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

Based on www.netterimages.com and www.beliefnet.com

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

Suturing techniques use needle and suture material (either absorbable or non-absorbable) to appose subepithelial connective tissue layers neatly and without undue tension. The surface skin layer requires very accurate apposition. Skin sutures, in contrast to sutures uniting connective tissue layers, should evert the wound edges slightly. This is best achieved by the sutures on either side of the wound picking up a cone of tissue, with the base of the cone situated deeply. A reverse type of suture with the apex of the cone placed deeply tends to invert the cut edges. This may be desirable or acceptable for mesothelial surfaces but is disastrous for epithelial wounds. A vertical mattress suture may also be used to achieve eversion of skin edges. Skin staples are useful in some circumstances.

Vacuum-assisted closure (VAC™). The VAC™ system of wound closure utilises continuous negative pressure applied to a foam dressing. It is effective in managing exudative wounds; large open wounds can thus be closed by second intention, delayed primary closure or by subsequent skin grafting following VAC™ therapy.

Repair of defects. Free skin grafts will not take on bared bone, cartilage or tendon. Vascularised tissues must be transferred to the defect by flaps. Flaps can be of local or distant origin and are used extensively in plastic surgery.

Local flaps (Figs 13.5 and 13.6). Advancement describes the situation where one edge of a flap is simply advanced to cover the defect. Undermining the skin edges around a wound before suturing it effectively forms two advancement flaps. With larger defects, local flaps may be moved by rotation or transposition as illustrated. Rotation flaps rotate in the arc of a circle of which the primary defect is a segment; skin closure redistributes tension over a much more extensive suture line. Transposition flaps are pivoted to fill the gap, leaving a secondary defect that may require grafting or may be closed directly. Combined rotation–transposition flaps are common. A Z-plasty (Fig 13.6) redistributes wound tension by transposing two triangular flaps, bringing in tissue from the sides to lengthen the wound and break up tension across it. It is more commonly used as a secondary procedure to relieve contractures than in primary wound closure. It can be helpful in wounds with unequal sides and may be used to advantage to break up tension across the defect left after excision of a skin lesion. Particularly when wounds cross skin lines or cleavage lines, a Z-plasty may be used to stagger the line of the scar and place a portion of it in the crease line.

Figure 13.5 Local wound flaps

In random flaps without an axial blood supply the ratio of length to width should not exceed 1:1.

Figure 13.6 Local flaps: Z-plasty flap

Source: www.wheelessonline.com

Distant flaps are used if local tissue rearrangement is impossible or inappropriate. They may be directly applied to the defect without an appreciable pedicle or they may require a long carrier vascular pedicle. The vascular pedicle may be tubed or may be buried or tunneled to insert the flap as an island into the defect. The anatomy of flaps and their vascularity enable distinctions to be made between randomly or axially supplied flaps that determine their safe limits. A transverse rectus abdominis myocutaneous (TRAM) flap is one type of distant flap (Fig 13.7).

Figure 13.7 TRAM flap used for reconstruction after mastectomy

Based on Mayo Foundation for Medical Education and Research, and BRO Development

Free grafts. Free skin grafts may be split skin (Thiersch) or whole thickness (Wolfe). Skin grafting remains the most common, most simple and usually the best technique of covering a well-vascularised defect.

More complex free transfer of composite tissues may be performed by direct microvascular anastomosis of the blood supply of the composite graft to local vessels. These free flaps often involve combinations of skin, fat, muscle or bone or other vascularised tissues.

Closed soft tissue (sporting) injuries

Soft tissue (including sporting) injuries can be classified into three groups:

Severe closed visceral injuries often produce life-threatening complications. Direct contusion to the quadriceps, gluteal and gastrocnemius muscles are common sites of sporting injuries. They require immediate recognition and care if morbidity is to be kept to a minimum. A direct blow to the quadriceps can, unless treated early, lead to severe muscle contusion with secondary haemarthrosis (which may be confused with an injury of the knee joint), periosteal contusion and sometimes muscular calcification. Severe direct injury to the buttock — another common sporting injury — may cause rupture of the superior gluteal vessels and sciatic nerve contusion. Subcutaneous haematomas and fat necrosis can cause large fluid collections that take weeks or months to resolve.

