Patients scheduled for elective surgery are usually in optimal physical and mental condition, with a definitive surgical diagnosis; any coexisting medical disease is defined and well controlled. In contrast, the patient with a surgical emergency may have an uncertain diagnosis and uncontrolled coexisting medical disease, in addition to any physiological derangements resulting from their surgical pathology. Thus, a major principle governing the practice of emergency anaesthesia is to identify and, if time permits, correct any major physiological abnormalities preoperatively. In addition, the anaesthetist must be prepared for potential complications arising as a consequence of anaesthetizing a patient in sub-optimal condition. These include vomiting and regurgitation, hypovolaemia and haemorrhage, and abnormal reactions to drugs in the presence of electrolyte disturbances and renal impairment.
The objective of emergency anaesthesia is to permit correction of the surgical pathology with the minimum risk to the patient. This requires adequate and accurate preoperative evaluation of the patient’s general condition, with particular attention to specific problems that may influence anaesthetic management.
The likely surgical diagnosis, and the extent and urgency of the proposed surgery must be discussed with surgical and medical colleagues preoperatively. The urgency for surgery is most helpfully conveyed using a recognized classification system, such as the one created by the National Confidential Enquiry into Patient Outcome and Death (NCEPOD) (Table 37.1). The nature and urgency of the planned surgery dictate the extent of preoperative preparation and anaesthetic technique. They also influence plans for postoperative care, which may include transfer to a HDU/ICU facility.
During the preoperative visit a past medical and drug history is elicited. In particular, the patient’s degree of cardiorespiratory reserve should be established, even if there is no formal diagnosis of cardiovascular or respiratory disease. The presence and severity of symptoms suggestive of reduced reserve such as angina, productive cough, orthopnoea or paroxysmal nocturnal dyspnoea should be sought. The patient’s functional capacity is of useful prognostic value and can be simply quantified in terms of metabolic equivalents (METs). 1 MET is a unit of resting oxygen consumption and appropriate questioning can allow an estimate of the patient’s maximal oxygen consumption capacity (VO2 max) (Table 37.2 and Ch 18 [Table 18.1]). A patient who is unable to perform activity at 4 METs or more is at increased risk of perioperative cardiac complications.
|MET Score||Approximate Level of Activity|
|1||Dress, walk indoors|
|2||Light housework, slow walk|
|4||Climb one flight of stairs|
|6||Moderate sport eg golf or dancing|
|10||Strenuous sport or exercise|
Depending upon the urgency of surgery, the physical examination may be targeted to identify significant cardiorespiratory dysfunction or any abnormalities that might lead to technical difficulties during anaesthesia. Basal crepitations, pitting oedema and raised jugular venous pulse signify impaired ventricular function and limited cardiac reserve, which significantly increase the risk of anaesthesia. It is also important to exclude arrhythmias and heart sounds indicative of valvular heart disease, as these influence the patient’s response to physiological challenges and thus anaesthetic management. Assessment of respiratory function is particularly difficult, as the patient in pain (with or without peritoneal irritation) may be unable to cooperate with pulmonary function testing.
Valuable information about the patient’s condition can also be obtained from the bedside observations chart. In particular, trends in physiological variables such as arterial pressure, heart rate and respiratory rate may signal a deteriorating condition, and even impending decompensation.
Preoperative evaluation of the airway is always important. The standard clinical tests of airway assessment should be used (see Ch 21: The practical conduct of anaesthesia) and any previous anaesthetic charts consulted if available. A history of difficult intubation is of considerable significance; however, a past record of easy tracheal intubation does not guarantee future success. In emergency anaesthesia, airway difficulties may be caused by the patient’s usual anatomy, but also surgical pathology such as dental abscesses, trauma and bleeding or haematoma. If a rapid-sequence induction is contemplated, then contingency plans are required for management of the patient in the event of failure to intubate the trachea. If a high degree of difficulty in tracheal intubation is anticipated then an awake technique may be necessary.
The final stage of the preoperative assessment is to review any laboratory investigations, including ECGs, radiological imaging and arterial blood gases where appropriate. The availability of blood products should be checked if necessary and urgent requests should be made for any additional tests which may influence patient management.
Assessment of intravascular volume is essential, as underestimated or unrecognized hypovolaemia may lead to circulatory collapse during induction of anaesthesia, which attenuates the sympathetically mediated increases in arteriolar and venous constriction as well as reducing cardiac output. In any patient in whom fluid is sequestered or lost (e.g. peritonitis, bowel obstruction) or in whom haemorrhage has occurred (e.g. trauma), the anaesthetist should try to quantify the circulating/intravascular blood volume or extracellular fluid volume, and correct any deficit.
