• Simultaneously feel for a carotid pulse and, if present, obtain a BP measurement as soon as practical. If there is no pulse, call for assistance, initiate chest compressions and follow basic and advanced life support algorithms (p. 704, 705). If there is a pulse, but no respiratory effort, call for assistance and supply rescue ventilation, ideally with a bag mask valve system connected to high-flow oxygen. Again, follow life support algorithms. If there is some respiratory effort, determine the adequacy by clinical examination, by attaching a pulse oximeter and, if practical, by obtaining an arterial blood gas (ABG) specimen. Be aware of the limitations of pulse oximetry, especially in hypotensive patients. Arterial blood needs to be sampled into an anticoagulated syringe and any air in the sample should be expelled before the sample is safely capped. The sample should be analysed immediately or transported in ice to minimize cellular metabolism in the sample from consuming oxygen and producing carbon dioxide.

The immediate management of cardiovascular and neurological abnormalities is discussed in later sections.

Guidelines for initial and daily patient assessment

Initial assessment

Dying patients and end-of-life care

• In the terminal phase of a patient’s illness, ensure optimal palliation of any/all sources of distress. Ensure that the family are fully aware of the situation.

• After discussion, withhold/withdraw any unnecessary interventions, including continuous monitoring.

• If appropriate, always discuss organ/tissue donation and adhere strictly to protocols (p. 562).

• If uncertain how to complete the death certificate, discuss this with a senior colleague. In the UK, many patients will require discussion with the coroner prior to completion of the death certificate.

• Whenever possible, inform the patient’s GP/primary care physician.

Transportation of the critically ill patient

Transfer of any critical ill patient out of the critical care environment requires planning and specialist skills. Even short journeys may provoke significant deterioration.

• The team escorting the patient must ensure that all necessary equipment is taken on the transfer, including sufficient supplies to deal with all predictable adverse events. In particular, the quantity of oxygen and battery power required for ventilators, monitors and infusion pumps must be in place.

• Patients who are intubated should always be escorted by a doctor with established airway skills and a nurse.

• Try to minimize the amount of equipment taken with the patient. For example, disconnect from feeding pumps and non-essential infusions.

• Prior to leaving, work through the NEWS (necessary, enough, working, secure) checklist.

General considerations for patient care in the critical care environment

Many of the items detailed below are being brought together in so-called care bundles. This approach has been shown to increase compliance.

• Take a holistic approach.

• Always introduce yourself to patients and their visitors, and explain what you are about to do. The patient’s comfort and dignity should be everybody’s priority; be conscious of the loss of the patient’s privacy and autonomy.

• Review the effectiveness of management plans at frequent intervals. If you initiate or change something, record it in the notes/chart and decide when you will need to review the patient’s response.

Infection control

• Before entering a critical care environment, remove white coats and jackets. Roll up sleeves to above the elbow and remove all hand and wrist jewellery. Wash hands and/or use an alcohol gel-based disinfectant.

• Before approaching the patient, hands should be washed or disinfected, and a plastic disposable apron or non-sterile gown and non-sterile gloves should be put on. When finished with a patient, remove gloves/gowns/aprons and wash or disinfect your hands again.

• To avoid cross-contamination between patients, all equipment should be dedicated for specific bed space use only.

• Barrier nursing is sometimes used for patients who are thought to have, or are colonized with, a communicable infection. Whenever practical, the patient should be isolated and the above guidelines strictly observed.

Patient care

• To prevent passive aspiration and enhance respiratory mechanics, all sedated patients should be positioned at least 30° head up. As soon as practical, sit patients out of bed for a portion of every day. Prescribe a simple eye ointment 6-hourly for all unconscious, sedated and/or mask/helmet-ventilated patients. Check the eyes daily for injury or inflammation in sedated or unconscious patients.

• Always examine the mouth and nose of patients with endotracheal and naso-gastric/naso-jejunal tubes. Look for signs of pressure necrosis, oral colonization and sinusitis. Start a chlorhexidine mouthwash with or without oral nystatin (topical antifungal) and discuss changing the offending tube. Topical antiseptics are increasingly being adopted as primary prophylaxis and added to existing care bundles.

Gastrointestinal care

• Oro-/naso-gastric tubes. All intubated patients, those receiving mask/helmet positive pressure ventilatory assistance and any other patient not able to eat should have either an oro-gastric or a naso-gastric tube.

• Stress ulcer prophylaxis. This is used for patient who are not receiving naso-gastric feeding, are shocked or on vasopressors, have a coagulopathy (including uraemia) or are anticoagulated, or are receiving gastric mucosal irritants, e.g. steroids, NSAIDS. Patients with burns/polytrauma or those who have had prolonged intubation and are sedated should also receive prophylaxis.

• Regimen. Oral ranitidine 150 mg 12-hourly; IV ranitidine 50 mg 8-hourly is given (reduce to 12-hourly in renal failure) if the enteral route is unavailable.

• High-risk patients or those with proven untreated peptic ulcer disease. Use an oral proton pump inhibitor (PPI), e.g. omeprazole 20 mg daily. For IV PPIs in patients with proven upper gastrointestinal bleeding, see p. 145.

• Bowel care. Constipation and diarrhoea are common complications of critical illness and most patients benefit from stool softeners, e.g. sodium docusate 200 mg twice daily, and mild aperients, e.g. sennakot 5–10 mL twice daily. Osmotic laxatives, e.g. lactulose, are avoided, as they can significantly contribute to bowel gas formation.

Nutritional support

Early enteral feeding

• Early initiation (within 12 hours) is the significant nutritional factor influencing clinical outcome, as ‘late’ feeding (i.e. feeding commenced within 36 hours of admission) is associated with increased gut permeability and an increase in late multi-organ failure.

• Timing, rather than amount/volume of feed administered, is the key factor.

Prokinetic therapy/enteral feeding failure

• If delayed gastric emptying is present (gastric aspirates > 200 mL after 4 hours), commence prokinetic therapy, e.g. metoclopramide 10 mg IV 8-hourly; erythromycin 250 mg IV 8-hourly is an alternative.

• Prokinetics should be stopped once patients have been absorbing for 24 hours.

• If enteral feeding cannot be established within 12 hours of admission, use a hypertonic glucose IV infusion, either 25 mL/hour of 20% or 10 mL/hour of 50% into a large vein.

• Post-pyloric feeding is used if gastric aspirates remain > 200 mL every 4 hours, or > 48 hours with regular prokinetic administration.

Total parenteral nutrition (TPN)

• To be of benefit, TPN has to given for a minimum of 10–14 days. It should only be used if enteral feeding cannot be successfully established.

• A dedicated central line or lumen should be set aside for TPN. Closely monitor electrolytes, liver biochemistry (for cholestatic jaundice) and line-related sepsis (p. 129).

