Intravascular Volume 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.

Extracellular Volume Deficit

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.

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.

 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.

Rapid-Sequence Induction

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.

For rapid-sequence induction to be consistently safe and successful, it should be performed with meticulous attention to detail and preparation is necessary. The patient must be on a tipping trolley or table, preferably with an adjustable headpiece so that the degree of neck extension/flexion may be altered quickly. Ideally the patient’s head should be in the classic ‘sniffing position’ with the neck flexed on the shoulders and the head extended on the neck. Failure to appreciate this point increases the likelihood of difficult intubation. The optimal incline of the operating table is debatable: some authorities recommend the reverse Trendelenburg (head-up) position (to prevent regurgitation) and others the classic Trendelenburg position (to prevent aspiration of any regurgitated or vomited material). In general, the optimum position is that in which the trainee anaesthetist has gained greatest experience in performing intubation.

The anaesthetist must be aided by at least one skilled assistant to perform cricoid pressure, assist in turning the patient, obtain smaller tracheal tubes, supply stylets for tubes, etc. High-volume suction apparatus must be functioning and the suction catheter should be within easy reach of the anaesthetist’s hand (commonly placed under the patient’s pillow). As with any anaesthetic, the machine should have been checked before starting, the ventilator adjusted to appropriate settings and all drugs drawn up into labelled syringes before induction. An i.v. cannula should be sited and connected to running fluid, to aid circulation of drugs to the brain. Appropriate monitoring devices should be attached.

Before inducing anaesthesia, it is essential to pre-oxygenate the patient’s lungs with 100% oxygen. The aim is to denitrogenate the lungs and maximize the oxygen reservoir available to the patient from their functional residual capacity, which will delay the onset of hypoxia if difficulty is encountered whilst securing the airway. The patient should breathe 100% O₂ for 3–5 min, or until the end-tidal oxygen concentration is > 85%. In extreme emergencies this process can be quickened by asking the patient to make 8 vital capacity breaths.

Heart rate, arterial pressure (and, when appropriate, central venous pressure) and ECG are monitored before induction of anaesthesia, and a skilled assistant is in position at the patient’s side to perform Sellick’s manoeuvre (cricoid pressure). It is important that the assistant can identify the cricoid cartilage, as compression of the thyroid cartilage distorts laryngeal anatomy and may render tracheal intubation very difficult. To perform Sellick’s manoeuvre correctly, the thumb and forefinger press the cricoid cartilage firmly in a posterior direction with a force of 20–40 N, thus compressing the oesophagus between the cricoid cartilage and the vertebral column. Because the cricoid cartilage forms a complete ring, the tracheal lumen is not distorted (Fig. 37.1).

Opinions differ with regard to the time at which cricoid pressure should be applied. Some prefer to inform the patient and apply it just before administration of the i.v. induction agent; others apply it as soon as consciousness is lost.

With the assistant in position, a predetermined sleep dose of i.v. anaesthetic induction agent is injected. This is followed immediately by the administration of a paralysing dose of succinylcholine (1.5 mg kg^–1) without waiting to assess the effect of the induction agent. Manually ventilating the patient’s lungs whilst waiting for muscle paralysis is sometimes avoided for fear of causing gastric insufflations and increasing the risk of aspiration. As soon as the jaw begins to relax or fasciculations have ceased, laryngoscopy is performed and the trachea intubated. Cricoid pressure is maintained until the cuff of the tracheal tube is inflated and correct placement of the tube has been confirmed, by auscultation of both lungs and the presence of end-tidal carbon dioxide. The exception to this rule is in instances of vomiting after induction, where maintenance of cricoid pressure could lead to oesophageal rupture.

After successful intubation, the lungs are gently ventilated by hand, as excessive increases in intrathoracic pressure may have harmful effects on circulatory dynamics. One of the main disadvantages of the rapid-sequence induction technique is the haemodynamic instability that may result if the dose of induction agent is excessive (hypotension, circulatory collapse) or inadequate (hypertension, tachycardia).

