(BQ) Part 2 book Critical care medicine at a glance presents the following contents: Cardiac, respiratory, renal and metabolic, gastrointestinal, neurological, infective, other systems, surgical, self‑assessment.
Medical Chapters Cardiac 30 Acute coronary syndromes I: clinical pathophysiology 60 31 Acute coronary syndromes II: investigations and management 62 32 Arrhythmias: tachyarrhythmias 64 33 Arrhythmias: bradyarrhythmias 67 34 Heart failure and pulmonary oedema 68 35 Cardiac emergencies 70 36 Deep venous thrombosis and pulmonary embolism 72 Respiratory 37 38 39 40 41 42 43 44 Chest imaging and bronchoscopy 74 Community-acquired pneumonia 76 Hospital-acquired (nosocomial) pneumonia 78 Asthma 80 Chronic obstructive pulmonary disease 82 Acute respiratory distress syndrome 84 Pneumothorax and air leaks 86 Respiratory emergencies 88 Renal and metabolic 45 Acute kidney injury: pathophysiology and clinical aspects 90 46 Acute kidney injury: management and renal replacement therapy 92 47 Electrolyte disturbances: sodium and potassium 94 48 Electrolyte disturbances: calcium 96 Part 49 Electrolyte disturbances: magnesium and phosphate 98 50 Diabetic emergencies 100 51 Endocrine emergencies 102 Gastrointestinal 52 53 54 55 56 57 58 59 Gastrointestinal haemorrhage 104 Jaundice 106 Acute liver failure 108 Acute pancreatitis 110 Vomiting and intestinal obstruction 112 Diarrhoea 114 Ascites 116 Abdominal imaging 117 Neurological 60 Acute confusional state, coma and status epilepticus 118 61 Stroke 120 62 Other cerebral vascular disorders 122 63 Infective neurological emergencies 123 64 Neuromuscular conditions 124 Infective 65 66 67 68 Specific bacterial infections 126 Common adult viral infections 128 Common fungal and protozoal infections 130 The immune compromised patient 132 Other systems 69 Coagulation disorders and transfusion 134 70 Drug overdose and poisoning 136 59 60 Part Medical 30 Acute coronary syndromes I: clinical pathophysiology Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd Epidemiology Pathophysiology Figure 30a illustrates the effects of coronary artery occlusion and factors that cause myocardial ischaemia Figure 30b illustrates the classification, characteristics and management of myocardial ischaemia Chronic stable (exertional) angina (SA) occurs when fixed, stable coronary artery occlusions (>70%) limit blood flow causing ‘predictable’, reversible cardiac ischaemia during exercise These stenoses are due to smooth, often circumferential atherosclerotic plaques with thick fibrous caps that are unlikely to rupture Resulting ischaemia is usually subendocardial because systolic compression mainly affects endocardial arterioles Variant (Prinzmetal’s) angina is uncommon and caused by transient coronary artery vasospasm or impaired vasodilation It often occurs in the vicinity of atherosclerotic plaques, but there may be no association with atherosclerosis Acute coronary syndrome (ACS) describes a spectrum of ischaemic events, of varying severity, that follow sudden coronary artery occlusion (±vasoconstriction) ACS is initiated by stressinduced rupture of small, eccentric (i.e non-circumferential), non-occlusive (i.e 70% stenoses in all three main, left main or proximal left anterior descending (LAD) coronary arteries Investigations In UA/NSTEMI thrombolytic therapy (TT) is not beneficial As in stable angina (SA), therapy includes nitrates, beta-blockers (±CCA) and additional: • Antiplatelet therapy: give all patients 300 mg aspirin imme diately and continue 75 mg/day indefinitely Irreversible cyclooxygenase inhibition prevents platelet aggregation 0.1 mV in two chest leads or >0.2 mV in two limb leads) is diagnostic of acute myocardial infarction (MI) (Chapter 4) and suggests the need for immediate revascularization However, ST segment depression (ST↓) and T-wave inversion occur in ∼20% of MIs with raised CE Patients with non-ST segment elevation MI (NSTEMI) not benefit from thrombolysis ACS patients with ST↓ have lower early mortality than those with ST↑but survival at >6 months is similar • Cardiac enzymes: a ≥2-fold increase in plasma CE concentration indicates myocardial damage (Figure 31c) Cardiac troponins (CTs) measured at 12 hours are sensitive, specific markers of myocardial necrosis and can detect MI after surgery or when the ECG is non-specific (e.g left bundle branch block [LBBB]) • Chest radiography detects heart failure and aortic dissection • Echocardiography assesses contractility and reveals dyskinesia, thrombus, septal defects and papillary muscle rupture • Incremental exercise stress tests (EST) reveal cardiac ischaemia as angina, ECG changes (i.e >2 mm ST↓, arrhythmias) or inappropriate heart rate or BP responses (Figure 31e) • Myocardial perfusion scans (MPS) detect reduced isotope uptake in underperfused myocardium using a gamma camera (Figure 31g) It is an alternative to EST in the immobile or those with LBBB • Coronary angiography provides radiographic imaging and assessment of coronary artery disease severity Management Treatment aims to reduce myocardial oxygen consumption (MOC) by decreasing heart rate (e.g beta-blockers) and afterload (e.g antihypertensives) while increasing myocardial oxygen supply with pharmacotherapy (±oxygen) Essential risk factor reduction includes smoking cessation, low fat diet, weight loss, exercise and control of diabetes or hypertension Most patients require anti-platelet agents (e.g aspirin), lipid-lowering drugs (e.g statins to reduce low-density lipoprotein [LDL] to 50 and >75 years old respectively Ventricular arrhythmias cause 15–40% of deaths from ischaemic heart disease (IHD) Automaticity describes the normal diastolic membrane depolarization in heart cells that triggers an electrical discharge (i.e action potential [APo]) at a threshold voltage HR is determined by the fastest pacemaker, usually the sinoatrial node (SAN) Tachyarrhythmias (Figure 32a) suppress SAN pacemaker activity and are caused by: • Ectopic pacemakers: increased automaticity due to faster spontaneous membrane depolarization, lower threshold potentials or repolarization oscillations (e.g digoxin toxicity) triggers early APo They often arise in damaged tissue (e.g myocardial infarction [MI] scars) • Re-entry circuits (Figure 32b): a depolarization wave travels around a circuit of abnormal myocardial tissue; if the initiating tissue is not refractory when the impulse returns, it will depolarize again, creating a recurring circuit and a faster pacemaker Re-entry circuits cause most paroxysmal tachycardia They develop in scar tissue, the atrioventricular node (AVN) and abnormal ‘accessory/ AVN’ or ‘atrial/AVN’ pathways The AVN is normally the only atrioventricular (AV) connection Accessory pathways are Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd 65 Chapter 32 Arrhythmias: tachyarrhythmias common, additional tracts of abnormal AV conducting tissue, which, with the AVN, form re-entry circuits Tachyarrhythmias are classified as: • Supraventricular tachycardia (SVT) if they originate in the atria or AVN Ventricular rate is determined by the arrhythmia, AVN conduction and/or prolonged post-depolarization refractory periods • Ventricular tachycardia (VT) if they start in the ventricles Mechanisms and electrocardiograms (ECGs) are illustrated in Figure 32a Clinical features Tachyarrhythmias may be asymptomatic or cause intermittent