W. Acute menningococcaemia: recent advances in management (with particularreference to children). Anaesthesia and Intensive Care 1996; 24: 197-216.

Tunkel A.R., Scheld W.M. Acute bacterial Meningitis. Lancet 1995; 346: 1675-80.




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Case 7

A 69 year old man was admitted to the coronary care unit with a history of severe chest pain unresponsive tohis usual GTN spray. Past medical history revealed 10 years of ischaemic heart disease and a coronary arterybypass grafting procedure for triple vessel disease seven years previously. Saphenous vein grafts had beenperformed, bypassing stenoses in his left anterior descending (LAD), circumflex and right coronary arteries.Left ventricular function had been described as good at that time. He reported he had been symptom free untilsix months previously when he could no longer play a full round of golf without experiencing several episodesof anginal-type pain and breathlessness. During the two weeks prior to admission he had also experienced somerest and night pain. Current drug therapy consisted of a b-blocker, calcium channel blocker and nitrates.

What is your differential diagnosis and how would you investigate this patient?

Serial electrocardiographs and cardiac enzymes revealed no evidence of a myocardial infarction. He continuedto experience episodes of angina at rest and was commenced on intravenous heparin and nitrate therapy. Anurgent coronary angiogram was performed which revealed a deterioration in left ventricular function withanterior apical hypokinesis, elevation of the left ventricular end diastolic pressure at 22 mmHg and occlusion ofthe circumflex and right coronary grafts. The LAD graft was providing the only significant myocardialperfusion.

This patient has been diagnosed as having unstable angina. Discuss the methods of treating this problem. Whatis the rationale




Page 36

of using GTN, heparin and aspirin at this time in the disease process?

Urgent coronary artery bypass grafting was scheduled for later that week. As this was a "redo" case, the surgeonrequested he receive a bolus and then infusion of aprotinin. Unfortunately the administration of just a fewmillilitres of this was associated with a marked fall in systolic blood pressure, rise in ventilation inflationpressure, and the patient became very flushed. Auscultation of the chest revealed widespread wheezing. Theaprotinin was immediately discontinued, the inspired oxygen increased to 100% and fluids rapidly infused.Boluses of adrenaline were given and an infusion commenced. He stabilised during the next 15 minutes and thesurgeon was able to proceed with the operation.

Anaphylaxis is an ever present hazard of both anaesthetic and ITU treatment.

Discuss how it should be managed and investigated.

How should a patient who has had an anaphylactic episode be managed after the acute event?

What would you discuss with the patient afterwards and would you arrange any follow up investigations?

Prior to re-sternotomy, he was heparinised and a femoral arterial cannula inserted. His left internal mammaryartery was anastomosed to his LAD, and saphenous veins to his obtuse marginal and distal right coronary arterybranches. Surgery was prolonged and difficult with a bypass time of over 2 hours and a blood loss of 1800ml.During bypass it was noticed that his urine had become tinged pink, and inotropic support was required to




Page 37

come off bypass. Despite adequate reversal of heparin, assessed by an activated clotting time, he continued toooze from the wound margins. Blood was sent for clotting studies, but while awaiting these results he wasgiven tranexamic acid, two units of fresh frozen plasma and six units of platelets empirically. Following chestclosure, he was taken to the cardiac ICU for postoperative care.

In the first 30 minutes after surgery 900ml of blood was lost from the drains and a further 3 units of bloodtransfused. His chest was reopened and a bleeding point on an anastamosis found and controlled.

The clotting results are shown below:

Table 7.1

Platelets45 x 109/1

PT25 seconds

APTT60 seconds

Why do cardiac surgical patients bleed?

What measures can be taken to minimise bleeding and decrease the need for transfusion not only in cardiac butin other types of surgery?

What is the rationale behind using aprotinin?

What are the hazards of aprotinin therapy other than anaphylaxis?

What other drugs can be given to decrease bleeding following cardiac surgery?

How should bleeding be managed in the ICU following cardiac surgery?

