A Airway and cervical spine

A compromised airway may occur secondary to maxillofacial or neck trauma, foreign body obstruction or simply from anatomical narrowing of the airway in the flexed neck (Fig 13.1a). In assessing the airway it is essential to simultaneously protect the cervical spine and spinal cord by avoiding excessive movement or rotation and by using an immobilising device such as a cervical collar. If the patient needs to be moved, it is important to stabilise the cervical spine with manual in-line immobilisation, which should be the sole focus of one member of the trauma team. The cervical collar should remain in place until radiological clearance has been obtained.

Figure 13.1a In the unconscious patient the tongue falls back

Simple measures to obtain a patent airway include the head tilt, chin lift and jaw thrust (protraction by lifting the angles of the mandible forwards) (Fig 13.2a). The mouth and pharynx are cleared manually of blood, vomitus or other foreign bodies (e.g. false teeth) if necessary (Fig 13.1b). An oropharyngeal (Guedel) or nasopharyngeal airway may be inserted.

Figure 13.2a Head tilt, chin lift and jaw thrust manoeuvres

Figure 13.1b Adequate airway

In the unconscious patient the airway is first cleared by making sure that the tongue is forward and that the pharynx is clear of foreign bodies.

In the unconscious patient, a definitive airway is required. This is achieved with tracheal intubation using an inflatable cuffed tube (Fig 13.2d). If the means of intubation are not available in the presence of an obstructed airway, surgical cricothyroidotomy may be required to secure a definitive airway. The procedure is not without hazard (especially in the very young, where the brachiocephalic vein may be inadvertently damaged) and requires a careful technique.

Figure 13.2d Endotracheal intubation: passage of an endotracheal tube

Nasotracheal intubation is preferable when there is a danger of cervical spine injury.

B Breathing and ventilation

Once airway patency and cervical spine protection have been confirmed the patient’s chest should be assessed. Adequate exposure will facilitate inspection, palpation, auscultation and percussion. Thoracic injuries that may compromise ventilation include open pneumothorax, tension pneumothorax, fractured ribs or flail chest, pulmonary contusion or massive haemothorax. The clinical signs and emergency management of these conditions are indicated in Table 13.2.

Table 13.2 Recognition and initial management of life-threatening thoracic injuries

Condition	Clinical signs	Initial management
Tension pneumothorax	↓ chest wall excursion, neck vein distension/cyanosis, tracheal deviation to opposite side, unilateral absent breath sounds, hyperresonant percussion note	The diagnosis is clinical — there is no time for a chest X-ray Insert large-bore (12–14G) needle into second intercostal space in the mid-clavicular line
Open pneumothorax	‘Sucking chest wound’, decreased breath sounds, hyperresonant percussion note	Close the defect in the chest wall with occlusive dressing that is taped only on three sides (to create a one-way valve)
Flail chest	Paradoxical/asymmetrical movement of chest wall Crepitus over ribs/cartilage	Analgesia Meticulous fluid balance May need to consider intubation and ventilation
Massive haemothorax	↓ chest wall excursion, tracheal deviation to opposite side, decreased breath sounds, stony dull percussion note	Insert 28 or 32G intercostal catheter
Cardiac tamponade	Beck’s triad (↓ arterial pressure, distended neck veins from ↑ venous pressure, muffled heart sounds) Kussmaul’s sign (↑ venous pressure with inspiration)	Pericardiocentesis via subxyphoid approach

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Oxygenation

Supplemental oxygen should be administered to all trauma patients. The conscious patient with a nasopharyngeal or oropharyngeal airway should receive oxygen via a bag-valve mask. The use of an oxygen reservoir device maximises oxygen delivery to the patient (Fig 13.2b and c) and is therefore strongly recommended.

Figure 13.2b Nasopharyngeal airway with bag-valve mask and reservoir device

Figure 13.2c Oropharyngeal airway with bag-valve mask

C Circulation and control of haemorrhage

The most likely cause of hypotension in the multiply injured trauma patient is hypovolaemia secondary to haemorrhage. Haemorrhage is the most common cause of death in these patients. Useful indicators of a patient’s circulatory status include vital signs (pulse and blood pressure), skin colour and level of consciousness. The normovolaemic patient would be expected to have a pink, well-perfused face and peripheries with a full, regular pulse. In contrast, the unconscious patient with cold, mottled peripheries and tachycardia is on the verge of hypovolaemic circulatory collapse.