Maintenance fluids — IV and enteral

Inputs

Patients with normal losses will require 2000–3000 mL per day. Whenever possible, this should be administered enterally. Additional losses are usually replaced intravenously to maintain adequate intravascular volume, patient hydration and normal electrolyte concentrations.

Losses

Losses may take place via normal routes (quantities may be low, normal or high): renal, gastrointestinal, respiratory and intact skin (sweat). Additional losses occur with bleeding, wounds/burns and third space accumulation due to leaky microvasculature and reduced oncotic pressure.

Assessing the adequacy of fluid replacement

• For intravascular volume, see the later section on cardiovascular support (p. 552).

• Plasma/serum biochemistry should be measured at least daily.

• Urine output should be at least 0.5–1 mL/kg/hour, except in oliguric or anuric renal failure.

• Accurate measurement of fluid input and output is very helpful but difficult to achieve.

• Achieving the target balance may require regular low doses or continuous infusion of loop diuretics or renal replacement therapy.

• Serum concentrations of sodium and chloride are monitored. Both tend to accumulate as a result of IV fluids and drugs, e.g. piperacillin. Iatrogenic hyperchloraemic acidosis is a common problem.

• Daily electrolyte requirements for a normal adult are: sodium 1–1.5 mmol/kg/day and potassium 1 mmol/kg/day.

Packed red cell transfusion

• The optimal haemoglobin (Hb) concentration is a balance of rheology and oxygen-carrying capacity. A target value is usually set at 8–10 g/dL, even in patients with critical myocardial or other organ ischaemia.

• A transfusion trigger of 7.5 g/dL is common. Most blood gas analysers are significantly less accurate at Hb measurement than formal haematology laboratories (errors as much as ± 2 g/dL).

• Try to minimize iatrogenic losses, in particular from blood sampling and during line insertion. Be conscious of the effects of iatrogenic haemodilution.

• Transfusion is not a benign intervention. Stored red blood cells become 2,3 diphosphoglycerate (2,3-DPG)-depleted, resulting in higher O₂ avidity, which causes a leftward shift in the oxygen dissociation curve, i.e. a reduction in oxygen release to the tissues. In addition, cells lose their highly deformable biconcave morphology and come to resemble spiky balls, which fail to enter capillaries and can become impacted, obstructing the micro-circulation. There is also the potential risk of disease transmission and allergic reactions.

Glycaemic control

• There is evidence now to suggest that tight glycaemic control (blood glucose levels between 4.0 and 6.0 mmol/L) in all critically ill patients is detrimental; instead, the blood sugar should be controlled < 10 mmol/L or 180 mg/dL. IV insulin infusion should be used with glucose as required.

• Keep a close watch on serum potassium concentration and supplement intake to maintain levels > 4.0 mmol/L.

• Avoid hypoglycaemia; if present, treat aggressively. Continuous feeding regimes, or dextrose infusions, should be used to reduce/avoid this problem.

Thrombo-prophylaxis

• All patients should receive an appropriate prophylactic dose of low molecular weight heparin (LMWH), unless they have a coagulopathy/thrombocytopenia or are receiving therapeutic anticoagulation or heparin/epoprostenol as anticoagulation for renal replacement therapy.

• Patients with severe acute, chronic or acute on chronic renal impairment should have unfractionated heparin 5000 U SC 12-hourly, as LMWHs accumulate in renal failure.

• Once daily LMWH should be prescribed at 18:00 h, so that any necessary surgical procedures (e.g. removal of epidural catheters, tracheostomies, line insertions or removals) are not delayed the following day.

• Appropriately sized TED stockings should be fitted to all patients where possible. Compression boots are also useful.

Analgesia and sedation

Analgesia, with or without sedation, is an essential component of the holistic care of critically ill patients. With the exception of immediate life-saving interventions, patient comfort should be the priority. Ideally, patients should be calm, co-operative, and able to communicate and to sleep when undisturbed.

Guidelines

• The commonest indication for the initiation of analgesia/sedation is endotracheal intubation and ventilation. Some patients may tolerate this without any drugs but most will require analgesia and suppression of airway reflexes.

• Most ICUs employ continuous infusions of opiates and sedatives. The choice of agents depends on a number of factors, including drug pharmacokinetics, cost and personal preference (Tables 14.1a and b).

• Start with a small bolus dose prior to commencing an infusion. If this is insufficient to achieve the desired level of analgesia/sedation, repeat the small bolus prior to each increase in infusion rate. This is to allow steady state drug levels to be achieved more quickly and reduces total cumulative dosage.

• Neuromuscular blockade (Table 14.2) should only be used in patients when sedation/analgesia does not achieve the defined goals: most commonly, failure to achieve adequate ventilation or as part of a cooling protocol. Intermittent bolus dosing is usually preferable to IV infusions. If given by infusion, daily cessation is mandatory. Prolonged use of neuromuscular blocking agents is associated with a higher incidence of critical illness neuromyopathy.

• Sedative drugs do not achieve physiological sleep (as assessed by EEG); sleep deprivation is probably one of the principal causes of ICU delirium.

• Prolonged use of sedation/analgesia drugs is associated with a degree of neurochemical dependence/withdrawal syndromes. Weaning from prolonged use may require staged reduction over a period of days.

• Over-sedation is associated with a higher incidence of ventilator-associated pneumonia, prolonged weaning from mechanical ventilation, colonization with multiply resistant organisms, an increased requirement for neurological investigations, prolonged ICU stay and death.

Table 14.1a Continuous infusion sedative analgesic regimens

Drug	Regime	Notes
Morphine	Loading 5–15 mg Maintenance 1–12 mg/hour	Slow onset. Long-acting. Active metabolites. Accumulates in renal and hepatic impairment
Fentanyl	Loading 25–100 mcg Maintenance 25–250 mcg/hour	Rapid onset. Modest duration of action. No active metabolites. Renally excreted
Alfentanil	Loading 15–50 mcg/kg Maintenance 30–85 mcg/kg/hour (1–6 mg/hour)	Rapid onset. Relatively short-acting. Accumulates in hepatic failure
Remifentanil	Maintenance 6–12 mcg/kg/hour	Rapid onset and offset of action, with minimal if any accumulation of the weakly active metabolite. Significant incidence of problematic bradycardia. Expensive
Clonidine	Maintenance 1–4 mcg/kg/hour	An α₂ agonist. Has marked sedative and atypical analgesic effects
Ketamine	Analgesia Induction 0.2 mg/kg/hour Maintenance 0.5–2.0 mg/kg 1–2 mg/kg/hour	Atypical analgesic with hypnotic effects at higher doses. Sympathomimetic; associated with emergence phenomena when given at hypnotic doses when usually co-administered with a benzodiazepine. Contraindicated in raised intracranial pressure

Table 14.1b Continuous infusion sedative regimens

Drug	Regime	Notes
Propofol 1%	Loading 1.5–2.5 mg/kg Maintenance 0.5–4 mg/kg/hour (0–200 mg/hour)	IV anaesthetic agent. Causes vasodilatation and hence hypotension. Extrahepatic metabolism, thus does not accumulate in hepatic failure. Has no analgesic properties
Midazolam	Loading 30–300 mcg/kg Maintenance 30–200 mcg/kg/hour (0–14 mg/hour)	Short-acting benzodiazepine. Used with morphine. Active metabolites accumulate in all patients, esp in renal failure

Table 14.2 Neuromuscular blocking drugs

Respiratory failure

There are two principal functions of the respiratory system: uptake of oxygenation and elimination of carbon dioxide; respiratory failure can result in hypoxaemia, hypercapnia or both.