A further six units of platelets and two units of fresh frozen plasma were transfused and vitamin K given. Thebleeding decreased over the following




Page 38

three hours, but his urine output had been minimal despite apparently adequate filling pressures. The inotropicsupport was increased. Six hours postoperatively, the systemic blood pressure fell precipitously and there was amarked rise in central venous pressure. There had been less bleeding from his chest drains during the last twohours.

His chest was reopened again and there was a sudden gush of blood from around the heart associated with arapid improvement in blood pressure and central venous pressure. There was generalised ooze of blood aroundthe heart but no specific bleeding points could be identified. Further platelets and fresh frozen plasma weregiven and the chest was again closed. Blood loss from his drains was now much less, he was cardiovascularlystable although still requiring inotropic support and his urine output had increased. During the following sixhours it was possible to begin to slowly decrease his inotropic support, and the sedation was lightened briefly inorder to assess his neurological status. His mental status was found to be appropriate and he was able to obeycommands. Thirty hours after surgery, he required minimal inotropic support and all sedation was stopped andonce he was fully awake and breathing spontaneously he was extubated and later that day returned to thecardiac high dependency unit. He was discharged from the acute ward to convalescence 10 days later.

This patient eventually developed a cardiac tamponade.

What is the pathophysiology of tamponade?

How can it be diagnosed?




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Further Reading

McMurray J. Rankin A. Recent Advances. Cardiology - I: Treatment of myocardial infarction, unstable angina,and angina pectoris. British Medical Journal 1994; 309: 1343-9.

Woodman R.C., Harker L.A. Bleeding complications associated with cardiopulmonary bypass. Blood 1990; 76:1680-97.

Mongan P.D. Optimizing erythrocyte conservation and transfusion practices in cardiac surgery. CurrentOpinion in Anaesthesiology 1995; 8: 41-8.

Pakalnis R. O'Hara I.B, Campbell F.W. Prevention and treatment of post-cardiopulmonary bypass bleeding.Current Opinion in Anaesthesiology 1995; 8: 49-55.

Davis R, Whittington R. Drug evaluation - Aprotinin. Drugs 1995; 49: 954-83.

Horrow J.C. Hemostatic therapy revisited. Anesthesiology Clinics of North America 1994; 12: 9-117.

Despotis G.J, Santoro S.A., Spitznagel E, Kater K.M., et al. Prospective evaluation and clinical utility of on-sitemonitoring of coagulation in patients undergoing cardiac operations. Thoracic and Cardiovascular Surgery1994; 107: 271-9.

McKinnon R.P., Wildsmith J.A.W. Histaminoid reactions in anaesthesia. British Journal of Anaesthesia 1995;74: 21-8.

Fowler N.O. Cardiac tamponade. A clinical or an echocardiographic diagnosis. Circulation 1993; 87: 1738-41.




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Case 8

A 19 year old primigravida at 33 weeks gestation underwent artificial rupture of membranes for induction oflabour because of deteriorating pre-eclampsia. She had been found to have proteinuria, platelets of 157 x 109/land a blood pressure of 160/115 mmHg.

What is understood about the pathophysiology of pre-eclampsia?

Which organ systems does the disease affect and how?

What are the therapeutic options for controlling this patient's blood pressure?

Describe the advantages and disadvantages of each therapy.

Her blood pressure was controlled with an infusion of labetolol and when she was in established labour, anepidural catheter was sited and analgesia provided by this route.

Six hours later she was delivered by forceps of a live male infant. The APGAR scores at one and five minuteswere eight and nine. Two hours after delivery of the infant her placenta was still retained and so she wastransferred to theatre for removal. On arrival in theatre routine monitoring was established and it was noted herblood pressure was 125/80 mmHg and heart rate was 100 beats/minute. She was bleeding steadily per vagina.Two large bore peripheral venous cannulae were inserted and as the epidural block had been patchy, generalanaesthesia was induced following pre-oxygenation. A rapid sequence intravenous induction technique wasemployed and her trachea intubated with the aid of a gum elastic bougie. It was noted she had oedema of heroropharynx and epiglottis.




