Clinical Scenarios in ICU

cover
next page>
title: author: publisher: isbn10 | asin: print isbn13: ebook isbn13: language: subject publication date: lcc: ddc: subject: Clinical Scenarios in Intensive Care Patey, Rona E. Greenwich Medical Media Limited 1900151650 9781900151658 9780511043116 English Critical care medicine, Critical care medicine--methods-problems. 1998 RC86P297 1998eb 616.028076 Critical care medicine, Critical care medicine--methods-problems.
cover
next page>
http://makolaiwy.blogspot.com
<previous page
page_i
next page>
Page i
Clinical Scenarios in Intensive Care
<previous page
page_i
next page>
<previous page
page_ii
next page>
Page ii
Greenwich Medical Media 1998 Greenwich Medical Media Ltd 219 The Linen Hall 162-168 Regent Street London W1R 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 permitted under the UK Copyright Designs and Patents Act, 1988, this publication may not be reproduced, stored, or transmitted, in any form or by any means, without the prior permission in writing of the publishers, or in the case of reprographic reproduction only in accordance with the terms of the licences issued by the Copyright Licensing Agency in the UK, or in accordance with the terms of the licences issued by the appropriate Reproduction Rights Organization outside the UK. Enquiries concerning reproduction outside the terms stated here 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 information contained in this book and cannot accept any legal responsibility or liability for any errors or omissions that may be made. A catalogue record for this book is available from the British Library. Distributed worldwide by Oxford University Press Designed and Produced by Diane Parker, Saldatore Limited Printed in Great Britain by Ashford Colour Press
<previous page
page_ii
next page>
<previous page
page_iii
next page>
Page iii
Clinical Scenarios in Intensive Care by Rona E. Patey MbChB, FRCA, FRCS Nigel R. Webster BSc, MB ChB, PhD, FRCA, FRCP
<previous page
page_iii
next page>
<previous page
page_v
next page>
Page v
Preface This book gathers together clinical problems, many of which are common and often found on the general intensive care unit. Although there are many tomes both large and small which detail the process of intensive care and the knowledge base on which to place such practice, there are few books which set about the task in a problem 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 the end of each case. These suggestions are not exhaustive, but have been included as they supplement information readily 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 the structured teaching sessions on intensive care for trainees. However it may also provide a useful framework for discussion by other staff who work on the intensive unit. Hopefully, it will provide a basis for discussion of the common problems and act as a forum to raise questions. Patients do not always survive treatment and outcome may well be different in your unit! R.E.P. R.R.W. 1997
<previous page
page_v
next page>
<previous page
page_vii
next page>
Page vii
Acknowledgements We acknowledge the considerable support given to us by all members of the department at Aberdeen Royal Hospitals 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 Robb for assistance with the radiological illustrations. RONA E. PATEY NIGEL R. WEBSTER
<previous page
page_vii
next page>
<previous page
page_ix
next page>
Page ix
Contents Case 1 Asthma Case 2 Community Aquired Pneumonia Case 3 Cardiac Arrest Case 4 Aquired Immune Deficiency Syndrome Case 5 Acute Myocardial Infarction Case 6 Meningitis Case 7 Redo Cardiac Surgery Case 8 Pre-Eclampsia Case 9 Acute Respiratory Distress in a Child Case 10 Hypothermia Case 11 Coma Case 12 Acute Head Injury Case 13 Diabetes Mellitus Case 14 Acute Respiratory Distress Syndrome Case 15 Tetanus Case 16 Acute Renal Failure Case 17 Guillan-Barr Syndrome Case 18 Road Traffic Accident Case 19 Acute Pancreatitis 1 7 13 19 25 31 35 41 47 51 57 63 67 73 77 81 85 89 95
Case 20 Trans Urethral Resection of Prostate Case 21 Post Operative Septicaemia
99 103
<previous page
page_ix
next page>
<previous page
page_xi
next page>
Page xi
List of Abbreviations aHCO3 APTT BE CI CO CVP ECG ESR FDP FIO2 gGT GTN LDH MAP MPAP MCH PaO2 PAOP PT Bicarbonate Activated partial thromboplastin time Base excess Cardiac Index Cardiac output Central venous pressure Electrocardiograph Erythrocyte sedimentation rate Fibrin degradation products Fractional inspired oxygen tension g Glutamyl transferase Glyceryl trinitrate Lactate dehydrogenase Mean arterial pressure Mean pulmonary artery pressure Mean cell haemoglobin Partial pressure of arterial oxygen Pulmonary artery occlusion pressure Prothrombin time
Haemoglobin oxygen saturation - arterial and SaO2/SvO2mixed venous sHCO3 SpO2 SVR TT WCC Standard bicarbonate Haemoglobin oxygen saturation - pulse Systemic vascular resistance Thrombin time White cell count
<previous page
page_xi
next page>
<previous page
page_1
next page>
Page 1
Case 1 A 19 year old woman was admitted to the respiratory unit with a suspected exacerbation of long-standing asthma, presumably due to an acute infection. She had required admission to hospital on three previous occasions. Her medication presently consisted of regular b-agonist and steroid inhalers, but no theophylline derivatives. She had received short courses of oral steroids during previous severe exacerbations. On this occasion she gave a three day history of increasing wheeze, a cough with little sputum, i.e., she had been unable to sleep well and was very tired. She had been using her inhalers increasingly frequently, and said she felt 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 was using accessory muscles of respiration. She complained of thirst, had a dry mouth and looked centrally cyanosed. Her pharynx was red and inflamed and on auscultation her chest was quiet with little wheeze. Blood pressure was measured at 100/80 mmHg, pulse 125 beats/minute, temperature 38 C, respiratory rate 36 breaths/minute and she was noted to have pulsus paradoxus of 20 mmHg. Humidified high-flow oxygen therapy was commenced and hydrocortisone and a loading dose of aminophylline (5mg/kg) given intravenously. Her peak flow was 70 1/minute and FEV1 600ml.
<previous page
page_1
next page>
<previous page
page_2
next page>
Page 2
Initial results are recorded below. On admission 0.21 5.6 kPa 6.9 kPa 68% Table 1.1 One hour after admission 0.6 9.0 kPa 8.6 kPa 82%
FIO2 PaO2 PaCO2 SpO2
Haemoglobin WCC Platelets Chest X-ray ECG
156g/l 15.3 x 109/l 468 x 109/l clear with significant hyperinflation sinus tachycardia - 125 beats/minute
This patient's asthma might be described as status asthmaticus. That is, either very severe asthma at its onset or asthma 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 differential diagnoses or complicating conditions which must be considered in patients at different ages
<previous page
page_2
next page>
<previous page
page_3
next page>
Page 3
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 these therapies and how can they be minimised? The decision to intubate and ventilate an asthmatic patient can be difficult. How can one initially assess the severity of an asthma attack and should the patients progress be monitored thereafter if ventilation is not immediately required? <><><><><><><><><><><><> An assessment from the medical staff in the Intensive Care Unit (ICU) was requested. She was becoming increasingly exhausted and urgent transfer was arranged to the ICU. On arrival an arterial cannula was inserted and 1200ml of intravenous fluid infused. Following pre-oxygenation anaesthesia was induced with ketamine and fentanyl. Suxamethonium provided rapid muscle relaxation, facilitating tracheal intubation followed by positive pressure ventilation. Inflation pressures after intubation were measured at 56 cmH2O but reduced to 32 cmH2O over the next two hours with alteration of ventilatory parameters, nebulised b-agonists and an intravenous aminophylline infusion (0.5 mg/kg/hour). Sedation was maintained with propofol and alfentanil infusions. In an attempt to minimise ventilation inflation pressure, neuromuscular blockade was continued initially. 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 to the bronchodilator therapy already underway. Two hours after intubation and ventilation, PaO2 was 17kPa with FIO2 0.5. She was normocapnic with tidal volumes between 700 and 900ml and a respiratory rate of 12 breaths/minute. Invasive monitoring of central venous pressure was commenced and was initially measured at zero. Seven
<previous page
page_3
next page>
<previous page
page_4
next page>
Page 4
litres of intravenous fluid were infused in the first 24 hours to correct dehydration and maintain circulatory status. Her central venous pressure rose to 5 cmH2O during this period. Blood, sputum and throat swabs were sent 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 whilst minimising peak airway pressures and intrinsic positive end expiratory pressure. Discuss the problems achieving 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 then discontinued with no increase in inflation pressure. She began to produce thick mucous plugs with chest physiotherapy 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 the respiratory 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 are important - why?
<previous page
page_4
next page>
<previous page
page_5
next page>
Page 5
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 Thoracic Society, Research Unit of the Royal College of Physicians of London, Kings Fund Centre, National Asthma Campaign. 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 America 1990; 74: 779-95. Hemming A., Mackenzie I., Finfer S. Response to ketamine in status asthmaticus resistant to maximal medical therapy. 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.
<previous page
page_5
next page>
<previous page
page_7
next page>
Page 7
Case 2 A 60 year old previously fit man was admitted to a general medical ward for investigation of pyrexia of unknown origin. He was slightly confused, and gave little history other than a recent generally non-productive cough and feeling generally unwell and thirsty. On examination his temperature was 39 C, he had a heart rate of 116 beats/minute and was sweaty. Examination of his chest revealed dullness to percussion and bronchial breathing at the right apex with vesicular breath sounds and crepitations at the left base. The only abnormality on abdominal examination was a slightly enlarged non-tender liver. His sputum was noted to be purulent and rusty coloured, and he had proteinuria. A chest X-ray revealed extensive consolidation in the right upper and left lower lobes. <><><><><><><><><><><><> This man was diagnosed has having a community-acquired acute pneumonic process. How should this be investigated? 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 2.1 145 g/l 129 mmol/l 10.1 x 109/l 4.2 mmol/l 486 x 109/l 24 mmol/l 50 mm/hr 8.9 mmol/l 110 micromol/l
Haemoglobin Na+ WCC K+ Platelets HCO3ESR Urea Creatinine
gram positive coccus Sputum gram stain Generally deranged liver function tests.
<previous page
page_7
next page>
<previous page
page_8
next page>
Page 8
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 was commenced on intravenous antibiotic treatment, maintenance fluid intravenously and oxygen by mask (6 1/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 be investigated 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 from the ICU. At assessment he was confused, but answered simple questions, tachypnoeic (45 breaths/minute) and centrally cyanosed, despite increasing his oxygen to 12 1/minute. Arterial blood was taken for gas estimation and showed PaO2 6kPa and PaCO2 3.4 kPa whilst he was breathing oxygen at 12 1/minute through a face mask. He was transferred to ICU to permit invasive monitoring and ventilatory support. <><><><><><><><><><><><> On what do you base the decision to ventilate such patients?
<previous page
page_8
next page>
<previous page
page_9
next page>
Page 9
On arrival at the ICU he was noted to be cold and clammy, responding only to pain, in atrial fibrillation (144 beats/minute), tachypnoeic (48 breaths/minute), hypotensive (90/70 mmHg) and centrally cyanosed. A pulse oximeter could pick up no trace. While he was pre-oxygenated with a non rebreathing bag, a radial arterial line was 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 pressure ventilation commenced with an FIO2 of 1.0. With the addition of 10 cmH2O of positive end expiratory pressure 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 PaO2 PaCO2 pH Base excess Haemoglobin WCC Platelets Haematocrit Na+ K+ Urea Creatinine 10.6 kPa 5.7 kPa 7.27 - 5.3 135 g/l 12 x 109/l 590 x 109/l 40% 129 mmol/l 3.9 mmol/l 7.2 mmol/l 125 micromol/l
He remained unstable after ventilation, requiring infusion of fluid and then commencement of dopamine to maintain systolic blood pressure above 100 mmHg. A pulmonary artery flotation catheter was inserted and after initial measurements and calculations, a noradrenaline infusion added to the dopamine infusion and he was digitalised.
<previous page
page_9
next page>
<previous page
page_10
next page>
Page 10
Heart rate MAP CVP PAOP MPAP CO2 CI SaO2 SvO2
Table 2.3 135 beats/minute 65 mmHg 12 mmHg 9 mmHg 22 mmHg 5.5 1/minute 3.2 1/minute/m2 96% 71%
What is your interpretation of these results? Can you calculate the vascular resistances, stroke work indices and oxygen 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 worst results 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?
<previous page
page_10
next page>
<previous page
page_11
next page>
Page 11