• Arterial oxygen tension is principally determined by the fraction of inspired oxygen (FiO₂), ventilation/perfusion matching and the oxygen-carrying capacity of the blood (essentially Hb concentration).

• Arterial carbon dioxide tension is primarily determined by minute volume, i.e. the tidal volume × the respiratory rate.

Respiratory support

Continuous positive airway pressure (CPAP)

This is used for patients with an acute exacerbation of chronic obstructive pulmonary disease (COPD) or those in respiratory failure with a PaO₂ of < 8 kPa (60 mmHg). The patient must be conscious and co-operative. CPAP may delay (or avoid) the necessity for invasive ventilation. CPAP has also been demonstrated to be efficacious in the management of atelectasis, pneumonia and pulmonary oedema.

• A tight-fitting helmet, nasal or full-face mask is used. The patient interface device is the primary determinant of patient tolerability.

• CPAP is a high-flow circuit providing a variable fraction of inspired oxygen (FiO₂) delivered at a set pressure.

• The pressure remains constant during the patient’s respiratory cycle, providing positive end expiratory pressure (PEEP). The advantage of this system is that it recruits and retains the patency of smaller airways and alveoli by splinting them open. This process principally improves oxygenation.

• Failure to achieve a sustained clinical improvement within 1 hour should prompt the clinician to change therapy, usually by intubation and mechanical ventilation.

• Therapy is usually commenced at +5 cmH₂O and escalated to a maximum of +15 cmH₂O.

• Insert a naso-gastric tube if necessary to mitigate against aerophagia and gastric distension, which can result in nausea, vomiting, aspiration and ventilatory failure secondary to diaphragmatic splinting.

• Problems and complications include impediment to patient communication, ocular injury, nasal injury, facial injury (from straps), and secretion drying and retention. The latter may result in proximal airway obstruction.

• Contraindications to CPAP include a Glasgow coma score < 14, an uncooperative patient, recent upper airway or upper gastrointestinal surgery, and severe respiratory acidosis (commonly pH < 7.2).

Non-invasive ventilation

Non-invasive ventilation is used in patients with acute exacerbations of COPD and as a weaning strategy from invasive ventilation. The broad indications are mild to moderate hypercapnia with or without hypoxaemia.

• This technique adds some form of ventilatory assistance to CPAP. Most commonly, this takes the form of patient-triggered inspiratory pressure support (PS). Alternatively, a time-cycled bilevel of CPAP is delivered (BiPAP).

• All of the same precautions and contraindications for CPAP apply.

• There are a wide range of delivery devices available, ranging from small domiciliary units that merely provide a set expiratory and inspiratory pressure (EPAP and IPAP respectively), to full ICU ventilators, which have the ability to deliver a set FiO₂, higher levels of IPAP, continuous monitoring and alarms. At the simplest end of this range, supplemental oxygen can be provided by mask entrainment.

• Therapy is usually commenced with an IPAP of 8–10 cmH₂O and an EPAP of 4–5cmH₂O. These settings are then incremented, based upon efficacy and tolerability.

N.B. Non-invasive ventilation and CPAP provide supportive care; you must determine the cause of the respiratory failure and initiate definitive therapy.

Endotracheal intubation (Box 14.1)

Unless you are experienced in advanced airway skills, call for assistance whilst maintaining airway patency, delivering high-flow oxygen at maximal concentration and providing rescue ventilation as described above. Ensure all necessary equipment is available and functioning.

• Indications. Indications for endotracheal intubation include:

• protection of the airway

• preventing or relieving airway obstruction

• respiratory failure requiring mechanical ventilation.

• Sedation and suppression of the airway reflexes. The choice of drug/s with which to sedate the patient for intubation must be tailored to the individual patient’s needs. Many critically ill patients require minimal, and sometimes no, sedation. Whichever drug/s are used, be very familiar with their pharmacodynamics, pharmacokinetics and side-effects. Be prepared to deal with immediate haemodynamic instability, in particular hypotension, by having fluid resuscitation and vasopressor therapy immediately available. Drugs include propofol, thiopentone, ketamine, fentanyl and alfentanil (see Table 14.1 a and b).

• Muscle relaxants. Onset and duration of action and side-effects are shown in Table 14.2.

Box 14.1 Endotracheal intubation and tracheostomy

Technique

• Pre-oxygenate the patient with 100% oxygen and a tight-fitting face mask. This should take at least 3 mins and is intended to achieve complete nitrogen washout. Ensure that the patient is optimally positioned, and if practical, is placed in the ‘sniffing the morning air’ position

• Ask an assistant to apply cricoid pressure to reduce the risk of aspiration. Be prepared to deal with secretions, passive regurgitation and vomiting

• To visualize the larynx, insert an appropriately sized laryngoscope into the right side of the mouth and sweep the tongue to the left. While advancing the scope blade, be careful not to damage the teeth or lips. By advancing the scope blade along the tongue, the epiglottis should come into view. Gently apply pressure along the axis of the handle until the optimal view of the vocal cords is achieved

• Insert the cuffed endotracheal tube through the cords, noting the distance the cuff is below them. Inflate the cuff and manually ventilate to check endotracheal location and optimal position above the main carina (bilateral chest movement, equal air entry, absence of gastric ventilation and a classic capnograph trace)

• A bougie or airway exchange catheter can be used if the view of the vocal cords is limited. If this is successfully placed, a lubricated endotracheal tube may be placed over the bougie

• The cuff balloon inflation pressure should be checked. High inflation pressures may lead to tracheal injury

• A naso-gastric tube should be passed and a CXR ordered to check endotracheal and naso-gastric tube position

Tracheostomy

• In patients who require prolonged support (> 5–7 days), tracheostomy is often performed. This can invariably be done by utilizing a percutaneous technique on the ICU. The optimal timing and individual patient’s risks and benefits are assessed daily

Mechanical ventilation

The mainstay of respiratory support is intermittent positive pressure ventilation (IPPV).

Modern ICU ventilators are complex devices, which provide continuous monitoring. Alarms must be checked regularly for appropriate settings.