Page 42

Table 8.1

PT20.2 seconds

APTT50 seconds

Fibrinogen1.3 g/l

Haemoglobin83 g/l


WCC7.8 x 109/l

Samples of blood were sent after delivery to haematology for full blood count estimation and a coagulationscreen.

Discuss these results and how you would proceed.

Two units of cross matched blood and two units of fresh frozen plasma were administered over the next 45minutes. Manual removal of placenta failed to slow the bleeding and so an infusion of syntocinon wascommenced. She was transfused a further two units of blood.

Review the current guidelines for management of major obstetric haemorrhage. This patient goes on to have amassive blood transfusion, which is a significant factor in the decision to refer her for intensive care.

What are the complications of massive blood transfusion and how would you minimise them?

What are the particular problems associated with fluid resuscitation in the pregnant and also pre-eclampticpatient?

Despite this she continued to bleed significantly per vagina. Fluid resuscitation




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continued while central venous and radial arterial cannulae were inserted to assist monitoring. Her conditionwas discussed with intensive care medical staff at this time and arrangements were made for her trnasfer to ICUafter leaving theatre.

Further blood samples were sent to haematology.

Table 8.2

PT43.6 seconds

APTT134 seconds

Fibrinogen0.8 g/l

Haemoglobin5.3 g/l

Platelets52 x 109/l

WCC4.5 x 109/l

Her condition was discussed with the haematologist on-call and further fresh frozen plasma was supplied, inaddition to cryoprecipitate and platelets. She continued to be transfused blood. In a further attempt to controlthe bleeding she received an intramyometrial injection of prostaglandin F2a.

Following this and the infusion of clotting factors, the haemorrhage appeared to be under control. She had nowbeen transfused eight units of packed red cells, received four units of fresh frozen plasma, six units ofcryoprecipitate, six units of platelets and 2000 ml of crystalloid. Her oropharyngeal temperature was 35.3 C ondeparture from theatre.

She was ventilated with an FIO2 of 1.0 and 10 cmH2O positive end expiratory pressure on arrival in ICU.

Her initial blood results were:

Table 8.3

PaO210.3 kPa

PaCO25.1 kPa

pH7.24

Base Deficit-8.6 mmol/l

Actual Bicarbonate16 mmol/l

K+6.7 mmol/l




Page 44

What do you think has happened and what would you do now?

A chest X-ray revealed pulmonary oedema (Fig. 8.1) and her central venous pressure was measured at 17mmHg.

Fig. 8.1

A bolus intravenous injection of a loop diuretic was given and followed by an infusion. This produced a briskdiuresis followed by an improvement in gas exchange and her serum potassium fell. She also received calciumgluconate. Electrolytes were within normal limits, but urea and creatinine were elevated (9.8 mmol/l and 112micromol/l). She was actively rewarmed.

Pulmonary oedema is a not uncommon, but serious complication in pre-eclampsia. Do you consider themonitoring in this patient was adequate?

Explain your answer.




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She remained hypertensive. The labetolol infusion continued and infusion of magnesium started. Liver functiontests remained normal throughout. Coagulation returned to normal within eight hours of her admission to theICU. She was extubated 24 hours after admission after direct laryngoscopy confirmed minimal laryngealoedema. She was monitored in the ICU for several hours after extubation but had no further airway problems.The epidural cannula was removed when coagulation and platelets were normal.

HELLP syndrome is being sought when checking this patients liver function. Why is this significant?

How does this condition present and what are the complications?

Magnesium sulphate was used in the management of this patient in ICU. What are the current indications formagnesium use in the pre eclamptic or eclamptic patient and are there problems with its use?

Can you discuss other potential uses of magnesium in the critically ill patient?




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Further Reading

Report on Confidential Enquiries into Maternal Deaths in the UK, 1988-1990 Department of Health. RevisedGuidelines for the Management of Massive Obstetric Haemorrhage.