His therapy was reviewed with the microbiologists and antibiotics changed. Thus far all microbial culture and autoantibody screens were negative, and the gram positive coccus reported on the initial sputum sample was reported as Staphylococcus epidermidis of doubtful significance. Diffuse alveolar infiltrates were now apparent in addition to the lobar consolidation on his chest X-ray. A nasogastric tube was inserted and he began to receive enteral nutrition. His condition steadily improved from this point, allowing steady reduction in the cardiovascular and ventilatory support. On the fifth day of intensive care, his gas exchange and general condition were such that his sedation was reduced. He was gradually weaned from ventilation over the next two days, extubated and then transferred back to the general medical ward. Shortly after arrival in the medical ward he was noted to have profuse diarrhoea. Nasogastric feeding was stopped, intravenous fluid replacement recommenced and stool was sent for culture. This grew Clostridium difficile 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 enterally fed. Discuss the causes of diarrhoea in the ICU patient and how you would proceed in the patient who had no growth 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 recently purchasing a bird table and regularly feeding the local pigeons.
<previous page
page_11
next page>
<previous page
page_12
next page>
Page 12
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 acquired pneumonia with emphasis on outcome. Chest 1993; 103: 232-5. American Thoracic Society: Guidelines for the Initial Management of Adults with Community-acquired Pneumonia: Diagnosis, Assessment of severity and Initial antimicrobial therapy. American Review of Respiratory Disease 1993; 148: 1418-26. Tabagcahli S., Jumaa P. Diagnosis and management of Clostridium Difficile infection British Medical Journal 1995; 310: 1375-80. Levinson M., Bryce A. Enteral feeding, gastrci colonisation and diarrhoea in critically ill patients; is there a relationship 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 classification system. 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.
<previous page
page_12
next page>
<previous page
page_13
next page>
Page 13
Case 3 A 27 year old woman was rushed to the resuscitation room of the local hospital by paramedic staff. On arrival she had a pulse rate of 170 beats/minute and her blood pressure was 85/40 mmHg. She was intubated and breathing spontaneously. Her pupils were fixed and dilated. Her Glasgow Coma Score was recorded as three. It was reported that she had collapsed suddenly at work and was in ventricular fibrillation when the paramedic staff 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 for management 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 the scene seven minutes after receipt of the call. There had been no basic life support carried out prior to their arrival, but the patient had been turned into the recovery position. Basic life support was commenced by one paramedic as the other attached the woman to a semi-advisory defibrillator monitor. Ventricular fibrillation was diagnosed and, prompted by the defibrillator, two DC shocks at 200J were administered. After the second shock a pulse could be felt in the region of the carotid artery and the monitor
<previous page
page_13
next page>
<previous page
page_14
next page>
Page 14
showed a supraventricular tachycardia of 170 beats/minute. Prior to transfer, her trachea was intubated and ventilation was assisted using a non rebreathing bag with supplemental oxygen although she was making some respiratory effort. Arrival in the resuscitation room was 22 minutes 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 a cardiac arrest. How is this manoeuvre optimally performed and how successful is it at maintaining organ blood flow? 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 blockade and continue supplemental oxygen. Arrangements were made to transfer her to the ICU after a computerised tomography (CT) scan of her head. While awaiting transfer to the CT room, adenosine was given in increments in 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 arterial pressure monitoring was established and revealed an elevated blood pressure at 220/120 mmHg. This was treated with increments of a beta blocker and her rhythm returned to sinus at 86 beats/minute and blood pressure settled at 110/80 mmHg.
<previous page
page_14
next page>
<previous page
page_15
next page>
Page 15
It is stated this patient had a supraventricular tachycardia following her cardiac arrest. How would this conclusion 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 be able to tell him whether she will survive and what quality of survival she will make. How will you council him? <><><><><><><><><><><><> Initial investigations included full blood count, urea and electrolytes, cardiac enzymes, chest X-ray, twelve lead ECG and echocardiography. The results of these were unremarkable other than an initial serum potassium of 2.8 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 it continue? <><><><><><><><><><><><> Her past medical records revealed a three year history of investigation of palpitations for which no cause had been found. She was currently being treated for hypertension with a calcium channel blocking agent.
<previous page
page_15
next page>
<previous page
page_16
next page>
Page 16
Estimation of cardiac enzymes was repeated during the period of sedation and ventilation but results remained within normal limits, however her serum potassium levels were persistently low. Several grams of potassium were infused to bring the level within the normal range. This was investigated further and revealed a high urinary excretion of potassium. On day three sedation was withdrawn and she rapidly recovered consciousness and returned to a general medical ward later that day. Further investigations included 24 hour Holter monitoring and extensive investigation of potassium handling. A diagnosis of primary ventricular fibrillation was made and an implantable 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 this contraindicated after cardiopulmonary resuscitation?
<previous page
page_16
next page>
<previous page
page_17
next page>
Page 17
Reading Ballew K.A., Cardiopulomonary Resuscitation. British Medical Journal 1997; 314: 1462-5. Emergency cardiac care committee and subcommittee, American Heart Association. Guidelines for cardiopulmonary 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 life support. 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 initiate cardiopulmonary 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 Topics in 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 in British hospitals (the BRESUS study): methods and overall results. British Medical Journal 1992; 304: 134751.
<previous page
page_17
next page>
<previous page
page_19
next page>
Page 19
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 a paramedic and given intermittent positive pressure ventilation with supplemental oxygen and maintained a spontaneous cardiac output at all times. An ambulance had been called by friends as they had become scared by his rapidly progressing breathlessness over the preceding few days. Apparently he had complained of a dry cough for one month and night sweats and fever 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 investigations were performed. Arterial blood gas results on admission were: Table 4.1 FIO2 SaO2 PaO2 PaCO2 pH 0.6 86% 8.0 kPa 6.2 kPa 7.23
Further examination revealed lymphadenopathy of his neck, axillae and groins and he had evidence of an oral candida infection. His temperature was 39.3 C. His friends revealed that the man was homosexual and had spent some years in the United States of America. His partner had lost
<previous page
page_19
next page>
<previous page
page_20
next page>
Page 20
weight over the last five months and so the patient had had an HIV antibody test 3 months earlier, though he had 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 end expiratory 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 few tracheobronchial secretions broncho alveolar lavage (BAL) was performed and a specimen sent for examination. His admission white cell count was 3.4 x 109/1 (15% lymphocytes). His Tcell subset CD4 count was 180 x 106/1 and HIV antibody test was confirmed positive by antigen tests. BAL specimen confirmed Pneumocystis 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 HIV infected individuals in North America. It would have been unusual for Pneumocystis carinii to occur had the CD4 count been greater than 250 x 106/1 cells/mm3. However other aetiologies must be considered.
<previous page
page_20
next page>
<previous page
page_21
next page>
Page 21
What in particular would you consider? Lactate dehydrogenase is characteristically elevated in patients with this pathology, and the level will correlate with the severity and the course of the infection. However this enzyme can be elevated in a number of other pathologies. 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 the technique? Would a trans-bronchial biopsy have been appropriate in this patient? <><><><><><><><><><><><> High dose intravenous cotrimoxazole, intravenous steroid and nebulised pentamidine were commenced. In addition, he received intravenous diuretic therapy and nebulised bronchodilators to manage intermittent bronchospasm. 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, then progressing 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 8.0 kPa (FIO2 1.0, PEEP 15 cmH2O) with pressure controlled mode of ventilation. He was sedated and neuromuscular blockade continued to facilitate ventilation. All bacteriological investigations were reviewed as there had been no improvement, however all other results were negative. In particular, there was no evidence of legionella or mycobacteria. Serology and a sample of diarrhoea on day five
<previous page
page_21
next page>
<previous page
page_22
next page>
Page 22
were positive for cytomegalovirus. Gancyclovir was commenced but as he developed a generalised erythematous rash, this was changed to Foscarnet. 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 when discharged to the infectious diseases unit he was commenced on anti-HIV therapy, acyclovir and oral septrin as Pneumocystis 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?
<previous page
page_22
next page>
<previous page
page_23
next page>
Page 23
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 with HIV infection. Chest 1995; 107: 506-10. Gachot B., Clair B., Wolff M., Regnier B., Vachan F. Continuous positive airway pressure by face mask or mechanical ventilation in patients with human immunodeficiency virus infection and severe Pneumocystis carinii 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 Journal 1995; 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 Medical Association 1992; 267: 541-7.
<previous page
page_23
next page>
<previous page
page_25
next page>
Page 25
Case 5 A 60 year old man complained of sudden severe gripping chest pain while participating in a bowls match and then collapsed on the green. An ambulance was called and he was transferred to the local hospital. On arrival he was noted to be distressed, pale, cold, clammy and breathless. He was able to report that he had recently had increasingly frequent chest discomfort, but had thought this was indigestion. He had smoked 30 cigarettes per day 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 flow oxygen 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 in leads V1-V3 (Fig. 5.1), and a chest X-ray was clear.
Fig. 5.1
<previous page
page_25
next page>
<previous page
page_26
next page>
Page 26
The working diagnosis was acute myocardial infarction and the patient was transferred to the coronary care unit. 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 hours after this he again complained of chest pain and became extremely dyspnoeic. His pulse rate was 125 beats/minute and his blood pressure 80/60 mmHg. A twelve lead ECG revealed sinus tachycardia with evidence of the recent infarct and generalised ischaemia. A chest X-ray was performed which revealed widespread pulmonary oedema. Acute left ventricular failure with cardiogenic shock was diagnosed and he was transferred back to the coronary care unit. <><><><><><><><><><><><> Discuss the pathophysiology of left ventricular failure and cardiogenic shock. Describe how these conditions can be treated.
<previous page
page_26
next page>
<previous page
page_27
next page>
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 were commenced and an intravenous bolus dose of loop diuretic given. One hour later his blood pressure remained low despite increasing rate of infusion of inotrope and only 30mls of urine had been passed after insertion of a urinary 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 short episodes of ventricular tachycardia (VT). A bolus dose of an anti-arrythmic agent was then given, but despite this, 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, despite increased inotropic support, his blood pressure remained low, a pulse oximeter could not pick up a reading and he had passed no further urine. <><><><><><><><><><><><> Which inotropic agents are you aware of and what is the mechanism of action of these agents?
<previous page
page_27
next page>
<previous page
page_28
next page>
Page 28
He was transferred to the ICU and after intravenous induction of anaesthesia, intubated and intermittent positive pressure ventilation commenced. His inotropic support was increased and a trans-oesophageal echocardiography performed which revealed severe mitral regurgitation resulting from a flail posterior valve leaflet. His left ventricular function was described as good and he was referred for emergency mitral valve replacement. <><><><><><><><><><><><> Trans-oesophageal echocardiography is increasingly used in cardiology and cardiac surgery/anaesthesia. What advantages 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 mmHg and pulmonary artery occlusion pressure of 23 mmHg. He was receiving significant inotropic support, but had only passed 50 mls of urine during the preceding 4 hours. During surgical preparation of the skin there was an episode of ventricular fibrillation which rapidly reverted to sinus tachycardia with a 200J DC shock. Surgery proceeded but during aortic cannulation he again became unstable with runs of ventricular and supraventricular tachycardia. This was rapidly followed by ventricular fibrillation and after a brief period of internal cardiac massage cardiopulmonary bypass was rapidly instituted. The aorta was cross-clamped and cardioplegia administered, whereupon the heart was opened and a flail anterior valve leaflet resulting in severe mitral regurgitation was revealed. The papillary muscle had ruptured and the chordae and papillary muscle were prolapsing 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 was inserted via the left femoral artery whereupon he was weaned from bypass with significant inotropic support.