palpitations, cardiovascular failure, ‘blackouts’ or cardiac arrests Diagnosis can be difficult ECG interpretation is complicated by electrical artifacts, shivering, seizures and tremor Oesophageal or right-sided ECG leads occasionally aid diagnosis • Narrow QRS complex (NC) tachycardias are usually SVTs Intravenous (i.v.) adenosine boluses transiently (but sometimes permanently) terminate SVTs and confirm the diagnosis • Wide QRS complex (WC) tachycardias are usually due to VT but can be difficult to differentiate from SVT with abnormal conduction (SVT/AbC) After excluding AVN block, treat SVT/AbC as VT if haemodynamic instability co-exists Lack of response to direct current (DC) cardioversion and/or i.v lignocaine suggests an SVT/AbC, which is confirmed (±cardioverted) with i.v adenosine Treatment failure is managed with i.v amiodarone (Figure 32c; Appendix 1) and repeated cardioversion General management Rapid assessment is essential but not all arrhythmias need immediate intervention Asymptomatic or stable rhythms (e.g AF, SVT) can be observed while the cause (e.g hypokalaemia) is corrected Symptomatic tachyarrhythmias with hypotension, pulmonary oedema or tissue hypoperfusion (e.g angina) are detrimental and require immediate termination (i.e cardioversion, drugs) Prevention: correct hypoxaemia, electrolyte disturbances (e.g hypokalaemia, hypomagnesaemia), acid–base imbalance, cardiac ischaemia and arrhythmogenic factors including vagal stimulation (e.g suctioning, pain), drugs (e.g theophylline) or cardiac irritants (e.g central lines) Prophylaxis: β-blockers reduce IHD mortality but anti-arrrhythmics not always improve outcome (e.g lignocaine after MI) Treatment options include: • Vagal stimulation (e.g carotid sinus massage): slows HR, aids diagnosis and may cardiovert some SVT • Antiarrhythmic drugs: classified by mechanism and site of action (Figure 32c; Appendix 1) and selected according to rhythm and pathophysiology Therapeutic windows are often narrow, sideeffects common and therapy is frequently ineffective (e.g ∼50% of VT) Paradoxically, treatment causes new arrhythmias in ∼20% ‘Proarrrhythmic’ effects are common Class 1a and III drugs prolong duration (i.e QT interval), trigger automaticity and can precipitate VT (e.g ‘Torsade de pointes’) • Non-pharmacological therapies are often more successful than drugs and may be required in emergencies In haemodynamically unstable VT or SVT, DC cardioversion using 50–360J shocks delivered through sternal and cardiac apex electrodes, in anaesthetized patients, achieves rapid cardioversion (Chapter 6) In recurrent VT, implantable defibrillators improve survival by >30% compared with drug therapy Radiofrequency catheter ablation (RFCA) delivers radiofrequency energy through a catheter tip and safely destroys >90% of treatable accessory pathways or ectopic pacemakers In refractory SVT, overdrive atrial pacing may restore sinus rhythm (SR) Types of tachyarrhythmia Premature ectopic beats may be: • Supraventricular: with abnormal P waves (i.e inverted or absent if the ectopic focus is near the AVN) that not arise from the SAN but normal QRS complexes (i.e normal ventricular conduction) They are benign and often followed by a ‘sinus’ pause before SR is reasserted • Ventricular: with wide QRS complexes (i.e abnormal and/or slow ventricular conduction route) They occur randomly or follow every (bigeminy), or every second (trigeminy), normal beat Although usually benign, they predispose to arrhythmias after MI and if they occur during the T wave of preceding beats 66 Supraventricular tachyarrythmias Part Medical SVT originates above or within the AVN and presents with dizziness, palpitations and dyspnoea Although rarely life-threatening, sudden death can occur • Sinus tachycardia (i.e SR with a HR > 100/min) is a normal SAN physiological response to stress (e.g exercise, emotion) or disease (e.g fever, hypovolaemia) • Atrial tachycardia (AT; HR 120–240/min) occurs in chronic cardiorespiratory disease due to ectopic atrial pacemaker activity caused by atrial surgery and metabolic, acid–base or drug (e.g digoxin) toxicity Treatment: use adenosine to terminate the AT, followed by class 1c (e.g flecanide) or III (e.g sotalol) drugs to prevent recurrence Correct the underlying metabolic defects and/or consider RFCA • Atrial fibrillation may occur in isolation but is common in cardiac disease (e.g heart failure), pneumonia, thyrotoxicosis and thromboembolism Spontaneous, chaotic, atrial depolarization produces an irregular atrial rate >300/min, but refractory AVN conduction limits ventricular rate to 20–25 mmHg, fluid filters into alveolar spaces Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd intervention By contrast, tachycardia usually accompanies anterior MI, and heart block in these patients suggests a particularly large infarct and requires early pacemaker insertion In this case, second-degree heart block followed the MI This occurs when some atrial beats are not conducted to the ventricles Mobitz AVN block (Wenkebach) causes progressive PR interval lengthening, culminating in failure of transmission of an atrial impulse This sequence is repetitive Treatment is rarely required Mobitz II block originates below the AVN in the His–Purkinje system Every second or third atrial impulse initiates ventricular contraction (2 : 1; 3 : 1 block) In this situation, pacemaker insertion may be required (e.g following an anterior MI) because symptoms or complete heart block may follow (Chapter 33) 7 Risk factors must be reduced following recovery from the initial MI Hypertension, hypercholesterolaemia and diabetes mellitus are treated and smoking cessation is strongly encouraged The family history of IHD in this patient suggests the possibility of familial hypercholesterolaemia and cholesterol levels should be checked and followed up in other family members Patients with IHD should be treated with lipid-lowering drugs (e.g statins) to reduce the risk of future ischaemic episodes Patients with unstable angina or at high risk of MI on exercise testing should be referred for angiography and early revascularization procedures (e.g angioplasty, surgical coronary artery bypass grafting) Warfarin is administered for 3-months after a large, usually anterior MI, to prevent mural clot forming on akinetic heart wall and embolizing into the systemic circulation causing strokes, ischaemic legs or bowel Aspirin should be continued indefinitely but beta-blockers and ACE inhibitors may be discontinued after 6–52 weeks in lowrisk patients (Chapter 31) Case 4: COPD and Type respiratory failure 1 Clinically the history and examination suggest an infective exacerbation of chronic obstructive pulmonary disease (COPD) with Type respiratory failure The raised bicarbonate on ABG analysis suggests an acute on chronic increase in Paco2 Peak expiratory flow rate (PEFR) and lung function testing will aid the diagnosis of COPD However, this patient also has a previous history of left ventricular failure (LVF) and the clinical features of pulmonary oedema can be surprisingly difficult to differentiate from COPD (Chapter 34) B-type natriuretic peptide (BNP) has been particularly useful in detecting heart failure in patients with lung disease, especially when combined with echocardiography (Chapter 34) Most BNP is released from the ventricular myocardium The serum BNP