Mushambi M.C, Halligan A.W, Williamson K. Recent developments in the pathophysiology and managementof pre eclampsia. British Journal of Anaesthesia 1996; 76: 133-48.

Gambling D.R, Laird Birmingham C, Jenkins L.C. Magnesium and the anaesthetist. Canadian Journal ofAnaesthesia 1988; 35: 644-54.

Donaldson M.D.J, Seaman M.J, Park G.R. Massive blood transfusion. British Journal of Anaesthesia 1992; 69:621-30.

Broughton Pipkin F. The hypertensive disorders of pregnancy. British Medical Journal 1995; 311: 609-13.




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Case 9

A five year old boy was admitted to the accident and emergency department with an acute episode of stridor.His mother reported that two days prior to admission he had complained of being unwell and she thought hehad a temperature and noted his nose was runny, he had a barking cough and was hoarse. On arrival at hospitalhe appeared unwell and his temperature was 38 C. His blood pressure was 100/40 mmHg, pulse rate 110beats/minute, respiratory rate 30/minute. There was marked use of accessory respiratory muscles, slight trachealdescent on inspiration and mild inspiratory and expiratory stridor. He also had palpable cervical lymph nodes.

What is the differential diagnosis?

Outline the initial management necessary for this child.

He was treated initially with nebulised adrenaline and intravenous steroid, but after one hour his condition hadnot improved and he was becoming cyanosed. Oxygen saturation was measured as 90% with a pulse oximeter.Senior anaesthetic and ENT surgical assistance was requested and he was transferred to the ICU. A gaseousinduction of anaesthesia was performed, intravenous access obtained and laryngoscopy then performed. Atlaryngoscopy, copious secretions were seen which had to be removed by suction prior to obtaining a good viewof the larynx, revealing a normal epiglottis.

What is your diagnosis now?




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He was then intubated with a size 4.0 oral uncuffed endotracheal tube and ventilated with an FIO2 of 1.0.Oxygen saturation did not immediately improve and copious frothy pink secretions welled up from theendotracheal tube. Ventilation was difficult by hand and when placed on a ventilator, the tidal volume was poordespite inflation pressures of 35-40 cmH2O.

What has happened and what action would you take?

Describe the pathophysiology causing this problem.

He was ventilated with humidified gases and positive end expiratory pressure applied. His compliance andblood gases gradually improved during the next 12 hours. He was commenced on intravenous sedation, steroidand antibiotic therapy and intravenous dextrose 4%, saline 0.18% was given at 65 mls per hour (weight 20 kg).His haemoglobin was 116 g/l, platelets 199 x 109/l, WCC 14.1 x 109/l with a neutrophil count of 9.8 x 109/l(70%).

Discuss the need for, and the problems with, sedation for children in ICU.

After 24 hours his oral endotracheal tube was exchanged for a nasal tube and he was allowed to breathspontaneously with continuous positive airway pressure. The following day copious purulent secretions wereproduced on tracheal suctioning, he was noted to be working harder to breath and his respiratory rate rosesteadily. He was sedated and ventilated, but his airway pressure was high and it became progressively moredifficult to maintain adequate ventilation. A chest X-ray was essentially normal but his gas exchange haddeteriorated.




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Table 9.1

FIO20.8

PaO27.3 kPa

PaCO27.5 kPa

pH7.23

HCO3-20 mmol/l

The nasal endotracheal tube was removed and replaced with a fresh one and ventilation was immediatelyimproved. The tip of the original endotracheal tube was partially clogged with thick purulent secretions. It waspresumed he had developed secondary bacterial tracheitis. Bronchoscopy was performed with a rigidbronchoscope to enable tracheal toilet. Over the next three days despite frequent suctioning by nursing andphysiotherapy staff, bronchoscopy was required to remove secretions on a daily basis. Culture of the trachealaspirate grew Staphylococcus aureus sensitive to his existing antibiotic therapy.

This case was atypical as it was a bacterial croup.

Outline the differences in management of viral and bacterial croup. How does this compare to epiglottitis orretropharyngeal abscess?

