Death following trauma has a trimodal distribution: the first peak of fatality occurs within seconds or minute of injury; the second peak occurs during the next few minutes to hours following injury and includes the so-called ‘golden hour’ which affords the clinician the best opportunity to safeguard the patient's life; the third peak occurs after several days and is a consequence of sepsis and multiple organ system failure. Clearly, the deaths occurring in the second and third periods may be influenced by the critical care clinician. A systematic approach to improving survival during the first hour has been the aim of the Advanced Trauma Life Support courses developed and sponsored by the American College of Surgeons. The basic philosophy of these courses carries through to intensive care management of trauma. Intensive care is generally required for patients requiring high levels of observation or organ system support such as mechanical ventilation. Retrospectively, the Injury Severity Score (ISS) correlates with the need for organ system support such as mechanical ventilation: patients requiring admission to a critical care unit usually have scores above 20. The aim of trauma critical care is to resuscitate and sustain the trauma victim while avoiding secondary complications.

Intensive care management can be considered in three phases. An acute resuscitative phase, an intermediate or consolidating phase and a late phase associated with secondary complications.

This phase begins as soon as the patient is transferred to intensive care from the emergency room, trauma unit or referring hospital. While it is the responsibility of the referring physician to ensure that such transfers are conducted safely with the patient as stable as possible, the receiving physician should participate in defining standards of care prior to initiating transfer. Most urgent investigations will have already been performed but others may still be required after admission to the intensive care unit. During the first few minutes on the intensive care unit the patient will be rapidly reassessed by the receiving physician. Simultaneously the transferring physician provides a brief, verbal review of prehospital history and subsequent management.

The following initial evaluation plan is based upon the Advanced Trauma Life Support Instructor Manual (American College of Surgeons Committee on Trauma 1988)

If the patient is not intubated, the airway should be checked. In intubated patients, patency of the airway, the position of the endotracheal tube, and cuff pressure of the tube should be ascertained.

Any difficulty or complications associated with intubation should be known, and the endotracheal tube should be examined to determine whether size and length are appropriate. If there are any causes for concern over the position or function of the endotracheal tube it should be changed. Procedures, including endotracheal intubation, can only be performed while control of the cervical spine is maintained.

The cervical spine must be stabilized until a cervical spine fracture can be excluded. All cervical spine films should be reviewed personally: the cervical spine should be assumed to be unstable until proven otherwise. The patient may be received in the critical care unit on a full spinal board, with stiff neck collar with sandbag support. This should be retained until the cervical spine can be cleared or a suitable replacement instituted.

If chest movement and air entry are not adequate and symmetrical, the reason should be determined. Signs of cyanosis should also be looked for.

The position of the endotracheal tube should be confirmed to exclude endobronchial intubation, and pneumothorax or haemothorax that could have developed since the initial evaluation should be excluded. If chest drains are already in situ they should be functioning normally; if not, there may be a need for a new thoracostomy tube.

If the patient is mechanically ventilated, any change in inflation pressures since initial assessment should be recorded. A sudden rise in peak inflation pressure may suggest pneumothorax, haemothorax or airway obstruction. The latter may take the form of a local obstruction due to kinked endotracheal tube, mucus or a foreign body, or generalized obstruction with wheezing, consistent with asthma.

All trauma patients must receive supplemental oxygen, and this should continue until any possible causes of hypoxaemia have been excluded. Pulse oximetry is an ideal way of monitoring oxygenation. Unless there are reasons to suspect chronic obstructive pulmonary disease the concentration of oxygen need not be restricted.

There is good evidence that oxygen uptake is increased during the immediate post-traumatic period, resulting in reduced mixed venous saturation. Supplemental oxygen, mechanical ventilation and inotropic support may therefore be required to ensure adequate oxygen delivery. It is essential that inotropic support is not confused with the need for adequate volume replacement.