Treatment during the acute inflammatory phase of injury aims to minimise bleeding and oedema formation by methods described by the acronym RICE:

Rest of the injured part

Ice application for 20–30 minutes every few hours

Compression bandaging for 48 hours after the injury

Elevation to minimise oedema

Local heat should not be applied for at least 24 hours after injury, as this will increase blood flow, bleeding and oedema formation. Alcohol should also be avoided, as it is a potent vasodilator. Intramuscular injections of local anaesthetic or steroids are of no benefit and may introduce infection. If complete muscle or ligament rupture has occurred, early surgical repair is indicated. Fasciotomy may sometimes be necessary for compartment syndrome with impending muscle necrosis.

Later treatment during the phase of fibrous repair of the muscle or ligament requires maintenance of muscle mobility as repair proceeds. Graduated increase in use of the injured part is combined with passive and active exercises. Attention must also be given to strengthening adjacent muscle groups, particularly those that act as joint stabilisers. Early physiotherapy involvement is essential to prevent long-term limitation of movement.

Local response to burns: Jackson’s burn zones

In 1947 DM Jackson described the three zones of a burn and this still forms the foundation of our understanding today (Fig 13.8). The zone of coagulation is the area where the most severe thermal injury occurs: cells are necrotic and irreversible tissue loss necessitates debridement. Surrounding this area is the zone of stasis, which is characterised by decreased tissue perfusion due to changes in the microcirculation. The viability of tissue in this zone may be preserved by restoring perfusion through appropriate resuscitation. Suboptimal fluid resuscitation or subsequent infection may, however, convert the zone of stasis into one of coagulation and necrosis, resulting in a larger and deeper burn. The outermost area is the zone of hyperaemia, where tissue perfusion is increased secondary to the release of inflammatory mediators from viable cells. This area usually recovers fully in burns.

Figure 13.8 Jackson’s burn zones

Based on firstaidwarehouse.co.uk

Systemic response to burns: SIRS and MODS

The release of inflammatory mediators causes an increased capillary permeability with significant fluid shifts from the intravascular to the extravascular space. A reduction in the plasma volume contributes to hypovolaemia, which leads to shock and a reduction in end-organ perfusion. Other organ systems may be affected; bronchoconstriction and a reduction in splanchnic perfusion may exist. The resultant systemic inflammatory response syndrome (SIRS) is defined as two or more of: patient temperature >38°C or <36°C; heart rate >90 beats/minute; respiratory rate >20/min or PaCO₂ <32 mmHg or leucocyte count >12,000/mm³; <4,000/mm³ or >10% immature (band) cells. Multiple organ dysfunction syndrome (MODS) exists when there is organ dysfunction in an acutely ill patient, such that homeostasis cannot be maintained without intervention.

Extent of burns

The burnt area is established as a percentage of body surface area (BSA), using the ‘rule of nines’ (Fig 13.9). A cross-check is always done by estimating the area not burnt. It is important to recognise that children have different proportions to adults and paediatric charts displaying body surface area estimations are useful in more accurately estimating burn extent.

Figure 13.9 ‘Rule of nines’ — calculating the percentage distribution of burnt skin in the adult and child

A: adult burns chart B: paediatric burns chart

Classification of burn depth

Burns are most helpfully considered as either shallow or deep. Shallow burns are further classified as epidermal (first-degree) or superficial partial-thickness (second-degree). Deep burns comprise deep partial-thickness (second-degree) and full thickness (third-degree). In areas where the skin is thick (e.g. palm, sole, back, buttock) burns are more likely to be partial thickness. Where skin is thin (dorsum of hands and feet, skin around the eyes), deep burns are more likely.

Epidermal burns (first-degree). These are minor burns (e.g. sunburn) involving only the superficial epidermis. Pain and erythema result from inflammation but blistering does not occur. Healing usually occurs over days to one week, with complete regeneration of a normal epithelium.

