Published on

1 Like
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide


  1. 1. 8 D.F. TREACHER I.S. GRANT Critical care and emergency medicine Clinical examination of the critically ill Presenting problems in Discharge from intensive care 200 patient 176 critical illness 186 Withdrawal of care 200 Circulatory failure: ‘shock’ 186 Brain death 200 Provision of critical care 178 Respiratory failure including Organisation of critical care 178 Scoring systems in critical care 200 ARDS 187 Critical care ‘outreach’ 178 Renal failure 189 Costs of intensive care 201 Admission guidelines 178 Neurological failure (coma) 189 Transport of the critically ill Outcome from critical care 201 Sepsis 189 patient 179 Disseminated intravascular Monitoring 179 coagulation (DIC) 190 General principles 179 General principles of critical care Monitoring the circulation 179 management 190 Monitoring respiratory function 182 Management of major organ Physiology of the critically ill failure 191 patient 182 Circulatory support 191 Oxygen transport 182 Respiratory support 193 Oxyhaemoglobin dissociation Renal support 197 curve 184 Gastrointestinal and hepatic Oxygen consumption 184 support 197 Relationship between oxygen Neurological support 198 consumption and delivery 184 Management of sepsis 199 Pathophysiology of the inflammatory response 185 175
  2. 2. CRITICAL CARE AND EMERGENCY MEDICINE CLINICAL EXAMINATION OF THE CRITICALLY ILL PATIENT 1 Initial assessment 2 Immediate management A irway Airway: ? Clear Support, ? Intubate Breathing: Oxygen B reathing Continuous positive airway 8 Distress pressure (CPAP), non-invasive Rate ventilation (NIV) Chest movement Intubate and ventilate Auscultation Circulation: Venous access Fluids C irculation Vasoactive drugs Pulse: Rate Rhythm 3 Monitoring Volume Heart rate; ECG Blood pressure: Respiratory rate; Sp O2 Direct arterial BP— arterial line pressure Temperature GCS; pupil size, reaction Peripheral perfusion: Urine output Peripheral pulses Central venous pressure Temperature Colour Capillary refill 4 Initial investigations D isability Full blood count Conscious level: Urea and electrolytes Glasgow Coma Scale Creatinine Pupil responses Glucose Localising signs Arterial blood gas lactate Coagulation Cultures: blood, urine, sputum Chest X-ray ECG Recognising the critically ill patient Cardiovascular signs Respiratory signs Neurological signs • Cardiac arrest • Threatened or obstructed airway • Threatened or obstructed airway • Pulse rate < 40 or > 140 bpm • Stridor, intercostal recession • Absent gag or cough reflex • Systolic blood pressure • Respiratory arrest • Failure to maintain normal PaO2 (BP) < 100 mmHg • Respiratory rate < 8 or > 35/min and PaCO2 • Tissue hypoxia • Respiratory ‘distress’: use of • Failure to obey commands Poor peripheral perfusion accessory muscles; unable to • Glasgow Coma Scale Metabolic acidosis speak in complete sentences (GCS) < 10 Hyperlactataemia • SpO2 < 90% on high-flow O2 • Sudden fall in level of consciousness • Poor response to volume • Rising PaCO2 > 8 kPa (> 60 mmHg), (GCS fall > 2 points) resuscitation or > 2 kPa (> 15 mmHg) above • Repeated or prolonged seizures • Oliguria: < 0.5 ml/kg/hr ‘normal’ with acidosis (check urea, creatinine, K+) 176
  3. 3. C L I N I C A L E X A M I N AT I O N O F T H E C R I T I C A L LY I L L PAT I E N T Monitor displaying blood pressure/ Intravenous fluids right atrial pressure/heart rate/Sp O2 Infusion Nitric pumps oxide cylinder 8 Intra-aortic Pacemaker Ventilator Haemofiltration balloon pump (behind machine haemofiltration machine) A patient with multi-organ failure supported by haemodynamic monitoring, cardiac pacing, a counterpulsation aortic balloon pump, haemofiltration and nitric oxide therapy. Shock Multi-organ failure Central nervous system Sweating Confusion Coma Reduced conscious level Intracerebral bleeding Confused, unresponsive Acute respiratory distress syndrome Tachypnoea Myocardial depression Liver failure with hyperbilirubinaemia Hypotension Gastrointestinal tract Ileus Mucosal damage Tachycardia with Haemorrhage low-volume pulse Endotoxin leak to portal vein Disseminated intravascular coagulation Bleeding from vessel puncture sites Cold cyanosed peripheries Skin Haemorrhages and infarcts secondary to disseminated intravascular coagulation Poor urine output Meningococcal sepsis: rash Ischaemia, gangrene secondary to decreased flow and intravascular coagulation Some features of shock. 177
  4. 4. CRITICAL CARE AND EMERGENCY MEDICINE A critically ill patient is one at imminent risk of death; the teams (PARTs). In some hospitals the medical emergency severity of illness must be recognised early and appropriate team may be the cardiac arrest team but with a wider measures taken promptly to assess, diagnose and manage remit, while in others this service is provided by the ICU or the illness. HDU team. The approach required in managing the critically ill Criteria that identify deranged physiology (p. 176) are patient differs from that required in less severely ill patients used to alert the ward nursing and junior medical staff to with immediate resuscitation and stabilisation of the impending problems so that they can summon the outreach patient’s condition taking precedence: team to assess the patient, institute initial resuscitation and Priorities are: supervise transfer to ICU or HDU as appropriate. ● prompt resuscitation, adhering to advanced life support guidelines (p. 556) and the principles of ADMISSION GUIDELINES cardiorespiratory management explained in this chapter 8 ● urgent treatment of life-threatening emergencies such as Rigid rules to determine admission to ICU/HDU are hypotension, hypoxaemia, hyperkalaemia, destined to fail because every case must be evaluated on its hypoglycaemia and dysrhythmias own merits. Nevertheless, broad guidelines are required ● analysis of the deranged physiology to avoid unnecessary suffering and the waste of valuable ● establishing the complete diagnosis in stages as further resources caused by admitting patients who have nothing to history and the results of investigations become available gain from intensive care because they either are too well or ● careful monitoring of the patient’s condition and have no realistic prospect of recovery. The existence of an response to treatment. empty bed does not justify admission. The guiding principle when considering ICU/HDU admission should be the timely use of this resource in patients who have a realistic PROVISION OF CRITICAL CARE prospect of recovering to achieve a quality of life that they would value. Patients who do warrant admission should ORGANISATION OF CRITICAL CARE be identified early and admitted without delay since this improves survival and reduces the length of stay on the ICU. Critical care embraces both intensive care and high- The wishes of the patient, if known, should be respected and dependency care. Intensive care units (ICUs) are for the whatever decision is made should be carefully explained to care of very ill patients with potential or established organ the patient’s family. failure. Initially established for the provision of mechanical If the appropriateness of admission remains uncertain, ventilation for patients with respiratory failure, ICUs now as may occur in the A&E department when little history is monitor and support all the major organ systems. High- available, the patient should be given the benefit of the doubt dependency care provides an intermediate level of care at a and the indication for continued active treatment reviewed point between intensive care and general ward care; it is as further information becomes available (Box 8.1). appropriate both for patients who have had major surgery There is now evidence that for patients undergoing and for those with single-organ failure. Ideally the ICU high-risk elective or emergency surgery the mortality, should be adjacent to the high-dependency unit (HDU), morbidity and both ICU and hospital length of stay are allowing the critical care medical team to manage a reduced by pre-operative admission to ICU/HDU to combined critical care department. improve cardiorespiratory status (‘pre-optimisation’). Such The intensive care specialist (intensivist) should provide a patients are often elderly with cardiorespiratory disease and holistic approach that coordinates expert opinions from poor physiological reserve, and benefit from a protocol of other specialties (surgeons, physicians, microbiologists) to intensive perioperative care. At present many hospitals have produce an integrated plan of management that recognises major problems in implementing this strategy due to a the priorities in the treatment of multiple organ failure. shortage of critical care beds. Specific indications for admission to ICU and HDU are given in Box 8.2. CRITICAL CARE ‘OUTREACH’ Critically ill patients can be found throughout the hospital, in post-operative recovery areas, coronary care units, the acute medical and surgical wards and accident and 8.1 FACTORS IN THE ASSESSMENT OF A POSSIBLE ICU ADMISSION emergency (A&E) departments. The purpose of ‘outreach’ is to achieve earlier identification of these patients so that ● Primary diagnosis and other active medical problems assessment and, if appropriate, transfer to ICU/HDU is ● Prognosis of underlying condition ● Severity of physiological disturbance—is recovery still possible? arranged before deterioration occurs to the point of ● Life expectancy and anticipated quality of life post-discharge imminent or actual cardiorespiratory arrest. Prompt ● Wishes of the patient and/or relatives identification and treatment may even avert the need for ● Availability of the required treatment/technology admission to ICU/HDU. Many hospitals are now setting up N.B. Age alone should not be a contraindication to admission. 178 medical emergency teams or ‘outreach’/‘patient at risk’
  5. 5. MONITORING 8.2 ADMISSION CRITERIA FOR ICU AND HDU attaching each patient to a battery of ‘alarming’ machines (p. 177). Much of the bedside nurse’s time is spent observing, recording and reacting to the information displayed by these Admission to ICU monitors, particularly the electrocardiogram (ECG), CVP, ● Patients requiring or likely to require endotracheal intubation and arterial blood pressure (BP), temperature and ventilator invasive mechanical ventilatory support data. The trends observed over time, interpreted in relation ● Patients requiring support of two or more organ systems (e.g. to changes in therapy, are an important guide to the patient’s inotropes and haemofiltration) ● Patients with chronic impairment of one or more organ systems progress. (e.g. chronic obstructive pulmonary disease (COPD) or severe The critically ill patient should be monitored according to ischaemic heart disease (IHD)) who also require support for acute the following principles: reversible failure of another organ system ● Regular clinical examination should never be neglected. Admission to HDU ● Simple physical signs such as respiratory rate, the ● Patients who require far more detailed observation or monitoring appearance of the patient, restlessness, conscious level 8 than can be safely provided on a general ward and indices of poor peripheral perfusion (pale, cold Direct arterial blood pressure (BP) monitoring Central venous pressure (CVP) monitoring skin, delayed capillary refill in the nail bed) are just as Fluid balance important as a set of blood gases or numbers Neurological observations, regular Glasgow Coma Scale impressively displayed on expensive monitors. (GCS) recording ● If there is conflict between clinical assessment and the ● Patients requiring support for a single failing organ system but information on a monitor, the monitor should be excluding invasive ventilatory support Mask continuous positive airway pressure (CPAP) or presumed to be wrong until all potential sources of error non-invasive (mask) ventilation (NIPPV)—Box 8.17, page 193 have been checked and eliminated. For example, CVP Low- to medium-dose inotropic support measurement may be erroneous because the line is Renal replacement therapy in an otherwise stable patient blocked, the system has not been reset to zero after a ● Patients no longer requiring intensive care but who cannot be safely managed on a general ward change in the patient’s position, the tip of the cannula is lying in the right ventricle, or another infusion has been attached to the same central line. ● Changes and trends are more important than any single TRANSPORT OF THE CRITICALLY ILL measurement. PATIENT ● Many monitors have alarms which will activate if certain maximum and minimum values are breached. This is a Critically ill patients should be transported to the most crucial safety feature and may, for example, help to appropriate clinical area for their continuing care. Before identify the fact that a patient has become disconnected intra- or inter-hospital transfer is undertaken, the patient’s from the ventilator. Despite the understandable desire to condition must be stabilised. Appropriate monitoring should avoid extra noise, the alarm limits should always be set be set up and if there is clinical evidence of progressive to define physiologically ‘safe’ limits for the variable respiratory failure or inability to protect the airway, being monitored. endotracheal intubation and ventilation are indicated. ● Sophisticated monitoring systems are often invasive and Intubation, while often essential, may be hazardous in the pose certain hazards, particularly infection (Box 8.3). patient with cardiorespiratory failure, and full monitoring Always ask ‘Is it necessary?’, and cease monitoring as and resuscitation facilities must be available. Hypovolaemia soon as possible. and hypotension should be corrected and this will often require monitoring of the central venous pressure (CVP). Transfer to another hospital may be necessary for further investigations (such as computed tomography, CT), or to MONITORING THE CIRCULATION specialist liver failure, neurosurgical or cardiac surgical units. The urgency of providing the specialist treatment has Electrocardiogram (ECG) to be balanced against the stability of the patient’s condition. Standard monitors display a single-lead ECG, record heart It may be more appropriate to admit the patient to the local rate and identify rhythm changes. More sophisticated ICU for initial stabilisation before transfer. All critically ill machines can print out rhythm strips and monitor ST patients should be accompanied during transfer by an segment shift, which may be useful in patients with appropriately trained medical escort. ischaemic heart disease. Blood pressure MONITORING This may be measured intermittently using an automated sphygmomanometer but in critically ill patients continuous intra-arterial monitoring, using a line placed in the radial GENERAL PRINCIPLES artery, is preferable. It is important to appreciate that when there is systemic vasoconstriction the mean arterial pressure On entering an ICU, relatives, students and even clinicians may be normal or even high although the cardiac output is may be intimidated by the numerous tubes and cables low. Conversely, if there is peripheral vasodilatation, as in 179