By the sixth day after admission the secretions had become less copious and gas exchange was improving. Hewas again allowed to breath spontaneously with continuous positive airway pressure and nasogastric feedingwas established. He was extubated under direct vision on day nine while deeply anaesthetised. There was nostridor or indrawing observed. After a further 12 hours of observation he was discharged to the paediatric wardand after observation for 2 hours oral fluids were commenced. The following day he was discharged home onoral antibiotics and a decreasing dose of oral steroids.




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Croup is a common problem in the 1-5 age group with 3-5% of all children having at least one episode. Themajority of cases are treated outwith the ICU.

What criteria exist for deciding to intubate a child with suspected croup?

Many scoring systems have been developed to predict outcome in adult patients who require intensive care. ThePaediatric Risk of Mortality is such a scoring system for paediatric ICU patients. Which parameters aremeasured for calculating this score?

Further Reading

Walker P, Crysdale W.S. Croup, epiglottitis, retropharyngeal abscess, and bacterial tracheitis: evolving patternsof occurrence and care. International Anesthesiology Clinics 1992; 30: 57-70.

Matthews A.J. An audit of sedation, analgesia and muscle relaxation in paediatric intensive care in the UnitedKingdom. Paediatric Anaesthesia 1993; 3: 107-15.

McDonogh A.J. The use of steroids and nebulised adrenaline in the treatment of viral croup over a seven yearperiod at a district hospital. Anaesthesia and Intensive Care 1994; 22: 175-8.

Jacobs S, et al. Validation of a croup score and its use in triaging children with croup. Anaesthesia 1994; 49:903-6.

Doull I. Corticosteroids in the management of croup. British Medical Journal 1995; 311: 1244.

Pollack M.M., Ruttimann U.E., Getson P.R. Pediatric risk of mortality (PRISM) score. Critical Care Medicine1988; 16: 1110-6.




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Case 10

A 72 year old, 76 kg man was taken by ambulance to the local hospital after being found unconscious in a coldbath by a neighbour. Two empty wine bottles were found on the floor beside the bath, the shower curtain wasripped and the left temporal area of his head was contused and lacerated. It was assumed he had struck his headon the side of the bath when he had attempted to get out.

On admission, his Glasgow coma scale was recorded as 6 (E1, M3, V2) and his pupils were fixed and dilated.His blood pressure was recorded at 85/40 mmHg, pulse rate 45 beats/minute, respiratory rate 8 breaths/minuteand on listening to his abdomen, no bowel sounds were heard. He was connected to the ECG monitor revealingprolonged PR interval and J waves (Fig. 10.1). His core temperature was measured at 29 C. Shortly afteradmission he became apnoeic and was rapidly intubated without the aid of sedation or neuromuscular blockade.

Fig 10.1




Page 52

This intervention precipitated ventricular fibrillation which was successfully treated by the administration ofthree DC countershocks (200J, 200J, 360J) followed by intravenous adrenaline 1 mg.

He was transferred to the ICU where a side room had been warmed in preparation for his arrival. Continuousinvasive monitoring of the central venous and systemic arterial pressure was commenced. Blood was sent forfull blood count, urea, electrolytes, glucose, amylase, liver function tests and blood cultures. Active rewarmingwas started by ventilation with warmed humidified respiratory gases and peritoneal lavage with warmed fluid.The fluid was heated to 40 C in a microwave oven and six litres of exchange fluid was used per hour. He wascovered in a warming blanket set at 37 C and intravenous fluid was given through a countercurrent fluidwarmer. He required initial rapid administration of fluid to stabilise his central venous pressure at 10 cmH2O.A lignocaine infusion, commenced after the period of ventricular fibrillation was continued, and after hiscentral venous pressure stabilised an infusion of dopamine was started to maintain his systolic blood pressure at115 mmHg. Sedation was assured with a propofol infusion running at a low rate. No neuromuscular blockadewas used.