The value of regular review, including respiratory examination, cannot be overstated. Minimizing ventilator-induced lung injury (VILI), rather than trying to normalize gas exchange, should be the main priority.

Regional lung ventilation and perfusion are not homogenous and this heterogeneity increases in disease. Positive pressure ventilation can cause lung injury via over-distension (volutrauma), excessive pressure (barotrauma), and cyclical recruitment and derecruitment.

• Patient position. Sit the patient up as far as possible to maximize functional residual capacity; turn the bad side down to ventilate it or the good side down to maximize oxygenation in severe hypoxaemia. In resistant hypoxaemia, the patient can be ventilated in the prone position.

• Types of ventilation. IPPV can be set up as either volume-controlled (pressure-monitored) or pressure-controlled (volume-monitored) (Table 14.3). This somewhat arbitrary distinction has become blurred with the advent of complex software in modern ventilators and the development of such concepts as volume-targeted pressure control, pressure-limited volume control, volume support, proportional assist and assisted spontaneous ventilation. In essence it does not matter which mode of ventilation you select as long as you understand what you need to set and what you need to monitor.

• Goals of supportive care. The goal is a spontaneously breathing, conscious patient who is able to cough and protect his/her airway with a PaO₂ > 8 κPa (> 60 mmHg) and a PCO₂ < 6 κPa (< 45 mmHg).

Table 14.3 Mechanical ventilation guidance

• To treat hypoxaemia

• Increase the FiO₂.

• Increase the CPAP/PEEP.

• Increasing the I:E ratio.

• Perform a recruitment manœuvre.

• Change the patient’s position.

• To fix hypercapnia

• Do not proceed if the pH is normal or within acceptable limits (permissive hypercapnia).

• Increase tidal volume and/or respiratory rate — watch the effect on peak pressures and on inspiratory and expiratory flows. Remember that the volume of dead space ventilation is fixed; hence increasing the rate at the expense of tidal volume will result in a reduction in alveolar minute ventilation and a rise in PaCO₂.

• Unconventional ventilation

• Time-cycled, bilevel pressure ventilation provides two levels of CPAP sequentially. It can be useful in patients who exhibit ventilator dyssynchrony or as a weaning mode.

• Airway pressure release ventilation (APRV) provides CPAP, often at a high level, with periodic, very short reductions in distending pressure to facilitate the washout of dead-space gas. It can be useful as a form of recruitment manœuvre, as a method of minimising VILI or as a weaning mode. It is most effective when there is some spontaneous breathing effort and especially if the tidal volumes are small.

• High-frequency oscillatory ventilation (HFOV) requires a specialist ventilator. CPAP is provided with the addition of a piston-driven diaphragm in the circuit, which oscillates at frequencies of 3–6 Hz. This results in the generation of multiple forms of gas diffusion and effective ventilation. HFOV is currently used as a second-line therapy in severe lung injury, although its optimal use remains controversial.

Complications associated with mechanical ventilation

• Airway complications. There may be complications with tracheal intubation or with additional local complications of a tracheostomy (see above).

• Disconnection, failure of gas or power supply, mechanical faults. These are unusual but dangerous. A method of manual ventilation, such as a self-inflating bag, and oxygen must always be available by the bedside.

• Cardiovascular complications. The application of positive pressure to the lungs and thoracic wall impedes venous return and distends alveoli, thereby ‘stretching’ the pulmonary capillaries and causing a rise in pulmonary vascular resistance. Both these mechanisms can produce a fall in cardiac output.

• Respiratory complications

• Ventilator-induced lung injury (VILI) and barotrauma. Mechanical ventilation can be complicated by a deterioration in gas exchange because of

mismatch and collapse of peripheral alveoli. Traditionally, the latter was prevented by using high tidal volumes (10–12 mL/kg), but high inflation pressures, with over-distension of compliant alveoli, perhaps exacerbated by the repeated opening and closure of distal airways, can disrupt the alveolar–capillary membrane. There is an increase in microvascular permeability and release of inflammatory mediators, leading to VILI. Extreme over-distension of the lungs during mechanical ventilation with high tidal volumes and PEEP can rupture alveoli and cause air to dissect centrally along the perivascular sheaths. This ‘barotrauma’ may be complicated by pneumomediastinum, subcutaneous emphysema, pneumoperitoneum, pneumothorax and intra-abdominal air. The risk of pneumothorax is increased in those with destructive lung disease (e.g. necrotizing pneumonia, emphysema), asthma or fractured ribs.

• Tension pneumothorax. A tension pneumothorax can be rapidly fatal in ventilated patients. Suggestive signs include the development or worsening of hypoxia, hypercarbia, respiratory distress and an unexplained increase in airway pressure, as well as hypotension and tachycardia, sometimes accompanied by a rising CVP. Examination may reveal unequal chest expansion, mediastinal shift away from the side of the pneumothorax (deviated trachea, displaced apex beat) and a hyper-resonant hemithorax. Although, traditionally, breath sounds are diminished over the pneumothorax, this sign can be extremely misleading in ventilated patients. If there is time, the diagnosis can be confirmed by CXR prior to definitive treatment with chest tube draining.

• Ventilator-associated pneumonia. Hospital-acquired pneumonia occurs in as many as one-third of patients receiving mechanical ventilation and may be associated with a significant increase in mortality. It can be difficult to diagnose. Multiple organisms have been isolated, such as aerobic Gram-negative bacilli, e.g. Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, Acinetobacter spp and Staphylococcus. Leakage of infected oro-pharyngeal secretions past the tracheal cuff is thought to be largely responsible. Bacterial colonization of the oropharynx may be promoted by regurgitation of colonized gastric fluid and the risk of pneumonia can be reduced by nursing patients in the semi-recumbent, rather than the supine, position and by oro-pharyngeal decontamination. Treatment is complicated by multiple drug resistance to many antibiotics and mortality is high.

• Gastrointestinal complications. Initially, many ventilated patients will develop abdominal distension associated with an ileus. The cause is unknown, although the use of opiates may in part be responsible.

• Salt and water retention. Mechanical ventilation, particularly with PEEP, causes increased ADH secretion and possibly a reduction in circulating levels of atrial natriuretic peptide. Combined with a fall in cardiac output and a reduction in renal blood flow, these can cause salt and water retention.

Weaning from IPPV

The weaning process starts the moment IPPV is initiated.

• Allow the patient to make spontaneous breathing efforts (albeit assisted) at the earliest possible stage of respiratory support.

• As oxygenation improves, wean FiO₂ and PEEP sequentially.

• As hypercapnia improves, wean from mandatory ventilation (MV)/synchronized intermittent mandatory ventilation (SIMV) to PS. Then gradually reduce PS.

• Once established on PS, consider a daily trial of support withdrawal. This needs to be coordinated with daily sedation holds. Three methods are widely used:

• CPAP +5 cmH₂O

• PS +5–7 5 cmH₂O with 0 PEEP

• just a T-piece.