Monitoring of vital signs, pulse, skin capillary refill, and blood pressure will determine whether there is continued blood loss: multiple fractures can be responsible for effective blood losses of over 40 per cent of total blood volume, and intra-abdominal bleeding should also be considered. Peritoneal lavage or abdominal CT may be performed if this was not carried out in the emergency room.

The total transfused volume of fluid should be determined, including crystalloid, colloid, and blood products. The availability of type-specific or cross-matched blood and quantity should be determined.

All patients suffering major trauma should have good venous access established during initial resuscitation, with at least two 14-gauge venous catheters. A single lumen central line may provide a satisfactory portal for drug administration and central venous pressure monitoring but is inadequate for aggressive volume resuscitation.

Is the patient alert? Does the patient respond to verbal commands or is the patient unconscious? This simplified ATLS neurological score (alert, responds to voice, responds to pain, unresponsive; AVPU) should be repeated to detect any change since admission and then replaced by the Glasgow Coma Score. Any change in pupil size and reactivity since admission should be recorded.

The patient should be examined from top to toe, and any further injuries identified. Results should be correlated with earlier findings.

The entire surface of the patient must be inspected on admission to the critical care unit, especially the head and back. The history of the trauma event and the resulting injuries should be reviewed carefully. Could there be any other injuries that have not been excluded?

Formal internal fixation and stabilization of fractures will often be undertaken during the first 24 h to facilitate nursing care and reduce the risk of fat embolus.

Anticipation of events related directly to the original injury and unrelated complications is the key to good management. Table 1 72 lists some of these events in order to their probable chronology.

During the 24 h following injury, changes in neurological and endocrine activity have a significant effect on the clinical course. Activation of the sympathetic nervous system defends the circulation against hypovolaemia by venous and arteriolar vasoconstriction and by increasing the rate and force of myocardial contraction. Metabolically there is glycogenolysis, fat mobilization, and reduced insulin secretion. Decreased blood volume leads to decreased perfusion of the kidney and increased renin secretion, which in turn activates angiotensin II and stimulates aldosterone release. Consequently, the circulation is further protected by vasoconstriction and salt and water retention. In response to pain, nausea, or any reduction in left atrial filling pressure, ADH secretion is also promoted, increasing the resorption of water from the distal renal tubules and collecting ducts. The adrenocortical response to severe trauma consists of an increase in ACTH from the anterior pituitary. Cortisol levels increase three- or four-fold unless there is adrenal insufficiency.

After the first 24 h most direct effects of injury will have declared themselves and will have been treated. Patients are typically haemodynamically stable, may have some degree of gas exchange impairment (due to lung contusion) and a proportion will require mechanical ventilation. If intubation is indicated in patients who have suffered crush injury, burns, or spinal cord injury, the use of depolarizing muscle relaxants should be avoided in view of the risk of sudden hyperkalaemia. Gastric paresis and a full stomach may be present 24 h after trauma and represent a significant hazard during intubation. Analgesia should be maintained to keep the patient comfortable and sedation should be used judiciously, particularly following head injury. Renal function is usually unimpaired at this stage unless there has been outflow obstruction or renal damage due to crush injury and myoglobinuria. Nutritional support is commenced, preferably as enteral feeding, but as total parenteral nutrition if necessary. If enteral feeding is not possible stress ulcer prophylaxis is required, preferably with a cytoprotective agent such as sucralfate.

Selective digestive tract decontamination has been recommended to reduce the rate of upper gastrointestinal tract colonization by Gram-negative organisms. Despite its rather marginal benefits in routine use, trauma patients may benefit most from such treatment. The focus of critical care management in the intermediate consolidating phase is to avoid iatrogenic complications and limit the risk of subsequent nosocomial infection.

Secondary complications begin to appear towards the end of the first week of admission, but may occur within 48 h.