<previous page
page_28
next page>
<previous page
page_29
next page>
Page 29
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 open and 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 massage commenced. There was no evidence of an acute tamponade. He failed to respond to fluids or further inotropes and 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 myocardial infarction. 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 England Journal 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 Drugs ed. Skarvan K. Bailliere's Clinical Anaesthesiology 1994; 8: 215-42.
<previous page
page_29
next page>
<previous page
page_30
next page>
Page 30
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. Clinical Applications. 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.
<previous page
page_30
next page>
<previous page
page_31
next page>
Page 31
Case 6 A previously well 18 year old male was admitted as a medical emergency with a two day history of fever and six hour history of severe "bursting" headache and photophobia. When seen at home by his general practitioner he displayed cervical rigidity and a positive Kernig's sign. The general practitioner administered 2.4g of benzyl penicillin 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 Score was 11 (E3, M5, V3). He was pyrexial (axillary temperature 38.8 C), his systolic blood pressure was 100 mmHg 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 procedure he further deteriorated and had a grand mal convulsion which resolved with bolus intravenous benzodiazepine treatment. Neuromuscular blockade was established to permit protection of his airway by tracheal intubation and he was transferred to the ICU. On arrival in the ICU, invasive monitoring was established and a lumbar puncture performed. The CSF was turbid and under pressure (not measured). CSF glucose was 1.8 mmol/l (serum glucose 7.8 mmol/l) and protein
<previous page
page_31
next page>
<previous page
page_32
next page>
Page 32
was 3 g/l. The cell count was 300, predominately polymorphonuclear leukocytes and a film revealed gram negative 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 the commonly 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 all negative. Sedation was maintained with propofol, benzodiazepine and opioid infusions. His respiratory function was good and he was ventilated with an F1O2 of 0.35 to maintain a PaCO2 of 3.8 kPa. Enteral feeding was commenced after insertion of an orogastric tube. He remained cardiovascularly stable and developed no rash indicative 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 with control of PaCO2 was continued
<previous page
page_32
next page>
<previous page
page_33
next page>
Page 33
until 48 hours after ICU admission. His sedation was reduced and he quickly weaned from assisted ventilation and 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 work colleagues received rifampicin as prophylaxis. Further Reading Strang J, Pugh E. Meningococcal infections: Reducing the fatality rate by giving penicillin before admission to hospital. 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 Infectious Diseases 1995; 20: 685-90. Kennedy N.J., Duncan A.W. Acute menningococcaemia: recent advances in management (with particular reference to children). Anaesthesia and Intensive Care 1996; 24: 197-216. Tunkel A.R., Scheld W.M. Acute bacterial Meningitis. Lancet 1995; 346: 1675-80.
<previous page
page_33
next page>
<previous page
page_35
next page>
Page 35
Case 7 A 69 year old man was admitted to the coronary care unit with a history of severe chest pain unresponsive to his usual GTN spray. Past medical history revealed 10 years of ischaemic heart disease and a coronary artery bypass grafting procedure for triple vessel disease seven years previously. Saphenous vein grafts had been performed, 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 until six months previously when he could no longer play a full round of golf without experiencing several episodes of anginal-type pain and breathlessness. During the two weeks prior to admission he had also experienced some rest 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 continued to experience episodes of angina at rest and was commenced on intravenous heparin and nitrate therapy. An urgent coronary angiogram was performed which revealed a deterioration in left ventricular function with anterior apical hypokinesis, elevation of the left ventricular end diastolic pressure at 22 mmHg and occlusion of the circumflex and right coronary grafts. The LAD graft was providing the only significant myocardial perfusion. <><><><><><><><><><><><> This patient has been diagnosed as having unstable angina. Discuss the methods of treating this problem. What is the rationale
<previous page
page_35
next page>
<previous page
page_36
next page>
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 surgeon requested he receive a bolus and then infusion of aprotinin. Unfortunately the administration of just a few millilitres of this was associated with a marked fall in systolic blood pressure, rise in ventilation inflation pressure, and the patient became very flushed. Auscultation of the chest revealed widespread wheezing. The aprotinin 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 the surgeon 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 mammary artery was anastomosed to his LAD, and saphenous veins to his obtuse marginal and distal right coronary artery branches. 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
<previous page
page_36
next page>
<previous page
page_37
next page>
Page 37
come off bypass. Despite adequate reversal of heparin, assessed by an activated clotting time, he continued to ooze from the wound margins. Blood was sent for clotting studies, but while awaiting these results he was given tranexamic acid, two units of fresh frozen plasma and six units of platelets empirically. Following chest closure, 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 blood transfused. His chest was reopened and a bleeding point on an anastamosis found and controlled. The clotting results are shown below: Table 7.1 Platelets PT APTT 45 x 109/1 25 seconds 60 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 but in 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. The bleeding decreased over the following
<previous page
page_37
next page>
<previous page
page_38
next page>
Page 38
three hours, but his urine output had been minimal despite apparently adequate filling pressures. The inotropic support was increased. Six hours postoperatively, the systemic blood pressure fell precipitously and there was a marked rise in central venous pressure. There had been less bleeding from his chest drains during the last two hours. His chest was reopened again and there was a sudden gush of blood from around the heart associated with a rapid improvement in blood pressure and central venous pressure. There was generalised ooze of blood around the heart but no specific bleeding points could be identified. Further platelets and fresh frozen plasma were given and the chest was again closed. Blood loss from his drains was now much less, he was cardiovascularly stable although still requiring inotropic support and his urine output had increased. During the following six hours it was possible to begin to slowly decrease his inotropic support, and the sedation was lightened briefly in order to assess his neurological status. His mental status was found to be appropriate and he was able to obey commands. Thirty hours after surgery, he required minimal inotropic support and all sedation was stopped and once he was fully awake and breathing spontaneously he was extubated and later that day returned to the cardiac 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?
<previous page
page_38
next page>
<previous page
page_39
next page>
Page 39
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. Current Opinion 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-site monitoring of coagulation in patients undergoing cardiac operations. Thoracic and Cardiovascular Surgery 1994; 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.
<previous page
page_39
next page>
<previous page
page_41
next page>
Page 41
Case 8 A 19 year old primigravida at 33 weeks gestation underwent artificial rupture of membranes for induction of labour because of deteriorating pre-eclampsia. She had been found to have proteinuria, platelets of 157 x 109/l and 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, an epidural 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 minutes were eight and nine. Two hours after delivery of the infant her placenta was still retained and so she was transferred to theatre for removal. On arrival in theatre routine monitoring was established and it was noted her blood 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, general anaesthesia was induced following pre-oxygenation. A rapid sequence intravenous induction technique was employed and her trachea intubated with the aid of a gum elastic bougie. It was noted she had oedema of her oropharynx and epiglottis.
<previous page
page_41
next page>
<previous page
page_42
next page>
Page 42
Table 8.1 PT APTT Fibrinogen Haemoglobin Platelets WCC 20.2 seconds 50 seconds 1.3 g/l 83 g/l 102 x 109/l 7.8 x 109/l
Samples of blood were sent after delivery to haematology for full blood count estimation and a coagulation screen. 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 45 minutes. Manual removal of placenta failed to slow the bleeding and so an infusion of syntocinon was commenced. 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 a massive 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-eclamptic patient? <><><><><><><><><><><><> Despite this she continued to bleed significantly per vagina. Fluid resuscitation
<previous page
page_42
next page>
<previous page
page_43
next page>
Page 43
continued while central venous and radial arterial cannulae were inserted to assist monitoring. Her condition was discussed with intensive care medical staff at this time and arrangements were made for her trnasfer to ICU after leaving theatre. Further blood samples were sent to haematology. Table 8.2 PT APTT Fibrinogen Haemoglobin Platelets WCC 43.6 seconds 134 seconds 0.8 g/l 5.3 g/l 52 x 109/l 4.5 x 109/l
Her condition was discussed with the haematologist on-call and further fresh frozen plasma was supplied, in addition to cryoprecipitate and platelets. She continued to be transfused blood. In a further attempt to control the 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 now been transfused eight units of packed red cells, received four units of fresh frozen plasma, six units of cryoprecipitate, six units of platelets and 2000 ml of crystalloid. Her oropharyngeal temperature was 35.3 C on departure 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 PaO2 PaCO2 pH Base Deficit Actual Bicarbonate K+ 10.3 kPa 5.1 kPa 7.24 -8.6 mmol/l 16 mmol/l 6.7 mmol/l
<previous page
page_43
next page>
<previous page
page_44
next page>
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 17 mmHg.
Fig. 8.1 A bolus intravenous injection of a loop diuretic was given and followed by an infusion. This produced a brisk diuresis followed by an improvement in gas exchange and her serum potassium fell. She also received calcium gluconate. Electrolytes were within normal limits, but urea and creatinine were elevated (9.8 mmol/l and 112 micromol/l). She was actively rewarmed. <><><><><><><><><><><><> Pulmonary oedema is a not uncommon, but serious complication in pre-eclampsia. Do you consider the monitoring in this patient was adequate? Explain your answer.
<previous page
page_44
next page>
<previous page
page_45
next page>
Page 45
She remained hypertensive. The labetolol infusion continued and infusion of magnesium started. Liver function tests remained normal throughout. Coagulation returned to normal within eight hours of her admission to the ICU. She was extubated 24 hours after admission after direct laryngoscopy confirmed minimal laryngeal oedema. 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 for magnesium 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?
<previous page
page_45
next page>
<previous page
page_46
next page>
Page 46
Further Reading Report on Confidential Enquiries into Maternal Deaths in the UK, 1988-1990 Department of Health. Revised Guidelines for the Management of Massive Obstetric Haemorrhage. Mushambi M.C, Halligan A.W, Williamson K. Recent developments in the pathophysiology and management of 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 of Anaesthesia 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.
<previous page
page_46
next page>
<previous page
page_47
next page>
Page 47
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 he had a temperature and noted his nose was runny, he had a barking cough and was hoarse. On arrival at hospital he appeared unwell and his temperature was 38 C. His blood pressure was 100/40 mmHg, pulse rate 110 beats/minute, respiratory rate 30/minute. There was marked use of accessory respiratory muscles, slight tracheal descent 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 had not 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 gaseous induction of anaesthesia was performed, intravenous access obtained and laryngoscopy then performed. At laryngoscopy, copious secretions were seen which had to be removed by suction prior to obtaining a good view of the larynx, revealing a normal epiglottis. <><><><><><><><><><><><> What is your diagnosis now?