Superficial partial-thickness burns (second-degree). Tissue death involves both the epidermis and the upper layers of the dermis. Superficial (subepithelial) blisters occur that contain fluid and electrolytes. Beneath the blisters the tissue is painful (hypersensitive) and usually has a pinkish appearance owing to an intact blood supply. Complete regeneration can occur in two to three weeks from viable dermal elements, with little scarring.

Deep partial-thickness burns (second-degree). Involvement of the deeper (reticular) layers of the dermis may also cause blistering of the skin but the underlying tissue has a mottled pinkish-white appearance. This reflects variable damage to the deeper dermis, with blood supply to some areas still viable, interspersed among islands of non-viable tissue. Left

Figure 13.10 Depth of burns

A: full thickness (deep) burn; B: partial thickness (superficial) burn

Based on Williamson & Waxman, 1998

untreated, these wounds may heal spontaneously (over three months) by surface re-epithelialisation from surviving hair follicle, sebaceous and sweat gland remnants but with a considerable degree of subepidermal scarring. Surgical excision combined with conventional skin-grafting methods will achieve a better cosmetic result.

Full-thickness (third-degree). All epithelial elements, including dermal elements, are destroyed. Such burns will heal spontaneously very slowly. A dead eschar or slough forms, which ultimately separates. Excessive granulation tissue and scarring occur; slow re-epithelialisation occurs from the periphery. Gross scarring and crippling deformities are common.

Assessment of burn depth

This may be easy with severe burns with charring and evident necrosis, but often depth is difficult to diagnose with absolute certainty on first examination. Demonstration of viability depends on detecting sensitivity to sterile pin prick (dermal viability) and demonstration of an active circulation.

Partial-thickness burns. These cause erythema, blistering and moist exudate, are soft, painful to pinprick and touch and show a circulation with blanching on pressure and refilling on release.

Full-thickness burns. These are dull white or opaque or brown and charred with visible thrombosed veins beneath a transparent glassy panniculus. They are dry without blistering or moist exudate, firm and inelastic, painless to pinprick and touch and show no capillary response on pressure. Accurate clinical assessment of depth requires a thorough and skilful examination and a cooperative and alert patient.

Burns to the respiratory tract

Singed eyelashes and eyebrows are a clue to anticipating respiratory tract burns. The mouth and nose is carefully inspected for mucosal oedema, erythema, blistering, and for carbon particles in the sputum, and the patient is observed for any stridor or dyspnoea. Evidence of upper airway thermal injury (nasopharynx oropharynx, trachea) should prompt early (immediate) intubation. Absence of these signs does not exclude a respiratory burn; frequent reassessment is necessary, as oedema may develop over a short period. Injury to the lower airway usually manifests as tracheobronchitis; these patients often have wheeze, shortness of breath and cough.

General management

Pain and analgesia. Severe pain is less of a problem with full thickness burning. Extensive partial-thickness burns can be extremely painful and require an adequate dose of narcotic analgesia. These patients may experience severe pain even with air currents passing across the burn surface.

Antibiotics. Antibiotic prophylaxis is not indicated, their use reserved until required for management of an established infection.

Tetanus prophylaxis is as essential in the management of burns as in management of any other traumatic wound.

Resuscitation. Large volumes of water, electrolytes, plasma and sometimes blood are lost from the burnt surface, and also into the surrounding normal tissue, due to a systemic increase in microvascular permeability. Fluid replacement must start as soon as possible after burning to prevent hypovolaemic shock. Burns over 10–15% BSA will require intravenous fluid replacement. A secure intravenous line must be established without delay in such patients. Fluid loss begins immediately after burning and is maximal during the first few hours, then gradually slows until reabsorption from tissues commences after 48 hours. Large burn wounds can thus cause the loss of many litres from the circulatory blood volume. Once the intravenous line is in place, fluid resuscitation can be planned and monitored. Delays of more than one hour should be avoided in burns over 20% BSA. The patient should be nursed in a warm environment. A urethral catheter is also inserted in patients with burns of 20% or more to help monitor fluid replacement.

Many formulae have been used as guides to initial replacement. Whatever guidelines are used, resuscitation is tailored to individual needs and the results of continuing monitoring. Resuscitation volumes and intravenous replacement derived from formulae start from the time of burning and not from the time of insertion of the intravenous line. A commonly used regimen is based on the Parkland formula:

volume replacement for the first 24 hours

= 4 mL Hartmann solution/kg weight/percentage burn BSA.