level, and its breakdown product NT-BNP, increases during myocardial wall stress and major studies demonstrate a high sensitivity (73–99%) and specificity (60–97%) for heart failure Occasionally, invasive measurements of pulmonary artery wedge pressure and cardiac output may be required to confirm the diagnosis of heart failure (Chapter 3) Alternatively, a trial of therapy (e.g diuretic) is less invasive and often the most effective means to establish or exclude the presence of pulmonary oedema 2 The alveolar–arterial (A–a) gradient is calculated from the difference between the alveolar oxygen partial pressure and the arterial blood oxygen partial pressure (Chapter 13) Alveolar oxygen tension (PAo2) is calculated from the simplified alveolar gas equation: PA O2 = PIO2 − (1.25× Pa CO2 ) where PIo2 is the inspired oxygen partial pressure corrected for barometric pressure and water vapour pressure: PIO2 = Fi O2 ×(barometric pressure (kPa) − water vapour pressure (kPa)) 158 Case studies answers Thus: breathing air: PIO2 = 0.21×(101 − 6.2) = 19.9 kPa Thus: PA O2 (breathing air) = 19.9 − (1.25×8.5) = 19.9 −10.63 = 9.3 kPa The alveolar − arterial oxygen tension difference is P(A−a)O2 = PA O2 − Pa O2 = 9.3 − 7.5 = 1.8 kPa The A–a gradient determines efficiency of gas exchange By incorporating PAco2 into the alveolar gas equation, it is possible to determine when hypoventilation or hypercapnia are the cause of hypoxaemia (i.e a high PAco2 lowers PAo2) Shunts, V/Q mismatch and diffusion impairment increase the A–a gradient The normal A–a gradient is ∼0.2–0.4 kPa but increases with age and Fio2 In this case, although the Pao2 is 7.5 kPa, the A–a gradient is only 1.8 kPa, indicating that a large component of the hypoxaemia is due to hypercapnia or hypoventilation rather than V/Q mismatch or shunt, and suggests that improving alveolar ventilation (i.e bronchodilation, use of NIV) is important 3 In patients with Type respiratory failure, low-dose oxygen therapy should be delivered through fixed performance, Venturi masks aiming for a target saturation of 88–92% (Chapters 13, 14) A higher Sao2 has no advantages, but, in chronically hypoxaemic patients dependent on hypoxic ventilatory drive, it can instigate hypoventilation, further hypercapnia and respiratory acidosis Recheck ABG at hour after starting oxygen therapy and at regular intervals while on oxygen, particularly after oxygen dose changes In the absence of an air compressor, nebulizers are driven with oxygen but only for minutes to limit the risk of further hypercapnic respiratory failure NIV should be considered in hypercapnic (Paco2 >6 kPa) patients with acidosis (pH 35/min, Pao2 < 8 kPa on >50% Fio2; Paco2 > 7.5 kPa, pH 7 mmol/L), suggesting the need for hospital admission but not necessarily HDU However, in this case the hypoxaemia, raised white cell count and multilobar involvement on clinical examination would alert the clinician to the potential severity of the CAP (Chapter 38) 2 The A–a gradient is calculated from the difference between the alveolar oxygen partial pressure and the arterial blood oxygen partial pressure (Chapter 13) Alveolar oxygen tension (PAo2) is calculated from the simplified alveolar gas equation: PA O2 = PIO2 − (1.25× Pa CO2 ) where PIo2 is the inspired oxygen partial pressure corrected for barometric pressure and water vapour pressure: PIO2 = Fi O2 ×(barometric pressure (kPa) − water vapour pressure (kPa)) Thus: breathing air: PIO2 = 0.21×(101 − 6.2) = 19.9 kPa Thus: PA O2 (breathing air) = 19.9 − (1.25×5.3) = ~13.5 kPa The alveolar − arterial oxygen tension difference is: P(A−a)O2 = PA O2 − Pa O2 (in n this case Pa O2 is 6.6 kPa at admission on air) =~13.5 − 6.6 = 6.9 kPa The A–a gradient differentiates between hypoxaemia due to: (i) hypoventilation and alveolar hypercapnia (i.e a high PAco2 lowers PAo2); and (ii) V/Q mismatch, shunt or diffusion impairment (Chapter 13) In this case, the A–a gradient is 6.9 kPa (normally 90% They also allow visualization of parenchymal abnormalities and are useful in patients with COPD or extensive CXR abnormalities when V/Q scanning will be indeterminate (Chapter 36) In less severe cases with a normal CXR, a V/Q scan may be the initial diagnostic investigation A negative perfusion scan rules out a PE whereas a ‘high probability’ scan (i.e multiple segmental perfusion defects and associated normal ventilation) has a >85% probability of a PE With a high clinical suspicion, a high probability V/Q scan has a positive predictive value >95% Unfortunately, most V/Q scans are not diagnostic or are indeterminate with a 15–50% likelihood of PE, necessitating further imaging Absence of a DVT combined with a low probability V/Q scan permits withholding treatment whereas a negative Doppler ultrasound scan with an intermediate probability V/Q scan (or underlying cardiac or pulmonary disease) necessitates further imaging Pulmonary angiography remains the diagnostic standard but is invasive Case studies answers 159 6 Patients with PE may present with pleuritic pain and haemoptysis in about 65% of cases, isolated dyspnoea in about 25% and circulatory collapse in ∼10% of cases Dyspnoea is not present in ∼30% of patients with confirmed PE Other non-specific features include apprehension, tachypnoea, tachycardia, cough, sweating and syncope Following a large PE, features of right ventricular failure (e.g hypotension, jugular venous distension) may occur 7 Anticoagulation stops propagation of existing lower limb thrombus and allows organization of the remaining clot, which reduces the risk of further PE Immediate therapy in patients with a high suspicion of a PE prevents further life-threatening emboli Unfractionated heparin (UFH) or low molecular weight heparin (LMWH) for 5–7 days, is followed by warfarin for 4–6 weeks when temporary risk factors (air travel in this case) are the cause and 3–6 months in idiopathic cases UFH and warfarin must be monitored, because subtherapeutic levels increase the risk of recurrent PE LMWH is more bioavailable and does not require monitoring About 20% of patients with thromboembolic disease have inherited or acquired hypercoagulation problems (e.g antithrombin III deficiency, protein C deficiency, lupus anticoagulant) and may require lifelong therapy If contraindications prevent anticoagulation (e.g recent surgery, haemorrhagic stroke, central nervous system metastases) or PE occurs while on therapeutic anticoagulation, an inferior vena cava filter may prevent further PE 8 Venous admixture (QS/QT) can be calculated from the Sao2 (70% or 0.7) and Svo2 (40% or 0.4) on air and the haemoglobin concentration as illustrated in Chapter 13 QS /Q T = (Cc O2 − Ca O2 )/(Cc O2 − CV O2 ) when C c,a,v O2 = [(Hb×Sa O2 × k) + (Pa O2 ×0.023)] C denotes oxygen content and c, a and v denote end capillary, arterial and venous (note that end capillary and calculated alveolar oxygen tensions are assumed to be equivalent; thus on air end capillary Sao2 is expected to be 0.98); Hb = haemoglobin (g/L); k = coefficient of Hb oxygen binding capacity (1.36 ml O2/g Hb); Pao2 × 0.023 = oxygen dissolved in plasma (usually so small as to be insignificant) Thus: QS /Q T = ([100×0.98×1.36]−[100×0.70×1.36])/ ([100×0.98×1.36]−[100×0.4 ×1.36]) = (133 − 95)/(133 − 54) = 38/79 = 0.48 = 48% venous admixture ‘True shunt’ (i.e corrected for partial V/Q mismatch) is calculated from the Sao2 (95%) and Svo2 (65%) when on 100% oxygen (i.e Fio2 1.0) (Note that end capillary Sao2 would be expected to be 100% or 1.0 on 100% oxygen) Thus: QS /Q T = ([100×1×1.36]−[100×0.95×1.36])/ ([100×1×1.36]−[100×0.65×1.36]) = (136 −129)/(136 − 88) = 7/48 = 0.15 = 15% true shunt 9 The CT scan in Case Figure 1b, (p 156) demonstrates consolidation consistent with pneumonia and also shows a cavitating wedge infarct following a PE in a left segmental pulmonary artery A single, sudden, large PE with marked obstruction of pulmonary blood flow is the likely cause of the cardiac arrest In general, circulatory collapse occurs with >50% obstruction of the pulmonary arterial bed Smaller emboli may be fatal when pre-existing lung or heart disease co-exist Cardiopulmonary resuscitation must be started immediately The cardiac massage may help break up a large clot into smaller segments that travel distally and reduce the degree 160 Case studies answers of pulmonary bed occlusion Following intubation high-dose oxygen must be administered Immediate plasma expanders and inotropic support are often given in an attempt to increase right ventricular pressure and to displace clot distally, but risk severe right ventricular distension and subsequent myocardial damage 10 Thrombolytic therapy is recommended in severe life-threatening massive PE with cardiovascular collapse Thrombolytics hasten resolution of perfusion defects and correct right ventricular dysfunction but there is limited evidence of survival benefit Nevertheless, thrombolytic therapy would be appropriate in this patient with life-threatening cardiovascular collapse In patients without massive PE, there is no survival benefit with thrombolysis and there is a substantial increase in bleeding complications, including a 0.3–1.5% risk of intracerebral haemorrhage Consequently thrombolysis is not recommended in these patients This patient was thrombolysed and survived Case 6: Diabetic emergencies 1 A bedside blood sugar (BS) level must be checked at admission in every confused, agitated or unconscious patient The brain is dependent on glucose for its metabolism and severe hypoglycaemia results in permanent brain damage within a matter of minutes Every year hypoglycaemic patients fail to be recognized despite protocols, education and the legal consequences 2 The first patient is hypoglycaemic If he were able to swallow safely, he would be given a glucose drink or ‘carbohydrate snack’ However, as his conscious level is severely depressed, intravenous glucose (e.g 50 ml 20% dextrose) is given Provided the glucose has been given before significant cerebral damage has occurred, the patient will often ‘wake up’ within a few minutes Glucagon (1 mg i.v./i.m.) or hydrocortisone therapy is occasionally required in severe or refractory hypoglycaemia, as in sulphonylurea overdoses These patients should be admitted for blood sugar monitoring (± glucose infusions) If BS measurement is not available (e.g sudden onset of confusion in a diabetic while out hill walking), glucose should be given empirically as a sugary drink Supplemental thiamine prevents Wernicke’s encephalopathy (i.e eye movement paralysis, ataxia, confusion) in hypoglycaemic malnourished patients, especially alcoholics 3 The second patient is hyperglycaemic An ABG test will establish that he is acidotic (in this case the ABG was pH 6.95, Pao2 14 kPa, Paco2 3.2 kPa, bicarbonate 3 mmol/L and base excess −21), a biochemical profile confirms he is dehydrated and hyperkalaemic (urea 20 mmol/L, creatinine 140 μmol/L and K+ 6.9 mmol/L) and a urine dipstix will demonstrate the presence of ketones This patient is hyperventilating to blow off carbon dioxide in an attempt to correct the metabolic acidosis; consequently his Paco2 is low Similarly, the bicarbonate buffer has been depleted and the base excess is high 4 The diagnosis is diabetic ketoacidosis (DKA) The immediate threats to this patient’s life are the dehydration, acidosis and rapid ion fluxes that cause haemodynamic instability, with hypotension due to hypovolaemia, and reduced myocardial contractility and cardiac arrest due to hyper- or hypo-kalaemia Rapid fluid replacement with ∼3–5 L normal saline (NS) in 100 mmHg Pulse > 100/min CF, IHD All other diagnoses Renal/liver failure Upper GI malignancy Blood in upper GI tract; adherent clot; visible vessel Metastases Notes: Rockall score assists prediction of rebleeding risk and death after upper GI bleeding A score >6 suggests surgery may be required, but the decision is rarely taken on the basis of the Rockall score alone CF = cardiac failure, GI = gastrointestinal, IHD = ischaemic heart disease, OGD = oesophagogastroduodenoscopy, SBP = systolic blood pressure Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd Appendix V: Child–Pugh grading: A = 5–6; B = 7–9; C = 10–15 Risk of variceal bleeding increases ≥8 Bilirubin (μmol/L) Albumin (g/L) Prothrombin ratio (s >normal) Ascites Encephalopathy (grade) point points points 35 1–3 None None 34–51 28–35 4–6 Minor 1–2 >51 6 >Moderate 3–4 Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd Appendix VI: Typical criteria for liver transplantation Paracetamol poisoning Other pathologies (e.g drugs, viruses) pH 6.5 Creatinine > 300 μmol/L Hepatic encephalopathy (grade 3–4) INR > 6.5 or any of: Drug or non-A, non-B virus aetiology Age 40 years old Jaundice for >7 days before encephalopathy INR > 3.5 Bilirubin > 300 µmol/L Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd Appendix VII: Royal College of Physicians’ top nutrition tips Royal College of Physicians’ ‘Ten Top Tips’ for oral nutrition NUTRITION IS IMPORTANT: it improves healthcare morbidity and mortality The Malnutrition Universal Screening Tool (MUST) should be used to identify malnourished or ‘at risk’ patients at admission to any healthcare facility Nutritional status should be assessed regularly in all healthcare settings Refer malnourished or ‘at risk’ patients to the dietician for specialist dietary advice Record food intake in malnourished or ‘at risk’ patients while in hospital or care homes Check that the swallowing reflex is safe to avoid aspiration (e.g following strokes) Occupational therapy assessment may be required in disabled or elderly patients (e.g feeding aids, such as large-handle cutlery) ‘Red trays’, ‘protected’ mealtimes and eating assistance improve food intake in vulnerable patients Consider oral nutritional supplements (e.g ‘high calorie drinks’) if normal oral food intake remains inadequate (e.g poor appetite) 10 Ensure community follow-up in nutritionally ‘at risk’ patients discharged from inpatient facilities Royal College of Physicians’ ‘Ten Top Tips’ for nasogastric tube feeding Consider nasogastric tube (NGT) feeding if a patient has a functional gut but poor oral intake or unsafe swallow Assessment, calculation of requirements and feed choice need appropriate advice (e.g dietician) NGT placement must be performed by trained, experienced staff using radio-opaque tubes with external length markings Use pH testing with CE marked indicator paper to assess NGT tip position A pH between and 5.5 is safe Keep the NGT clean and flush regularly with water using a 50 ml syringe (e.g before/after feeding, between medications and 4–6 hourly if used continuously) Position patients at 30–45 degrees to the horizontal during NGT feeding or hydration and keep raised for ≥1 