The usual duration is a maximum of 15 mins; if successful, it should prompt extubation.

• In tracheostomized patients, ‘training periods’ of reduced or absent support can be employed as part of a daily weaning routine. The routine should be reviewed at least daily and titrated according to progress. Complete rest overnight and establishing a day/night cycle are essential.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)

ALI and ARDS are syndromes and represent a spectrum of disease. The syndrome is defined as a specific form of lung injury with diverse causes, characterized pathologically by diffuse alveolar damage and pathophysiologically by a breakdown in both the barrier and gas exchange functions of the lung, resulting in proteinaceous alveolar oedema and hypoxaemia.

Diagnostic criteria

• Hypoxaemia (usually refractory to supplemental oxygen).

• Bilateral, diffuse, interstitial and alveolar infiltrates on CXR (and/or CT).

• Reduced respiratory compliance (optional).

• No evidence for cardiac factors as the principle cause of the pulmonary oedema (pulmonary artery occlusion pressure (PAOP) ≤ 18 mmHg).

• Pulmonary hypertension (common).

• ALI — PaO₂/FiO₂ < 40 kPa; ARDS — PaO₂/FiO₂ < 26 kPa.

Outcome

Mortality is 35–60%, possibly falling due to improved general care. ARDS/ALI is still the commonest cause of death in multiple organ failure. It is the failure to improve over the first 7 days and not the initial severity that indicates prognosis. In survivors the long-term lung function returns to pre-morbid levels. However, the long-term quality of life and morbidity are worse than severity-matched critically ill patients without ARDS.

Pathophysiology

Changes include alveolar flooding with proteinaceous fluid (exacerbated by reduced clearance); decreased surfactant production, resulting in atelectasis and decreased compliance; and hyaline membrane formation and interstitial oedema, leading to impaired gaseous diffusion. There is increased intrapulmonary shunt and loss of mechanical defence barrier; hence the high risk of sepsis.

Management

• Early and aggressive treatment of the underlying condition.

• Optimal cardiovascular support with fluid restriction, diuretics and, if necessary, haemofiltration in order to achieve a consistently negative fluid balance.

• Early enteral nutrition.

• Minimal sedation and neuromuscular blockade is usually recommended although a recent trial has shown benefit of neuromuscular blockade given for 48 hours early in the disease.

• Adherence to the ventilator care bundle.

• Ventilatory strategy: ‘open the lung and keep it open’ and minimize VILI.

• Low tidal volumes 6–8 mL/kg ideal body weight

• ‘Adequate’ (high) PEEP

• Minimal peak/plateau pressures (≤ 30 cmH₂O)

• Minimal FiO₂

• Maintenance of spontaneous breathing.

• Unproven ventilatory rescue therapies: unconventional ventilation, in particular HFOV; extracorporeal lung assist.

• Adjunctive therapies with no evidence of benefit: inhaled nitric oxide, nebulized prostacyclin, almitrine and recombinant surfactant.

• Adjunctive therapies under active investigation: sildenafil and salbutamol.

• Controversies: whether an open lung biopsy should be performed and the role of high-dose corticosteroids.

Cardiovascular failure

The principal roles of the cardiovascular system are to deliver oxygen and glucose to the tissues and to remove carbon dioxide and other waste products. Failure to do this is termed ‘shock’.

• Clinical manifestations of cardiovascular insufficiency/shock include:

• low-volume peripheral pulses

• cold peripheries, especially with proximal extension/peripheral capillary refill > 2 s (except in distributive shock states, where peripheries may be warm with capillary refill time < 2 s)

• tachycardia and hypotension (not invariable and the least reliable signs)

• altered mental function, confusion or diminished level of consciousness (cerebral hypoperfusion)

• urine output < 0.5 mL/kg/hour (renal hypoperfusion).

• Cardiovascular support is achieved by assessing and optimizing four key components of the cardiovascular system in strict order (Table 14.4). More than one component failure may exist. Inotropic and/or vasopressor support should only be instituted after volume resuscitation. Exceptions to this suggestion include severe or drug-induced hypotension.

• At an organ level, shock may result in micro-circulatory failure. This complex phenomenon arises from, among other processes, endothelial cell damage, formation of capillary occlusive micro-thrombi and neutrophil margination. This results in arterio-venous shunting and tissue ischaemia. This phenomenon is hard to monitor in almost all organs and no specific therapy exists to treat it.

• Measures of global oxygen delivery (DO₂) and consumption (VO₂) are useful in assessing the adequacy of resuscitation and include the direct measurements of DO₂ and VO₂, central or mixed venous oxygen saturations (ScvO₂ and SvO₂ respectively) and blood pH, lactate levels and calculated base excess.

Table 14.4 The four key assessable and treatable components of shock

Terminology and normal values

Note that these are normal value ranges for healthy human adults at rest. There are no normal ranges for shocked patients. Therapeutic targets are best considered by assessing the dynamic response to an intervention and using all available measures of both organ-specific and global hypoperfusion.

• Stroke volume = 70–100 mL.

• Cardiac output = Stroke volume × heart rate (normal range at rest 4–6 L/min).

• Oxygen delivery (DO₂) is the total amount of oxygen delivered to the tissues per minute.

• DO₂ = Cardiac output × arterial oxygen content.

• DO₂ = CO × ((SaO₂ × [Hb] × 1.34) + (PaO₂ × 0.003)).

• DO₂ = 950–1300 mL/min.

• Oxygen consumption (VO₂) is the amount of oxygen consumed by the tissues per minute.

• VO₂ = Cardiac output × (arterial oxygen content) − (mixed venous oxygen content − SvO₂).

• VO₂ = 180–320 mL/min.

• Mixed venous saturation (SvO₂) is a guide to the difference between oxygen being delivered to the tissues and its extraction or use. This is measured by taking a sample of blood from the distal port of a pulmonary artery catheter (PAC) and measuring the saturation using a blood gas analyser. If a PAC is not available, samples from a central venous catheter in the superior vena cava will provide an approximate guide. This variable is called central venous oxygen saturation (ScvO₂). The normal value is 70–75%. This measurement has been successfully used to guide resuscitation, resulting in improved morbidity and mortality.

Methods of continuous haemodynamic monitoring

The insertion of peripheral arterial and central venous lines is the first step in the monitoring of critically ill patients.

Invasive arterial and venous pressure monitoring

• Arterial cannulation. Insert arterial cannulation. This allows real-time BP measurement and beat-to-beat display of the arterial waveform, and facilitates regular arterial blood sampling.

• A modified Seldinger technique or direct cannulation can be used.

• Favoured sites are the radial and femoral arteries.

• The complication of distal ischaemia is rare. Infection is always a risk with invasive lines. Suspicion of colonization should prompt early line cultures and removal/change of lines if possible.