Although the body’s physiological response to hypovolaemia is predictable, this statement needs qualification. At extremes of age (i.e. the elderly and the young child or toddler) tachycardia may be absent in the setting of hypovolaemia. One possible reason for this is polypharmacy; it is not uncommon to find elderly patients taking beta-blockers for cardiovascular disease. Other contributing factors include chronic illness and age-related blunting of the sympathetic response to hypovolaemia. By virtue of their large physiological reserves, children (and athletes) are well able to compensate for significant reductions in blood volume. Clinical signs of hypovolaemia may be initially absent. If these patients are severely injured, decompensation is often precipitous. In caring for such patients, one cannot afford to be solely comforted by the presence of a ‘normal’ heart rate or blood pressure. Frequent reassessment during resuscitation is mandatory.

Fluid resuscitation

A minimum of two large-bore intravenous cannulas (14 or 16G) should be placed percutaneously in peripheral veins and blood should be obtained for baseline investigations and for cross-matching type-specific blood.

When percutaneous access is difficult, a venous cutdown technique should be considered. The best sites are the long saphenous vein on the medial side of the ankle or any vein in the cubital fossa (Fig 13.3). Intra-osseous access in children over the upper tibia using an intra-osseous needle is very effective.

Figure 13.3 Venous cutdown

A: incision above and anterior to the medial malleolus; B: the vein margins are defined; C: a length of vein is cleared; D: the vein is elevated and ligated; E: a bevelled incision is made and the vein is cannulated; F: the catheter is tied in and infusion begins

When the rapid infusion of large volumes of fluid is anticipated the percutaneous insertion of a large bore cannula (8G) in the femoral vein in the groin is indicated. The insertion of a central venous catheter in the subclavian or internal jugular vein is more useful in monitoring the response to fluid resuscitation than in gaining access for the rapid infusion of fluids.

Intravenous fluid therapy is now commenced via a giving set with a pump, using a balanced salt solution (Hartmann’s solution) with 2 L given rapidly to achieve an appropriate response. All fluids used should be pre-warmed (37–40° C) or administered via a blood-warming device.

Blood transfusion may be necessary in the patient who fails to respond or in whom there is massive blood loss. Type-specific blood is preferred but if this is not available then type O-negative can be used. When more than four units of blood are transfused or anticipated consider the use of other blood products to prevent coagulopathy, particularly fresh frozen plasma, platelets and prothrombin. There are specific guidelines for the use of recombinant factor V and vitamin K.

During the resuscitative phase of circulation management it is vital to keep the patient warm with: pre-warmed intravenous fluid, external space blankets and/or specific devices with circulating warm air (Bair hugger).

The lethal triad that complicates the management of the severely injured patient: coagulopathy, acidosis (from poor tissue circulation/perfusion) and hypothermia, can be prevented in the primary survey by following the principles outlined above.

Surgical intervention may in some circumstances be the only effective method to stabilise the circulation.

D Disability and neurological assessment

An assessment of the central nervous system is crucial in detecting secondary brain injury. Two simple tools may be utilised — the AVPU method and the Glasgow coma scale (GCS). The AVPU method is a simple mnemonic that enables a rapid assessment of the level of consciousness:

Alert

Vocal response

Pain response only

Unresponsive

The cooperative, conscious patient may be asked to identify the site of the injuries, whereas the drowsy, head-injured patient who only responds to painful stimuli warrants reassessment of airway patency and consideration of intubation. This is seen particularly in patients with extradural haematomas, where approximately one-third will have the classic ‘lucid interval’ (see Ch 13.5).

The GCS is more commonly used during the secondary survey and will be discussed later.

E Exposure and environmental control

Complete removal of the patient’s garments is necessary to facilitate a thorough inspection and examination. Equally as important is the conservation of core body temperature. As such, once a thorough examination has been conducted, it is important to use a warming blanket to prevent the loss of body heat. Exposure to the cool of the ground, the wind or rain prior to retrieval — combined with blood loss and polytransfusion — lead to core body temperatures well below normal. The surgeon dealing with ongoing ooze during emergency laparotomy knows only too well the effect of hypothermia on the coagulation cascade. The use of pre-warmed intravenous fluids for resuscitation should be standard procedure. Patient temperature should be monitored and documented, alongside blood pressure and heart rate; it should be regarded as an important part of the vital statistics.

1 Clean wounds

These comprise uninfected surgical wounds in which no inflammation is encountered and the respiratory, alimentary, genital or uninfected urinary tracts are not entered. In addition, clean wounds are closed primarily and, if necessary, drained with closed drainage. Surgical incisional wounds that occur with nonpenetrating (i.e. blunt) trauma should be included in this category if they meet the criteria.

2 Clean–contaminated wounds

A surgical wound in which the respiratory, alimentary, genital or urinary tracts are entered under controlled conditions and without unusual contamination. Specifically, procedures involving the biliary tract, appendix, vagina and oropharynx are included in this category, provided no evidence of infection or major breaks in technique are encountered.