<previous page
page_47
next page>
<previous page
page_48
next page>
Page 48
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 the endotracheal tube. Ventilation was difficult by hand and when placed on a ventilator, the tidal volume was poor despite 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 and blood gases gradually improved during the next 12 hours. He was commenced on intravenous sedation, steroid and 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 breath spontaneously with continuous positive airway pressure. The following day copious purulent secretions were produced on tracheal suctioning, he was noted to be working harder to breath and his respiratory rate rose steadily. He was sedated and ventilated, but his airway pressure was high and it became progressively more difficult to maintain adequate ventilation. A chest X-ray was essentially normal but his gas exchange had deteriorated.
<previous page
page_48
next page>
<previous page
page_49
next page>
Page 49
Table 9.1 FIO2 PaO2 PaCO2 pH HCO30.8 7.3 kPa 7.5 kPa 7.23 20 mmol/l
The nasal endotracheal tube was removed and replaced with a fresh one and ventilation was immediately improved. The tip of the original endotracheal tube was partially clogged with thick purulent secretions. It was presumed he had developed secondary bacterial tracheitis. Bronchoscopy was performed with a rigid bronchoscope to enable tracheal toilet. Over the next three days despite frequent suctioning by nursing and physiotherapy staff, bronchoscopy was required to remove secretions on a daily basis. Culture of the tracheal aspirate 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 or retropharyngeal abscess? <><><><><><><><><><><><> By the sixth day after admission the secretions had become less copious and gas exchange was improving. He was again allowed to breath spontaneously with continuous positive airway pressure and nasogastric feeding was established. He was extubated under direct vision on day nine while deeply anaesthetised. There was no stridor or indrawing observed. After a further 12 hours of observation he was discharged to the paediatric ward and after observation for 2 hours oral fluids were commenced. The following day he was discharged home on oral antibiotics and a decreasing dose of oral steroids.
<previous page
page_49
next page>
<previous page
page_50
next page>
Page 50
Croup is a common problem in the 1-5 age group with 3-5% of all children having at least one episode. The majority 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. The Paediatric Risk of Mortality is such a scoring system for paediatric ICU patients. Which parameters are measured for calculating this score? Further Reading Walker P, Crysdale W.S. Croup, epiglottitis, retropharyngeal abscess, and bacterial tracheitis: evolving patterns of 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 United Kingdom. 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 year period 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 Medicine 1988; 16: 1110-6.
<previous page
page_50
next page>
<previous page
page_51
next page>
Page 51
Case 10 A 72 year old, 76 kg man was taken by ambulance to the local hospital after being found unconscious in a cold bath by a neighbour. Two empty wine bottles were found on the floor beside the bath, the shower curtain was ripped and the left temporal area of his head was contused and lacerated. It was assumed he had struck his head on 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/minute and on listening to his abdomen, no bowel sounds were heard. He was connected to the ECG monitor revealing prolonged PR interval and J waves (Fig. 10.1). His core temperature was measured at 29 C. Shortly after admission he became apnoeic and was rapidly intubated without the aid of sedation or neuromuscular blockade.
Fig 10.1
<previous page
page_51
next page>
<previous page
page_52
next page>
Page 52
This intervention precipitated ventricular fibrillation which was successfully treated by the administration of three 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. Continuous invasive monitoring of the central venous and systemic arterial pressure was commenced. Blood was sent for full blood count, urea, electrolytes, glucose, amylase, liver function tests and blood cultures. Active rewarming was 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 was covered in a warming blanket set at 37 C and intravenous fluid was given through a countercurrent fluid warmer. 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 his central venous pressure stabilised an infusion of dopamine was started to maintain his systolic blood pressure at 115 mmHg. Sedation was assured with a propofol infusion running at a low rate. No neuromuscular blockade was used.
<previous page
page_52
next page>
<previous page
page_53
next page>
Page 53
His blood results were as follows (arterial blood gases are corrected for temperature): Haemoglobin Haematocrit WCC Platelets Clotting screen Blood alcohol Na+ K+ Urea Creatinine Glucose Amylase FIO2 pH PaO2 PaCO2 Base excess HCO3Table 10.1 141 g/l 44% 7.4 x 109 /l 82 x 109/ll normal 220 mg/dl 137 mmol/l 3.8 mmol/ 7.6 mmol/l 102 micromol/l 14.8 mmol/l 78 U/l 1.0 7.52 18.4 kPa 28 kPa -6.9 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?
<previous page
page_53
next page>
<previous page
page_54
next page>
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 pressure measurements. Urine output was maintained at 0.5 ml/kg. Specific gravity was low initially. The core temperature did not rise in the first hour of ICU but thereafter rose by 0.8 C for the following 4 hours. As the patient's core temperature rose, renal tubular function improved. Peritoneal lavage was discontinued once the core temperature rose above 32 C. Despite this, the pupils remained fixed and dilated and therefore a CT scan was arranged to assess any intracranial pathology which had resulted from the fall. The scan was reported as normal 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 of arousal for six hours, whereupon he woke steadily. He was weaned easily from the ventilator and was extubated after a short period of spontaneous ventilation with minimal assist from the ventilator. Despite being in a thermoneutral environment and receiving warmed fluids and respiratory gases his temperature had not risen above 36 C and remained at this level for a further 48 hours after his discharge to a general medical ward. <><><><><><><><><><><><> 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.
<previous page
page_54
next page>
<previous page
page_55
next page>
Page 55
Using the equation Q = mc (t2-t1), where Q = heat loss, m = mass and c = specific heat, calculate the heat deficit of this patient. Assuming peritoneal lavage is the only rewarming measure in this patient, what volume of fluid at 40 C will be 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 exchanged each 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 cardiovascular instability. It was not considered as an option on this occasion in case of intracranial bleeding with concurrent heparinisation. 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 temperatures below 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 you aware of current areas of research into induced hypothermia as therapy in the critically ill patient?
<previous page
page_55
next page>
<previous page
page_56
next page>
Page 56
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 fifteen year survey. Danish Medical Bulletin 1992; 39:190-3. Bernard S. Induced hypothermia in intensive care medicine. Anaesthesia and Intensive Care 1996; 24: 382-8.
<previous page
page_56
next page>
<previous page
page_57
next page>
Page 57
Case 11 A 19 year old male was found lying on his bedroom floor, unrouseable with noisy breathing in the morning by his 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 episode while 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 dilated and 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 were placed in the groin and axillae, blood was sent for toxicology and intravenous N-acetyl cysteine was commenced. 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 temperature was measured with an oesophageal probe and found to be 40.2 C. Dantrolene was administered and further blood samples were taken for full blood count, urea, electrolytes, glucose, amylase, liver function tests and blood cultures. In addition, a viral screen
<previous page
page_57
next page>
<previous page
page_58
next page>
Page 58
was performed with a view to dialysing for temperature control. A nasogastric tube was passed and some altered blood was aspirated. Normal saline was infused intravenously and a broad spectrum antibiotic administered. His core temperature began to fall 20 minutes after administration of the dantrolene and returned to normal in 1 hour. However, despite the infusion of 500ml of saline, he had passed no urine. His blood test results were as follows: Na+ K+ HCO3Urea Creatinine Glucose Mg2+ Phosphate 136 mmol/l 6.2 mmol/l 18 mmol/l 6.1 mmol/l 172 micromol/l 9.4 mmol/l 0.63 mmol/l 1.82 mmol/l Table 11.1 Ca2+ Amylase Total protein Albumin Bilirubin LDH AAT Alk phos gGT FIO2 pH PaCO2 HCO3Base excess 1.96 mmol/l 163 U/l 55 g/l 55 g/l 26 micromol/l 690 U/l 155 U/l 54 U/l 47 U/l 0.8 7.33 3.28 kPa 13.3 mmol/l -10.7
PT 28.5 seconds TT 1 8.8 seconds APTT 60.5 seconds PaO2 27 kPa Fibrinogen 1.3 g/l Platelets 101x109/l FDPs > 200 Urine positive for myoglobin. Paracetamol not detected. Salicylate not detected.
Review these laboratory findings and outline the action you would take.
<previous page
page_58
next page>
<previous page
page_59
next page>
Page 59
What is the corrected calcium level? <><><><><><><><><><><><> His blood pressure fell progressively for the first few hours after admission despite significant fluid administration. After administration of fresh frozen plasma and cryoprecipitate, a pulmonary artery catheter was inserted. Initial measurements are shown in Table 11. Table 11.2 140 beats/minute 70/35 mmHg 8.4 l/min 10 mmHg 550 dyne.cm-5s-1 12 mmHg
Pulse rate
Blood pressure Cardiac output CVP SVR PAOP
Vasoactive drugs were commenced, his blood pressure rapidly rose to acceptable levels and after diuretic therapy he began to pass large volumes of urine. His cardiac output was maintained. During the first 24 hours oxygenation 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 on the admission samples. He required a further three days of ventilation and cardiovascular support. All sedation was discontinued and he began to breath spontaneously with continuous positive airway pressure, but he did not wake up. A CT scan was performed which was normal and 24 hours later he was awake enough to be extubated.
<previous page
page_59
next page>
<previous page
page_60
next page>
Page 60
This patient had ingested a significant amount of alcohol which would have contributed to his dehydration and subsequent hyperthermia. Outline the management of a patient with severe alcohol intoxication occurring in isolation. Discuss the main objectives of treatment in any case of acute poisoning. Describe how you would specifically treat 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 of action 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 the dantrolene? What is the differential diagnosis of hyperthermia occurring in a patient in ICU?
<previous page
page_60
next page>
<previous page
page_61
next page>
Page 61
Further Reading O'Connor B. Hazards associated with the recreational drug ecstasy. British Journal of Hospital Med i cine 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 Pediatrics 1994; 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 amphetamine deriviatives. 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.
<previous page
page_61
next page>
<previous page
page_63
next page>
Page 63
Case 12 A 45 year old woman was taken by ambulance to the local hospital emergency department after falling 40 feet from the second floor of her home. She had been cleaning a window, and was seen to fall by her neighbours who alerted the emergency services. On arrival at hospital, her respiratory rate was 18 breaths/minute, pulse rate 100 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 lateral cervical spine film revealed a fracture of the spinous process of C7 and on her chest X-ray there were changes consistent with aspiration at the right base. The on-call anaesthetic and neurosurgical teams were contacted and after rapid neurosurgical assessment, she was intubated and ventilated before transfer to the radiology department. CT scan of her head confirmed a severe injury. There was a compound left petrosal bone fracture with a small subdural haematoma and slight midline shift, a contra coup injury on the right, bilateral frontal contusions, cerebral oedema and small amounts of subarachnoid and intra ventricular blood. Surgical intervention was not thought appropriate and she was transferred to the ICU after wound debridement, insertion of 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.
<previous page
page_63
next page>
<previous page
page_64
next page>
Page 64
This patient has sustained a significant primary brain injury. Currently there is no treatment for primary damage, and resources are aimed at injury prevention. Management after an injury has been sustained is directed 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 also commenced intravenous antibiotics and H2 antagonist. Ventilation was adjusted to keep the PaCO2 at 4 kPa for the first 48 hours. A right subclavian central line and radial arterial line were inserted and vasoactive agents used to maintain the cerebral perfusion presure above 50 mmHg. Although initially the intracranial pressure remained around 15 mmHg after an hour in ICU there were several sustained rises above 25 mmHg. <><><><><><><><><><><><> Describe your immediate management of these changes in intracranial pressure? What is the role of sedation and neuromuscular blockade in the management of the patient being ventilated with a serious head injury? What types of monitor are available for measurement of intracranial pressure? How is cerebral perfusion pressure calculated? How can cerebral perfusion be monitored?