A burn of 30% BSA in a 70-kg adult may therefore require over 8L of fluid in the first 24 hours after burning. Of this replacement volume, half should be given in the first eight hours and the remaining half in the next 16 hours. For children, the same formula may be used but an additional maintenance infusion (by weight) of glucose-containing fluid (e.g. 4% NSaline and 1/5 dextrose solution) may be required to maintain the specified urine output. The addition of glucose reflects the decreased glycogen reserves in children and tendency towards hypoglycaemia.

In practice, some clinicians may reduce the amount of resuscitation fluid administered to 2 mL/kg/percentage burn in various clinical circumstances and reserve resuscitation with 4 mL/kg/percentage burn for inhalational injury, prolonged patient exposure or delayed retrieval time. The crucial point to make is that fluid resuscitation must be adequate; both under- and overresuscitation may be detrimental to the patient and should be avoided. Resuscitation formulae are limited by the accuracy of BSA calculations (which may be difficult to estimate in some circumstances) and also do not account for patients with inhalational injury (who require more fluid volumes). Monitoring urinary output with the insertion of a catheter is an invaluable clinical aid and provides an objective measure of the adequacy of fluid resuscitation.

For burns exceeding 30% BSA, a central venous line is additionally inserted and is very helpful for monitoring response. A nasogastric tube may be required to decompress the stomach in patients with severe burns, as gastric stasis is initially common. Later, it can be used for enteral feeding. For burns exceeding 50% BSA, the initial calculation is made as for 50% and modified according to clinical assessment and response. These patients should be transferred to the intensive care unit (of a specialised burns centre) for monitoring and further management.

Monitoring

Fluid replacement is monitored by the following observations.

Pulse, blood pressure, respiration rate. These will usually show no worrying changes. Hypotensive hypovolaemic shock should be preventable, provided resuscitation begins within one hour of burning. Agitation and restlessness indicate hypoxia, which should be treated with oxygen delivered by face mask at 4–6 L/minutes to give an FiO₂ of 40–50%.

Urine output. This is the best guide to adequate replacement. Sufficient fluid should be given to provide for sensible and insensible losses from the burn wound and into the tissues, and to provide for a continuing urinary output of 30 mL/hr in adults (0.5 mL/kg/hr) or 1.0mL/kg/hr in young children who weigh 30 kg or less. The urine should be regularly tested for albumin, haemoglobin and myoglobin. Evidence of myoglobinuria requires urine output to be maintained at a higher level (i.e. 0.5–1 ml/kg/hr).

Central venous pressure. Central venous pressure monitoring is essential in patients with burns greater than 30% BSA. It is only occasionally necessary in burns of lesser extent. A progressively falling central venous pressure (CVP), below the normal range of 0–10 cmH₂O relative to the right atrium, indicates hypovolaemia. A progressively rising CVP above 15 cmH₂O indicates hypervolaemia.

Other biochemical analyses. Frequent arterial blood gas analyses and serum electrolyte (particularly serum K⁺) and creatinine levels are required for patients with severe burns over 30%. Carboxyhaemoglobin and random blood glucose should also be performed.

After the first 24 hours, capillary stability begins to return. Colloid (usually in the form of albumin) may be administered sparingly, although no consensus exists as to whether this is of any significant clinical benefit. Maintenance fluid replacement should continue following successful burns fluid resuscitation.

After the first 48 hours, total fluid therapy can be gradually regulated to allow a return to normal intake. Fluid reabsorption from oedematous tissues begins by the third to fifth day and is associated with diuresis and weight loss. Blood is generally not required in the early post-burn period but blood transfusion will be necessary to cover major burn wound excisional surgery.

Respiratory care: management of the airway. In severe facial burns, gross oedema of the face occurs in the first 24 hours and the adequacy of the airway must be carefully monitored, preferably by serial blood gas analyses. Intubation will be required for progressive hypoxia unresponsive to oxygen delivery by face mask. The oedema will subside within a few days; tracheostomy remains controversial and is to be avoided if possible.