Page 53

His blood results were as follows (arterial blood gases are corrected for temperature):

Table 10.1Haemoglobin 141 g/lHaematocrit 44%WCC 7.4 x 109 /lPlatelets 82 x 109/llClotting screen normalBlood alcohol 220 mg/dlNa+ 137 mmol/lK+ 3.8 mmol/Urea 7.6 mmol/lCreatinine 102 micromol/lGlucose 14.8 mmol/lAmylase 78 U/lFIO2 1.0pH 7.52PaO2 18.4 kPaPaCO2 28 kPaBase excess -6.9HCO3- 14 mmol/l

Describe the abnormalities in these results and explain why they have occurred?

What is meant by alpha stat strategy for managing acid base imbalances in hypothermia?




Page 54

How would these blood gases be different if they had not been corrected for temperature?

Fluid resuscitation with both colloid and crystalloid continued according to central venous pressuremeasurements. Urine output was maintained at 0.5 ml/kg. Specific gravity was low initially. The coretemperature did not rise in the first hour of ICU but thereafter rose by 0.8 C for the following 4 hours. As thepatient's core temperature rose, renal tubular function improved. Peritoneal lavage was discontinued once thecore temperature rose above 32 C. Despite this, the pupils remained fixed and dilated and therefore a CT scanwas arranged to assess any intracranial pathology which had resulted from the fall. The scan was reported asnormal and over the next few hours, his pupils became reactive and smaller.

Sedation was continued until the following morning when the propofol infusion ceased. There were no signs ofarousal for six hours, whereupon he woke steadily. He was weaned easily from the ventilator and wasextubated after a short period of spontaneous ventilation with minimal assist from the ventilator. Despite beingin a thermoneutral environment and receiving warmed fluids and respiratory gases his temperature had notrisen above 36 C and remained at this level for a further 48 hours after his discharge to a general medicalward.

Comment on the timing of the CT scan. Should this have been performed on hospital admission?

What do you understand by the term afterdrop and how can it be avoided?

How does this differ from post-immersion collapse?

We know that the specific heat of the body is 0.83 kcal/kg/ C and that of water is 1.0 kcal/kg/ C.




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Using the equation Q = mc (t2-t1), where Q = heat loss, m = mass and c = specific heat, calculate the heatdeficit of this patient.

Assuming peritoneal lavage is the only rewarming measure in this patient, what volume of fluid at 40 C willbe required to replace the deficit, if the fluid is returned at 35 C?

Given an aim of increasing the core temperature by 1 C/ hour what volume of fluid needs to be exchangedeach hour?

This patient had three predisposing factors to hypothermia, namely, old age, alcohol and water exposure.

What other factors predispose to hypothermia?

Cardiopulmonary bypass has been recommended for rewarming hypothermia victims with cardiovascularinstability. It was not considered as an option on this occasion in case of intracranial bleeding with concurrentheparinisation.

What other methods of rewarming could have been used in this case?

Is there a maximum rate of rewarming?

Describe the cardiovascular effects of worsening hypothermia. Why does cooling or rewarming at temperaturesbelow 30 C cause atrial and ventricular irritability? At what temperature would you expect asystole to occur?

Hypothermia has been induced as a adjunct to therapy in critical illnesses for more than 50 years. Are youaware of current areas of research into induced hypothermia as therapy in the critically ill patient?




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Further Reading

Larach M.G. Accidental hypothermia. Lancet 1995; 345: 493-8.

Danzl D.F., Pozos R.S. Accidental hypothermia. New England Journal of Medicine 1994; 331: 1756-60.

Stoneham M.D., Squires S.J. Prolonged resuscitation in acute deep hypothermia. Anaesthesia 1992; 47: 784-8.

Gentilello L.M. Advances in the management of hypothermia. Surgical Clinics of North America 1995; 75:243-55.

Neilsen H.K, Toft P, Koch J, Andersen P.K. Hypothermic patients admitted to an intensive care unit: a fifteenyear survey. Danish Medical Bulletin 1992; 39:190-3.