hour after feeding Document refeeding risk in the medical notes and follow appropriate refeeding guidelines (e.g NICE CG32) Review medications to be administered via an NGT with a pharmacist or the nutrition support team Gastrointestinal disturbances: (i) Diarrhoea (e.g infection, malabsorption, drug causes, constipation with overflow diarrhoea): consider reducing feed osmolality, remove fibre and decrease feed rate; (ii) Nausea/vomiting requires exclusion of obstruction/ ileus: correct electrolyte imbalances, review drug prescriptions and consider pro-motility agents or post-pyloric feeding; reduce feeding rate 10 Tube difficulties: (i) Blocked tubes: flush (i.e push/pause technique) with warm water using 50 ml syringe; (ii) Repeated NGT displacement: consider NGT bridle/bolus feeding/early gastrostomy Royal College of Physicians’ ‘Ten Top Tips’ for intravenous fluid administration Determine whether intravenous (IV) fluid administration is required (e.g coma) When possible, oral (or nasogastric) fluid is preferable IV fluid administration should follow clinical assessment including biochemical and fluid balance review (e.g input/output measurement, weight) IV fluid and/or electrolyte administration should be supervised by a senior clinician because inadequate or excessive therapy is associated with excess morbidity and mortality The three main IV fluid regimens are: (a) resuscitation; (b) maintenance; or (c) maintenance with correction for ongoing losses, redistribution or fluid/electrolyte imbalance Fluid resuscitation regimens aim to restore haemodynamic stability and maintain tissue perfusion following excessive fluid losses (e.g haemorrhage) or critical illness (e.g sepsis) Maintenance fluid regimens aim to replace normal daily fluid and electrolyte losses (i.e L of water and 1 mmol/kg NaCl and KCl) Fluid regimes that address ongoing fluid/electrolyte losses or correct previous fluid/electrolyte imbalance are determined from measured fluid inputs/outputs and biochemical assessment of serum or ‘lost’ fluids Correct the normal fluid maintenance regime for the additional (or reduced) fluid/electrolyte requirements Large volume IV fluid resuscitation may be associated with excess electrolyte administration and has physiological consequences (e.g hyperchloraemic acidosis) or causes complications (e.g pulmonary oedema) Resuscitation to haemodynamic stability may be achieved with slightly lower volumes of colloid, compared with crystalloid fluids; but has no clear morbidity or mortality benefits 10 Stop IV fluids when oral (or nasogastric) intake is possible, or when the patient is haemodynamically stable, to reduce associated complications (e.g line sepsis) Royal College of Physicians’ ‘Ten Top Tips’ for parenteral nutrition Parenteral nutrition (PN) is most safely given through a dedicated single lumen catheter When feeding through a central vein the catheter tip should be at the vena cava/right atrial junction Before starting PN there should be an assessment of the risk of re-feeding problems PN is not an emergency treatment and should be started electively with clear aims PN should always include vitamins and trace elements The volume of PN must be included on fluid balance charts Patients having PN in hospital should be clinically monitored every day (especially fluid balance) Catheter-related sepsis (CRS) usually originates from the hub connection so surgical aseptic non-touch techniques are needed for all procedures that access the catheter* SVC thrombosis is an emergency that needs treatment to reestablish venous patency 10 Abnormal LFTs on PN more commonly relate to pre-existing liver disease, drugs or sepsis than to the parenteral nutrition solutions Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd Index Page numbers in italics denote figures, those in bold denote tables Abbreviated Injury Scale ABCD system abdominal emergencies, acute 146–7, 146 abdominal imaging CT 117, 117 radiation doses 117 X-ray 112, 117, 117 abscess 54 ACE inhibitors 63, 69, 157 acid-base balance 38–9, 38 acidosis 38, 39 Acinetobacter spp 78 A baumanii 50 acquired immunodeficiency syndrome (AIDS) 132, 133 ACTH stimulation 102 activated charcoal 137 activated clotting time 135 activated partial thromboplastin time (APTT) 134, 135 activated protein C 49 acute bowel ischaemia 147 acute confusional state 118–19, 118 acute coronary syndromes clinical pathophysiology 60–1, 60 investigations and management 62–3, 62 see also specific conditions acute kidney injury (AKI) 90–1, 90 management 92–3, 92 staging 164 acute liver failure 108–9, 108 acute pancreatitis 110–11, 110 acute respiratory distress syndrome see ARDS acutely ill patients 2, Addisonian crisis 102, 103 adenosine 162 admission adrenal emergencies 102, 103 adrenocortical excess 103 adult advanced life support 10, 11 advanced trauma life support (ATLS) 141 African trypanosomiasis 52 afterload 16 air leaks 86–7, 86 airway 2, 3, 141 burn injuries 151 examination 33 inflammation see asthma management 37 obstruction 3, 28–9, 28, 151 see also ventilatory support albumin 22 albumin cycle 18 albuterol 81 alcohol intoxication 136 alfentanil 40 alkalosis 38, 39 allergic bronchopulmonary aspergillosis 130, 131 alpha-1-antitrypsin deficiency 107 alveolar gas equation 38 alveolar oxygen tension 24, 150 alveolar recruitment 27 alveolar-arterial oxygen gradient 24, 25 amaurosis fugax 121 aminophylline 81 amiodarone 11, 65, 162 amniotic fluid embolism 148, 149 amoxicillin 77 anaemia 27 anaesthetic facemasks 29 analgesia 40–1, 40 non-opioid 41 opioid 41 see also individual drugs anaphylactic shock 15 angina 70 Prinzmetal’s 61 stable 60, 61, 63 unstable 61, 63 anion gap 38, 39 drug overdose 136 antepartum haemorrhage 149 antiarrhythmic drugs 65 Vaughan Williams classification 65, 162 antibiotics gonorrhoea 127 listeriosis 127 meningitis 123 pancreatitis 111 toxic shock syndrome 127 anticholinergic overdose 136 anticholinesterases 125 anticoagulants 135 heart failure 69 stroke 121 supraventricular tachycardia 66 unstable angina 63 antihypertensives, stroke 121 antiplatelet therapy 63 antivirals 129 aortic rupture 144, 145 APACHE II apnoea test 56 ARDS 84–5, 84 arrhythmias bradycardias 17, 67, 67 tachycardias 17, 64–6, 65 arterial blood gases 7, 38–9, 38 asthma 81 pulmonary embolism 73 arterial carbon dioxide partial pressure (PaCO2) 39 arterial oxygen partial pressure (PaO2) 38, 39 arterial oxygen saturation ascites 116, 116 aspergilloma 130, 131 aspergillosis allergic bronchopulmonary 130, 131 chronic necrotising pulmonary 131 Aspergillus spp 130, 131 aspiration pneumonia 77, 79 aspiration syndromes 89 aspirin myocardial infarction 63 overdose 136 stroke 121 asthma 80–1, 80 at-risk patients atenolol 162 atracurium 40, 41 atrial fibrillation 64, 66 atrial flutter 65, 66 atrial myxoma 54 atrial tachycardia 64, 66 atrioventricular see AV atropine 11 auscultation 17 AV heart block 67, 67 AV re-entrant tachycardias 65, 66 bacteraemia 48–9, 48 bacteria, classification 126 bacterial infections 128–9, 128 see also specific infections bag-valve mask 11 balloon tamponade 104, 105 barbiturate overdose 136 barium enema 117 barotrauma 35 base excess 39 Battle’s sign 143 benzodiazepines 41 overdose 136 berry aneurysm 122 beta-blockers 63, 65, 69 beta2-agonists 81 bi-level positive pressure ventilation (BIPAP) 37 bicarbonate 21 buffer system 38, 39 bilirubin metabolism 