  6. 6. CRITICAL CARE AND EMERGENCY MEDICINE 8.3 COMPLICATIONS AND PITFALLS OF CENTRAL Hypervolaemia VENOUS AND PULMONARY ARTERY (PA) CANNULATION Normovolaemia At insertion Hypovolaemia ● Pneumothorax—more likely with subclavian than with internal jugular approach ● Haematoma from accidental arterial puncture CVP ● Air embolism ● Dysrhythmia ● Damage to thoracic duct with left internal jugular or subclavian approach ● Knotting of catheter* ● Pulmonary artery rupture* 8 In situ 0 15 30 ● Sepsis Time (min) ● Endocarditis ● Thrombosis Fig. 8.1 The different responses observed in central venous ● Pulmonary infarct* pressure (CVP) after a fluid challenge of 250 ml, depending on the ● Pulmonary artery rupture* intravascular volume status of the patient. ● Erroneous information ● Inappropriate response to information * Risk associated specifically with PA catheterisation. In severe hypovolaemia the RAP may be sustained by peripheral venoconstriction, and transfusion may initially sepsis, the mean arterial pressure may be low although the produce little or no change in the CVP (Fig. 8.1). cardiac output is high. Pulmonary artery ‘wedge’ pressure (PAWP) Central venous pressure (CVP) and PA catheterisation CVP or right atrial pressure (RAP) is monitored using a In most situations the CVP is an adequate guide to the filling catheter inserted via either the internal jugular or the pressures of both sides of the heart; however, certain subclavian vein with the distal end sited in the upper right conditions such as pulmonary hypertension or right atrium. Although on general wards and some HDUs ventricular dysfunction may lead to raised CVP levels even measurements may be made using a saline-filled manometer in the presence of hypovolaemia. If this is suspected, it may tube, in ICU the line is transduced as for arterial pressure be appropriate to insert a pulmonary artery flotation catheter measurement. The zero reference point used is normally the (Fig. 8.2) so that pulmonary artery pressure and PAWP, mid-axillary line (MAL), which approximates to the level of which approximates to left atrial pressure, can be measured. the tricuspid valve or mid-right atrium with the patient lying The mean PAWP normally lies between 8 and 12 mmHg semi-supine. All intravascular pressures quoted in this (measured from the mid-axillary line) but in left heart failure chapter are referenced to that point. The classical bedside it may be grossly elevated and even exceed 30 mmHg. clinical examination uses the ‘sternal angle’ as the zero Provided the pulmonary capillary membranes are intact, the reference point and this lies approximately 6–8 cm optimum PAWP when managing acute circulatory failure in (depending on the antero-posterior chest diameter) the critically ill patient is generally 12–15 mmHg because vertically above MAL. (Values of CVP measured from this this will ensure good left ventricular filling without risking reference point will therefore be 6–8 cm lower than values hydrostatic pulmonary oedema. recorded from MAL.) These catheters may also be used to measure cardiac The CVP is a useful means of assessing the need for output, sample blood from the pulmonary artery (‘mixed intravascular fluid replacement and the rate at which it venous’ samples) and, by oximetry, provide continuous should be given. If the CVP is low in the presence of a low monitoring of the mixed venous oxygen saturation (SvO2). mean arterial pressure (MAP) or cardiac output, fluid Measurement of SvO2 gives an indication of the adequacy of resuscitation is necessary. However, a raised level does not cardiac output in relation to the body’s metabolic require- necessarily mean that the patient is adequately volume ments and is especially useful in low cardiac output states. resuscitated. It must be remembered that right heart function, pulmonary artery pressure, intrathoracic pressure Cardiac output and venous ‘tone’ also influence CVP and may lead to a The most widely used method for cardiac output measure- raised CVP even when the patient is hypovolaemic. In ment is the thermodilution technique using a PA catheter. A addition, positive pressure ventilation raises intrathoracic bolus of cold 5% dextrose is rapidly injected into the right pressure and causes marked swings in atrial pressures and atrium via the CVP line and mixes with the total venous systemic blood pressure in time with respiration. Pressure return in the right ventricle, producing a drop in the measurements should be recorded at end-expiration or, if pulmonary artery temperature that is sensed by a thermistor safe, off the ventilator because these values provide the most at the tip of the PA catheter. The cardiac output is derived reliable measure of ventricular end-diastolic transmural from the volume and temperature of the injectate and the 180 pressure. resulting change in temperature measured in the pulmonary
  7. 7. MONITORING A Pulmonary artery Aorta LA B mmHg Balloon RA Right Pulmonary ventricular pressure artery pressure 8 30 LV Wedge 20 (left atrial) RV pressure Right atrial 10 pressure Balloon inflated 0 Fig. 8.2 A pulmonary artery catheter. A There is a small balloon at the tip of the catheter and pressure can be measured through the central lumen. The catheter is inserted via an internal jugular, subclavian or femoral vein and advanced through the right heart until its tip lies in the pulmonary artery. When the balloon is deflated the pulmonary artery pressure can be recorded. B Advancing the catheter while inflating the balloon will ‘wedge’ the catheter in the pulmonary artery. In this position blood cannot flow past the balloon so the tip of the catheter will now record the pressure transmitted from the pulmonary veins and left atrium. This is known as the pulmonary artery wedge pressure and provides an indirect measure of the left atrial pressure. artery; it is inversely related to the area under the temperature–time curve. Although generally viewed as the ‘gold standard’ for clinical measurement of cardiac output, the error may be 10–15%. Thermodilution cardiac output measurement has been refined by the development of PA catheters incorporating a heating element, which raises blood temperature at frequent intervals, with the resultant temperature change also Oesophageal detected by the thermistor. These ‘continuous’ cardiac Doppler probe output catheters dispense with the need for injections of cold dextrose. Increasingly less invasive methods for monitoring cardiac Stroke Peak output are being used, such as oesophageal Doppler distance velocity ultrasonography. This involves inserting a 6 mm probe into the distal oesophagus to allow continuous monitoring of the aortic flow signal from the descending aorta (Fig. 8.3). From the stroke distance (area under velocity/time waveform), and using a correction factor that incorporates the patient’s age, height and weight, an estimate of left ventricular stroke volume and hence cardiac output can be made. Peak velocity is an indicator of left ventricular Flow performance while flow time is an indicator of left time ventricular filling and peripheral resistance. Oesophageal Doppler provides a rapid and clinically useful assessment of Fig. 8.3 Oesophageal Doppler ultrasonography. volume status and cardiac performance to guide early fluid and vasoactive therapy. Urine output Analysis of arterial pressure waveform is another means This is a sensitive measure of renal perfusion, provided that of continuously estimating cardiac output, and can be cali- the kidneys are not damaged (e.g. acute tubular necrosis) or brated either by transpulmonary thermodilution (PiCCO) or affected by drugs (e.g. diuretics, dopamine), and can be lithium dilution methods (LidCO). monitored accurately if a urinary catheter is in place. It is 181