Burns to the respiratory tract can be difficult to diagnose and progressive respiratory failure can result from smoke inhalation with minimal skin burning. Regular chest X-rays, blood gas and carbon monoxide estimations help in diagnosis. Severe pulmonary insufficiency will require assisted ventilation and the use of positive end expiratory pressure (PEEP) will improve oxygenation by reversing atelectasis.

Nutritional support. A major burn can result in the death of kilograms of tissue and if invasive infection supervenes, continued loss of body energy stores and weight losses and a hypercatabolic state persist. Adequate nutrition is vital. In patients with burns less than 20% oral intake is usually adequate after the first 24 hours. With burns more than 20–30%, nutritional support should be delivered through a nasogastric or nasojejunal feeding tube in preference to the parenteral route. The advantages of this are well documented: gut mucosal integrity is preserved and the incidence of bacterial translocation is significantly reduced. Where significant burnt tissue exists, maintenance of nutrition is best achieved by timely excision and early skin cover by skin grafting to avoid invasive infection. Overall patient management and burn wound management are thus intimately linked. Uncontrolled sepsis is the major cause of morbidity and mortality and can rapidly lead to a vicious circle of weight loss and further depletion of protein stores in an already immunocompromised host, with exacerbation of invasive infection.

Burn wound management

The patient is admitted to hospital (burn unit) or treated as an outpatient.

Admission is required for burns >10% in a child and >15% in adults, all deep burns, and all burns of vital or difficult areas such as face, hands and perineum.

Outpatient treatment is appropriate for superficial burns of small extent suitable for treatment by dressings.

Early wound care. The burn wound is covered with a temporary sterile dressing; local cleansing is performed as soon as the patient is stable. Cleansing and subsequent dressings are best performed in a warm environment (25–30°C) to help reduce evaporative losses. The initial cleansing of the burn wound is done gently using sterile swabs moistened with antiseptic-detergent solutions ‘aqueous chlorhexidine’ or ‘Betadine’ (povidone iodine). Adequate analgesia is essential. Obviously nonviable shards or shreds of dermal elements are excised, blisters are left unbroken unless very large and tense. Ingrained dirt and carbon are wiped gently away. Classification of some wounds may be difficult; dermal viability of wounds with uncertain burn depth may only be discovered with the passage of time or response to grafting.

Superficial (first-degree) burns. These wounds normally heal spontaneously over a week or so and require little else except simple non-adherent dressings and analgesia.

Superficial partial-thickness (second-degree) burns. If relatively clean, these wounds should be treated with paraffin-gauze dressings and left to heal over a period of two weeks. Dressings may be changed daily or every second day. In wounds with more contamination or suspected infection, the topical antibacterial cream, silver sulfadiazine (SSD), has a broad antibacterial and antifungal profile and may be used. All burn areas, including the margin with surrounding normal skin, are smeared with cream, applied with the sterile gloved hand or spatula as a buttered layer 3 mm thick, over the whole burn surface. After application of the antibacterial cream, the burnt area can be treated by one of two techniques.

Deep partial-thickness (second-degree) or full-thickness (third-degree) burns. Obviously deep burns (i.e. involving deeper layers of the dermis) should be excised as soon as possible and a split skin graft applied to the fresh surface. Left untreated, such wounds heal with significant scarring that may lead to contractures, deformity and subsequent loss of function. Tangential excision is the process whereby the burnt area is progressively sliced, using a skin graft knife (dermatome) set to take very fine surface shavings, and the exposed surface is observed for the presence of bleeding. The presence of circulation confirms viable tissue and a meshed split skin graft can be applied to the surface that first shows punctate haemorrhages, to facilitate healing and return of function. This process is used predominantly in partial-thickness burns. For full-thickness burns, fascial excision is more commonly used and involves the removal of the burnt tissue down to the level of the underlying fascia.

Escharotomy and fasciotomy. Escharotomy (Fig 13.11) involves an incision through burnt skin (eschar), to release any constriction that may compromise circulation. It is urgently indicated in burns that encircle the body wall (leading to abdominal compartment syndrome or restriction of respiration) or limb (threatening neurovascular supply). Electrical burns causing injury to deeper tissues may lead to significant swelling and increased compartment pressures and may require fasciotomy.