106 bladder care blastomycosis 130 bleeding disorders 135 blood 21, 135 blood components 135 blood count 47 blood gas analysis 25 blood transfusion 134–5, 134 blue bloaters 83 blunt chest trauma 145 body water distribution 18 Borrelia burgdorferi 127 botulism 88, 123 bradycardias 17, 67, 67 brainstem death 56, 57 breathing 2, 3, 141 bronchial artery embolization 89 bronchitis 82, 83 bronchoalveolar lavage 81 bronchodilators 69 bronchoscopy 74–5, 75, 85 brucellosis 52 buffers 39 buffer line 38, 39 bundle branch block 67 Critical Care Medicine at a Glance, Third Edition Richard Leach © 2014 John Wiley & Sons, Ltd Published 2014 by John Wiley & Sons, Ltd burns 150–1, 150 burst fracture 140 C-reactive protein 47 calcium 96–7, 96 homeostasis 96–7 hypercalcaemia 96, 97 hypocalcaemia 97, 136 calcium channel antagonists 63, 69 calcium sensitizers 69 Campylobacter spp 115 Campylobacter jejuni 115 Candida spp 50, 131 oral infection 130 capnography carbon monoxide poisoning 150, 151 cardiac arrest out of hospital 10 in pregnancy 149 cardiac contusion 145 cardiac emergencies 70–1, 70 cardiac enzymes 62, 63 cardiac function 16–17 cardiac output heart failure 68 thermodilution technique and venous return 16 cardiogenic shock 14, 15 cardiopulmonary resuscitation 10–11, 10 adult advanced life support 10, 11 cardiovascular care case studies 152–61 Castleman’s disease 54 central venous catheter central venous pressure 7, 16 cerebral oedema 108, 142 cerebral perfusion pressure 143 cerebral vascular disorders 122, 122 see also stroke cerebral venous sinus thrombosis 122 chemical burns 151 chest compressions 11 chest drainage 85, 86 chest trauma 144–5, 144 chest X-ray 63, 74–5, 75 aspergillosis 130 community-acquired pneumonia 153 heart failure 68 hospital-acquired (nosocomial) pneumonia 78 P jiroveci infection 132 pneumothorax 86 pulmonary embolism 73 trauma 144 Child-Pugh grading system 166 Chlamydia pneumoniae 77 cholangitis 147 cholecystitis 147 cholestatic jaundice 107 Chovsteck’s sign 96, 97, 98 chronic kidney disease (CKD) 97 chronic necrotising pulmonary aspergillosis 131 chronic obstructive pulmonary disease see COPD circulation 2, 3, 141 assessment 16–17, 16 circulatory hydrostatic pressure 19 cirrhosis 116, 116 clarithromycin 77 clopidogrel 63 Clostridium difficile 50, 51 Clostridium tetani 123, 127 CNS depression 88 coagulase negative staphylococcus 50 coagulation disorders 134–5, 134 coagulation tests 134, 135 coagulopathies 135 coccidioidomycosis 130 codeine 41 colloids 21, 22 coma 118–19, 118 hyperosmolar non-ketotic (HONK) 101 myxoedema 102, 103 combitube 29 communication with patients with relatives community-acquired pneumonia 76–7, 76, 153–4, 153, 159–60 computed tomography (CT) abdomen 117 abdominal 117, 117 ARDS 84 aspergillosis 130 chest 74–5, 75 head injury 142 pancreas 110 subdural haematoma 122 toxoplasmosis 132 constrictive pericarditis 71 continuous positive airways pressure (CPAP) 31, 37, 69 COPD 82–3, 82, 153, 158–9 cor pulmonale 69, 83 core-peripheral temperature corneal reflex 56, 57 coronary angiography 63 coronary arteries 60 corticosteroids see steroids costs cough reflex 56, 57 CPAP see continuous positive airways pressure cricothyroidotomy 29 Crigler-Najjar syndrome 107 critical illness polyneuropathy 125 critically ill patients 4–5, Crohn’s disease 54 cryoprecipitate 135 Cryptococcus neoformans 123, 131 crystalloids 21, 22 CT see computed tomography Cullen’s sign 110 cyanide poisoning 151 cytomegalovirus 129 D-dimer 73, 135 daily checklist dantrolene 45 deep venous thrombosis 72–3, 72 prophylaxis 4, 72 dengue 52 dextrans 22 diabetic emergencies 100–1, 100, 154, 154, 160–1 170 Index diabetic ketoacidosis 100, 101 dialysis 15, 92–3, 92 drug overdose 137 diamorphine 69 diaphragm air under 146 injuries 145 diarrhoea 114–15, 114 chronic 115 drug overdose 136 diastolic dysfunction 17, 69 difficult intubation 33 digoxin 69, 162 overdose 136 dihydrocodeine 41 diltiazem 65, 162 diphtheria 88 disability 2, discharge disopyramide 65, 162 disseminated intravascular coagulation (DIC) 134, 135 diuretics 69, 93, 116 dobutamine 23, 49 dopamine 23, 49, 93 Doppler ultrasound 73 doxycycline 77 drug effects acute kidney injury 91 acute liver failure 108 hyperthermia 45, 54 drug overdose 136–7, 136 Dubin-Johnson syndrome 107 early warning score ECG 7, 8–9, acute coronary syndromes 62 interpretation leads 8, and plasma potassium 94 pulmonary embolism 73 echocardiography 63 mitral valve endocarditis 70 pulmonary embolism 73 eclampsia 70 ectopic pacemakers 64 edrophonium (Tensilon) test 125 Einthoven’s equilateral triangle 8, electrical burns 151 electrocardiogram see ECG electrolytes acute kidney injury 93 daily requirements 19, 43 electrolyte disturbances calcium 96–7, 96 magnesium 98–9, 98 phosphate 98–9, 98 potassium 94–5, 94 sodium 94–5, 94 embolic stroke 121 embolism amniotic fluid 148, 149 fat embolism syndrome 145 pulmonary 72–3, 72, 149, 159–60 emphysema 82, 83 encephalitis 123 encephalopathy 70 hepatic 108, 109 end of life issues 56–7, 56 endocarditis 54 infective 70, 71 mitral valve 70 endocrine emergencies 88, 102–3, 102 endoscopy 117 endotracheal intubation 29, 32–3, 32 difficult 33 failed 33 energy expenditure 43 enoximone 23 enteral nutrition 42–3, 42 Enterobacter spp 50 Enterococcus faecalis 50 enteroviruses 128 epinephrine 11, 23, 49 Epstein-Barr virus 129 erythema migrans 126 Escherichia coli 50, 115 ethylene glycol poisoning 136 exercise testing 62 extension injuries 140 extracellular fluid 18 extradural haematoma 122 extubation 36–7, 36 factitious fever 54 faecal elastase/chymotrypsin 115 failed intubation 33 familial Meditarranean fever 54 fat embolism syndrome 145 fentanyl 40 ferritin 107 fever 46–7, 46 returning travellers 52–3, 52 of unknown origin 54–5, 54 fibrinogen degradation products 135 flail chest 145 flecainide 162 Flenley acid-base nonogram 38, 39 fluids choice of 22, 22 restriction 27 retention 35 types of 21 fluid aspiration 89 fluid challenge 17 fluid management 17 acute kidney injury 93 acute pancreatitis 111 assessment and prescription 20–1, 20 burn injuries 150 pathophysiological factors 18–19, 18 replacement/redistribution 21 resuscitation 15, 20, 21 routine maintenance 20, 21 flumazenil 41 foetor hepaticus 108, 109 forced diuresis 137 fracture dislocations 140 Frank-Starling curve 16 fresh frozen plasma 135 functional bowel disturbance 115 fungal infections 130–1, 130 see also specific infections gag reflex 56, 57 gallstones 111 gastric lavage 137 gastric tonometry gastroenteritis 115 gastrointestinal haemorrhage 104–5, 104 Rockall risk-scoring system 165 gastrointestinal/nutritional care see also nutrition gelatins 22 German measles 128 Gilbert’s syndrome 107 Gitelman’s syndrome 98 Glasgow Coma Score (GCS) 3, 5, 7, 25, 33, 119, 141, 142, 143 global oxygen consumption (VO2) 12, 13 global oxygen delivery (DO2) 12, 13 glucose hyperglycaemia 101 hypoglycaemia 100, 101 glyceryl trinitrate 71 goal-directed therapy 13 gonorrhoea 127 Guillain-Barré syndrome 88, 124, 125 gunshot wounds 145 gut dialysis 137 haematemesis 105 haematoma 54 haemocynamic monitoring haemofiltration 92 haemoglobin 39 haemoglobin saturation (SO2) 12, 13, 24 arterial 25 haemophilia 135 Haemophilus influenzae 70, 77, 78, 123 haemoptysis 88–9, 88 haemorrhage gastrointestinal 104–5, 104 obstetric 148, 149 severity classification 140 haemorrhagic stroke 121 haemothorax 145 