  8. 8. CRITICAL CARE AND EMERGENCY MEDICINE normally measured hourly and the lower limit of normal Arterial blood gases is 0.5 ml/hr/kg body weight. These are usually measured several times a day in a ventilated patient so that inspired oxygen (FIO2) and minute Fluid balance volume can be adjusted to achieve the desired PaO2 and Assessing fluid balance in critically ill patients is a difficult PaCO2 respectively. Analysis of arterial blood gas results is but important discipline. Weighing the patient daily can be also a useful means of monitoring disturbances of acid–base helpful but is extremely difficult, and assessment is usually balance (Ch. 16). based on fluid balance charts which record: ● inputs: oral, nasogastric and intravenous, classified as Lung function crystalloid and colloid In ventilated patients lung function is monitored by: ● outputs: urine, nasogastric, fistulae, vomiting, diarrhoea ● alveolar–arterial PO2 gradient and hypoxaemia index and surgical drain losses. (PaO2/FIO2), both measures of gas exchange 8 ● arterial and end-tidal CO2, reflecting alveolar The insensible loss from skin, respiration etc. is normally 500–1000 ml/day but can exceed 2 litres/day in a pyrexial ventilation patient with open wounds. ● tidal volume (VT), respiratory rate (f), minute volume (VT × f), airway pressure and compliance, reflecting Peripheral/skin temperature airways resistance, the ‘stiffness’ of the lungs and the This is conventionally measured over the dorsum of the ease with which the patient can meet the required work foot and reflects cutaneous blood flow and venous filling. of breathing. The gradient between peripheral and central or ‘core’ temperature (from rectal, oesophageal or tympanic probes) Capnography may be used to assess peripheral perfusion; a difference of The CO2 concentration in inspired gas is zero, but during < 3°C suggests that both intravascular fluid replacement and expiration, after clearing the physiological dead space, it tissue perfusion are adequate. rises progressively to reach a plateau which represents the alveolar or end-tidal CO2 concentration. This cyclical change Blood lactate, hydrogen ion and base deficit in CO2 concentration or capnogram is measured using an A metabolic acidosis with base deficit > 5 mmol/l requires infrared sensor inserted between the ventilator tubing and explanation (p. 437). It often indicates increased lactic acid the endotracheal tube. With normal lungs, the end-tidal production in poorly perfused, hypoxic tissues and impaired CO2 closely mirrors PaCO2, and can be used to assess the lactate metabolism due to poor hepatic perfusion. Serial adequacy of alveolar ventilation. However, there may be lactate measurements may therefore be helpful in moni- considerable discrepancies if there is lung disease or impaired toring tissue perfusion and the response to treatment. Other pulmonary perfusion (for example, due to hypovolaemia). conditions such as acute renal failure, ketoacidosis and Trends in end-tidal CO2 are useful in head injury manage- poisoning may be the cause (p. 438). Large volume ment and during the transport of ventilated patients. infusions of fluids containing sodium chloride, e.g. in theatre In combination with the gas flow and respiratory or during resuscitation, may lead to a hyperchloraemic cycle data from the ventilator, CO2 production and hence acidosis. metabolic rate may be calculated. MONITORING RESPIRATORY FUNCTION PHYSIOLOGY OF THE CRITICALLY ILL Oxygen saturation (SpO2) PATIENT This is measured by a probe, usually attached to a finger or earlobe. Spectrophotometric analysis is used to determine OXYGEN TRANSPORT the relative proportions of saturated and desaturated haemoglobin. The technique is unreliable if peripheral The major function of the heart, lungs and circulation is perfusion is poor and may produce erroneous results in the provision of oxygen and other nutrients to the various the presence of nail polish, excessive movement or high organs and tissues of the body. During this process carbon ambient light. In general, arterial oxygenation is satisfactory dioxide and the other waste products of metabolism are if SpO2 is greater than 90%. In the ICU, sudden falls in SpO2 removed. The rate of supply and removal should match the may be caused by: specific metabolic requirements of the individual tissues. ● pneumothorax This requires adequate oxygen uptake in the lungs, global ● displacement of the endotracheal tube matching of delivery and consumption, and regional control ● disconnection from the ventilator of the circulation. Failure to supply sufficient oxygen to ● lung collapse due to thick secretions blocking the meet the metabolic requirements of the tissues is the proximal bronchial tree cardinal feature of circulatory failure or ‘shock’. ● circulatory collapse causing a poor signal due to The transport of oxygen from the atmosphere to the impaired peripheral perfusion mitochondria within individual cells is illustrated in Figure 182 ● error such as a detached probe. 8.4. The important points to note are that:
  9. 9. PHYSIOLOGY OF THE C R I T I C A L LY ILL PAT I E N T PaO2 P50 SaO2 (97) CaO2 (200) (13) (3.5) DO2 Hb (150) QT (5) (1000) P lO2 humidified (20) P lO2 dry (21) Diffusion of O2 in tissues Capillary P O2 Heart and Arterial Venous lungs (13) (5.3) Interstitial P O2 Expired dry ‘Shunt’ (5.3 – 2.7) V i/e (5) P EO2 (15.9) (2–3%) VO2 P ECO2 (4.2) Intracellular PO2 (250) 8 (2.7 – 1.3) VCO2 (200) Mitochondrial P O2 (1.3 – 0.7) PAO2 (14) P50 O2R Pv O2 Sv O2 (75) CvO2 (150) (750) (5.3) Hb (150) QT (5) Calculations CaO2 = (Hb x k x SaO2/100) + (PaO2 x 0.23) = 200 ml O2/l k = coefficient of haemoglobin oxygen-binding capacity = 1.36 ml O2/gram of 100% saturated Hb PaO2 x 0.23 = oxygen dissolved in plasma = 3 ml/l DO2 = QT x CaO2 = 1000 ml/min VO2 = QT (CaO2–CV O2) = 250 ml/min OER = VO2 /D O2 x 100 = 25% Fig. 8.4 Transport of oxygen from inspired gas to the cell, demonstrating the ‘oxygen cascade’, with equations for calculation of arterial oxygen content, global oxygen delivery, consumption and extraction. Values in parentheses for a normal 70 kg individual (body surface area: 1.67 m2) breathing air (F IO2: 0.21) at standard atmospheric pressure (PB: 101 kPa). Partial pressures of O2, CO2 in kPa; saturation in %; contents (CaO2, Cv O2) in ml/litre; Hb in g/l; blood/gas flows (QT, Vi/e) in litre/min; oxygen transport (DO2, O2R), VO2 and V CO2 in ml/min. To convert kPa to mmHg, multiply