Thiopental has long been regarded as the i.v. induction agent of choice for RSI. It provides a rapid loss of consciousness with a clearly defined end-point. A dose of 4–5 mg kg^–1 can reliably be predicted to be sufficient for healthy young patients, but much less (1.5–2 mg kg ^–1) is required in the elderly and frail or hypovolaemic patient. In the critically ill patient with a metabolic acidosis, the unbound fraction of the drug is increased and this will also reduce dose requirements. In comparison to thiopental, propofol 1.5–2 mg kg ^–1 causes greater suppression of laryngeal reflexes and may be more familiar to junior anaesthetists, owing to its everyday use in anaesthesia for elective procedures. However, propofol causes more cardiovascular depression than thiopental and should be used with caution. Another alternative is etomidate 0.1–0.3 mg kg^–1 which has the advantage of less cardiodepressant effects but its use is limited by adverse effects of adrenal suppression. Ketamine 1.5 mg kg ^–1 has a slower speed of onset and poorly defined end-point compared to thiopental. However, it causes the least cardiovascular depression of any induction agent and is often used in severely shocked patients.

It is sometimes inferred from the term RSI that the i.v. anaesthetic should be injected rapidly. This is not the case: RSI means that a predetermined dose of i.v. anaesthetic drug is immediately followed by injection of the neuromuscular blocking drug, and before waiting for signs of unconsciousness. Too rapid an injection of i.v. agent may exaggerate cardiovascular depression in the compromised patient, and bolus doses of all intravenous anaesthetics during RSI should be given over several seconds. Opioids are often injected along with intravenous anaesthetics at induction of anaesthesia for elective surgery, but ‘classical’ teaching suggests they should be omitted during RSI despite their potential benefits – for example attenuating the sympathetic response to intubation. This is largely because of concerns about delaying the onset of spontaneous respiration in the event of failed intubation. However, shorter acting drugs such as alfentanil are increasingly used as part of an RSI and may allow reduced doses of i.v. anaesthetic induction agents.

Succinylcholine is used as the neuromuscular blocker for RSI because it has two very desirable properties: a rapid onset of action facilitates speedy intubation and therefore minimizes the risk of aspiration, whilst a short duration of action allows for a quicker onset of spontaneous ventilation in the event of failed intubation. However, it also causes a number of undesirable effects including increased serum potassium concentrations, muscle pains and, rarely, malignant hyperthermia. The incidence of anaphylaxis is also higher than that of other neuromuscular blocking drugs. High-dose rocuronium (0.9–1.2 mg kg ⁻¹) achieves intubating conditions in a comparable time to succinylcholine but its use in RSI has been limited by a more prolonged duration of action. However, sugammadex allows rapid reversal of the effects of rocuronium through encapsulation of the rocuronium molecule. The availability of sugammadex may therefore enable high-dose rocuronium to be used as an alternative to succinylcholine in RSI.

Inhalational Induction

If there is reasonable doubt about the ability to perform intubation or to maintain a patent airway in a patient with a full stomach (e.g. the patient with facial trauma, epiglottitis or bleeding tonsil), an inhalational induction may be used with oxygen and halothane or sevoflurane. When the patient has reached a deep plane of anaesthesia, laryngoscopy is performed followed by an attempt at tracheal intubation during spontaneous ventilation. Normally, the patient should be placed in the left lateral, head-down position, but if circumstances do not allow the lateral position then the supine posture with cricoid pressure may have to be accepted. Indeed a modification of this technique may be used in any elderly, frail patient who may not tolerate i.v. induction agents. Anaesthesia may be induced by inhalational induction with the maintenance of cricoid pressure and, when the patient is sufficiently anaesthetized, succinylcholine injected and the trachea intubated.

Awake Intubation

Although blind nasal intubation is a valuable skill, the introduction of the narrow-gauge fibreoptic intubating laryngoscope has replaced it as the technique of choice in those patients who are likely to develop unrelievable airway obstruction when loss of consciousness occurs (e.g. trismus from dental abscess) or who are known or suspected to pose difficulties with intubation. Such endoscopic tracheal intubations may be performed via either the nasal route (more commonly used) or the oral route (see Ch 22: Management of the difficult airway). Before embarking on awake fibreoptic nasal intubation, the nasopharynx and, to a greater or lesser extent, the upper airway must be rendered insensitive, so that the patient can tolerate the introduction of a tracheal tube (see Ch 43: Complications during anaesthesia).