Figure 13.11 Locations for escharotomies

The incisions are placed along the mid-medial and mid-lateral lines of the extremities and the thorax (dashed lines). The skin is especially tight along major joints, and decompression at these sites must be complete (solid lines). Neck and digital escharotomies are rarely necessary.

Based on Brunicardi et al, 2005

Later care. The patient with a severe burn requires prolonged follow-up to prevent or treat late deformities and to aid rehabilitation. Skin destroyed by burns, even when excised early and replaced by a split skin graft, may never regain full function and convalescence is often slowed by painful and hypertrophic scars. A multidisciplinary approach to burn management is critical in improving patient outcomes and is the core strategy of burn units throughout the world. Physiotherapists and occupational therapists with training in burns physical therapy form an integral part of the team.

Primary injury: focal lesions

Contusions are brain surface bruises that occur mainly in the temporal and frontal lobes during acceleration/deceleration injury. Symptoms (most commonly prolonged confusion) usually persist for more than 24 hours. Depending on the site of contusion, focal neurological signs may be present. Most patients with cerebral contusion recover over a period of days, but some may develop secondary brain injury from raised intracranial pressure or cerebral oedema. Seizures may also occur.

Lacerations result from severe trauma to the brain; focal neurological deficit is invariable and is often permanent.

Skull fractures significantly increase the likelihood of underlying brain injury and may be classified according to whether they are open or closed, by morphology (linear vs stellate vs depressed) or by site (cranial vault vs base of skull). Depressed skull fractures imply a significant impact, with the potential for the fractured fragment to cause underlying dural penetration or brain laceration. Such injuries may increase the risk of infection (meningitis) by providing a portal of entry for bacteria. Basilar (base of skull) fractures usually involve the temporal bone and are characterised by the following clinical features: CSF otorrhoea or rhinorrhoea (from dural trauma); periorbital ecchymosis (raccoon eyes); ecchymosis around the mastoid process (Battle’s sign); haemotympanum (disruption of the temporal bone that houses the middle ear); and cranial nerve deficits (nerves III, IV and VI — from disruption of the cavernous sinus).

Intracranial haemorrhage may be extradural, subdural or intracerebral. Extradural haematomas (EDH) result, in most cases, from laceration of the posterior branch of the middle meningeal artery adjacent to a skull fracture. This leads to a unilateral increase in intracranial pressure. Only about one-third of patients have the classic ‘lucid interval’. There may be no initial loss of consciousness or minimal concussion with a rapid recovery of normal brain function. Prodromal features include increasing headache and restlessness, and oedema and bruising of the scalp over the fracture. With increasing size of the haematoma the temporal lobe is compressed, CN 3 palsy develops, increasing hemiparesis of the opposite side and eventually transtentorial herniation of the mid-brain occurs (Fig 13.12b). CT scanning typically reveals a biconvex, hyperdense, lenticular lesion that does not extend beyond the suture lines (sites of dural attachment).

Figure 13.12b Coronal section of a patient undergoing herniations of the brain caused by an EDH

A and B based on Williamson & Waxman, 1998

Subdural haematomas (SDH) are the most common intracranial space-occupying lesion complicating head injury. Unlike the arterial bleeding in EDH, the slower venous bleeding in SDH may delay clinical presentation. Classification of SDH is by time from injury: acute (<24 hours), subacute (24 hours to two weeks) and chronic (two weeks or more after trauma). Symptomatic acute SDHs are usually associated with severe brain damage and cortical lacerations, with bleeding from torn veins running from the cortex to the dural sinuses or from the venous sinuses themselves. Many patients with an acute SDH have a poor prognosis and surgical intervention is often not curative. Subacute and chronic SDH are a particular problem in the elderly, where poor memory for past events and injuries can delay diagnosis. Headache is the main presenting symptom. Features on CT scan include a hyperdense, crescentic lesion with associated mass effect and midline shift. The lesion often extends beyond the suture lines and may cover the surface of one hemisphere.