by 7.5. CaO2 = arterial O2 content O2R= oxygen return P I O2 = inspired PO2 SO2=oxygen saturation (%) CvO2 = mixed venous O2 content PaO2= arterial PO2 PO2 = oxygen partial pressure (kPa) SvO2 = mixed venous SO2 DO2 = oxygen delivery PAO2 = alveolar PO2 PvO2 = venous PO2 V CO2 = CO2 production Hb = haemoglobin P ECO2= mixed expired PCO2 QT = cardiac output Vi/e= minute volume: inspired/expired OER = oxygen extraction ratio P EO2 = mixed expired PO2 SaO2 = arterial SO2 VO2 = oxygen consumption ● The movement of oxygen from pulmonary capillary to patient who is both anaemic (Hb 60 g/l) and hypoxaemic systemic tissue capillary, referred to as the global (SaO2 75%) when breathing air (FIO2 0.21). oxygen delivery (DO2), relies on convection or bulk flow Supplementary oxygen at FIO2 0.4 will increase SaO2 to and is the product of cardiac output and arterial oxygen 93%; CaO2 will increase by 24% but further increases in content. FIO2 while increasing PaO2 cannot produce any further ● The regional distribution of oxygen delivery is vital. If useful increases in SaO2 or CaO2. However, increasing skin and muscle receive high blood flows but the Hb to 90 g/l by blood transfusion will result in a further splanchnic bed does not, the gut will become hypoxic 50% increase in CaO2. even if overall oxygen delivery is high. ● The movement of oxygen from tissue capillary to cell ● The major determinants of the oxygen content of arterial occurs by diffusion and depends on the gradient of blood (CaO2) are the arterial oxygen saturation of oxygen partial pressures, diffusion distance and the haemoglobin (SaO2) and the haemoglobin concentration ability of the cell to take up and use oxygen. Therefore (over 95% of oxygen carried in the blood is attached to microcirculatory, tissue diffusion and cellular factors, as haemoglobin). The shape of the oxyhaemoglobin well as DO2, influence the oxygen status of the cell. dissociation curve dictates that increases in PaO2 beyond ● Supranormal levels of oxygen delivery cannot the level that ensures SaO2 is > 90% produce relatively compensate for diffusion problems between capillary small additional increases in CaO2 (Fig. 8.5). Consider a and cell, nor for metabolic failure within the cell. 183
  10. 10. CRITICAL CARE AND EMERGENCY MEDICINE 100 approximately 250 ml/min for an adult of 70 kg undertaking normal daily activities. VO2 may be calculated indirectly from the product of cardiac output and the arterial mixed venous oxygen content difference (CaO2–CvO2), as shown Haemoglobin saturation SO2 (%) 80 in Figure 8.4, or directly by sampling the inspired and Temperature mixed-expired gases from the ventilator and measuring H+ inspired and expired minute volume using either a mass 60 PaCO2 spectrometer or metabolic cart. 2,3 DPG The oxygen saturation in the pulmonary artery, otherwise known as the mixed venous oxygen saturation (SvO2), 40 represents a measure of the oxygen not consumed by the P50 tissues (DO2–VO2). The saturation of venous blood from 8 different organs varies considerably; for example, the 20 hepatic venous saturation usually does not exceed 60% but the renal venous saturation may reach 90%, reflecting the great difference in both the metabolic requirements 1 2 3 4 5 6 7 8 9 10 11 12 13 kPa of these organs and the oxygen content of the blood 0 0 20 40 60 80 100 mmHg delivered to them. The SvO2 is influenced by changes PO2 (mmHg or kPa) both in oxygen delivery (DO2) and consumption (VO2) and, Fig. 8.5 The relationship between oxygen tension (PO2) and provided the microcirculation and the mechanisms for percentage saturation of haemoglobin with oxygen (SO2). The cellular oxygen uptake are intact, can be used to monitor dotted line illustrates the rightward shift of the curve (i.e. P50 increases) whether global oxygen delivery is adequate to meet overall caused by increases in temperature, PaCO2, metabolic acidosis and demand. 2,3 diphosphoglycerate (DPG). The reoxygenation of the blood that returns to the lungs and the resulting arterial saturation (SaO2) will depend on how closely pulmonary ventilation and perfusion are OXYHAEMOGLOBIN DISSOCIATION CURVE matched. If part of the pulmonary blood flow perfuses non-ventilated parts of the lung, there will be ‘shunting’, The oxyhaemoglobin dissociation curve (Fig. 8.5) describes and the blood entering the left atrium will be desaturated the relationship between the saturation of haemoglobin in proportion to the size of this shunt and the level (SO2) and the partial pressure (PO2) of oxygen in the blood. of SvO2. Due to the shape of the curve, a small drop in PaO2 below 8 kPa (60 mmHg) will cause a marked fall in SaO2. Its position and the effect of various physico-chemical factors are defined by the PO2 at which 50% of the haemoglobin is RELATIONSHIP BETWEEN OXYGEN saturated (P50), which is normally 3.5 kPa (26 mmHg). CONSUMPTION AND DELIVERY A shift in the curve will influence the uptake and release of oxygen by the Hb molecule; for example, if the curve The tissue oxygen extraction ratio (OER), which is 20–25% moves to the right, the haemoglobin saturation will be lower in a normal subject at rest, rises as consumption increases for any given oxygen tension and therefore less oxygen will or supply diminishes (Fig. 8.6). The maximum OER is be taken up in the lungs but more will be released to the approximately 60% for most tissues; at this point no further tissues. As capillary PCO2 rises, the curve moves to the right, increase in extraction can occur and any further increase increasing unloading of oxygen in the tissues—a phenomenon in oxygen consumption or decline in oxygen delivery will known as the Bohr effect. cause tissue hypoxia, anaerobic metabolism and increased Traditionally, the optimum haemoglobin concentration lactic acid production. for critically ill patients had been considered to be In sepsis the slope of maximum OER decreases, approximately 100 g/l, representing a balance between reflecting the reduced ability of tissues to extract oxygen maximising the oxygen content of the blood and avoiding (DE cf. AB on Fig. 8.6), but the curve does not plateau regional microcirculatory problems due to increased and oxygen consumption continues to increase even at viscosity. However, recent evidence suggests an improved ‘supranormal’ levels of oxygen delivery. This concept outcome in critically ill patients if the haemoglobin encouraged some physicians to treat septic shock using concentration is maintained between 70 and 90 g/l, with the vigorous intravenous fluid loading and inotropic support, exception of the elderly and patients with coronary artery usually with dobutamine, with the aim of achieving very disease, in whom a level of 100 g/l remains appropriate. high oxygen deliveries (> 600 ml/min/m2) in the belief that this strategy would increase oxygen consumption, relieve tissue hypoxia, prevent multiple organ failure and OXYGEN CONSUMPTION improve prognosis. Trials have demonstrated no benefit in ICU patients with established organ failure but suggest that The sum of the oxygen consumed by the various organs it may be worthwhile if applied before organ failure 184 represents the global oxygen consumption (VO2) and is supervenes (Box 8.4)