Regional Anaesthesia

The use of regional anaesthesia is increasing in the UK, partly because of the growth in the practice of ultrasound-guided regional anaesthetic techniques. Many regional techniques are eminently suitable for emergency procedures on the extremities (e.g. to reduce fractures or dislocations).

Brachial plexus block by the axillary, supraclavicular or interscalene approach is satisfactory for orthopaedic manipulations or surgical procedures involving the upper extremity. It satisfies surgical requirements for analgesia, muscle relaxation and immobility. There are minimal effects on the cardiovascular system and there is a prolonged period of analgesia postoperatively. Similarly, i.v. regional anaesthesia is useful for the manipulation or reduction of a fractured wrist; prilocaine 0.5% plain is the drug of choice as it is the least toxic local anaesthetic drug and has the largest therapeutic index. If prilocaine is not available, then lidocaine 0.5% plain is acceptable.

For regional anaesthesia of the lower extremity, available techniques include subarachnoid, epidural and sciatic/femoral blocks. Spinal and epidural blocks are contraindicated if there is doubt about the adequacy of extracellular fluid or vascular volumes, as large decreases in arterial pressure may result from the associated pharmacological sympathectomy.

It is a common surgical misconception that subarachnoid or epidural anaesthetic techniques are safer than general anaesthesia for patients in poor physical condition. It must be emphasized that for the inexperienced anaesthetist, these techniques are invariably more dangerous than general anaesthesia for the patient with moderate/major trauma or any intra-abdominal emergency condition.

Fluid Management

During emergency intra-abdominal surgery, there may be large blood and fluid losses, which exceed the patient’s maintenance fluid replacement. Hartmann’s solution (compound sodium lactate) is still the preferred i.v. fluid during surgery. More sophisticated methods of determining intravascular volume status and cardiac output are increasingly used. Although much of the work in this field has been performed in patients undergoing elective surgery, there are a few examples of fluid optimization using cardiac output monitoring proving beneficial in emergency patients (Sinclair et al 1997). Methods of determining cardiac output are covered in Chapter 16 (Clinical measurement and monitoring).

The requirement for blood transfusion varies in different groups of patients. In general the threshold for transfusion of blood (or more commonly packed red blood cells), the ‘transfusion trigger’, is a haemoglobin concentration 8 g dL ^–1 (Carless et al 2010). A higher transfusion trigger is often used for certain patient populations, for example 10 g dL ^–1 in patients with ischaemic heart disease, though the evidence for this is not established. Near-patient-testing devices, sampling from arterial or venous catheters are invaluable aids to guide transfusion during surgery.

Tracheal Extubation

If extubation is planned after emergency anaesthesia, this should take place in the operating room with the presence of a trained anaesthetic assistant. Immediately before tracheal extubation, the patient is turned to the lateral position (if possible) and asked to take a deep inspiration while gentle positive pressure is applied to the airway. At the peak of inspiration, the cuff is deflated and the tracheal tube removed as the patient exhales, thus assisting removal of any secretions which may have accumulated above the cuff. Oxygen 100% is administered until a regular respiratory rhythm is re-established and the patient has demonstrated an ability to cough and maintain a patent airway. Breathing 40% O₂, the patient is transported in the lateral position to the recovery room and remains there until all vital signs are stable.

Prophylactic Postoperative IPPV

Continuation of IPPV should be considered electively in several circumstances, some of which are listed in Table 37.6. There should be close cooperation between intensive care colleagues, surgeons and anaesthetists when the decision is made to continue ventilation.

 Is it likely that the patient will die with or without surgery? If the answer is yes, then surgery is not indicated unless it is likely that it will contribute to the physical comfort of the patient during the dying process, i.e. contribute to a ‘good death’.

 Is it likely that the patient would survive a laparotomy if the underlying cause were found to be curable/treatable (e.g. perforated duodenal ulcer, appendicitis)? If the answer is yes, then surgery is indicated and agreement on the appropriate level and duration of postoperative organ support must be reached.