Intracerebral haematomas (ICH) occur in severe trauma and comprise haemorrhage deep within the substance of the brain (usually frontal and temporal lobes). Secondary brain injury may occur with raised intracranial pressure and bleeding into ventricles may cause obstructive hydrocephalus.

Primary injury: diffuse lesions

Concussion is classically defined as a temporary disruption of neurological function associated with posttraumatic amnesia that usually resolves within six hours. There may be associated loss of consciousness and autonomic dysfunction. Common clinical features include retrograde amnesia, headache, dizziness and nausea. It is generally accepted that the duration of amnesia is an accurate reflection of the severity of concussion. On clinical examination, there are usually no focal neurological signs.

Diffuse axonal injury (DAI) is common after head injury and is defined as a coma that persists for at least six hours and occurs immediately after trauma. Classification is into mild, moderate or severe, depending on the duration of coma. The underlying cause for the condition is thought to be diffuse disruption of axonal white matter tracts secondary to shearing trauma. Patients with mild DAI regain consciousness between six and 24 hours and exhibit a relatively complete recovery. In severe cases the patient may be in a prolonged coma, suffer from secondary brain injury and never regain consciousness.

Primary survey and resuscitation

Airway management in the severely head-injured patient is vital. The patient should also be presumed to have a cervical spine injury and particular care must be taken to support and protect the cervical spine at the same time as maintaining airway patency. A poorly managed airway is the most common cause of secondary brain injury. Cerebral injury may lead to centrally mediated respiratory depression or coma and securing a definitive airway (early intubation) is crucial.

As a general rule shock is not due to the head injury alone. Hypotension in these patients should still be assumed to be secondary to hypovolaemia or haemorrhage, rather than from primary brain injury (which is possible but less likely). Intravenous access should be obtained and fluid resuscitation commenced while any obvious haemorrhage is controlled. Significant blood loss from scalp lacerations can occur before arrival at hospital. The combination of such lacerations with the vasodilation secondary to alcohol intoxication can lead to hypovolaemic shock. Cerebral perfusion pressure (CPP) is equal to the mean arterial pressure (MAP) minus the ICP. For this reason, hypotension (decreased mean arterial pressure) is not tolerated by the brain and results in cerebral injury.

Once the patient has been stabilised, a brief neurological examination should be performed. The level of consciousness is the most important measure of the patient’s progress and is graded by eye opening, verbal and pain response according to the GCS. Determination of the GCS enables stratification of the patient into the mild, moderate or severe head injury category.

Secondary survey

Trauma severe enough to cause head injury often results in additional injuries to other parts of the body. Systematic (head-to-toe) examination aims to exclude or diagnose other injuries — in particular injuries to the chest and abdomen. Such injuries often produce hypoxia and shock that, unless promptly dealt with, will significantly decrease the chance of neurological recovery.

Re-evaluation

A standard head injury observations chart is required so that progress of the patient’s consciousness, eye signs, pain response, motor function and vital signs is recorded. Any deviations in trends or changes in neurological status can thus be recognised and treated promptly (Figs 13.13 and 13.14). Clinical deterioration is best detected by serial examination.

Plain X-ray

Plain X-rays of the skull are only indicated when CT scanning is not available. They may also be used in the setting of penetrating head injury, where it may be useful to determine the number or characteristics of intracranial foreign bodies. CT scanning can then be used to ascertain the exact location of the penetrating objects. When performed, several varieties of skull fracture may be seen on plain X-ray; all signify that the patient has suffered a significant head injury. Simple linear non-displaced vault fractures require no specific treatment, although fracture lines that cross the middle meningeal groove or major dural venous sinuses raise the possibility of EDH or SDH, respectively. Depressed skull fractures are readily detected on X-rays and may require surgical elevation. Compound (open) fractures, where the skin is breached adjacent to a fracture, require wound debridement and closure. Basal fractures may be internally compound and complicated by CSF leak into the nose or ear, with the dangers of meningitis and brain abscess. The presence of skull fractures significantly increases the likelihood of underlying traumatic brain injury and is a strong indication for immediate CT scanning. Other plain X-ray findings requiring further evaluation with CT scanning include subarachnoid or intraventricular air. A normal skull radiograph does not exclude intracranial injury.