Blood loss may be assessed using the patient’s history and any measured losses, but more commonly the anaesthetist has to rely on clinical evaluation of the patient’s current cardiovascular status. Profound circulatory shock with hypotension, poor peripheral perfusion, oliguria and altered cerebration is easy to recognize. However, a more careful assessment is needed to recognise the early manifestations of haemorrhage, such as tachycardia and cutaneous vasoconstriction. Useful indices include heart rate, arterial pressure (especially pulse pressure), the state of the peripheral circulation, central venous pressure and urine output. Table 37.3 describes approximate correlations among these clinical indices and the extent of haemorrhage, but it should be stressed that these refer to the ‘ideal’ patient. In young, healthy adults, arterial pressure may be an unreliable guide to volume status because compensatory mechanisms can prevent a measurable decrease in arterial pressure until more than 30% of the patient’s blood volume has been lost. In such patients, attention should be directed to pulse rate, skin circulation and a narrowing pulse pressure. Tachycardia in the presence of a normal arterial pressure should never automatically be attributed to pain or anxiety if there is a clinical history consistent with the potential for intravascular volume loss. In elderly patients with widespread arterial disease, limited cardiac reserve and a rigid vascular tree (fixed total peripheral resistance), signs of severe hypovolaemia may become evident when blood volume has been reduced by as little as 15%. However, as baroreceptor sensitivity decreases with age, elderly patients may exhibit less tachycardia for any degree of volume depletion.
In general, hypovolaemia does not become apparent clinically until circulating blood volume has been reduced by at least 20% (approximately 1000 mL). A reduction by more than 30% of blood volume occurs before the classic ‘shock syndrome’ is produced, with hypotension, tachycardia, oliguria and cold, clammy extremities. Haemorrhage greater than 40% of blood volume may be associated with loss of the compensatory mechanisms that maintain cerebral and coronary blood flow, and the patient becomes restless, agitated and eventually comatose. In patients with major trauma, it is valuable to compare the clinical assessment of the extent of haemorrhage with the measured or assumed loss. A marked disparity between these two estimates often leads to a diagnosis of a further concealed source of haemorrhage.
Whilst clinical evaluation remains the most important and most frequently used guide to the management of intravascular volume deficit, the use of non-invasive and minimally-invasive methods of cardiac output measurement in this setting is growing. These techniques may be of particular benefit in guiding the immediate resuscitation of frail or critically ill patients.
Assessment of extracellular fluid volume deficit is difficult. Guidance may be obtained from the nature of the surgical condition, the duration of impaired fluid intake and the presence and severity of symptoms associated with abnormal losses (e.g. vomiting). At the time of the earliest radiological evidence of intestinal obstruction, there may be 1500 mL of fluid sequestered in the bowel lumen. If the obstruction is well established and vomiting has occurred, the extracellular fluid deficit may exceed 3000 mL. Table 37.4 describes some of the clinical features seen with varying degrees of severity of extracellular fluid losses. It is clear that considerable losses must occur before clinical signs are apparent, and that these signs are often subjective in more minor degrees of extracellular fluid deficit.
|Percentage Body Weight Lost as Water||mL of Fluid Lost per 70 kg||Signs and Symptoms|
|Over 4% (mild)||Over 2500||Thirst, reduced skin elasticity, decreased intraocular pressure, dry tongue, reduced sweating|
|Over 6% (mild)||Over 4200||As above, plus orthostatic hypotension, reduced filling of peripheral veins, oliguria, low CVP, apathy, haemoconcentration|
|Over 8% (moderate)||Over 5600||As above, plus hypotension, thready pulse with cool peripheries|
|10–15% (severe)||7000–10 500||Coma, shock followed by death|
In addition to clinical signs, laboratory investigations may also indicate extracellular fluid volume deficit. Haemoconcentration results in an increased haemoglobin concentration and an increased packed cell volume. As dehydration becomes more marked, renal blood flow diminishes, reducing renal clearance of urea and consequently increasing the blood urea concentration. Patients with moderate volume contraction exhibit a ‘pre-renal’ pattern of uraemia characterized by an increase in blood urea out of proportion to any increase in serum creatinine concentration. Under maximal stimulation from ADH and aldosterone, conservation of sodium and water by the kidneys results in excretion of urine of low sodium concentration (0–15 mmol L–1) and high osmolality (800–1400 mosmol kg–1).