<previous page
page_64
next page>
<previous page
page_65
next page>
Page 65
Sedation was increased and the patient repositioned with a 15 head up tilt. During the next eight hours her intracranial pressure remained below 18 mmHg. She then had a sudden significant rise in intracranial pressure to 55 mmHg for over ten minutes. Her blood pressure and pulse were unchanged. <><><><><><><><><><><><> What are the possible causes of a rise in intra-cranial pressure at this stage and how would you investigate this change? <><><><><><><><><><><><> After ascertaining that there was no change in her ventilation, sedation or positioning 25 grams of mannitol was infused intravenously and the neurosurgeon contacted. The pressure dropped quickly before the mannitol infusion was complete but B waves were noted on the ICP trace. Shortly after that, there was another large rise in intracranial pressure and her pulse rate slowed. She was rapidly transferred for a further CT scan of the head. Hydrocephalus was evident and so the patient underwent emergency insertion of a ventriculo-peritoneal shunt. Baseline intra-cranial pressure then remained below 15 mmHg for 24 hours. The pressure monitor was removed. <><><><><><><><><><><><> What other methods are available for monitoring cerebral status in such patients? <><><><><><><><><><><><> Enteral feeding was commenced via an orogastric tube. A chest X-ray revealed persistent right lower lobe consolidation and a coliform was grown in pathological quantities and antibiotic therapy was changed according to sensitivities. After six days, a percutaneous tracheostomy was formed, as all attempts at reduction in ventilatory support had been unsuccessful due to confusion and poor respiratory pattern. The following day ventilatory support was successfully withdrawn. When transferred to the neurosurgical ward for further care the following morning she remained confused and uncooperative.
<previous page
page_65
next page>
<previous page
page_66
next page>
Page 66
Patients with a head injury or mechanism of injury such as this patient are at risk of a cervical spinal injury. How can this be assessed and how should the patient be managed? Are there any concerns about semi rigid cervical collars in patients with raised intracranial pressure? Further Reading Teasdale G.M. Head Injury. Journal of Neurology, Neurosurgery and Psychiatry 1995; 58: 526-39. Gentleman D., Dearden N.M., Midgley S., Maclean D. Guidelines for resuscitation and transfer of patients with serious head injury. British Medical Journal 1993; 307: 547-52. Price D.J. Intracranial pressure monitoring. British Journal of Clinical Equipment 1980; May: 92-98. Jeevaratnam D.R, Menon D.K. Survey of intensive care of severely head injured patients in the United Kingdom. British Medical Journal 1996; 312: 944-6. Pickard J.D., Czosnyka M. Management of raised intracranial pressure. Journal of Neurology, Neurosurgery and Psychiatry 1993; 56: 845-58. Miller J.D. Vasoconstriction as head injury treatment - right or wrong? Intensive Care Medicine 1994; 20: 24950. Dearden N.M. Management of raised intracranial pressure after severe head injury. British Journal of Hospital Medicine 1986; August: 94-103.
<previous page
page_66
next page>
<previous page
page_67
next page>
Page 67
Case 13 A 21 year old student was admitted to the ICU from the emergency department. She had been found unconscious at home by friends. They reported she was an insulin dependent diabetic and they thought her blood sugar control was usually good. She had complained of flu-like symptoms during the preceeding two weeks and had been noticably short of breath when last seen 36 hours previously. On admission to ICU she had a Glasgow coma score of 6 (E1, M4, V1), her respiratory rate was 36 breaths/minute, blood pressure 73/46 mmHg and pulse rate 136 beats/minute. On auscultation of her chest, decreased air entry at the right base with bronchial breathing and inspiratory crackles were noted. Oxygen saturation on a pulse oximeter was 86% although 10 1/minute of oxygen was being administered through a face mask. After induction of anaesthesia, her trachea was intubated and her lungs ventilated. No neuromuscular blocking agent was used. Results of arterial blood gases and blood urea and electrolytes taken in the emergency department were now available (Table 13.1). Table 13.1 pH Na+ PaO2 K+ PaCO2 Cl HCO3 Urea Glucose Creatinine 7.01 131 mmol/l 7.9 kPa 8.3 mmol/l 2.6 kPa 100 mmol/l 12 mmol/l 20.1 mmol/l 38 mmol/l 197 mmol/l
What type of acid/base disturbance do these results indicate?
<previous page
page_67
next page>
<previous page
page_68
next page>
Page 68
What can produce this picture? Can you calculate the anion gap in this patient? What is the reason behind and the significance of an anion gap? What features would you expect on an ECG? Describe your immediate management and investigation of this patient. <><><><><><><><><><><><> Resuscitation was commenced with an intravenous infusion of normal saline. She was given 20 units of actrapid insulin and 10 millimoles of calcium gluconate intravenously. An intravenous infusion of insulin at 1015 units/hour was started. The rate was decided according to blood sugar level which was estimated every 30 minutes. Central venous access was gained via the internal jugular route and a radial arterial cannula and urinary catheter were inserted. The central venous pressure read 1 mmHg after infusion of three litres of normal saline during the first two hours. Potassium supplementation started when the serum potassium fell below 5 mmol/l. The initial chest X-ray had changes consistent with right middle lobe and apical segment of lower lobe pneumonia (Fig 13.1 and 13.2). Broad spectrum intravenous antibiotics were started. Six hours after ICU admission she had received 12 litres of normal saline. The blood glucose was now 18.6 mmol/l and 5% dextrose was added to the fluid regime. Her cardiovascular status had improved with fluid resuscitation however she had only passed 100 ml of urine since admission. A low dose infusion of dopamine was started. Further intravenous fluid and potassium were given, in addition to phosphate and magnesium supplemention during the next 24 hours. Urine production increased, and there was a gradual decrease in serum creatinine concentration. At the end of the first day in ICU she was producing 200-250 ml of urine each hour. Insulin infusion continued according to a sliding scale of blood sugar.
<previous page
page_68
next page>
<previous page
page_69
next page>
Page 69
Fig 13.1
Fig 13.2
<previous page
page_69
next page>
<previous page
page_70
next page>
Page 70
Copious tracheobronchial secretions were suctioned with chest physiotherapy and her oxygenation steadily improved. Her sedation was decreased on the second day of admission to facilitate weaning from artificial ventilation. With this, spontaneous respiration quickly resumed, but there were no other signs of the patients conscious level improving. By day three she was still tolerating the endotracheal tube without sedation. She had received no long-acting sedative drugs. <><><><><><><><><><><><> Are you concerned by the patient's conscious level? What is your differential diagnosis and how would you proceed? What is the role of low dose dopamine to produce a urine output? <><><><><><><><><><><><> A CT scan of the head was performed which was consistent with marked cerebral oedema and raised intracranial pressure (Fig. 13.3). Intravenous sedation was recommenced and the lungs ventilated for a further 48 hours. Urine and plasma osmolality were measured as the urine output continued to be high.
Fig 13.3 The results strongly suggested diabetes insipidus. No specific treatment was given for this, but fluid balance was strictly controlled and the urine output decreased during the next 24 hours. The CT scan was repeated and
<previous page
page_70
next page>
<previous page
page_71
next page>
Page 71
showed apparent resolution of the cerebral oedema. Sedation was again withdrawn and she was weaned from the ventilator over the following six days. However, she continued to show evidence of cerebral impairment. This cerebral impairment seemed to improve over a further 48 hours and she was discharged to a general medical ward, on a twice daily insulin regimen. <><><><><><><><><><><><> Why did this patient develop cerebral oedema and diabetes insipidus? Could anything have been done to prevent this happening? Discuss the pathophysiology and causes of diabetes insipidus. How is a diagnosis made? What is the pathophysiology of diabetic ketoacidosis? How do other life threatening complications of diabetes mellitus present and how should they be treated? Further Reading Blevins L.S.Jr., Wand G.S. Diabetes insipidus. Critical Care Medicine 1992; 20: 69-79. Kitabchi A.E., Wall B.M. Diabetic ketoacidosis. Medical Clinics of North America 1995; 79: 9-37. Gonzalez-Campon J.M., Robertson R.P. Diabetic ketoacidosis and hyperosmolar non ketotic state: gaining control over extreme hyperglycaemic complications. Post Graduate Medical Journal 1996; 99: 143-52. Lorber D. Nonketotic hypertonicity in diabetes mellitus. Medical Clinics of North America 1995; 79: 3-52.
<previous page
page_71
next page>
<previous page
page_73
next page>
Page 73
Case 14 A 45 year old 70kg man was admitted to the ICU from the general surgical ward with increasing respiratory distress. Seven days previously he had undergone elective total pancreatectomy and splenectomy because of chronic pancreatitis and persistent pain. Initial progress after this procedure had been satisfactory, but on the sixth postoperative day he became increasingly tachypnoeic with clinical signs of infection in the right lower zone of his chest. Consolidation of the right lower lobe was evident on a chest X-ray. Intravenous antibiotic therapy was commenced, but his condition continued to deteriorate and he was transferred the following day to the ICU. On arrival he was distressed with a respiratory rate of 35 breaths per minute. Arterial blood gas analysis was performed whilst he was breathing oxygen, FIO2 0.6 (Table 14.1). He was becoming increasingly tired, tachypnoeic and confused. Following induction of anaesthesia, his trachea was intubated to permit artificial ventilation of his lungs. Sedation was continued by intravenous infusion. He was ventilated initially in a volume controlled mode with an I:E ratio of 1:2, PEEP of 2 cmH2O and an FIO2 of 0.6. The peak inflation pressure was measured at 27 cmH2O. Copious tracheobronchial secretions were suctioned and sent for microbiological analysis. Table 14.1 FIO2 pH PaO2 PaCO2 Base excess SaO2 0.6 7.19 7.5 kPa 2.5 kPa 9.9 86%
Over the next 24 hours his condition continued to deteriorate. He required 100% oxygen and PEEP increased to 10 cmH2O to maintain a PaO2 of greater than 10kPa. Neuromuscular blockade was commenced at this stage and continued by infusion.
<previous page
page_73
next page>
<previous page
page_74
next page>
Page 74
Throughout this period his cardiovascular status was good, he produced good volumes of urine and maintained normal serum biochemistry. As gastric aspirates were high and no bowel sounds were heard, parenteral nutrition was commenced. Broad spectrum antibiotic therapy continued, although all microbiological results were negative for organisms. <><><><><><><><><><><><> What do you understand by the term ''best PEEP"? What are the detrimental effects of PEEP? What is "auto PEEP"; how can it be measured and how is it delivered? <><><><><><><><><><><><> By the third day in ICU there was bilateral opacification throughout both lung fields on the chest X-ray and PaO2 was now persistently below 10kPa despite ventilation with 100% oxygen. The peak airway pressure had risen to 42 cmH2O with a plateau pressure of 35 cmH2O and a tidal volume of 800ml. A pressure controlled mode of ventilation was instituted with a pressure limit of 38cm H2O, I:E ratio 2:1 and PEEP of 15 cmH2O. Despite altered ventilator settings PaO2 remained below 10kPa and there was progressive rise in PaCO2 to 8kPa. This was judged acceptable in the face of poorly compliant lungs and a stable cardiovascular system. <><><><><><><><><><><><> What was the patient's dynamic compliance? Discuss the pathophysiology of acute respiratory distress syndrome. What investigations could be undertaken to help confirm the diagnosis? This man had several changes to his ventilatory mode and pattern.
<previous page
page_74
next page>
<previous page
page_75
next page>
Page 75
What other modes/manoeuvres are available to try to maintain oxygenation in patients with this problem? What is the proposed mechanism for each of these? <><><><><><><><><><><><> His condition remained unchanged until a sudden fall in oxygen saturation, accompanied by a fall in blood pressure, was noticed on day eight in intensive care. Tension pneumothorax was suspected and confirmed by chest X-ray. This was drained with an apical intercostal chest tube. A further pneumothorax developed on the opposite side in the next 24 hours and this too was drained. Repeated chest radiographs over the following three days revealed multiple loculated pneumothoraces, which were drained according to clinical indication. All antibiotic therapy had been stopped as there were no positive microbiological results. <><><><><><><><><><><><> Does the development of pneumothoraces influence the outcome from acute respiratory distress syndrome? What pharmacological treatments of the acute respiratory distress syndrome have you heard of and how might these work? <><><><><><><><><><><><> Some improvement in oxygenation was noted by day 12 in ICU and PEEP was reduced to 12 cmH2O. A tracheostomy was performed and nasogastric feeding was established. All central lines were removed and some resolution of the opacification in the lower zones was noted on a chest X-ray. This improvement continued during the following days enabling further reductions in F1O2, PEEP and ventilation pressure limit. Neuromuscular blockade was reversed, and as sedation was reduced, the patient began making spontaneous respiratory efforts. On the 25th day of ICU he was breathing spontaneously through a T-piece with an F1O2 of 0.35 giving a PaO2 of 12kPa.