  11. 11. PHYSIOLOGY OF THE C R I T I C A L LY ILL PAT I E N T F 8.5 TERMINOLOGY USED TO DESCRIBE THE 300 INFLAMMATORY STATE E Infection B C ● Invasion of normally sterile host tissue by microorganisms 200 Bacteraemia Oxygen consumption ● Viable bacteria in the blood (VO2) ml/min Systemic inflammatory response syndrome (SIRS) 100 ● Encompasses inflammatory response to both infective and A non-infective causes such as pancreatitis, trauma, D cardiopulmonary bypass, vasculitis etc. ● Defined by presence of two or more of: Temperature > 38.0°C or < 36.0°C 8 0 0 400 800 1200 Heart rate > 90/min Oxygen delivery (DO2) ml/min Respiratory rate > 20/min PaCO2 < 4.3 kPa (< 32 mmHg) or ventilated Fig. 8.6 The effects of changing oxygen delivery on consumption. White blood count > 12 × 109/l or < 4 × 109/l The solid line (ABC) represents the normal relationship and the dotted line (DEF) the altered relationship believed to exist in sepsis. Sepsis ● Systemic inflammatory response caused by documented infection EBM 8.4 EARLY GOAL-DIRECTED THERAPY IN Severe sepsis/SIRS SEVERE SEPSIS ● Sepsis/SIRS with evidence of early organ dysfunction or ‘In patients with severe sepsis or septic shock managed initially in hypotension A&E, early goal-directed therapy (EGT) reduced 60-day mortality Septic/SIRS shock from 57% to 44%. Both groups were resuscitated with similar targets for CVP, arterial blood pressure and urine output, but in the ● Sepsis associated with organ failure and hypotension (systolic EGT group additional goals were central venous oxygen saturation BP < 90 mmHg or > 40 mmHg fall from baseline) unresponsive > 70% and haematocrit > 30%, resulting in more rapid fluid to fluid resuscitation resuscitation and higher RBC transfusion rates in the first 6 hours.’ Multiple organ dysfunction syndrome (MODS) ● Rivers E, et al. N Engl J Med 2001; 345:1368–1377. ● Development of impaired organ function in critically ill patients with SIRS ● If prompt treatment of underlying cause and suitable organ support are not achieved, then multiple organ failure (MOF) will ensue PATHOPHYSIOLOGY OF THE INFLAMMATORY RESPONSE oxygen radicals and particularly pro-inflammatory cytokines The mediators and clinical manifestations of the inflam- (p. 66) are released into the circulation. matory response are described on pages 75–76. In critically The inflammatory and coagulation cascades are ill patients these processes have important consequences intimately related. The process of blood clotting not only (Box 8.5). involves platelet activation and fibrin deposition but also Fever, tachycardia with warm peripheries, tachypnoea causes activation of leucocytes and endothelial cells. and a raised white cell count traditionally prompt a diag- Conversely, leucocyte activation induces tissue factor nosis of sepsis with the implication that the clinical picture expression and initiates coagulation. Control of the is caused by invading microorganisms and their breakdown coagulation cascade is achieved through the natural anti- products. However, other conditions such as pancreatitis, coagulants antithrombin (AT) III, activated protein C (APC) trauma, malignancy, tissue necrosis, aspiration syndromes, and tissue factor pathway inhibitor (TFPI) which not only liver failure, blood transfusion and drug reactions can all regulate the initiation and amplification of the coagulation produce the same clinical picture in the absence of infection. cascade but also inhibit the pro-inflammatory cytokines. Deficiency of ATIII and APC (features of disseminated Local inflammation intravascular coagulation (DIC), see below) facilitates The body’s initial response to a noxious local insult is to thrombin generation and promotes further endothelial cell produce a local inflammatory response with sequestration dysfunction. and activation of white blood cells and the release of a variety of mediators to deal with the primary ‘insult’ and Systemic inflammation prevent further damage either locally or in distant organs. During a severe inflammatory response systemic release Normally, a delicate balance is achieved between pro- and of cytokines and other mediators triggers widespread anti-inflammatory mediators. However, if the inflammatory interaction between the coagulation pathways, platelets, response is excessive, local control is lost and a large array endothelial cells and white blood cells, particularly the of mediators including prostaglandins, leukotrienes, free polymorphonuclear cells (PMNs). These ‘activated’ PMNs 185
  12. 12. CRITICAL CARE AND EMERGENCY MEDICINE express adhesion factors (selectins) causing them initially to hypovolaemia due to venodilatation and fluid loss through adhere to and roll along the endothelium, then to adhere the leaky vascular endothelium) are promptly controlled firmly and finally to migrate through the damaged and before significant organ failure occurs (‘early’ shock), the disrupted endothelium into the extravascular, interstitial prognosis is good. However, if the global and peripheral space together with fluid and proteins, resulting in tissue circulatory failure is not corrected promptly, and particularly oedema and inflammation. A vicious circle of endothelial if the underlying cause is not effectively treated, progressive injury, intravascular coagulation, microvascular occlusion, deterioration in organ function occurs and multiple organ tissue damage and further release of inflammatory failure (MOF) ensues (‘late’ shock). mediators ensues. The mortality of MOF is high and increases with the All organs may become involved. This manifests in the number of organs that have failed, the duration of organ lungs as the acute respiratory distress syndrome (ARDS) failure and the patient’s age. Failure of four or more organs and in the kidneys as acute tubular necrosis (ATN), while is associated with a mortality > 80%. 8 widespread disruption of the coagulation system results in the clinical picture of DIC. The endothelium itself produces mediators that locally PRESENTING PROBLEMS IN control blood vessel tone: endothelin 1, a potent vaso- CRITICAL ILLNESS constrictor, and prostacyclin and nitric oxide (NO, p. 76) which are systemic vasodilators. NO (which is also generated outside the endothelium) is implicated in both the CIRCULATORY FAILURE: ‘SHOCK’ myocardial depression and the profoundly vasodilated circulation (both arterioles and venules) that causes the Circulatory failure or ‘shock’ exists when the oxygen relative hypovolaemia and systemic hypotension found in delivery (DO2) fails to meet the metabolic requirements of septic/SIRS shock. the tissues. In the context of critical illness, ‘shock’ is often A major component of the tissue damage in septic/SIRS considered to be synonymous with hypotension and to shock is the inability to take up and use oxygen at define the state of circulatory failure. While hypotension is mitochondrial level even if global oxygen delivery is a sinister development and requires urgent attention, it is supranormal. This effective bypassing of the tissues results most important to appreciate that hypotension is often a late in a reduced arteriovenous oxygen difference, a low oxygen manifestation of circulatory failure or shock and that the extraction ratio, a raised plasma lactate and a paradoxically cardiac output and oxygen delivery may be critically low high mixed venous oxygen saturation (SvO2). even though the blood pressure remains normal (Box 8.6); If both the precipitating cause and accompanying the problem should be identified and treatment instituted circulatory failure (hypotension and frequently severe before the blood pressure falls. 