Hospital-acquired infection by endogenous bacteria is a continual threat, to the patient. The incidence of nosocomial infection increases with increasing severity of injury, the number and level of invasive clinical procedures, and the length of admission. After 10 days of critical care admission very few patients escape some form of hospital-acquired infection. The systemic signs of infection, fever, and leucocytosis may herald the appearance of the sepsis syndrome with organ system failure, although leucocytosis may be absent in the severely injured patient. In many patients the type of injury will suggest the source of infection, while in ventilated patients nosocomial pneumonia must always be considered. The stress of trauma and gastrointestinal tract colonization with Gram-negative organisms may result in bacterial or endotoxin translocation across the intestinal wall into the circulation, precipitating the sepsis syndrome.

The respiratory system is commonly involved with differing degrees of respiratory impairment. The most severe examples are manifest as the adult respiratory distress syndrome, which requires a prolonged period of mechanical ventilation. Adult respiratory distress syndrome following trauma may result from lung contusion, fat embolism, massive blood transfusion, aspiration of gastric contents, or in association with the sepsis syndrome. Lung contusion and, by the same token, myocardial contusion, must be suspected in any patient with fractured ribs, sternal fracture, or anterior flail segment. Ventilator management is directed at maintaining adequate arterial oxygenation without circulatory embarrassment, oxygen toxicity, or barotrauma.

In its classical form, fat embolism syndrome presents with dyspnoea, skin petechiae, hypoxaemia, thrombocytopenia, falling haemoglobin, and fat globules in the urine. It is most common in patients with extensive and multiple fractures, occurring in up to 5 per cent of patients with combined pelvic and femoral fractures. Fat droplets may activate platelet aggregation with resultant consumption coagulopathy. Fat lodging in the lung is converted by lipase to free fatty acid that causes acute lung injury. Petechial haemorrhages over the torso, axillae, and conjunctivae probably result from a combination of thrombocytopenia and circulating fatty acids. Treatment is supportive and includes vasopressors, inotropes, and mechanical ventilation. There is some evidence to suggest that treatment with high-dose corticosteroids may reduce platelet aggregation. Other agents such as aspirin and heparin carry a significant risk of haemorrhage and are not recommended.

In the oliguric patient prerenal azotaemia and obstructive uropathy must be excluded before attributing renal failure to vasomotor nephropathy (acute tubular necrosis). Haemofiltration or haemodialysis should be commenced once reversible renal impairment has been excluded.

Most cardiovascular problems relate to the initial acute resuscitative phase. However, during the late phase the effects of myocardial contusion and sepsis syndrome may be associated with impaired myocardial contractility and hypotension. Appropriate use of inotropes and vasoactive agents may be required to support the circulation. Late hypovolaemia resulting from secondary haemorrhage or delayed rupture of the spleen should always be considered.

American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Instructor Manual. Chicago: ACS, 1988.

Chandrasekar, PH, Kruse JA, Mathews MF. Nosocomial infection among patients in different types of intensive care units at a city hospital. Crit Care Med, 1986; 14: 508–10.

Cournard A, et al. Studies of the circulation in clinical shock. Surgery, 1943; 13: 964–95.

Cowan BN, Burns HJG, Boyle P, Ledingham I. McA. The relative prognostic value of lactate and haemodynamic measurements in early shock. Anaesthesia, 1984; 39: 750–5.

Craven DE, et al. Nosocomial infection ad fatality in medical and surgical care unit patients. Arch Intern Med 1988; 148: 1161–8.

Edwards JD. Oxygen transport following major trauma. In: Vincent, J. L. (ed. Update in Intensive Care and Emergency Medicine. Berlin: Springer Verlag, 1988; 5: 25–31.

Shoemaker WC, et al. Pathogenesis of respiratory failure (ARDS) after haemorrhage and trauma. Crit Care Med, 1980; 8: 504–12.

Stoutenbeck CP, et al. The effect of selective decontamination of the digestive tract on colonization and the infection rate in multiple trauma patients. Intensive Care Med, 1984; 10: 185–92.