<previous page
page_75
next page>
<previous page
page_76
next page>
Page 76
His mental condition was unimpaired, but there were problems with the withdrawal of opioid which had been used for sedation. This was managed with further small doses of opioid and a low dose infusion of benzodiazepine. The final chest drain was removed after complete radiological resolution of all pneumothoraces, although widespread opacification remained. The following day he was discharged back to the surgical ward. Further Reading Chapman M.J. Adult respiratory distress syndrome an update. Anaesthesia and Intensive Care 1994; 22: 25566. Gattinoni L, Bombino M, Pelosi P, Lissoni A., et al. Lung structure and function in different stages of severe adult respiratory distress syndrome. Journal of the American Medical Association 1994; 271: 1771 - 9. Schuster D.P. What is acute lung injury? What is ARDS? Chest 1995; 107: 1721-6. Vincent J-L. Is ARDS usually associated with right ventricular dysfunction or failure? Intensive Care Medicine 1995; 21: 522-36.
<previous page
page_76
next page>
<previous page
page_77
next page>
Page 77
Case 15 A 50 year old man was admitted to the ICU from theatre following an emergency procedure for formation of tracheostomy. Five days previously he had been admitted as an emergency to the ENT ward, complaining of difficulty in opening his mouth and moving his tongue. Further questioning revealed he had experienced some abdominal muscle spasms, and that all these symptoms were subsequent to a minor foot injury whilst gardening five days previously. Examination at the time of admission to hospital revealed trismus and painless nuchal rigidity. The presumptive diagnosis was tetanus and intravenous benzylpenicillin was commenced. He had no record of tetanus immunisation so a course of anti tetanus toxoid was also started and he received Humotet. Intravenous diazepam was given for muscle spasms, and he was nursed in a single room. <><><><><><><><><><><><> The diagnosis of tetanus is made on clinical grounds only, and is now a rare condition in this country. The world-wide incidence is around one million cases per year, but most of these occur in the developing nations with there only being around 15 cases reported in the United Kingdom each year. The history given above of trismus, painless nuchal rigidity, and other spasms is typical of generalised tetanus. What is the infecting organism and the pathophysiology of the disease? Describe the range of autonomic dysfunction you might see in a patient with generalised tetanus. Why is it necessary to immunise the patient now he has contracted the disease?
<previous page
page_77
next page>
<previous page
page_78
next page>
Page 78
His condition steadily deteriorated over the next two days, with worsening abdominal spasms, increased difficulty in breathing, swallowing and mouth opening, despite increasing benzodiazepine therapy. It was decided to perform a tracheostomy and then transfer him to ICU. At the same time a radial arterial line, urinary catheter and fine bore nasogastric feeding tube were inserted. <><><><><><><><><><><><> The interval between injury and onset of clinical symptoms can range from three to thirty days, but in general the shorter this incubation period the more severe the disease. The period of onset of the disease is defined as the time from presence of first symptom to a generalised spasm e.g. the abdominal spasms in this patient. This time ranges from less than one day to twelve days. Again a shorter time indicates more severe disease. Both times would appear to be short in this case. Can you comment on the initial management of the patient in light of this? It is likely that the patient will require a prolonged period of ICU. What problems are associated with prolonged periods of intensive care and how would you aim to prevent them? <><><><><><><><><><><><> On arrival in the ICU a benzodiazepine infusion was commenced and he was allowed to breathe spontaneously as he awoke from anaesthesia. However, due to frequent severe abdominal spasms, doses of sedation were increased (benzodiazepine and opioid infusions). Despite this, spasms continued; a neuromuscular blocking agent was therefore given and artificial ventilation re-instituted. The following day nasogastric feeding was commenced, and sub-cutaneous heparin was given as prophylaxis for deep venous thrombosis. Benzylpenicillin therapy continued for two weeks and he was given glycopyrrolate regularly for excessive salivation. <><><><><><><><><><><><> Benzylpenicillin has been used in the management of tetanus for
<previous page
page_78
next page>
<previous page
page_79
next page>
Page 79
many years. What alternatives are there? Magnesium sulphate has been suggested as a useful adjunct to treatment. Why is this? <><><><><><><><><><><><> On day 15 in ICU he became pyrexial and chest X-ray revealed right upper lobe consolidation. Pneumococcus was grown from tracheal aspirates and appropriate antibiotic cover was commenced and chest physiotherapy targeted. This improved over the next week. He remained sedated and fully ventilated for five weeks as he continued to have spasms, at times requiring additional large bolus doses of benzodiazepine. Neuromuscular blockade was reversed and sedation reduced several times during this time, however he quickly developed distressing spasms on each occasion. After stopping neuromuscular blockade, sedation was successfully reduced on day 33 in ICU without him experiencing any spasms. All sedation was then discontinued and he steadily became more awake over three days and weaned without difficulty from ventilatory support. Two days later his tracheostomy was removed and he was transferred to a surgical high dependency ward the following day. He was discharged from hospital to home one week later. <><><><><><><><><><><><> This patient was sedated with high dose benzodiazepines and opioids for approximately five weeks and in addition required neuromuscular blockade in order to allow his care in ICU and to control his muscle spasms. What complications should you be aware of associated with the use of these types of agents for prolonged periods in the critically ill?
<previous page
page_79
next page>
<previous page
page_80
next page>
Page 80
Further Reading Edmonson R.S., Flowers M.W. Intensive care in tetanus: management complications and mortality in 100 cases. British Medical Journal 1979; 1: 1401-04. Harding-Goldson H.E, Hanna W.J. Tetanus: a resurring intensive care problem. Journal of Tropical Medicine and Hygiene 1995; 98: 173-8. Sandford J.P Tetanus Forgotten but not gone. Editorial. New England Journal of Medicine 1995; 332: 812-813. Todd Smith A, Drew S.J. Tetanus: A case report and review. Journal of Oral and Maxillofacial Surgery 1995; 53: 77-80. Udwadia F.E, Sunavala J.D, Jain M.C, D'Costa R., et al. Haemodynamic studies during the management of severe tetanus. Quarterly Journal of Medicine 1992; 302: 449-60. Prielipp R.C., Coursin D.B., Wood K.E and Murray M.J. Complications associated with sedative and neuromuscular blocking drugs in critically ill patients. Chapter in Critical Care Clinics Sedation of the Critically Ill Patient, 11(4), October 1995. Editor Cheng EY. Publishers: WB Saunders Company.
<previous page
page_80
next page>
<previous page
page_81
next page>
Page 81
Case 16 A 33 year old obese man was admitted to a general medical ward with a 24 hour history of haemoptysis. His only past medical history was of two episodes of pneumonia in the last year. On admission he appeared breathless, his respiratory rate was 28 breaths/minute and his pulse rate was 110 beats/minute. Auscultation of his chest revealed generalised late inspiratory and expiratory crepitations and chest X-ray showed widespread bilateral alveolar consolidation. <><><><><><><><><><><><> What is your differential diagnosis and what investigations would you perform? Initial laboratory results were: Table 16.1 Na+ 137 mmol/l FIO2 0.21 K+ 6.5 mmol/l pH 7.41 HCO3 23 mmol/l PaO2 6.0 kPa Urea 13.6 mmol/l PaCO2 4.1 kPa Creatinine 296 micromol/l sHCO3 23 mmol/l Albumin 31 g/l aHCO3 23 mmol/l Bilirubin 12 micromol/l Base excess 1.0 Haemoglobin 100 g/l MCH 30 pg Haematocrit 30% WCC 10.5 x 109/l MCV 89 fl Platelets 352 x 109/1 Urine microscopy: coarse granular casts, red blood cells What is your diagnosis now?
<previous page
page_81
next page>
<previous page
page_82
next page>
Page 82
The presumptive diagnosis was glomerulonephritis and he was transferred to the care of the renal physicians. A renal biopsy was performed and was reported as showing crescentic glomerulonephritis, consistent with Goodpasture's syndrome. Intravenous steroid and cyclophosphamide and a course of plasma exchange treatments were commenced. A double lumen renal dialysis line was inserted into the left subclavian vein for this purpose. <><><><><><><><><><><><> Discuss the aetiology of acute renal failure. What methods are available to treat a patient with hyperkalaemia? What are the advantages and disadvantages of these therapies? His parents are extremely concerned about his condition. How would you council them? <><><><><><><><><><><><> The haemoptysis continued and his respiratory function deteriorated further, so he was transferred to the ICU. Following induction of anaesthesia his trachea was intubated and infusions of sedative drugs commenced to permit ongoing mechanical ventilation. He became hypotensive and increasingly tachycardic after induction of anaesthesia and despite 100% inspired oxygen the pulse oximeter only read 85%. Rapid examination revealed no air entry on the left side of the chest and distended neck veins. <><><><><><><><><><><><> What is the differential diagnosis of this episode and how would you treat the patient? Discuss the complications of central line insertion. How does insertion site influence the complication rates?
<previous page
page_82
next page>
<previous page
page_83
next page>
Page 83
More thorough examination revealed hyperresonance on the left side of the chest and tracheal deviation to the right. Following insertion of a large bore cannula into the left second interspace in the midclavicular line there was a gush of air and the cardiovascular parameters and oxygen saturation improved. A 32FG intercostal drain was inserted into the fifth intercostal space anterior to the mid axillary line and connected to an underwater seal. This was seen to bubble vigorously. During the next 24 hours his renal function deteriorated further and renal replacement therapy was necessary. Daily haemodialysis commenced with a target weight loss of 2.5kg over four hours. During haemodialysis there were several episodes of hypotension which responded to rapid boluses of fluid. His serum potassium was 3.1 mmol/l after dialysis. <><><><><><><><><><><><> Discuss the advantages and disadvantages of this type of renal replacement therapy in the setting of acute renal failure in the intensive care unit. What other modes are available? When are these techniques appropriate and what are the relative advantages and disadvantages? <><><><><><><><><><><><> Blood loss continued from the lungs over the following five days and ten units of packed red cells were transfused during this time to maintain a haemoglobin of 100 g/l. Gas exchange improved as the pulmonary blood loss decreased and he was weaned from ventilation on the ninth day after intensive care admission and extubated shortly thereafter. He returned to the renal unit the following morning, where haemodialysis continued. He was reported to be positive for anti-glomerular basement membrane antibody. Ten days later he was discharged home with no evidence of return of renal function. He entered a chronic haemodialysis programme. One year later he received a sibling renal transplant which was rejected at three days. He remains on chronic haemodialysis therapy.
<previous page
page_83
next page>
<previous page
page_84
next page>
Page 84
How would you investigate a patient who presented five days post-operatively with anuria and a serum creatinine of 350 mmol/l? Discuss the prognostic significance of the development of acute renal failure in the critically ill. Discuss the use of pharmacological methods of ''renal rescue" in the critically ill. Does the infusion of small doses of dopamine have a renal protective effect? Further Reading Abbs I.C. Continuous haemofiltration for the treatment of acute renal failure. In: Intensive Care Britain 1994, 46-50. Grey Coat Publishing. Allon M. Treatment and prevention of hyperkalaemia in end stage renal disease. Kidney International 1993; 43: 1197-209. Bellama R, Ronco C. Acute renal failure in the ICU: adequacy of dialysis and the case for continuous therapies. Nephrology, Dialysis and Transplantation 1996; 11: 424-8. Bullingham, Palazzo. Renal rescue in the critically ill: The Charing Cross Protocol. In: Intensive Care Britain 1994, 51-5. Grey Coat Publishing. Chertow G.M, Christiansen C.L., Cleary P.D, Munro C, Lazarus J.M. Prognostic stratification in critically ill patients with acute renal failure requiring dialysis. Archives of Internal Medicine 1995; 155: 1505-11. Cottee D.B, Saul W.B. Is renal dose dopamine protective or therapeutic? No. Critical Care Clinics 1996; 12: 687-95. Daugiradas J.T, Ing T.S. Handbook of Dialysis (2nd Edition) Little, Brown and Co., Boston.
<previous page
page_84
next page>
<previous page
page_85
next page>
Page 85