8.6 TYPICAL CIRCULATORY MEASUREMENTS IN A NORMAL ADULT AND IN VARIOUS CARDIORESPIRATORY CONDITIONS THAT MAY CAUSE CIRCULATORY ‘SHOCK’ RAP/CVP LAP/PAWP PAP MAP Heart rate Cardiac CaO2 DO2 Clinical condition (mmHg) (mmHg) (mmHg) (mmHg) (/min) output (l/min) SVR* PVR* (ml/l) (ml/min) Normal 6 11 16 96 70 5 18 1 200 1000 Major haemorrhage 0 4 11 81 120 3 27 2.3 160 480 Left heart 8 20 24 96 100 3.7 24 1 180 670 failure Major pulmonary 12 6 36 81 110 2.5 28 12 160 400 embolism Exacerbation of 11 10 42 82 100 6 12 5 150 900 COPD Septic shock Pre-volume load 3 8 16 55 130 4.5 12 1.3 150 675 Post-volume load 9 15 23 60 120 7.5 7 1.1 140 1050 * Multiply by 80 to give SI units: dyn.sec/cm5. To adjust for the size of the patient, the measurements of flow and resistance are frequently indexed by dividing by the patient’s body surface area. (RAP/LAP = right/left atrial pressure; CVP = central venous pressure; PAWP = pulmonary artery wedge pressure; PAP/MAP = pulmonary artery/mean arterial pressure; SVR/PVR = systemic/pulmonary vascular resistance; Ca O2 = arterial oxygen content; DO2 = global oxygen delivery; COPD = chronic obstructive pulmonary disease) Note These values are merely examples. The severity of the condition and pre-existing cardiorespiratory disease will affect the precise figures obtained in individual cases. Note that in contrast to other conditions the oxygen delivery is high in septic shock after volume loading. When the circulatory abnormalities have been defined in this way, appropriate management may be planned. Pressures quoted referenced to zero at mid-axilla as is usual practice in ICU. Subtract vertical distance from mid-axilla to sternal angle (approx. 6–8 mmHg) if sternal angle used as reference point. 186
  13. 13. PRESENTING PROBLEMS IN CRITICAL ILLNESS The many causes of circulatory failure or ‘shock’ may 8.7 GENERAL FEATURES OF SHOCK broadly be classified into: ● hypovolaemic—any condition provoking a major ● Hypotension (systolic BP < 100 mmHg) reduction in blood volume, e.g. internal or external ● Tachycardia (> 100/min) haemorrhage, severe burns, dehydration ● Cold, clammy skin ● Rapid, shallow respiration ● cardiogenic—any form of severe heart failure, e.g. ● Drowsiness, confusion, irritability myocardial infarction, acute mitral regurgitation ● Oliguria (urine output < 30 ml/hr) ● obstructive—obstruction to blood flow around the ● Elevated or reduced central venous pressure (see text) circulation, e.g. major pulmonary embolism, cardiac ● Multi-organ failure tamponade, tension pneumothorax ● neurogenic—caused by major brain or spinal injury output. The central venous pressure (jugular venous producing disruption of brain stem and neurogenic pressure, JVP) is typically reduced in hypovolaemic and vasomotor control; may be associated with neurogenic anaphylactic shock but elevated in cardiogenic and 8 pulmonary oedema obstructive shock, and may be low, normal or high in ● anaphylactic—inappropriate vasodilatation triggered by neurogenic and septic shock. This is an important distinction an allergen (e.g. bee sting) and direct measurement of the CVP or PAWP (Fig. 8.2, ● septic/SIRS—infection or other causes of a systemic p. 181) may be very helpful if the physical signs are difficult inflammatory response that produce widespread to interpret. Figure 8.7 indicates how the likely diagnosis endothelial damage with vasodilatation, arteriovenous may be established by careful analysis of the CVP, shunting, microvascular occlusion and tissue oedema, peripheral perfusion, pulse volume and haematocrit. All resulting in organ failure. forms of shock require early identification and treatment because, if inadequate regional tissue perfusion and cellular Clinical assessment and complications dysoxia persist, multiple organ failure will develop. Although dependent to some extent on the underlying cause, a range of clinical features are common to most cases (Box 8.7 and p. 177). RESPIRATORY FAILURE INCLUDING ARDS Hypovolaemic, cardiogenic and obstructive causes of circulatory failure produce the ‘classical’ image of shock, The majority of patients admitted to ICU/HDU will have with cold peripheries, weak central pulses and evidence of a respiratory problems either as the primary cause of their low cardiac output. In contrast, neurogenic, anaphylactic admission or secondary to pathology elsewhere. Respiratory and septic shock are usually associated with warm failure is formally classified on the basis of blood gas peripheries, bounding pulses and features of a high cardiac analysis into: Measure CVP (mmHg from mid-axillary line) Raised Low Peripheral temperature Cold Warm Warm Cold Pulse volume Reduced Increased Increased Reduced Haematocrit Normal Normal Normal Normal Increased or reduced or increased or reduced Diagnoses to consider Myocardial infarct Sepsis Sepsis Haemorrhage Na/H2O loss Pulmonary embolus CO2 retention Anaphylaxis Tension Over-transfusion Drugs/overdose GI tract GI tract pneumothorax CNS lesions Trauma Ascites Cardiac tamponade Major vessel Renal Sepsis Thorax Sepsis Abdomen Retroperitoneal Fig. 8.7 A guide to the initial analysis and diagnosis of circulatory shock. 187
  14. 14. CRITICAL CARE AND EMERGENCY MEDICINE ● type 1—hypoxaemia (PaO2 < 8 kPa (< 60 mmHg) when ● Adequate supplemental oxygen to maintain SpO2 > 94% breathing air) without hypercapnia caused by a failure of should be provided. If the inspired oxygen concentration gas exchange due to mismatching of pulmonary required exceeds 0.6, refer to the critical care team. ventilation and perfusion ● Monitoring of SpO2 and arterial blood gases is helpful in ● type 2—hypoxaemia with hypercapnia (PaCO2 > 6.5 kPa documenting progress. (> 49 mmHg)) due to alveolar hypoventilation which ● Restless patients dependent on supplementary oxygen occurs when the respiratory muscles cannot perform or with deteriorating conscious level are at risk. If they sufficient effective work to clear the carbon dioxide remove the mask or vomit, the resulting hypoxaemia or produced by the body. aspiration may be catastrophic. ● An attempt should be made to reduce the work of Although this distinction is conceptually useful, it cannot breathing, e.g. by treating bronchoconstriction or using be applied too rigidly in critically ill patients since they CPAP (Box 8.17, p. 193). may change from type 1 to 2 as their illness progresses. 