• CVP line. Insert a CVP line (Fig. 14.1), guided by US. The CVP line provides information on right heart filling pressures; allows estimation of mixed venous saturations; and acts as a vascular access.

• Central venous pressures should correlate well with left ventricular filling pressures; however, this is not always so in the critically ill. Ischaemic cardiomyopathy, valvular pathology, pulmonary hypertension and pulmonary embolism are potential causes of disparity.

• The Seldinger technique is routine for multi-lumen catheters. Strict aseptic technique should be employed. Skin preparation with 2% chlorhexidine in 70% alcohol is recommended. Exit sites should be dressed so as to prevent contamination. Prior to any use, any access port should be cleaned with chlorhexidine. Lines should be removed at the earliest opportunity.

• Favoured sites are the internal jugular and subclavian. The latter has a lower risk of line-related bacteraemia but is associated with a high risk of complications at insertion and chronic stenosis and thrombosis. The femoral site should be avoided in the first instance.

Fig. 14.1 Cannulation of the right internal jugular vein.

Pulmonary artery catheterization and thermodilution

This is still the gold standard technique for measurement of haemodynamic status (see below).

• An introducer sheath is first placed into a central vein using the Seldinger technique. The flotation pulmonary artery catheter (PAC) is then inserted via the sheath into the cannulated vein. The PAC has a balloon on its tip. This is inflated in the cannulated vessel and the PAC is advanced slowly, its direction and location guided by the direction of blood flow. The pressure, measured at the tip of the PAC, is continuously transduced and should successively show the pressures within the right atrium, the right ventricle and the pulmonary artery. The PAC is further advanced until the balloon occludes a branch of the pulmonary artery, which is noted by a sudden change in pressure waveform. The pressure now transduced, known as the pulmonary artery wedge (or occlusion) pressure (PAWP or PAOP), should represent left atrial pressure. The balloon should be deflated and only re-inflated periodically to measure PAOP. A CXR should be obtained to ensure optimal position of the PAC tip. Optimal position is within West’s zone III (where the PAC tip communicates continuously with the distal vascular pressures during diastole) and < 5 cm from the hilum.

• The PAC can also provide an estimate of cardiac output using cold or warm thermodilution techniques. Injection of a 10 mL bolus of cold (~4°C) 5% glucose into the right atrium results in a transient decrease in blood temperature in the pulmonary artery. A thermistor at the catheter tip detects this change in temperature. The mean decrease in temperature is inversely proportional to the cardiac output, which can be derived using the modified Stewart–Hamilton equation. Warm thermodilution is a similar technique, with a downstream thermistor detecting heat pulses sent in binary code from a thermal filament placed in the right ventricle. The latter method is automated and semi-continuous. Thermodilution has its limitations. There are inaccuracies in both high and low cardiac output ranges, often as a result of operator error or errors from injectate temperature calibration. This is especially true when a patient is hypothermic or has significant tricuspid regurgitation or dysrhythmias.

• SvO₂ can be measured intermittently by blood sampling from the pulmonary artery or continuously using a specialist catheter.

• Complications of PACs, over and above central venous cannulation, include pulmonary infarction, pulmonary artery rupture and sustained arrhythmias.

• Due to the invasive nature of the PAC, a lack of evidence to demonstrate the benefit of therapy guided by the data that it can provide, and the development of less invasive alternative techniques of monitoring cardiac output, use of the PAC has declined dramatically over recent years. There is, however, overwhelming evidence that use of the PAC is safe.

Oesophageal Doppler

• This technique relies on the phenomenon that sound undergoes a frequency shift with respect to a fixed receiver when the source is moving at a different speed to the receiver. The degree of frequency shift is directly proportional to the speed of the sound source (the Doppler effect).

• A probe inserted 30–40 cm down the oesophagus and a US beam is focused on the blood flow in the descending aorta. In this area the aorta lies parallel to the oesophagus and has a predictable cross-sectional area. The frequency of reflected sound waves undergoes Doppler shift dependent on the speed of blood flow. By quantifying this shift and incorporating the estimated cross-sectional area and ejection time (stroke distance), the stroke volume can be calculated. The aortic stroke volume is a percentage of the actual cardiac output, which can be derived from patient nomograms based on height and weight.

• The advantages of this system include relative ease of use, minimal invasiveness and the fact that this is the only method of haemodynamic monitoring to provide real-time data based on the actual (and not derived) cardiac output.

• Conditions prohibiting use include severe aortic pathology, an intra-aortic balloon pump (IABP) and oesophageal disease.

Pulse contour analysis

The pressure wave displayed by an invasive arterial line is amenable to pulse contour analysis. The pressure waveform is converted to a volume–time waveform. The area under the curve gives a derived estimate of beat-to-beat stroke volume. Combination with the heart rate is used to calculate cardiac output. For accuracy, several of the systems calibrate the estimates of cardiac output using trans-pulmonary dilution methods.

Cardiovascular supportive therapies

Rate and rhythm control

• The target pulse rate is 90/min.

• If the patient is haemodynamically unstable, treat as per the Advanced Life Support algorithm. DC cardioversion is relatively straightforward in intubated patients and can be performed early.

• If the patient is haemodynamically stable, correct electrolytes and perform a dynamic fluid challenge prior to drug treatment and/or DC cardioversion.

• The commonest arrhythmia in critically ill patients is atrial fibrillation (AF). In the majority of cases there is an identifiable iatrogenic precipitant (e.g. furosemide, insulin, salbutamol, inotropes). Aim to keep serum Mg²⁺ > 0.9 mmol/L and K⁺ > 4.4 mmol/L to prevent arrhythmias.

• If the onset of AF is known to have been within 12–24 hrs, DC cardioversion is used. If the AF has been paroxysmal, has been present for > 24 hours or fails DC cardioversion, digoxin (may control rate), esmolol, metoprolol, sotalol or amiodarone is used. Verapamil and flecainide should be avoided, as they are both profoundly negatively inotropic.

IV fluid resuscitation, the dynamic fluid challenge or pre-load optimization

• These techniques are used to describe the assessment of fluid responsiveness rather than assessment of the adequacy of intravascular volume. They are performed by administering a rapid 100–500 mL bolus of IV fluid and measuring the instantaneous response in heart rate and stroke volume (and hence cardiac output), CVP and MAP. Of all of these variables, stroke volume is most useful measure.

• There is no proven benefit in using any particular crystalloid or colloid.

• With regard to CVP, three patterns of response (see Fig. 11.1) are looked for, in patients with a starting CVP in the normal range of 4–8 cmH₂O (caution in interpretation is required in patients receiving positive pressure ventilation).