3 Contaminated wounds

Contaminated wounds are open, fresh, accidental wounds. In addition, procedures that have major breaks in sterile technique (e.g. open cardiac massage) or gross spillage from the gastrointestinal tract and incisions in which acute, nonpurulent inflammation is encountered are included in this category.

4 Dirty–infected wounds

Old traumatic wounds that have retained devitalised tissue and those that involve existing clinical infection or perforated viscera. This definition suggests that the organisms causing postoperative infection were present in the surgical field before the procedure.

Phases in wound healing

There are three major phases in wound healing: haemostasis and inflammation (two to five days); proliferation (beginning from about three days); and maturation (extending over many months). Haemostasis occurs via platelet aggregation and activation of the clotting cascade. Following this, polymorphonuclear leucocytes (PMN) and macrophages migrate to the area of injury, followed by lymphocytes (inflammation). Proliferation involves fibroblastic proliferation and angiogenesis, with resultant collagen formation. During the final stage of wound healing, the collagen and extracellular matrix are remodeled (maturation). There is overlap in these phases and wound strength progressively increases. Epithelialisation over the defect begins from the first day after injury; in clean surgical wounds treated by primary closure this is completed by the second day. In large wounds left to heal by second intention the process is hastened by wound contraction but will nevertheless take significantly longer.

Local factors

Local factors are the most common causes of failure of wound healing. Bacterial contamination, particularly when combined with a nidus facilitating bacterial growth, is followed by infection. Common factors acting as niduses are areas of dead or dying tissue, foreign bodies (including suture materials) and collections of blood, serum and lymph. Other local tissue factors — such as the adequacy of the arterial and venous circulation and lymphatic drainage and previous irradiation damage — are extremely important. Excessive tension during repair of wounded tissues inevitably leads to local tissue ischaemia, subsequent necrosis and wound breakdown (Box 13.3).

Box 13.3

Local factors that interfere with wound healing

Bacterial contamination: the risk depends on number, duration of exposure, virulence of organism and antibiotic resistance

A persistent nidus or haematoma or foreign and devitalised material

Ischaemia

Tension

Chronic oedema

Extensive skin loss

General factors

Age, diabetes, malignancy. Advanced age is associated with impaired or delayed wound healing. This may be due to a higher prevalence of other adverse factors such as vascular insufficiency, metabolic disease, malnutrition, cancer and drugs. Diabetes may cause neuropathy and microvascular or macrovascular disease leading to tissue ischaemia. Defects in angiogenesis, granulocyte function and wound matrix formation have also been described. Patients with cancer may be malnourished and immunocompromised from treatment (chemoradiotherapy) or disease progression (Box 13.4)

Box 13.4

General or host factors that interfere with wound healing

Advanced age, especially with vascular insufficiency

Diabetes

Malignant disease

Renal failure

Steroids for chronic disease

Malnutrition: deficiency of protein, vitamins (C and K) and trace elements (Zn); seen especially in the aged and alcoholics

Post splenectomy

Shock and generalised tissue ischaemia at the time of injury

Renal insufficiency, steroid treatment, cytotoxic treatment. All markedly retard wound healing. Steroid administration inhibits the inflammatory phase of wound healing, whereas cytotoxic drugs interfere with cell proliferation and protein synthesis. Renal insufficiency may lead to uraemia or anaemia, both of which impair tissue regeneration.

Nutritional deficiencies. Adequate protein and haemoglobin levels are important nutritional factors. The wound maintains its individual energy requirements in the face of moderate body deficits. Gross deficiencies are relatively rare in surgical practice and are more likely to be found in those suffering from the chronic effects of alcohol or drug abuse or patients with prolonged malnutrition or sepsis. Vitamins (particularly A and C) and trace elements (particularly zinc) are also essential for wound healing but deficiencies are uncommon.

Wound care — debridement

A clean surgical wound treated by primary closure is expected to heal with a fine, thin, cosmetically and functionally acceptable scar. With contaminated non-surgical wounds, the aim of management is to gain wound closure as soon as possible by converting them to a state analogous to the clean surgical wound, that is, by removing dead and doubtfully viable tissue and foreign matter and by arresting haemorrhage. This procedure is called wound debridement, excision or toilet. (‘Débridement’, a term coined by Napoleon’s chief surgeon, literally means unbridling or opening up. It has no relation to the word debris.)