haloperidol 41 hand washing 4, 50 hangman’s fracture 140 head injury 142–3, 142 heart failure 68–9, 68 New York Heart Association classification 68 heart rate 16 heatstroke 44, 45 Heimlich manoeuvre 28, 29, 88 HELLP syndrome 148 Henderson-Hasselbach equation 38, 39 heparin 63, 135 hepatic encephalopathy 108, 109 hepatic foetor 108, 109 hepatocellular jaundice 106, 107 herpes simplex virus 129 herpes zoster 128, 129 histoplasmosis 130 Homan’s sign 73, 87 hospital-acquired (nosocomial) infections 50–1, 50 hospital-acquired (nosocomial) pneumonia 77, 78–9, 78 hydrocortisone 49 hydrogen breath test 115 hydroxyethyl starch 22 hyper-IgD syndrome 54 hypercalcaemia 96, 97 hypercapnia 25, 143 permissive 81 hypercoagulability 135 hyperglycaemia 101 hyperkalaemia 92, 95 hypermagnesaemia 99 hypernatraemia 94, 95 hyperosmolar non-ketotic coma (HONK) 101 hyperparathyroidism 96, 97 hyperphosphataemia 96, 97, 99 hypertension emergencies 70–1 pregnancy-induced 149 hyperthermia 44–5, 44 drug overdose 136 hyperthyroidism 102 hyperventilation 142 hypocalcaemia 97 drug overdose 136 hypocapnia 142, 143 hypoglycaemia 100, 101 hypokalaemia 94, 95 hypomagnesaemia 98 hyponatraemia 94, 95 hypophosphataemia 99 hypopituitary crisis 103 hypothermia 44–5, 44 hypothyroidism 102, 103 hypoventilation 25 controlled 81 drug overdose 136 hypovolaemic shock 14 hypoxaemia 25, 83 hypoxia 24–5, 24, 143 imaging see specific modes immune complex deposition 71 immune compromised patients 132–3, 132 immunonutrition 43 in-hospital arrests 10–11 in-line immobilization 140 infections 46–7, 46 bacterial 126–7, 126 fungal 130–1, 130 hospital-acquired (nosocomial) 50–1, 50, 77, 78–9, 78 neurological 123, 123 protozoal 130–1, 130 sepsis 48–9, 48 viral 128–9, 128 see also specific infections infective endocarditis 70, 71 inflammatory bowel disease 147 inflammatory markers 47 influenza 128–9 inhalation injuries 150–1, 150 inotropes 17, 23, 23 acute kidney injury 93 sepsis 49 shock 15 see also individual drugs internal jugular vein catheter intertrigo 131 intestinal obstruction 112–13, 112, 146, 147 intracranial bleed in pregnancy 149 intracranial pressure 142 intrathoracic pressure 145 intravascular volume 19 ipratropium bromide 81 irritable bowel syndrome 115 jacket (cuirass) ventilators 31 Jarisch-Herxheimer reaction 127 jaundice 106–7, 106 jaw lift 28 kerbstone fractures 144 ketoacidosis, diabetic 100, 101 ketogenesis 100 Kikuchi’s disease 54 Klebsiella spp 50 Klebsiella pneumoniae 78 Kussmaul’s sign 71 labetalol 71 lactic acidosis 101 Lambert-Eaton syndrome 124 laparotomy 113 laryngeal mask airways 29 laryngoscoppy 33 left ventricular afterload 35 left ventricular failure 68–9 Legionella spp 77 Legionella pneumophila 78 leishmaniasis, viral 52 leptospirosis 52 leukaemia 54 levosimendin 69 lidocaine 65, 162 life-threatening organ damage 70–1 lignocaine see lidocaine lines line-related sepsis 51 lipid emulsion therapy 137 Listeria monocytogenes 123, 127 listeriosis 127 lithium overdose 136 liver acute liver failure 108–9, 108 ascites 116, 116 liver function tests 107 transplantation 109, 167 loop diuretics 69 lorazepam 41 lower gastrointestinal bleeding 104, 105 lung compliance lung disease lung function lung torsion 145 Lyme disease 126, 127 lymphoma 54 magnesium 98–9, 98 hypermagnesaemia 99 hypomagnesaemia 98 magnesium sulphate 81, 149 malabsorption 115 malaria 52, 53 malignant hyperthermia 45 Mallory-Weiss syndrome 105 mask ventilation 28, 29 maternal death 148 measles 128 mechanical ventilation see ventilatory support melaena 105 meningitis 123, 123 meningococcal septicaemia 126–7, 126 metabolic acidosis 39, 93 metabolic alkalosis 38, 39 metabolic rate 12, 13 methanol poisoning 136 metoprolol 162 micronutrients 43 midazolam 40, 41 Miller Fisher syndrome 124 milrinone 23, 69 mini-tracheostomy 36, 37 miosis 136 mitral valve endocarditis 70 mixed venous oxygen saturation 7, 13 monitoring 6–7, morphine 40, 41 motor neurone disease 88 MRSA 50, 51 mucormycosis 131 multiple organ dysfunction 48 multisystem inflammatory disease 54, 55 mumps 128 mushroom poisoning 136 myasthenia gravis 88, 124, 125 Mycobacterium avium intracellulare 55 Mycobacterium catarrhalis 77 Mycobacterium tuberculosis 123 Mycoplasma pneumoniae 77 mydriasis 136 myocardial contractility 16 myocardial infarction 60, 152–3, 156–7 ECG 62 NSTEMI 61 STEMI 61 treatment 63 myocardial injury patterns 62 myocardial ischaemia 23, 60 myocardial oxygen consumption 63 myocardial perfusion scans 62, 63 myxoedema coma 102, 103 nasopharyngeal airways 29 near-drowning 89 needle pericardiocentesis 70 negative pressure ventilation 31 Neisseria gonorrhoeae 127 Neisseria meningitidis 123, 126–7 neurogenic (spinal) shock 15 neuroleptic malignant syndrome 45 neurological emergencies 124–5, 124 infections 123, 123 neurological monitoring neurological status 141 neuromuscular blockers 41 neuromuscular care nifedipine 63, 71 nil-by-mouth orders 112 nitrates 63, 69 nitric oxide, inhaled 85 nitrovasodilators 63 non-invasive ventilation 30–1, 30, 37 non-ST segment elevation MI (NSTEMI) 61 non-steroidal anti-inflammatory drugs (NSAIDs) 41 norepinephrine 23, 49 norovirus 115, 129 nosocomial infections see hospitalacquired (nosocomial) infections nutrition assessment 42–3, 42 enteral 42–3, 42 parenteral 42–3, 42 RCP top tips 168 obstetric emergencies 148–9, 148 obstetric haemorrhage 149 obstructive shock 14 oculocephalic reflexes 56, 57 odontoid process fracture 140 oesophageal rupture 145 oesophageal varices 104, 105 Child-Pugh grading system 166 opioid analgesics 40, 41 overdose 136 opportunistic pneumonia 77 organ donation 56, 57 organ function 19 organ oxygenation organophosphate poisoning 136 oropharyngeal (Guedel) airways 29 oropharyngeal obstruction 29 Osler’s nodes 71 osmolality 94 osmotic pressure 19 out-of-hospital arrests 10 oxygen consumption 13 oxygen delivery 12, 13 oxygen tension (PO2) 12, 24, 25 arterial 25 oxygen therapy 26–7, 26, 152, 155–6 COPD 83 heart failure 69 oxygen transport 12–13, 12 oxygen uptake 13 oxygenation see tissue oxygenation oxyhaemoglobin dissociation curve 12, 13 P wave pacemakers 163 packed red cells 135 palpation 17 pancreatic pseudocysts 111 pancreatitis acute 110–11, 110 chronic 111 severe necrotizing 111 paracentesis 116 paracetamol 41, 45 overdose 136, 137 paracoccidioidomycosis 130 paralysis 40–1, 40 parenteral nutrition 42–3, 42 parvovirus B19 128 patient comfort PEEP see positive end expiratory volume peptic ulceration 147 percutaneous coronary intervention 63, 157 pericardial effusion 71 pericardial tamponade 145 pericarditis 71 peripartum haemorrhage 149 peritoneal dialysis 92, 93 peritonitis, spontaneous bacterial 108, 109, 116 permissive hypercapnia 81 petechial skin rash 145 Peutz-Jegher’s syndrome 105 phaeochromocytoma 103 pharyngeal airways 28, 29 phenylephrine 23 phosphate 98–9, 98 hyperphosphataemia 96, 97, 99 hypophosphataemia 99 phosphodiesterase inhibitors 69 pink puffers 83 placenta praevia 148, 149 placental abruption 149 plasma oncotic (colloid) pressure 19 Plasmodium falciparum 53 platelet count 135 platelets 135 Pneumocystis jiroveci 130, 132, 133 pneumomediastinum 86, 87 pneumonia aspiration 77, 79 community-acquired 76–7, 76, 153–4, 153, 159–60 hospital-acquired (nosocomial) 77, 78–9, 78 immunosuppression-related 79 pneumopericardium 87 pneumothorax 86–7, 86, 144, 145 poisoning 136–7, 136 poliomyelitis 88, 123 portal hypertension 