Bernard S. Induced hypothermia in intensive care medicine. Anaesthesia and Intensive Care 1996; 24: 382-8.




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Case 11

A 19 year old male was found lying on his bedroom floor, unrouseable with noisy breathing in the morning byhis mother. He had been at a party the night before and his mother did not know what time he had come home.She also reported there was evidence he had been sick and she had witnessed a generalised twitching episodewhile waiting for the ambulance to arrive.

What is your differential diagnosis and how would you investigate the patient?

On arrival at hospital his Glasgow coma score was 7 (E1, V2, M4), and on examination, his pupils were dilatedand sluggishly reactive and he was noted to be generally hyper-reflexic. His pulse rate was 180 beats/minute,blood pressure 110/55 mmHg, respiratory rate 18 breaths/minute, and his axillary temperature was 39.5 C.Although ten litres of oxygen were delivered via a Hudson mask the pulse oximeter read 92%. Ice packs wereplaced in the groin and axillae, blood was sent for toxicology and intravenous N-acetyl cysteine wascommenced. After induction of anaesthesia he was intubated and transferred to the ICU.

Which drugs would you routinely screen for in cases of suspected drug abuse or overdose?

In the ICU invasive monitoring of central venous and arterial pressure was established and his core temperaturewas measured with an oesophageal probe and found to be 40.2 C. Dantrolene was administered and furtherblood samples were taken for full blood count, urea, electrolytes, glucose, amylase, liver function tests andblood cultures. In addition, a viral screen




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was performed with a view to dialysing for temperature control. A nasogastric tube was passed and somealtered blood was aspirated. Normal saline was infused intravenously and a broad spectrum antibioticadministered.

His core temperature began to fall 20 minutes after administration of the dantrolene and returned to normal in 1hour. However, despite the infusion of 500ml of saline, he had passed no urine.

His blood test results were as follows:

Table 11.1Na+ 136 mmol/l Ca2+ 1.96 mmol/lK+ 6.2 mmol/l Amylase 163 U/lHCO3- 18 mmol/l Total protein 55 g/lUrea 6.1 mmol/l Albumin 55 g/lCreatinine 172 micromol/l Bilirubin 26 micromol/lGlucose 9.4 mmol/l LDH 690 U/lMg2+ 0.63 mmol/l AAT 155 U/lPhosphate 1.82 mmol/l Alk phos 54 U/l

gGT 47 U/lPT 28.5 seconds FIO2 0.8TT 1 8.8 seconds pH 7.33APTT 60.5 seconds PaCO2 3.28 kPaPaO2 27 kPa HCO3- 13.3 mmol/lFibrinogen 1.3 g/l Base excess -10.7Platelets 101x109/lFDPs > 200Urine positive for myoglobin.Paracetamol not detected.Salicylate not detected.

Review these laboratory findings and outline the action you would take.




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What is the corrected calcium level?

His blood pressure fell progressively for the first few hours after admission despite significant fluidadministration. After administration of fresh frozen plasma and cryoprecipitate, a pulmonary artery catheter wasinserted. Initial measurements are shown in Table 11.

Table 11.2

Pulse rate140 beats/minute

Blood pressure70/35 mmHg

Cardiac output8.4 l/min

CVP10 mmHg

SVR550 dyne.cm-5s-1

PAOP12 mmHg

Vasoactive drugs were commenced, his blood pressure rapidly rose to acceptable levels and after diuretictherapy he began to pass large volumes of urine. His cardiac output was maintained. During the first 24 hoursoxygenation deteriorated and a chest X-ray showed patchy consolidation of the right middle and lower lobes.This was considered to be consistent with an aspiration pneumonia.

The laboratory phoned to say that an MDMA level was 1.09 mg/litre and his alcohol level was 150 mg/dl onthe admission samples.

He required a further three days of ventilation and cardiovascular support. All sedation was discontinued and hebegan to breath spontaneously with continuous positive airway pressure, but he did not wake up. A CT scanwas performed which was normal and 24 hours later he was awake enough to be extubated.