Once the extent of blood volume or extracellular fluid volume deficit has been estimated, deficits should be corrected with the appropriate intravenous fluid. The overall priority is to maintain adequate tissue perfusion and oxygenation, therefore correction of intravascular deficit takes precedence – hypovolaemia due to blood loss should be treated with either a balanced crystalloid solution (such as Hartmann’s solution) or a suitable colloid until packed red cells are available (see Ch 12: Fluid, electrolyte and acid–base balance). Resuscitation is usually guided by clinical indices of circulating volume status and organ perfusion. Central venous pressure (CVP) measurement has often been used to guide fluid therapy but CVP has limitations when used to predict intravascular volume status and responsiveness to infused fluids. High-risk surgical patients may benefit from the use of (non-invasive) cardiac output measuring devices to direct fluid resuscitation towards predetermined goals for cardiac output and systemic oxygen delivery.
Extracellular fluid deficit is usually corrected after the correction of any intravascular deficit, by adjusting maintenance fluid infusion rates. Losses from vomiting or gastric aspirates are best replaced by crystalloid solutions containing an appropriate potassium supplement. Hartmann’s solution is often used, although hypochloraemia is an indication for saline 0.9% (with additional potassium). Lower GI losses, such as those due to diarrhoea or intestinal obstruction, are normally replaced volume-for-volume with Hartmann’s solution.
Vomiting or regurgitation of gastric contents, followed by aspiration into the tracheobronchial tree whilst protective laryngeal reflexes are obtunded, is one of the commonest and most devastating hazards of emergency anaesthesia.
Vomiting is an active process that occurs in the lighter planes of anaesthesia. Consequently, it is a potential problem during induction of, or emergence from, anaesthesia, but should not occur during maintenance if anaesthesia is sufficiently deep. In light planes of anaesthesia, the presence of vomited material above the vocal cords stimulates spasm of the cords. This reflex provides a degree of protection against material entering the larynx and tracheobronchial tree. However, apnoea occurs as a consequence and may persist until severe hypoxaemia or even cardiac arrest occurs. If the spasm does resolve then aspiration may occur unless the supraglottic debris has been cleared by the anaesthetist before the resumption of ventilation.
In contrast to vomiting, regurgitation is a passive process that may occur at any time, is often ‘silent’ (i.e. not apparent to the anaesthetist) and, if aspiration occurs, may have clinical consequences ranging from minor pulmonary sequelae to fulminating aspiration pneumonitis and acute respiratory distress syndrome (ARDS). Regurgitation usually occurs in the presence of deep anaesthesia or at the onset of action of neuromuscular blocking drugs, when laryngeal protective reflexes are absent and so the risk of aspiration is increased.
The most important factors determining the risk and degree of gastric regurgitation are lower oesophageal sphincter function and residual gastric volume, which itself is largely determined by the duration of fasting and rate of gastric emptying.
The lower oesophageal sphincter (LOS) is a 2–5 cm length of oesophagus with higher resting intraluminal pressure situated just proximal to the cardia of the stomach. The sphincter relaxes during oesophageal peristalsis to allow food into the stomach, but remains contracted at other times. The structure cannot be defined anatomically but may be detected using intraluminal pressure manometry.
The LOS is the main barrier preventing reflux of gastric contents into the oesophagus. Many drugs used in anaesthetic practice affect the resting tone of the LOS. Reflux is related not to the LOS tone per se, but to the difference between gastric and LOS pressures; this is termed the barrier pressure. Drugs that increase the barrier pressure (e.g. cyclizine, anticholinesterases, α-adrenergic agonists and metoclopramide) decrease the risk of reflux. For many years it was thought that the increase in intragastric pressure during succinylcholine-induced fasciculations predisposed to reflux. However, LOS tone is also increased by succinylcholine and so barrier pressure is maintained.
Anticholinergic drugs, ethanol, tricyclic antidepressants, opioids and thiopental reduce LOS pressure and it is reasonable to assume that these drugs increase the tendency to gastro-oesophageal reflux.
Gastric emptying results from peristaltic waves sweeping from cardia to pylorus at a rate of approximately three per minute, although temporary inhibition of gastric motility follows recent ingestion of a meal. The gastric emptying of clear fluids is an exponential process, i.e. the rate of emptying at any given time is proportional to the volume of liquid in the stomach. The half-time for this process is about 20 min, so less than 2% of ingested clear fluid remains in the stomach at 2 h. The gastric emptying of solids is roughly linear, i.e. occurs at a constant rate, and usually begins about 30 min after ingestion of a meal. The rate of emptying varies depending on the composition of food ingested. Typically, about 50% of food reaches the duodenum within 2 h although meals high in fat content may take considerably longer. The rate of gastric emptying is also significantly delayed if the mixture reaching the duodenum is very acidic or hypertonic (the inhibitory enterogastric reflex), but both the nervous and humoral elements of this regulating mechanism are still poorly understood. Many pathological conditions reduce gastric emptying (Table 37.5). In the absence of any of these factors, it is reasonably safe to assume that the stomach is empty provided that solids have not been ingested within the preceding 6 h, or clear fluids consumed in the preceding 2 h, and provided that normal peristalsis is occurring. This is the usual case for elective surgical patients. However, in emergency surgery it may be necessary to induce anaesthesia urgently before an adequate period of starvation occurs. In addition, the patient’s surgical condition is often accompanied by delayed gastric emptying or abnormalities of peristalsis. In these circumstances, even if the usual period of fasting has been observed it cannot be assumed that the patient’s stomach is empty.