The wound must be thoroughly explored and should be enlarged on either side as far as is required to determine the extent of deeper damage. Excision of necrotic tissue proceeds in depth. Skin edges usually need only a narrow margin of excision. Partially avulsed and bruised skin flaps require complete defatting and excision of the apex of the flap back to the point of dermal bleeding. Subcutaneous fat is freely excised back to pristine bleeding fat. Deep fascia is split widely to expose underlying structures and damaged muscle is radically excised back to healthy tissue (which bleeds and contracts when cut). Free bone fragments devoid of periosteum are removed and foreign material and debris must be removed from bone ends and marrow cavities. Subsequent treatment of fractures and injuries to other deep tissues (major tendons, nerves and vessels) depends on the degree of damage and contamination.

Irrigation of the wound with warm saline should be performed during debridement and before closure. This helps remove foreign matter and blood clots; it has no additional antibacterial effect. Early administration of intravenous antibiotics is also indicated in heavily contaminated wounds, but systemic (or topical) antibiotic administration should never be used as justification for inappropriate primary wound closure. If doubt exists as to the wisdom of closing the wound, it should be left open in readiness for subsequent delayed closure.

Wound closure

Two questions are fundamental to wound closure: When should the wound be closed? and By what means? These are separate but interrelated aspects of wound closure. Timing of closure is determined mainly by the degree of bacterial contamination (risk of infection) and viability of tissue. Techniques of closure are influenced particularly by the different types of injured tissues and whether the wound involves a defect or loss of tissue.

Timing of wound closure

Immediate (primary) closure. Primary closure is preferred for clean surgical wounds and clean–contaminated wounds following debridement. For most wounds, layered anatomical closure is performed using sutures as fine as is compatible with the tensile forces acting on the wound. Absorbable sutures should be used for subepithelial tissues where possible, to minimise the risks of persisting infection due to foreign bodies. Deep repair of clean wounds may include primary tendon and nerve suture. Primary skin closure can be by suture, tapes, clips or bioglue. The wound edges can be brought together or a free graft can be used. If a defect cannot be closed without tension a skin graft can be applied or a flap repair may be required.

Delayed closure. The risks of infection and wound breakdown are high when gross and prolonged contamination is combined with severe local damage. It is safer to leave such a wound open after debridement. This allows the wound to drain freely; it can then be more safely closed at a later stage. Repair of deep tissues is also usually best deferred in dirty–infected wounds. Internal fixation of bones is inadvisable in such wounds because the risk of sepsis is high. However, external fixation using pins through normal tissue above and below the fracture site (skeletal transfixion) is permissible and may be performed. The stabilisation of the limb skeleton so achieved facilitates repair and promotes healing of the associated soft tissue injuries. This is particularly so when an accompanying arterial anastomosis is essential. The techniques of repair of tendons and nerves in dirty–infected wounds are, however, so critical that sometimes these are best delayed until the wound has healed and is free of infection.

When complex contaminated wounds breach body cavities (cranial, peritoneal, pleuropericardial or joint cavities) the linings of the cavity walls should be repaired and sealed if possible. The superficial layers should be left open, lessening the likelihood of infection in the surface wound. Deep infection must be prevented by meticulous debridement and by appropriate systemic antibiotic treatment. Deep drainage may be indicated in specific circumstances, for example, in the pleural cavity.

When the large bowel is also breached, the danger of severe infection of the peritoneal cavity is so great that it is preferable to make a deliberate enterocutaneous fistula — a stoma (colostomy) at the site of the damage. It is, for example, virtually mandatory to establish a colostomy for a gunshot wound of the colon. If the bowel is repaired, the consequences of failure are unacceptably high.

Open wounds treated by delayed closure under dressings heal by granulation tissue, forming a mesenchymal scar. Excessive scar is an acceptable price for low morbidity and mortality.

Delayed primary closure. The first few days of wound healing are phagocytic and preparative rather than fibroblastic and reparative — the continuing biological debridement complements the surgical procedure. Because of this, closure can be delayed for a few days without prejudice to the end result or to the speed of healing. If closure is performed within a few days, the tissues are still soft, with little fibroblastic activity, and the wound can readily be closed. Delayed closure is thus best done between the second and fifth days after wounding. The end result is similar to that of primary healing. If closure is deferred for more than five days, granulation tissue will have developed on the exposed wound surface. The tissues are stiffer and do not approximate well and the procedure then becomes one of secondary wound closure.

Secondary closure. A clean granulating wound can often be induced to heal more quickly by secondary closure after the first week or so. This can be achieved by either skin graft or apposition of granulating surfaces. The tissues are too rigid to allow neat or precise closure, but apposition of granulating surfaces diminishes the volume of scar tissue required to bridge the gap. The process of adherence of two granulating surfaces in such circumstances is sometimes called healing by third intention. If the defect is large and cannot be closed without tension, skin grafting of the granulating surface is, of course, preferred.

Wound closure techniques and materials