Case 17 A 32 year old woman was referred by the general physicians to the ICU because of increasing breathlessness. She had presented three days previously complaining of numbness in both feet and weakness in her legs. Examination revealed loss of vibration sense in her ankles, hyporeflexia in her lower limbs, and a seventh nerve palsy. <><><><><><><><><><><><> List the differential diagnoses, and discuss what investigations you think are indicated. Describe the initial management of this case. <><><><><><><><><><><><> During the twelve hours prior to ICU referral, the weakness in her legs had become more marked and she had increasingly complained of breathlessness. On admission to ICU her respiratory rate was 27 breaths/minute, her forced vital capacity was 30% of the predicted value and she had a weak cough. After induction of anaesthesia her trachea was intubated and mechanical ventilation started. All initial blood investigations were normal as was a lumbar puncture. She had given no history suggestive of diptheria or hexacarbon abuse, and an electromyograph showed slowing of transmission of impulses and denervation. A diagnosis of Guillain-Barr was made. <><><><><><><><><><><><> How is the diagnosis of Guillain-Barr syndrome confirmed? Discuss the options for definitive treatment of this woman. What evidence is there of their effectiveness? Describe how you would perform plasma exchange on a patient and what problems might be encountered?
<previous page
page_85
next page>
<previous page
page_86
next page>
Page 86
After securing large bore venous access in one subclavian vein, plasma exchange was performed thrice weekly for two weeks. Fresh frozen plasma was used as the replacement fluid. She was kept sedated for the first five days and then allowed to lighten intermittently to allow assessment of neurological function. There was no improvement in her condition after fifteen days and so elective percutaneous tracheostomy was performed. <><><><><><><><><><><><> What factors would influence your decision to arrange for a tracheostomy in the critically ill patient and at what stage in treatment would you consider this? Justify your answer. This patient had a percutaneous tracheostomy performed in the ICU. Is ICU the appropriate place to perform this, and is it always an appropriate technique or do you consider a formal surgical tracheostomy in an operating room is the optimal approach? What is the incidence of complications following tracheostomy, and is there a difference between the various techniques and complication rate? Patients suffering from severe Guillain-Barr commonly endure a prolonged period of immobility. This can lead to several complications. What are these complications and how would you aim to prevent their occurrence? How does Guillain-Barr affect the autonomic system and how would you manage the problems? <><><><><><><><><><><><> During her first two weeks on ICU there were repeated problems with cardiovascular instability, with episodes of both hyper and hypotension associated with a variety of rhythm disturbances. The hypertension frequently needed treatment with intravenous beta blocking agents and the hypotension responded to intravenous fluids and occasionally inotropic support. Enteral feeding was eventually established and a programme of aggressive physiotherapy instigated. After the tracheostomy and as she
<previous page
page_86
next page>
<previous page
page_87
next page>
Page 87
became tolerant to the ventilator breaths the sedation was stopped. However she required frequent night sedation and a course of anti-depressant treatment was necessary. Improvement in muscle strength started after 23 days and progressed so she was able to be weaned off the ventilator after 31 days. She was then discharged to the care of the physicians still with marked lower limb weakness, but was able to leave hospital two weeks later. <><><><><><><><><><><><> What is the prognosis for patients with Guillain-Barr Syndrome? Once a tracheostomy was performed this patient's sedation requirements changed. What are the varying reasons for using sedation in the intensive care patient and how can one try and reduce the requirement for sedation? Is pain a major problem in Guillan-Barr Syndrome? Further Reading French Cooperative Group on Plasma Exchange in the Guillain-Barr Syndrome. Ann. Neurol. 1987; 22: 753 61. Rees J. Guillain-Barr Syndrome: Clinical manifestations and directions for treatment. Drugs 1995; 49: 912 - 20. Winner J.B., Greenwood R.J., Hughes R.A.C., Perkin G.D, Healey M.J.R. Prognosis in Guillain-Barr Syndrome. Lancet 1985; 1: 1202-3. Zochodne D.W. Autonomic Involvement in Guillain-Barr Syndrome: A review Muscle and Nerve 1994; 17: 1145-55. Fischler M.P., Kuhn M, Cantieni R, Frutiger A. Late Outcome of percutaneous dilational tracheostomy in intensive care patients. Intensive Care Medicine 1995; 21: 475-481. Tung A., Rosenthal M. Patients requiring sedation. Chapter in Critical Care Clinics-Sedation of the Critically Ill Patient 1995; 11: 791-802. Howard R.S. Neurology. British Medical Journal 1994; 309: 392-5. Anonymous. Double blind trial of intravenous methylprednisolone in Guillain-Barr Syndrome. Lancet 1993; 341: 586-90.
<previous page
page_87
next page>
<previous page
page_89
next page>
Page 89
Case 18 A 27 year old woman was taken by paramedic staff to the local hospital following a road traffic accident involving two vehicles. She had been a front seat passenger, wearing seat restraint, in one car hit on the drivers side by the other car which was reported to have been travelling at speed. The emergency services had extricated her without difficulty, although all others involved had been killed. On arrival at hospital she was conscious, but in great distress with a respiratory rate of 36 breaths/minute. Her pulse was thready with a rate of 136 beats/minute and blood pressure was 77/40 mmHg. <><><><><><><><><><><><> This patient has sustained a significant traumatic insult. What will your immediate approach, initial management and investigation of this patient be? What information do you require to calculate the injury severity score (ISS) and the predicted risk of death in this patient? From the mechanism of injury what life threatening injuries might she have sustained? Can these be diagnosed in the resuscitation room? At what stage should she be transferred to another hospital area or hospital for care? <><><><><><><><><><><><> Examination and investigations revealed extensive injuries to the right side of the body. There were six fractured ribs posteriorly with a flail segment and pneumothorax. This was drained by insertion of a chest tube in the fifth intercostal space anterior to the the mid axillary line. Extensive bruising was
<previous page
page_89
next page>
<previous page
page_90
next page>
Page 90
evident on the right side of the abdomen, which was distended, tender and silent. Other injuries included fractures of the right superior pubic ramus and an undisplaced fracture of the right distal tibia. Radiography of the cervical spine did not reveal any abnormality and she was observed moving all four limbs in the initial assessment. Fluid resuscitation was commenced initially with crystalloid and then O Rhesus negative blood, however she remained tachycardic and hypotensive. She was transferred to the operating theatre, where she was anaesthetised and underwent laparotomy. She had been transfused six units of O Rhesus negative blood by this time. <><><><><><><><><><><><> Discuss the advantages of crystalloid as opposed to colloids as an initial resuscitation fluid. What are the problems of giving uncross-matched blood? In which circumstances should it be used, if at all? A flail segment is a significant injury. Why is this? What factors influence whether a patient will require a period of ventilation as part of their management if they have a flail segment? <><><><><><><><><><><><> At laparotomy the right lobe of the liver was found to be extensively lacerated, the right kidney macerated and about three litres of free blood were in the peritoneal cavity. A right lobe partial hepatectomy and right nephrectomy were performed. During this procedure there were two periods when the blood pressure had been documented as unrecordable in the anaesthetic record. Bleeding was profuse and a total of 42 units of blood were given, in addition to ten units of cryoprecipitate, six units of fresh frozen plasma and five units of platelets during the procedure. The measured blood loss was 18,800 mls.
<previous page
page_90
next page>
<previous page
page_91
next page>
Page 91
This patient has received a massive blood transfusion. This can be defined as the administration of more than 1.5 times the estimated blood volume or replacement of the patients blood volume by homologous blood within 24 hours. Describe your treatment approach to the patient with acute severe haemorrhage. What problems would you anticipate in the period after a massive transfusion and how might you minimise these? <><><><><><><><><><><><> She was transferred post-operatively to the ICU sedated and ventilated with an FIO2 of 0.7. Her nasopharyngeal temperature was 34.5 C, heart rate 110 beats/minute, blood pressure 110/80 mmHg and central venous pressure 12 mmHg. A chest X-ray was performed and blood sent for routine analysis. Urea and electrolytes were normal and the haematology results were: Haemoglobin Platelets WCC Table 18.1 82 g/l INR 27 x 109/l APTT 17.4 x 109/l Fibrinogen FDP 2.1 50s 1.1g/l >200
Further blood products were given. <><><><><><><><><><><><> What blood products do you consider necessary? What are the differences between fresh frozen plasma, cryoprecipitate and whole blood and when are these different products indicated?
<previous page
page_91
next page>
<previous page
page_92
next page>
Page 92
What is the significance of a widened mediastinum (Fig 18.1) in this patient? What other features would give you the same cause for concern on a chest X-ray?
Fig 18.1 What are the appropriate examinations to perform to look for abnormalities of the mediastinum and what are the relative sensitivities and specificities for each?
<previous page
page_92
next page>
<previous page
page_93
next page>
Page 93
This was investigated with transoesophageal echocardiography, but no abnormality was found. She remained stable and it was possible to reduce the F1O2 to 0.5 during the next 48 hours. Despite this she became increasingly jaundiced and her renal function deteriorated as shown by her biochemistry on day three. Table 18.2 Na+ K+ Urea Creatinine Ca2+ Albumin Bilirubin AAT Alkaline phosphatase g GT Lactate dehydrogenase Protein 148 mmol/l 4.8 mmol/l 21.4 mmol/l 176 micromol/l 2.24 mmol/l 30 g/l 277 micromol/l 194 micromol/l 126 micromol/l 117 micromol/l 604 micromol/l 56 g/l
Discuss the pathphysiology and management of altered liver function in the critically ill patient. What are the possible factors involved in this patients deranged liver function? <><><><><><><><><><><><> The liver and renal function continued to worsen and two days later she became anuric. Renal replacment therapy was commenced in the form of intermittent haemodialysis. On day eight the bilirubin level peaked at 376 micromol/l. Liver function slowly returned to normal during this time and dialysis was no longer necessary after day 30. Enteral nutrition was established by day 21. Until this time she had been fed parenterally. Several attempts were made to reduce the ventilatory support, however she became tachypnoeic and gas exchange deteriorated with each attempt. A tracheostomy was performed on her 18th day of intensive care. Weaning
<previous page
page_93
next page>
<previous page
page_94
next page>
Page 94
from ventilatory support was still prolonged due to generalised weakness, however by day 33 she had been breathing spontaneously through a T-piece unaided for 48 hours. She was discharged from ICU to the surgical high dependency unit where mobilisation was slow due to her fractures and general weakness. <><><><><><><><><><><><> Weakness after intensive care for severe multiple organ failure is not uncommon and often will present with difficulty in weaning from ventilation. What are the causes for this problem and what are the prognoses for the patients long term? Further Reading Bolton C.F. Neuromuscular conditions in the intensive care unit. Ed. Intensive Care Medicine 1996; 22: 841-3. Committee on Trauma, American College of Surgeons: Advanced Trauma Life Support Manual. Chicago, American College of Surgeons, 1993. Cowley H.C., Webster N.R. Management of liver disease on ICU. Care of the Critically Ill 1993; 9: 122-7. Donaldson M.D.J., Seaman M.J., Park G.R. Massive Blood Transfusion. British Journal of Anaesthesia 1992; 69: 621-30. Erbel R, Zamorano J. The Aorta: Aortic aneurysm, trauma and dissection. Critical Care Clinics 1996; 12: 73363. Shoemaker W.C., Peitzman A.B., Bellamy R., Ballano R., Brittig S.P., Capore A., Dubick M., Kramer G.C., et al. Resuscitation from severe haemorrhage. Critical Care Medicine 1996; 24: S12-23.
<previous page
page_94
next page>
<previous page
page_95
next page>
Page 95
Case 19 A 41 year old man was admitted to hospital with severe upper abdominal pain. The pain had started some days earlier but he thought that it was indigestion as it had not been relieved by the tablets the doctor had given him for his angina. The pain was now much worse. He was grey and sweaty and obviously in some distress. He had had angina diagnosed two years ago and was noted in the biochemical investigations performed at that time to have hypertriglyceridaemia. <><><><><><><><><><><><> What is your differential diagnosis? Initial investigations revealed: Na+ K+ HCO3 Urea Creatinine Bilirubin Amylase Table 19.1 130 mmol/l Haemoglobin 3.5 mmol/l Haematocrit 30 mmol/l WCC 14 mmol/l Platelets 165 micromol/l 13 mmol/l 345 IU 133 g/l 44% 17.3 x 109/1 120 x 109/l