• A rapid fluid bolus should not be given via an automated volumetric pump, which is too slow to assess volume responsiveness properly. (N.B. Do it yourself)

• In patients receiving positive pressure ventilation, who demonstrate no inspiratory effort and are in sinus rhythm, a maximum variation in systolic or pulse pressure of > 15% over each respiratory cycle is a validated method of predicting volume responsiveness.

• There is evidence to support the idea that early and aggressive fluid resuscitation is beneficial. In the short term, fluid administration is simple, quick and often effective; iatrogenic fluid overload is rare. In responsive patients, fluid therapy increases global oxygen delivery for the smallest increase in myocardial work.

Inotropes, vasopressors and other vasoactive drugs

• If rate and rhythm are acceptable and/or resistant to fluid and electrolyte resuscitation, estimation and continuous monitoring of cardiac output are highly desirable to guide pharmacological therapy.

• If there is a low or inadequate cardiac output and/or perfusion pressure (MAP), then vasoactive drugs should be commenced (Tables 14.5 and 14.6).

• Dobutamine is probably the inotrope of first choice. It is a strongly positive chronotrope and an arterial vasodilator. Alternatives include the inodilators, milrinone and levosimendan (available in some countries). Inodilators exert positive inotropic effects and induce systemic vasodilatation. Due to the vasodilatation that these drugs cause, combination with a vasopressor is often required. All are pro-arrhythmogenic.

• Dopamine and adrenaline (epinephrine), both inoconstrictors, are not so frequently used.

• In ischaemic cardiogenic shock, inotropic drugs should be used to provide a temporal bridge to definitive revascularization and/or mechanical support, most commonly an IABP.

• Noradrenaline (norepinephrine) is the first-choice vasoconstrictor with a weakly positive chronotropic and inotropic activity. Vasopressin analogues and methylene blue are also used. Excessive doses of vasopressors can lead to increased over-centralization of the circulation, left ventricular failure, and splanchnic and distal extremity ischaemia/infarction.

• In immediate resuscitation, ephedrine, phenylephrine, metaraminol and 1 : 100 000 adrenaline (epinephrine) can be given in small bolus doses to maintain BP.

• In the immediate management of decompensated left ventricular failure, IV nitrates are a useful first-line agent in offloading the left side of the heart. This is predominantly via venodilatation. Second-line agents in hypertensive cardiovascular crises include hydralazine and labetalol.

Table 14.5 Cardiovascular effects of vasoactive drugs and devices

Table 14.6 Dosage regimens of commonly used vasoactive drugs

Drug	Dosage range	Notes
Dopamine	1–20 mcg/kg/min	Dominant effect dependent on dose. Some evidence of worse outcome compared to other drugs, therefore out of favour
Dobutamine	5–20 mcg/kg/min	Inodilator (positive inotropic and causes systemic vasodilatation)
Dopexamine	0.25–2.0 mcg/kg/min	Positive chronotrope/inodilator/anti-inflammatory?
Adrenaline (epinephrine)	0.01–1 mcg/kg/min	Inoconstrictor (positive inotropic causing systemic vasoconstriction)
Noradrenaline (norepinephrine)	0.01–1 mcg/kg/min	Vasoconstrictor (some inotropic activity), first-line vasopressor
Milrinone (phosphodiesterase inhibitor)	150–750 ng/kg/min	Inodilator. Significantly longer onset and elimination half-life than dobutamine. Accumulates in renal failure. Do not give loading dose
Levosimendan (Ca sensitizer and K channel opener)	0.05–0.2 mcg/kg/min	Inodilator. Active metabolite with long elimination half-life, hence 24-hour infusion will have measurable effects for up to 7 days. Do not give loading dose
Vasopressin	0.01–0.05 U/min	Vasoconstrictor. Second-line vasopressor in noradrenaline-resistant shock (see also functional hypoadrenalism)
Terlipressin (vasopressin analogue)	0.25–2 mg bolus	Vasoconstrictor. Duration of action 4–6 hours. Alternative to vasopressin
Methylene blue (nitric oxide antagonist)	2 mg/kg loading 0.25–2 mg/kg/hour	Vasoconstrictor. 2^nd/3^rd line vasopressor in norepinephrine resistant shock (see also functional hypoadrenalism)

‘Low-dose’ corticosteroids and functional hypoadrenalism in shock

There is some evidence to suggest that a proportion of patients with distributive shock have functional hypoadrenalism. This is manifested as vasopressor resistance, with patients requiring rapidly escalating or high-dose infusions. Whether such patients have functional hypoadrenalism and/or peripheral resistance is unclear. ‘Physiological replacement’ dose hydrocortisone 200–240 mg/24 hrs, with or without fludrocortisone, has been demonstrated to be beneficial in some patients, both in terms of attenuating vasopressor requirements and outcomes.

In order to determine whether or not a patient is likely to benefit from such therapy, a short adrenocorticotrophic hormone (ACTH) stimulation test can be performed. A low baseline cortisol level, coupled with an attenuated or negligible response to ACTH, predicts patients who benefit from ‘low-dose’ corticosteroids. Outside of this profile, interpretation of the test remains an area of controversy.

Post-operative care of patients with a high risk of morbidity and mortality

The more extensive the surgery and the more physiologically deranged the patient, be it acute, acute on chronic or merely chronic, the higher the risk. Many such patients are often referred to critical care environments for their immediate post-operative care.

Survivors have a different physiological profile to non-survivors. The median value of DO₂I (I = index) in survivors was 600 mL/min/m². Maximizing a high-risk patient’s DO₂I in the immediate post-operative period (8 hours) using the therapies described above, in particular intravascular fluid responsiveness, with the addition of low-dose inodilators where necessary, in an attempt to reach 600 mL/min/m² has been demonstrated to be a successful strategy in reducing morbidity and mortality.

Systemic Inflammatory Response Syndrome (SIRS), Sepsis, Severe Sepsis and Septic Shock

Definitions

SIRS is triggered by localized or generalized infection, trauma, thermal injury or sterile inflammatory processes, e.g. acute pancreatitis. It is considered to be present when patients have more than one of the following clinical findings:

• body temperature > 38°C or < 36°C

• heart rate > 90/bpm

• hyperventilation evidenced by respiratory rate > 20/min or PaCO₂ < 4.2 kPa

• white blood cell count > 12 × 10⁹/L or < 4 × 10⁹/L.

Sepsis is defined as SIRS with a documented or suspected infection. Severe sepsis is sepsis with evidence of organ dysfunction (as defined by SOFA or equivalent, p. 31). Septic shock is defined as severe sepsis with hypotension despite adequate fluid resuscitation. Severe sepsis and septic shock are the commonest conditions requiring critical care. Their incidence is high and increasing. They are associated with a very high morbidity and an overall mortality of 30–60%.

The Surviving Sepsis campaign’s recommendations (2004) may be found at www.survivingsepsis.org.

Management goals within the first 24 hours (see Emergencies in Medicine, p. 718)

• Administer low-dose steroids for septic shock in accordance with a standardized ICU policy.