116 positive end expiratory pressure (PEEP) 35 positive pressure ventilation (PPV) 30, 31, 81 positron emission tomography (PET) 75 postpartum haemorrhage 148, 149 potassium 94–5, 94 hyperkalaemia 92, 95 hypokalaemia 94, 95 PR interval pre-eclampsia 70, 148, 149 pre-excitation syndromes 64 Index 171 precordial thump 11 pregnancy complications 149 see also obstetric emergencies preload 16, 68 preoxygenation 33 pressure support 31 pressure support ventilation 31, 37 pressure-controlled ventilation 31 Prinzmetal’s angina 61 propofol 40, 41 proteins 43 Proteus spp 50, 78 prothrombin time 134 protozoal infections 130–1, 130 see also specific infections pseudocholinesterase deficiency 41 Pseudomonas aeruginosa 50, 78 pulmonary angiography 72, 73, 75 pulmonary artery catheter pulmonary artery wedge/occlusion pressure pulmonary contusions 145 pulmonary embolism 72–3, 72, 159–60 in pregnancy 149 pulmonary hypertension 83 pulmonary infiltrates 133 pulmonary oedema 31, 68–9, 68, 70 pulse oximetry 25 pulsus paradoxus 80 pupillary responses 56, 57 pyrexia see fever Q wave QRS complex tachycardias 65 QT interval quinidine 65, 162 rabies 123 racoon eyes 143 Ramsey sedation score 40 Ranson’s score 110 rapid sequence induction 32, 33 re-entry circuits 64–5, 64 reassurance recognizing unwell patients 2–3, refeeding syndrome 43, 99 renal failure 70 renal function 19 renal protection 23 renal replacement therapy 15, 92–3, 92 respiratory acidosis 38, 39 respiratory alkalosis 38, 39 respiratory care respiratory emergencies 88–9, 88 respiratory failure 24–5, 24, 153, 158–9 respiratory management 36–7, 36 respiratory monitoring resuscitation adult advanced life support 10, 11 advanced trauma life support (ATLS) 141 burn injuries 151 cardiopulmonary 10–11, 10 retinopathy 70 revascularization 63 rib fractures 144, 145 right ventricular failure 69 right ventricular preload reduction 35 risus sardonicus 127 Rockall risk-scoring system for GI bleeds 165 172 Index rocking beds 31 rocuronium 40, 41 Roth spots 71 rotovirus 129 Royal College of Physicians, top nutrition tips 168 rubella 128 salbutamol 81 Salmonella spp 115 SAPS schistosomiasis 52 Schofield equation 42, 43 sclerotherapy 105 secretion retention 27 sedation 40–1, 40 ventilated patients 37 Seldinger technique 6, 86 Sengstaken-Blakemore tube 104 sepsis 48–9, 48, 152, 155 line-related 51 septic shock 14, 14, 23, 48 mortality 49 Serratia spp 78 S marcescens 50 severe necrotizing pancreatitis 111 severity of illness scores shear stress 145 Sheehan’s syndrome 149 Shigella spp 115 shock 14–15, 14, 152 anaphylactic 15 cardiogenic 14, 15 complications 15 haemorrhagic 121 hypovolaemic 14 neurogenic (spinal) 15 obstructive 14 septic 14, 14, 23, 48, 49 shunts 24, 25 SIADH 94 sick cell syndrome 19 sick euthyroid syndrome 103 sick sinus syndrome 67 sinus bradycardia 67, 67 sinus tachycardia 65, 66 SIRS 48–9, 48 skin care small bowel obstruction 146 sodium 94–5, 94 hypernatraemia 94, 95 hyponatraemia 94, 95 loss 18 retention 18 sodium nitroprusside 71 sotalol 65, 162 spinal stability 141 spiral CT scan 72, 73 spirometry 80 spontaneous bacterial peritonitis 108, 109, 116 ST segment ST segment elevation MI (STEMI) 61 stab wounds 145 Staphylococcus aureus 70, 78 gastroenteritis 115 meningitis 123 methicillin-resistant see MRSA toxic shock syndrome 127 Staphylococcus epidermidis 70, 123 status epilepticus 118–19, 118 steatorrhoea 115 Stenotrophomonas maltophilia 50 steroids 49, 55 asthma 81 Still’s disease, adult 54, 55 Streptococcus faecalis 70 uploaded by [stormrg] Streptococcus pneumoniae 77, 78, 123 Streptococcus pyogenes 127 Streptococcus viridans 70, 71 streptokinase 63 stress response 19 stroke 70, 120–1, 120 prognosis 120 risk factors 120 stroke volume 16 subarachnoid haemorrhage 122 subcutaneous emphysema 87 subdural haematoma 122, 122 suction 33 supportive care supraventricular tachycardia 65, 66 suxamethonium 41 Sweet’s syndrome 54 synchronized intermittent mandatory ventilation (SIMV) 35, 37 syndrome of inappropriate ADH secretion see SIADH syphilis 127 systemic inflammatory response syndrome see SIRS systolic dysfunction 16–17 systolic failure 69 systolic heart failure 23 T wave tachycardias 17, 64–6, 65 see also specific types tank ventilators (iron lungs) 31 tension pneumothorax 87 terlipressin 105 tetanus 88, 123, 127 tetany 96 theophylline overdose 136 Therapeutic Intervention Scoring System (TISS) thermodilution technique, cardiac output thrombocytopenia 135 thrombolytic therapy 63, 157 contraindications 62 stroke 121 thyroid emergencies 102–3, 102 thyrotoxic crisis 102–3, 102 tick typhus 52 tissue oxygenation 7, 13, 152, 155–6 failure of 24–5, 24 tissue plasminogen activator 63 TNF receptor-associated periodic syndrome 54 total parenteral nutrition 43 toxic inhalation 150–1, 150 toxic shock syndrome 127 toxoplasmosis 131, 132 tracheobronchial obstruction 29 tracheobronchial tears 145 tracheostomy 29, 36–7, 36 tramadol 41 transient ischaemic attacks 121 transjugular intrahepatic portal stents 105, 116 trauma 140–1, 140 see also specific types Trauma Score trauma team 141 travellers diarrhoea 115 fever in 52–3, 52 Treponema pallidum 127 tricyclic antidepressant overdose 136, 137 Trousseau’s sign 97, 98 tuberculosis 54, 88 tubulointerstitial disease 91 typhoid 52 ultrasound, abdominal 116, 117 upper airways obstruction 3, 28–9, 28, 88, 89 upper gastrointestinal bleeding 104–5, 105 urinalysis 91 urinary tract infections 51 urine flow uterine atony 149 uterine rupture 149 varicella-zoster 128, 129 vascular permeability 19 vasopressin 49 vasopressors 17, 23, 23, 49 see also individual drugs Vaughan Williams classification of anti-arrhythmic drugs 65, 162 venous admixture 24 venous blood saturation 13 venous return, and cardiac output 16 ventilation/perfusion mismatch 24, 25, 84 ventilation/perfusion scans 73, 75 ventilator dependence 37 ventilatory support 11, 15, 27, 34–5, 34, 69 ARDS 85 complications 35 COPD 82, 83 indications 25 laryngeal mask airways 29 mask ventilation 28, 29 non-invasive 30–1, 30 sedation, analgesia and paralysis 40–1, 40 ventilatory mode 35 weaning from 36–7, 36 ventricular fibrillation 64 ventricular tachycardia 64, 65, 66 verapamil 65, 162 vestibulo-ocular reflex 56, 57 Vibrio parahaemolyticus 115 viral haemorrhagic fever 52 viral hepatitis 108, 128 viral infections 128–9, 128 see also specific infections visiting hours vitamins 43 volutrauma 35 vomiting 112–13, 112 von Willebrand’s disease 135 Wallace’s rule of 9s 150 warfarin 66 water compartmental distribution 19 daily requirements 19, 43 loss 18 retention 18 Whipple’s disease 54 WHO analgesic ladder 40 whole blood 135 withdrawal of treatment 57 X-rays abdominal 112, 117, 117 air under diaphragm 146 cervical 140 chest see chest X-ray small bowel obstruction 146 Yersinia spp 115 ... abnormal ‘accessory/ AVN’ or ‘atrial/AVN’ pathways The AVN is normally the only atrioventricular (AV) connection Accessory pathways are Critical Care Medicine at a Glance, Third Edition Richard Leach... ventilation/perfusion (V/Q) mismatch and increased ventilatory dead space necessitates increased ventilation to maintain a normal Paco2 Reduced surfactant in affected areas causes atelectasis... Pulmonary angiography: a rarely used diagnostic standard Treatment Therapy is similar to that for established DVT: • Anticoagulation stops propagation of DVT and allows organization Immediate therapy