Which other investigations would you now require? <><><><><><><><><><><><> The patient was hypotensive and tachycardic and initial resuscitation was performed with a crystalloid infusion. An intensive care referral was made because of increasing respiratory distress. He was transferred to the ICU where ventilation was commenced and a central venous cannula inserted to permit further resuscitation. When a nasogastric tube was passed a large residual gastric content was drained. A presumed diagnosis of pancreatitis was made.
<previous page
page_95
next page>
<previous page
page_96
next page>
Page 96
How is the diagnosis of pancreatitis made and what are the best investigations to confirm this diagnosis? What are the surgical treatment options? What is the aetiology of pancreatitis and are there any important features in this patient? Which factors indicate a good or poor prognosis in a patient with pancreatitis? <><><><><><><><><><><><> By the third day in ICU he had gone into renal failure and was still being ventilated. His blood sugar had consistently been raised and he had recently required frequent injections of calcium gluconate to maintain a normal plasma calcium concentration. In addition his albumin had by now fallen to 21 g/l. He had been managed conservatively with nasogastric drainage, octreotide infusion and fluid therapy with crystalloid. <><><><><><><><><><><><> What is the best measure of plasma calcium to guide replacement? Are there any other electrolytes particularly important in pancreatitis? When is the ideal time to start feeding patients on ICU? What is the best route generally and in this specific patient for feeding? Which nutrients are required and in what quantities? In this patient what difference does the hypertriglyceridaemia make to the nutrition regimen and also to his sedation requirements? What is the place of glutamine supplementation in this patient? <><><><><><><><><><><><> On day seven a large quantity of fresh blood was aspirated from the nasogastric tube and a transfusion of five units of packed red cells was required over the next four hours to maintain a haemoglobin concentration above 90 g/l.
<previous page
page_96
next page>
<previous page
page_97
next page>
Page 97
What is the place of stress ulcer prophylaxis? Would you change your treatment now? <><><><><><><><><><><><> Upper gastrointestinal endoscopy revealed no localised source of bleeding but fortunately blood loss appeared to stop with the transfusion of a further two units of blood and five units of fresh frozen plasma. His plasma albumin had continued to fall despite total parenteral nutrition and was now 19 g/l, but other markers of hepatic synthetic function were satisfactory. <><><><><><><><><><><><> What is an acceptable albumin concentration? What does albumin do within and outside the circulation? How could you increase the albumin concentration? Does altering the albumin concentration affect outcome from ICU treatment? <><><><><><><><><><><><> Two days later he became pyrexial and his blood pressure fell to 85/45 mmHg and further blood loss was aspirated from the nasogastric tube. One litre of colloid was given rapidly and a pulmonary artery catheter inserted. CO CVP PAOP SVR Table 19.2 8 l/minute 4 mmHg 6 mmHg 520 dyne cm5 sec1
What has happened now and what are the treatment options? <><><><><><><><><><><><> Cross-matched blood was given when available and vasoconstrictor therapy started. The patient died six hours later with refractory hypotension.
<previous page
page_97
next page>
<previous page
page_98
next page>
Page 98
Further Reading Fernandez-del Castillo C, Rattner D.W., Warshaw A.L. Acute pancreatitis. Lancet 1993; 342: 475-9. Thomas P. Decision making in surgery: management of acute pancreatitis. British Journal of Hospital Medicine 1994; 51: 593-6. Forsmark C.E., Toskes P.P. Acute pancreatitis: Medical Management. Critical Care Clinics 1995; 11: 295-309. Baker C.C., Huynh T. Acute pancreatitis: Surgical management. Critical Care Clinics 1995; 11: 311-22. Formela L.J., Galloway S.W., Kingsnorth A.N. Inflammatory mediators in acute pancreatitis. British Journal of Surgery 1995; 82: 855. Berger R., Adams L. Nutritional support in the critical care setting (Part one). Chest 1989; 96: 139-150. Berger R., Adams L. Nutritional support in the critical care setting (Part two). Chest 1989; 96: 372 80.
<previous page
page_98
next page>
<previous page
page_99
next page>
Page 99
Case 20 A 61 year old man underwent transurethral resection of prostate under spinal anaesthesia. He had no previous hospital admissions, was on no medication but had smoked 10 cigarettes per day for over 30 years. Physical examination and pre-operative investigations were unremarkable. The procedure went smoothly until 50 minutes into the resection when the patient began to complain of feeling sick and having chest pain which radiated down his left arm. He was noted to be hypertensive (200/110 mmHg) and tachycardic (100 beats/minute). <><><><><><><><><><><><> What is your differential diagnosis? How would you investigate the problem and what immediate action would you take? <><><><><><><><><><><><> He continued to be hypertensive and complain of chest pain and his oxygen saturation as measured by pulse oximeter fell from 98% to 90% on 4 litres oxygen via a facemask. It was thought that some ST depression was evident on the ECG monitor. The flow rate of oxygen being delivered by face mask was increased to 10 litres, he was given a nitrate spray, intravenous opioid and surgery was terminated. The patient was transferred to the recovery room where a chest X-ray was ordered, twelve lead ECG performed and blood sent for arterial blood gas analysis, urea and electrolytes and cardiac enzymes. Examination of his chest revealed bilateral basal crepitations and pulmonary oedema was suspected. During this time the patient became increasingly confused and agitated. His ECG demonstrated T wave inversion in the lateral leads, which had not been present preoperatively. He was now maintaining an oxygen saturation, measured by the pulse oximeter of 92%, however he remained restless and confused and required constant reminding to keep his oxygen mask on. He was transferred to the ICU.
<previous page
page_99
next page>
<previous page
page_100
next page>
Page 100
On arrival in the ICU a radial arterial line was inserted and ECG and pulse oximeter monitoring continued. Return of the chest X-ray performed after surgery confirmed pulmonary oedema. The biochemical results became available. Table 20.1 before surgery Na+ K+ HCO3 Urea Creatinine Glucose Serum osmolality 141 mmol/l 3.9 mmol/l 27 mmol/l 6.2 mmol/l 77 micromol/l 4.8 mmol/l recovery room 120 mmol/l 4.5 mmol/l 21 mmol/l 4.3 mmol/l 72 micromol/l 5.6 mmol/l 290 mosmol/kg
Comment on these results and the diagnosis. What is the calculated serum osmolality? What is the significance of the measured serum osmolality? How would you manage this patient? <><><><><><><><><><><><> A bolus dose of intravenous diuretic was given and intravenous fluids given at a rate of 75 ml/hour of normal saline. His urine output was closely monitored and a further dose of diuretic given as the urine output tailed off four hours later. The confusion and agitation steadily improved during this time and his oxygen saturation improved. His electrolytes were repeated every two hours.
<previous page
page_100
next page>
<previous page
page_101
next page>
Page 101
Table 20.2 Hours Na+ K+ HCO3 Urea Creatinine post surgery mmol/l mmol/l mmol/l mmol/l micromol/l 2 4.8 22 4.5 125 72 4 3.9 22 5.4 129 88 6 3.6 25 7.6 13.4 No further treatment was required. His cardiac enzymes were reported as normal and a further twelve lead ECG the following day was no different from his pre-operative recording. He returned to the surgical ward the following morning. <><><><><><><><><><><><> This patient had an episode of acute hyponatraemia. What are the symptoms of this problem, and in what clinical situations will it be encountered? When would hypertonic sodium solution be an appropriate treatment? How quickly should acute hyponatraemia be corrected? Further Reading Anonymous. Walking on the moon. Lancet 1996; 347: 207. Dixon B, Ernest D. Hyponatraemia in the transurethral resection of prostate syndrome. Anaesthesia and Intensive Care 1996; 24: 102-3. Mulloy A.L., Caruana R.J. Hyponatraemic emergencies. Medical Clinics of North America 1995; 79: 155-168.
<previous page
page_101
next page>
<previous page
page_103
next page>
Page 103
Case 21 A 74 year old man was admitted to the ICU with a history of increasing tachypnoea and tachycardia over the preceding 24 hours. Five days previously he had undergone total cystectomy for bladder carcinoma. On admission he was breathing 10 litres oxygen through a face mask and intravenous fluids were running through an internal jugular central venous cannula. This had been inserted prior to surgery. His respiratory rate was 36 breaths/minute, heart rate 120 beats/minute and blood pressure 150/80 mmHg. An arterial blood gas sample had been obtained immediately prior to ICU admission and the results are shown below. Table 21.1 pH PaCO2 PaO2 HCO3 Base excess 7.18 7.6 kPa 9.5 kPa 17 mmol/l 9
Anaesthesia was induced and his trachea intubated and controlled ventilation commenced with an FIO2 of 1.0. His blood pressure fell to 80/60 mmHg after induction. Initially this responded to rapid intravenous fluid administration, however after 21 his central venous pressure had risen to 12 mmHg and his blood pressure was seen to fall each time the infusion rate was reduced. Inotropic support was commenced <><><><><><><><><><><><> What is your differential diagnosis and how would you investigate this patient? <><><><><><><><><><><><> Further blood was sent for arterial gas analysis and blood was taken from the central venous line for blood culture, routine biochemistry and haematology.
<previous page
page_103
next page>
<previous page
page_104
next page>
Page 104
Initial results were as follows FIO2 pH PaCO2 PaO2 12. HCO3 Base excess WCC Table 21.2 1.0 Na+ 7.29 K+ 5.5 kPa HCO3 9 kPa Urea 19 mmol/l Creatinine 6.4 Platelets 33.8 x 109/l Haemoglobin 129 mmol/l 3.6 mmol/l 17 mmol/l 17.6 mmol/l 200 micromol/l 150 x 109/l 10.4 g/dl
The differential blood count reported a neutrophilia. The inotropic support required to maintain an adequate blood pressure rapidly increased and so a pulmonary artery catheter was inserted. The existing central venous line was removed and the tip sent for culture. It was noticed at this time that the insertion site of this line was very inflamed. Blood cultures were taken from the new line and broad spectrum intravenous antibiotic therapy started. Initial measurements from the pulmonary artery catheter were taken and cardiovascular support then adjusted. Initial measurements: Table 21.3 53 mmHg 14 mmHg 21 mmHg 5 mmHg 119 beats/minute 6.1 l/min 3.6 l/min.m2
MAP CVP MPAP PAOP HR CO CI
What parameters can you derive from the results available so far?
<previous page
page_104
next page>
<previous page
page_105
next page>
Page 105
Which agents would you use to maintain perfusion and what goals would guide your therapy? Therapy for this patient has been guided by the insertion of and measurements made from a pulmonary artery catheter. Pulmonary artery catheters are commonly inserted in ICU patients. Do they commonly influence therapy and improve outcome? <><><><><><><><><><><><> He passed only 40 mls of urine during the first four hours in ICU, then produced large volumes (150-250 mls/hour) for several hours. A gram positive coccus was reported in the blood culture gram stain. The following morning he was stable but still required significant cardiovascular support. A gram positive coccus was also grown from the central line tip sent after admission to ICU and 24 hours later microbiology confirmed the presence of a single organism ( staphylococcus aureus). The central venous line was the presumed site of infection. His antibiotic therapy was altered according to sensitivities. Seventy two hours after admission to ICU his condition had improved such that the inotropic support was being steadily reduced and his gas exchange was now reasonable with an FIO2 of 0.5. His renal function was also improving. The sedation was then reduced and he began to wean from ventilation. It took another three days for the cardiovascular and respiratory support to finally be withdrawn. He was extubated on day 7 of intensive care and returned to the surgical ward the following day. <><><><><><><><><><><><> This patient became septicaemic due to an infected central venous line. How might this complication be minimised? What are the other complications of central venous lines? Other therapies common to intensive care units can result in iatrogenic problems e.g. arterial lines and pulmonary artery catheters.
<previous page
page_105
next page>
<previous page
page_106
Page 106
What are these problems and how would you minimise them? Intubation and ventilation have been implicated in the genesis of nosocomial infection in the ICU. What is the basis for this? Further Reading Del Guercio L.R.M. Does pulmonary artery catheter use change outcome? Yes. Critical Care Clinics 1996; 12: 553-7. Fabregas N., Torres A., El-Ebiary M., Ramirez J., et al. Histopathologic and microbiologic aspects of ventilator-associated pneumonia. Anesthesiology 1996; 84: 760-71. Leibowitz A.B. Do pulmonary artery catheters improve patient outcome? No. Critical Care Clinics 1996; 12: 559-67. Rouby J.J. Editorial - Nosocomial infection in the critically ill - The lung as a target organ. Anesthesiology 1996; 84: 757-9.
<previous page
page_106

Clinical Scenarios in ICU

Diunggah oleh

Informasi Dokumen

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Clinical Scenarios in ICU

Diunggah oleh

Hak Cipta:

Format Tersedia

cover

Clinical Scenarios in Intensive Care

Case 20 Trans Urethral Resection of Prostate Case 21 Post Operative Septicaemia

FIO2 PaO2 PaCO2 SpO2

Haemoglobin WCC Platelets Chest X-ray ECG

Haemoglobin Na+ WCC K+ Platelets HCO3ESR Urea Creatinine

Heart rate MAP CVP PAOP MPAP CO2 CI SaO2 SvO2

Blood pressure Cardiac output CVP SVR PAOP

What type of acid/base disturbance do these results indicate?

MAP CVP MPAP PAOP HR CO CI

Anda mungkin juga menyukai