• Administer drotrecogin alfa (recombinant human activated protein C) in accordance with a standardized ICU policy (see below).

• Maintain blood glucose at < 10 mmol/L (< 180 mg/dL).

• In mechanically ventilated patients, maintain the inspiratory plateau pressure at < 30 cmH₂O.

• Activated protein C or drotrecogin alfa. In severe sepsis/septic shock there is activation of the coagulation cascade, including the fibrinolytic pathway. This leads to a depletion of activated protein C; lower levels are associated with a worse outcome.

• Recombinant human activated protein C (rhAPC), drotrecogin alfa, is used in patients with severe sepsis and septic shock. Controversy continues over its use, as some trials and observational studies have raised doubts regarding both the safety and the efficacy of rhAPC.

• Current indications for its use are patients at high risk of death (APACHE II ≥ 25) from sepsis-induced multiple organ failure (two or more organs). It must be administered within 24 hours of the onset of organ dysfunction.

• It is contraindicated in patients with active internal bleeding, intracranial pathology, concurrent heparin use or significant thrombocytopenia (platelet count ≤ 30 × 10⁹/L).

Brain injury

Regardless of the nature of the brain injury, certain universal principles of care apply; minimize secondary brain injury and optimize any chance of penumbral recovery.

• Take an ABC approach to resuscitation.

• Aim for normoxia, normocarbia, normotension, normothermia, normoglycaemia and normonatraemia. In particular, hypercarbia, hyperthermia and both hypo- and hyperglycaemia are associated with secondary brain injury. There is no therapeutic benefit in hypocarbia. Mild hypothermia may be of benefit.

• Position the patient 30° head up. This is the best compromise between the increased gravitational gradient placed on the arterial pressure and enhanced gravitational gradient for venous drainage. Try to avoid any intervention that may reduce or obstruct cerebral venous return, e.g. internal jugular lines, or high intrathoracic pressures (high mean airway pressures) created by mechanical ventilation.

• As regards blood pressure, the concept of cerebral perfusion pressure (CPP) (mean systemic pressure — intracranial pressure (ICP)) is helpful. A minimum target CPP of 70 mmHg is optimal. A lower CPP is associated with a higher incidence and extent of secondary brain injury. If possible, measure and continuously monitor ICP.

• Medical management of raised ICP includes:

• aggressive normalization of PaCO₂ and core temperature

• patient positioning (see above)

• high-dose propofol or thiopentone infusion (barbiturate coma) to reduce cerebral metabolic demand

• aggressive management of seizures

• hypertonic saline and/or mannitol.

• Surgical management of raised ICP includes:

• CSF drainage (placement of an extraventricular drain)

• decompressive craniectomy.

Brainstem death

This is an emotive area that is often difficult to communicate and for family and staff at the bedside to understand.

The term may have different definitions in different countries. In the UK this term refers to ‘the irreversible loss of the capacity for consciousness combined with the irreversible loss of the capacity to breathe’. This may be anatomically defined as brainstem death. In some states in the USA brain death also encompasses cardiopulmonary death as part of the definition.

The process of diagnosing brain death is divided into three parts: pre-conditions, exclusions and tests.

Pre-conditions

• The patient must be in an apnoeic coma and on a ventilator, unable to make spontaneous breathing effort.

• The presence is required of irremediable structural brain damage contributing to brainstem death, e.g. traumatic head injuries or haemorrhage.

Exclusions

• Hypothermia: core temperature must be > 35°C.

• Metabolic or endocrine derangement must be excluded (e.g. hypoglycaemia).

• Poisoning and use of neuromuscular drugs and sedatives must be excluded and taken into account.

Brainstem death tests

These should be performed and repeated by two separate senior doctors (ideally one should be a consultant or equivalent). This may be done on separate occasions or together. The two doctors should not be part of a transplantation team and should be competent in the area. The time of death is when the first set of tests confirms the presence of brainstem death.

• Oculo-cephalic reflex. This should be absent. It is tested by rolling the head from side to side. In a functioning brainstem the eyes will move relative to the orbit (doll’s eyes present). In brainstem death the eyes move with the head in the direction of travel of the movement (doll’s eyes absent).

• Pupillary reflex. Pupils are fixed and unresponsive to light stimulus. Direct and consensual light reflexes are absent. Pupils may or may not be dilated.

• Corneal reflex. Cotton wool may be used to elicit a response to corneal stimulation by light touch. This response will be absent in brainstem death.

• Vestibulo-ocular reflexes. Caloric testing is used to assess function of the labyrinth; it is essential that the tympanic membrane is visualized prior to the test. Fifty mL of ice-cold water is injected into the left ear over 1 min. Intact brainstem response will elicit nystagmus with fast movements to the right (away from the injected ear). The opposite response will take place in the intact brainstem of an individual if water is injected into the right ear. In patients with brainstem death no response to ice-cold water injection is seen.

• Gag and cough reflex. Pharyngeal, laryngeal (throat spatula) and tracheal (suction catheter down the endotracheal tube to the carina) stimulation would normally elicit a cough/gag response. This is absent in brainstem death.

• Motor reflex. Centrally or peripherally applied painful stimulus would normally elicit a motor response in the cranial nerve territory. In brainstem death this is absent.

• Apnoea testing. Intact brainstems will initiate spontaneous respiratory effort in the presence of hypercarbia. The patient is placed on 100% oxygen on the ventilator and pre-oxygenated for 10 mins. The minute volume should be reduced to achieve a PaCO₂ > 5 kPa before the test. The patient is then disconnected from the ventilator and oxygen is attached to the endotracheal tube at 6 L/min (to maintain oxygenation in the presence of hypercarbia). The PaCO₂ must rise to > 6.65 kPa. The chest is visualized and inspected for movements. In brainstem death no movements are present and the patient is then re-connected to the ventilator.

Organ and tissue donation

Individual countries have their own processes. In the UK, organ and tissue donation are governed by the Human Tissue Act 2004 (see http://body.orpheusweb.co.uk/HTA2004/20040030.htm). Always consider donation in dying patients, especially in those with brainstem death and, in particular, if the brain injury is the sole organ failure. In the UK, to discuss any aspect of donation, contact your local transplant coordinator.

acute kidney injury

Acute kidney injury (p. 348) is a common complication of critical illness. Kidney injury is associated with increased morbidity and mortality regardless of the primary pathology, with a direct correlation between the severity of renal injury and poor outcome.

• Clinically, oliguria is the first presenting sign. This may lead promptly to anuric renal failure.

• Prevention, by maintaining intravascular volume and adequate renal perfusion pressure, together with the avoidance of nephrotoxic drugs, e.g. NSAIDs, in the at-risk population is well established.

• X-ray intravascular contrast is another potent precipitant of acute kidney injury (p. 351).