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This patient had ingested a significant amount of alcohol which would have contributed to his dehydration andsubsequent hyperthermia. Outline the management of a patient with severe alcohol intoxication occurring inisolation.

Discuss the main objectives of treatment in any case of acute poisoning. Describe how you would specificallytreat paracetamol and salicylate overdoses.

The main feature in this patient's presentation is hyperthermia. Why does this occur with MDMA ingestion?What are the possible long term sequelae of ingesting this drug?

Dantrolene has traditionally been used in the treatment of malignant hyperthermia. What is its mechanism ofaction and how does this assist in temperature reduction in MDMA overdose?

Dantrolene is kept in powder form in vials and requires to be reconstituted. The vials also contain mannitol.This patient was given 180 mg of dantrolene. How much mannitol would have been given along with thedantrolene?

What is the differential diagnosis of hyperthermia occurring in a patient in ICU?




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Further Reading

O'Connor B. Hazards associated with the recreational drug ecstasy. British Journal of Hospital Medicine 1994;52: 507-14.

Kulig K. Initial management of ingestions of toxic substances. New England Journal of Medicine 1992; 326:1677-81.

Lamminpaa A. Acute alcohol intoxication among children and adolescents. European Journal of Pediatrics1994; 153: 868-72.

Sue Y-J, Shannon M. Pharmacokinetics of drugs in overdose. Clinical Pharmacokinetics 1992; 23: 93-105.

Bodenham A.R, Mallick A. New dimensions in toxicology: hyperthermic syndrome following amphetaminederiviatives. Intensive Care Medicine 1996; 22: 622-4.

Hunter W.A.H, Randalls B, Grande C.M. Intraoperative hyperthermia. Problems in Anesthesia 1994; 8: 122-36.




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Case 12

A 45 year old woman was taken by ambulance to the local hospital emergency department after falling 40 feetfrom the second floor of her home. She had been cleaning a window, and was seen to fall by her neighbourswho alerted the emergency services. On arrival at hospital, her respiratory rate was 18 breaths/minute, pulse rate100 beats/minute, blood pressure 145/90 mmHg and axillary temperature 35.5 C. Her GCS was 6 (E1, M3,V2), her pupils were equal and reacted sluggishly to light and no focal neurological signs could be elicited.There was clinical evidence of a compound right tibial fracture.

With the mechanism of injury described, what serious injuries is this woman at risk of?

How would you investigate the patient at this stage?

Chest and lateral cervical spine radiographs were performed in the emergency room. Review of the lateralcervical spine film revealed a fracture of the spinous process of C7 and on her chest X-ray there were changesconsistent with aspiration at the right base. The on-call anaesthetic and neurosurgical teams were contacted andafter rapid neurosurgical assessment, she was intubated and ventilated before transfer to the radiologydepartment. CT scan of her head confirmed a severe injury. There was a compound left petrosal bone fracturewith a small subdural haematoma and slight midline shift, a contra coup injury on the right, bilateral frontalcontusions, cerebral oedema and small amounts of subarachnoid and intra ventricular blood. Surgicalintervention was not thought appropriate and she was transferred to the ICU after wound debridement, insertionof a subdural intracranial pressure monitor and a right tibial Denham pin for traction in theatre.

The intracranial pressure was recorded as 15 mmHg at the time of insertion.




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This patient has sustained a significant primary brain injury. Currently there is no treatment for primarydamage, and resources are aimed at injury prevention. Management after an injury has been sustained isdirected at the prevention of secondary injury.

Describe your approach to this with this patient in mind. Where should this patient be managed?

Neuromuscular blockade and sedation were maintained with intravenous infusions in ICU and she was alsocommenced intravenous antibiotics and H2 antagonist. Ventilation was adjusted to keep the PaCO2 at 4 kPa forthe first 48 hours. A right subclavian central line and radial arterial line were inserted and vasoactive agentsused to maintain the cerebral perfusion presure above 50 mmHg. Although initially the intracranial pressureremained around 15 mmHg after an hour in ICU there

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