 If, having embarked on surgery, the underlying cause is found to be treatable but not curable (e.g. perforated carcinoma with metastases, gangrenous bowel), would radical surgery be appropriate, given the patients overall state? If not, aggressive postoperative intensive care is not indicated. If yes, then what would be an appropriate level and duration of postoperative support? These questions need to be answered by experienced clinicians.

 Catastrophic haemorrhage control: less common in civilian than military trauma but does occur.

 Airway

 Breathing

 Circulation: haemorrhagic and non-haemorrhagic causes may co-exist. There is a strong emphasis on haemorrhage control.

 In the limbs apply direct pressure and elevate

 For continued bleeding use indirect pressure and apply a military tourniquet

 Pelvic binder – should have been applied pre-hospital; ensure correctly positioned

 Patient is conscious, alert, talking. Give high-flow oxygen via face mask. There is no need for immediate airway intervention and a full clinical evaluation can be done. Persisting signs of shock and/or the diagnosis of serious underlying injuries might be an indication for planned endotracheal intubation and mechanical ventilation

 Patient has a reduced conscious level but some degree of airway control and gag reflex still present. If the patient is maintaining the airway and breathing adequately then there is no need for immediate intervention. Endotracheal intubation will be necessary but a clinical evaluation can be done whilst equipment is being readied.

 Patient has a reduced conscious level, gag reflex absent. If the patient is unable to maintain the airway or is breathing poorly tracheal intubation and artificial ventilation should be carried out at once.

Damage Control Resuscitation

There has been a significant shift in management of major trauma away from ‘full’ resuscitation and ‘definitive’ surgery towards a concept of damage control resuscitation. This approach combines time-limited permissive hypotension, haemostatic resuscitation and damage control surgery. It is important to understand that permissive hypotension is not an end in itself. The presence of a peripheral pulse is deemed to be evidence of adequate perfusion only until the source of bleeding is controlled. The emphasis is on rapid and effective control of bleeding.

Circulation

Haemorrhage is the most common cause of shock in the injured patient and virtually all patients with multiple injuries have an element of hypovolaemia. Patients with major trauma often require urgent restoration of sufficient circulating blood volume to ensure:

Initial response to adequate boluses of warmed isotonic fluids may give some guide as to degree of hypovolaemia. However, if a patient has clear signs or a strong history suggestive of significant blood loss, there is nothing to be gained by administration of crystalloids. Blood should be given at the earliest opportunity.

All fluids given must be warmed as the triad of hypothermia, acidosis and clotting derangement can be lethal. At least two large (14-gauge) i.v. cannulae are inserted into peripheral veins in one or two limbs and both attached to infusions running through blood-warming coils.

Concurrently with administration of fluid replacement the team should be instituting measures to reduce further blood loss. The most important of these are:

Transfusion protocols have changed over the last few years, largely as a result of experience gained in conflict zones. Hospitals will have their own protocols for massive haemorrhage; these vary in their ratios of packed red cells: FFP: cryoprecipitate: platelets. However, the overall aim is the same: correction/avoidance of coagulopathy (haemostatic resuscitation) and adequate tissue oxygen delivery and perfusion. Good transfusion practice requires the use of near patient testing and close co-operation with haematology services. Further detail is given below (p 767).

Pump Function

Pump failure in major trauma is commonly due to the presence of a tension pneumothorax, but other possibilities include severe myocardial contusion and traumatic pericardial tamponade. Tension pneumothorax causes compression of the mediastinum (heart and great vessels) and presents with extreme respiratory distress, shock, unilateral air entry, a shift of the trachea towards the normal side and distension of the veins in the neck, although the last sign may not be seen in hypovolaemic shock. Tension pneumothorax is a clinical diagnosis, and should be treated if suspected. X-ray simply delays treatment. It may be relieved immediately by insertion of a 14-gauge cannula through the second intercostal space in the midclavicular line. This should be followed by standard chest drainage. Patients with blunt chest trauma and fractured ribs may develop a tension pneumothorax rapidly when positive-pressure ventilation is commenced, and the prophylactic insertion of a chest drain should be considered in such patients.