8 For example, hypercapnia may develop in pneumonia or pulmonary oedema as the patient tires and can no longer ACUTE RESPIRATORY DISTRESS sustain the increased work of breathing. SYNDROME (ARDS) Pulmonary problems in critically ill patients can also be This describes the acute, diffuse pulmonary inflammatory classified according to the functional residual capacity response to either direct (via airway or chest trauma) or (FRC, or the lung volume at the end of expiration). indirect blood-borne insults that originate from extra- Examples of low FRC include lung collapse, pneumonia and pulmonary pathology. It is characterised by neutrophil pulmonary oedema; examples of a high FRC (i.e. over- sequestration in pulmonary capillaries, increased capillary distended lungs) include asthma, COPD and bronchiolitis. permeability, protein-rich pulmonary oedema with hyaline This allows logical management directed at improving lung membrane formation, damage to type 2 pneumocytes compliance and reducing the work of breathing. leading to surfactant depletion, alveolar collapse and The more common causes of acute respiratory failure reduction in lung compliance. If this early phase does presenting to ICU/HDU for respiratory support are shown in not resolve with treatment of the underlying cause, a Box 8.8. fibroproliferative phase ensues and causes progressive The presentation, differential diagnosis and initial pulmonary fibrosis. It is frequently associated with other treatment of the primary respiratory conditions causing organ dysfunction (kidney, heart, gut, liver, coagulation) as acute respiratory failure are covered in Chapter 19. part of multiple organ failure. The term ARDS is often The assessment of respiratory failure in the critically ill limited to patients requiring ventilatory support on the ICU, patient should be guided by several important principles: but less severe forms, conventionally referred to as acute ● The patient’s appearance (tachypnoea, difficulty lung injury (ALI) and with similar pathology, occur on acute speaking in complete sentences, laboured breathing, medical and surgical wards. The clinical symptoms and exhaustion, agitation or increasing obtundation) is more important than measurement of blood gases in deciding when it is appropriate to provide mechanical respiratory support or intubation. 8.8 COMMON CAUSES OF RESPIRATORY FAILURE IN CRITICALLY ILL PATIENTS Type 1 respiratory failure ● Pneumonia ● Lung collapse,* ● Pulmonary oedema* e.g. retained secretions ● Pulmonary embolism ● Asthma ● Pulmonary fibrosis ● Pneumothorax ● ARDS* ● Pulmonary contusion ● Aspiration (blunt chest trauma) Type 2 respiratory failure ● Reduced respiratory drive,* ● COPD e.g. drug overdose, ● Peripheral neuromuscular head injury disease, e.g. Guillain–Barré, ● Upper airway obstruction myasthenia gravis (oedema, infection, ● Flail chest injury Fig. 8.8 Chest X-ray in acute respiratory distress syndrome foreign body) ● Exhaustion* (includes all (ARDS). This 22-year-old woman was involved in a road traffic ● Late severe acute asthma type 1 causes) accident. Note bilateral lung infiltrates, pneumomediastinum, * Secondary complications of other diseases. pneumothoraces with bilateral chest drains, surgical emphysema, and 188 fractures of the ribs, right clavicle and left scapula.
  15. 15. PRESENTING PROBLEMS IN CRITICAL ILLNESS 8.9 CONDITIONS PREDISPOSING TO ARDS 8.10 SYSTEMIC CAUSES OF COMA Inhalation (direct) Cerebral hypoxia; hypercapnia ● Aspiration of gastric contents ● Blunt chest trauma ● Respiratory failure ● Toxic gases/burn injury ● Near-drowning ● Pneumonia Cerebral ischaemia Blood-borne (indirect) ● Cardiac arrest ● Hypotension ● Sepsis ● Major blood transfusion Metabolic disturbance ● Necrotic tissue reaction ● Diabetes mellitus ● Uraemia (particularly bowel) ● Anaphylaxis (wasp, bee, Hypoglycaemia ● Hepatic failure ● Multiple trauma snake venom) Ketoacidosis ● Hypothermia ● ● Pancreatitis Cardiopulmonary bypass ● ● Fat embolism Carcinomatosis ● Hyperosmolar coma Hyponatraemia ● ● Drugs Sepsis 8 ● Severe burns ● Obstetric crises ● Drugs (heroin, barbiturates, (amniotic fluid embolus, thiazides) eclampsia) conscious level and management of airway, breathing and signs are not specific, sharing many features with other circulation are essential to prevent further brain injury, to pulmonary conditions. The criteria defining ARDS are: allow diagnosis and for definitive treatment to be instituted. Impairment of conscious level is objectively graded ● hypoxaemia, defined as PaO2/F IO2 < 26.7 kPa according to the Glasgow Coma Scale (GCS, p. 1186), (< 200 mmHg) which is also used to monitor progress. Although necessarily ● chest X-ray showing diffuse bilateral infiltrates (Fig. 8.8) limited, careful neurological examination is very important ● absence of a raised left atrial pressure: PAWP < 15 mmHg in the unconscious patient. Pupil size and reaction to light, ● impaired lung compliance. presence or absence of neck stiffness, focal neurological The term ARDS has severe limitations as a diagnostic signs and evidence of other organ impairment should be label since, like jaundice or a raised CVP, it represents a noted. After cardiorespiratory stability is achieved, the cause response to a variety of primary conditions (Box 8.9). of the coma must be sought from history (family, witness, general practitioner), examination and investigation, particularly CT. The possibility of drug overdose should RENAL FAILURE always be considered. The direct neurological causes of coma are listed and described in Chapter 26. Oliguria is frequently an early sign of systemic problems in critical illness and successful resuscitation is associated with restoration of good urine output, an improving acid– SEPSIS base balance and correction of plasma potassium, urea and creatinine. Acute renal failure (p. 481) in the context of Any or all of the features of SIRS (Box 8.5, p. 185) may be critical illness is usually due to pre-renal factors such as present, together with an obvious focus of infection such as uncorrected hypovolaemia, hypotension or ischaemia purulent sputum from the chest with shadowing on chest causing acute tubular necrosis (ATN). Sepsis is frequently a X-ray or erythema around an intravenous line. However, compounding factor, causing both global hypotension and severe sepsis may present as unexplained hypotension (i.e. local ischaemia that is often associated with DIC. In the septic shock) and the speed of onset may simulate a major presence of pre-existing chronic renal impairment or pulmonary embolus or myocardial infarction. The common nephrotoxic drugs, acute renal failure may result from sites of infection in critically ill patients and some of the relatively minor ischaemic or hypotensive insults. While appropriate investigations to consider are listed in Box 8.11. ATN is by far the most common cause of acute renal failure The patient may be admitted with infection from home in the ICU, it is essential not to overlook other causes, (‘community-acquired’) or may develop it after admission such as renal tract obstruction (including a blocked urinary to the unit (‘nosocomial’). The likely causative microorgan- catheter), drug toxicity, acute glomerulonephritis and ism and the antibiotic sensitivities will depend on this vasculitis associated with connective tissue diseases such as important distinction, which therefore directs the initial systemic lupus erythematosus. Appropriate investigations choice of antibiotics. Initial investigations should include: such as urinary microscopy, immunopathological tests and ● cultures of blood, sputum, intravascular lines, urine and abdominal ultrasound to exclude renal tract obstruction need any wound discharges to be carried out at an early stage. ● coagulation profile, plasma lactate, arterial blood gases, urinalysis and chest X-ray. NEUROLOGICAL FAILURE (COMA) As few as 10% of ICU patients with a clinical diagnosis of ‘septic’ shock will have positive blood cultures, due to the Impaired consciousness or coma is often an early feature effects of prior antibiotic treatment and the fact that a patient of severe systemic illness (Box 8.10). Prompt assessment of with an inflammatory state is not necessarily infected. 189