With absent or abnormal peristalsis
Peritonitis of any cause
Metabolic ileus: hypokalaemia, uraemia, diabetic ketoacidosis
Drug-induced ileus: anticholinergics, those with anticholinergic side-effects
With obstructed peristalsis
Small or large bowel obstruction
With delayed gastric emptying
Diabetic autonomic neuropathy
Fear, pain or anxiety
Oesophageal strictures – benign or malignant
In patients who have sustained a significant trauma injury, gastric emptying virtually ceases as a result of the combined effects of fear, pain, shock and treatment with opioid analgesics. In these patients, the interval between ingestion of food and the injury is a more reliable index of residual stomach volume than the period of fasting observed since injury. It is not uncommon to encounter vomiting 24 h or longer after ingestion of food when trauma has occurred very shortly after a meal. In these patients, a patient’s sensation of hunger should not be used to indicate an empty stomach: sensations of hunger and satiety are complex and are unreliable indicators of stomach volume. Bedside ultrasonography is a more objective tool for determining gastric content and its use may become more widespread.
Injury from aspiration of gastric contents results from three different mechanisms: chemical pneumonitis (from acid material), mechanical obstruction from particulate material and bacterial contamination. Aspiration of liquid with a pH < 2.5 is associated with a chemical burn of the bronchial, bronchiolar and alveolar mucosa, leading to atelectasis, pulmonary oedema and reduced pulmonary compliance. Bronchospasm may also be present. The claim that patients are at risk if they have more than 25 mL of gastric residue with a pH < 2.5 is based on data from animal studies extrapolated to humans and should not be regarded as indisputable fact. Day-case patients often have residual gastric volumes greater than 25 mL.
If aspiration of gastric contents occurs, the first manoeuvre after the airway is secured is to suction the trachea to remove as much foreign material as possible. If particulate matter is obstructing proximal bronchi, bronchoscopy may be necessary. Hypoxaemia is managed with O2, IPPV and PEEP. Steroids are not recommended and antibiotics are not given routinely unless the aspirated material is considered unsterile.
It is important to recognize any patient who may have significant gastric residue and who is in danger of aspiration. The anaesthetic management of such a patient may be described in five phases: preparation, induction, maintenance, emergence and postoperative management.
Whilst it may be necessary to postpone surgery in the emergency patient to obtain investigations and resuscitate with i.v. fluids, there is usually little benefit in terms of reducing the risk of aspiration of gastric contents; the risk of aspiration must be weighed against the risk of delaying an urgent procedure. However, two manoeuvres are available:
Although not completely effective, insertion of a nasogastric tube to decompress the stomach and to provide a low-pressure vent for regurgitation may be helpful. Aspiration through the tube may be useful if gastric contents are liquid, as in bowel obstruction, but is less effective when contents are solid. Cricoid pressure is still effective at reducing regurgitation even with a nasogastric tube in situ.
Clear oral antacids (e.g. sodium citrate) may be used to raise the pH of gastric contents immediately before induction. However, this also increases gastric volume. Particulate antacids should not be used, as they may be very damaging to the airway if aspirated. The preoperative administration of H2-receptor antagonists consistently raises gastric pH and may reduce the chance of chemical pulmonary injury occurring in the event of inhalation. Although this is standard practice in obstetric anaesthesia, few anaesthetists employ these measures for emergency general surgery. The regimens available are described in Chapter 35.
This is the technique used most frequently for the patient with a full stomach. The phrase ‘rapid-sequence’ hints at one of the fundamental goals of this technique, which is to minimize as much as possible the duration of time between loss of consciousness and tracheal intubation, during which the patient is at greatest risk of aspiration of gastric contents. In achieving this goal, this technique contravenes one of the fundamental rules of anaesthesia, namely that neuromuscular blockers are not injected until control of the airway is assured. The decision to employ the rapid-sequence induction technique balances the risk of losing control of the airway against the risk of aspiration. Therefore it is vital to assess carefully the likelihood of difficult laryngoscopy or tracheal intubation. The anaesthetist must have a contingency plan prepared for patient management should intubation fail. If preoperative evaluation indicates a particularly difficult airway, alternative methods should be considered, e.g. local anaesthetic techniques or ‘awake intubation’ under local anaesthesia.