Damage Control Surgery

An early decision by the team is needed regarding the most appropriate pathway for the patient. Urgent trauma CT provides important anatomical information about actual or potential threat to life and is indicated in patients with adequate perfusion. Patients with inadequate perfusion and not responding to resuscitation should go straight to the operating theatre. Patients intermediate between these two groups require a more complex decision. The most important action is to make a decision. Waiting in ED is not going to further the patient’s care. Well-run trauma units expect to have major trauma patients through CT and with initial reporting of major findings within 30 minutes of ED arrival.

A FAST (Focused Abdominal Sonography for Trauma) scan by a skilled operator may provide helpful information if positive. A negative FAST scan does not rule out significant injury. Based on the CT findings and clinical picture, senior members of the trauma team will make a prompt decision regarding intervention: operating theatre for damage control surgery; embolization; non-operative continued resuscitation (critical care).

The anaesthetist must be involved in ongoing discussions with the surgical teams about the extent and intent of surgery.

The aims of Damage Control Surgery are:

The duration of surgery is limited, and additional surgical trauma is minimised. During this time, particularly once haemorrhage has been controlled, the anaesthetist should be aiming to correct metabolic, fluid and haemostatic derangements. In particular:

For patients who do not require immediate surgery for haemorrhage, decontamination or decompression, a team decision may need to be made whether to proceed to Early Total Care (ETC: definitive treatment of all long-bone fractures) or Damage Control Orthopaedic Surgery. These decisions should be based on an overall assessment of patient condition, particularly the trend in arterial lactate. If lactate is < 2.0 mmol L^– 1 then ETC can be considered; if > 2.5 mmol L^– 1 then continued resuscitation is required.

It is often necessary to induce anaesthesia in a hypovolaemic patient; this requires meticulous attention to fluid and drug management. A controlled rapid-sequence induction using thiopental, propofol or ketamine should be performed, but with extreme care over the dose of induction agent. Often very small doses of ketamine (0.3–0.7 mg kg^–1) suffice. The use of etomidate in trauma is still contentious due to its metabolic effects. The depressant effects of i.v. induction agents are exaggerated because the proportion of the cardiac output going to the heart and brain is increased. In addition, the rate of redistribution and/or metabolism is decreased as a result of reduced blood flow to muscle, liver and kidneys and thus blood concentrations remain increased for longer periods in comparison with healthy patients. Ketamine can be used in patients with a significant head injury as the benefits of maintained arterial blood pressure outweigh any concerns about cerebrometabolic effects. Figure 37.2 illustrates monitoring often used for the management of major trauma. Particular care needs to be taken in the presence of hypovolaemia and severe traumatic brain injury as hypotension is associated with a doubling of mortality.

After tracheal intubation, the lungs are ventilated at the lowest peak airway pressure consistent with an acceptable tidal volume. Judicious doses of muscle relaxant and analgesia (usually fentanyl) are given as necessary. As the cardiovascular status normalises and systolic pressure exceeds 90 mmHg, anaesthesia should be deepened as tolerated. This should be undertaken cautiously and, in principle, agents which are rapidly reversible or rapidly excreted should be used. In the shock state, there is very rapid uptake of inhalational agents. Reduced cardiac output and pulmonary blood flow decrease the rate of removal of anaesthetic agent from the alveoli, producing a rapid increase in alveolar concentration. Thus, the MAC value is approached more rapidly than in normovolaemic patients.

Basic monitoring will have been instituted in the emergency department. Insertion of arterial lines should not delay time to CT or surgical control of haemorrhage. However, blood may be sampled from an arterial cannula to monitor changes in acid-base state, haemoglobin concentration, coagulation and electrolyte concentrations. Central venous access is not usually a high priority in trauma resuscitation, but may be essential for i.v. access in the presence of four limb trauma. Short wide cannulae (e.g. ‘Swan sheaths’) should be used. Urine output is a useful guide to adequacy of resuscitation.

When surgical bleeding has been controlled, the patient’s cardiovascular status should improve, but if hypotension persists despite apparently adequate fluid administration, other causes of haemorrhage should be sought (Table 37.7). It is important that the anaesthetist assesses the patient regularly during prolonged anaesthesia to exclude these latent complications of major trauma.