CT scan

A non-contrast CT scan is the ideal investigation in all cases of head injury, especially if accompanied with a history of loss of consciousness or amnesia. The scan can be acquired rapidly and most emergency departments have protocols in place to determine which head-injured patients require CT scanning. These algorithms take into account GCS, presence of fracture, amnesia, seizure activity, focal neurological deficit, age, presence of coagulopathy and mechanism of injury. CT scanning may demonstrate skull fractures (on bone windows) or intracranial haematomas (on tissue windows). Other important radiological features include midline shift, herniation, petechial haemorrhage, hydrocephalus, intraventricular blood or air and cerebral oedema. There is no further benefit in ordering skull X-rays once CT scanning has been performed.

Lumbar puncture

There is very little place for lumbar puncture in the patient with head injury. In the patient with increased ICP, lumbar puncture may induce fatal brain herniation.

Magnetic resonance imaging (MRI)

MRI is not usually indicated in the immediate assessment of the head injured patient; it is time consuming, may not adequately define acute haemorrhage and lacks sensitivity in detecting bony injury. It is, however, useful in patients with persistent neurological dysfunction despite normal CT scan results. MRI is superior to CT scanning in detecting abnormalities associated with diffuse axonal injury and may demonstrate small cerebral contusions not otherwise detected by CT.

Cerebral angiography

Angiography is rarely indicated in the patient with an acute head injury. It is only indicated when CT scanning is not available and a vascular injury (i.e. dissection) is suspected.

General principles of management

Intravenous fluid resuscitation. The treatment of hypotension in head injury should be with intravenous infusions of normal saline or Hartmann’s solution. Hypotonic solutions such as 5% dextrose should not be used; hyponatraemia may lead to cerebral oedema and subsequent coma or death.

Mannitol. The use of osmotic agents such as mannitol (a sugar alcohol or polyol) is indicated in patients with increased ICP who demonstrate deterioration in neurological status. Intravenous bolus administration causes water to be drawn into the intravascular space by osmosis; this reduces cerebral oedema and brain volume, with a resultant decrease in pressure. Dosages of intravenous mannitol range from 0.25–1 g/kg and administration should be in consultation with a neurosurgeon. Urine output, blood pressure and serum electrolytes should be monitored closely.

Ventilation. Hypoxia must be avoided so that optimum cerebral oxygenation is maintained. An increase in PaCO₂ causes cerebrovascular dilatation and an increase in cerebral blood flow, which tends to increase ICP. A fall in PaCO₂ on the other hand causes cerebral vasoconstriction that can reduce ICP. In the patient with persistently raised ICP despite sedation, a limited period of hyperventilation (to keep PaCO₂ in the range of 30–35 mmHg) may be used in the acute setting to reduce the pressure. It is generally accepted that a PaCO₂ of less than 25 mmHg may cause significant cerebral ischaemia from vasoconstriction and should be avoided.

Steroids. There has been no convincing evidence in the literature to support the use of steroids in the management of acute head injury or raised ICP. They are not recommended.

Seizure prophylaxis. Approximately 10% patients who sustain a significant head injury develop early posttraumatic seizures. Early seizure activity in these patients may additionally traumatise the brain through secondary mechanisms and raised ICP, and anticonvulsant therapy is an effective preventative strategy. Drugs such as diazepam or phenytoin may be used in the acute setting. The long-term risk of posttraumatic seizure development, however, is not reduced by early administration of anticonvulsants.

Management of mild head injury (GCS 14–15)

The vast majority (approximately 75–80%) of all patients presenting to the emergency department with head trauma will have a minor injury. Most of these patients will recover completely and only a small minority will develop complications. At the very least, patients with mild head injury should be kept in the emergency department and observed for 12–24 hours and subsequently discharged with written advice if they remain asymptomatic, not intoxicated and when there is no clinical deterioration. In practice it is not possible to perform a CT scan on all patients with minor injury; risk stratification dictates which patients should be scanned. In general, those who present with loss of consciousness and amnesia for the traumatic event should be scanned, whereas the asymptomatic patient with GCS 15, alert and non-intoxicated may simply be observed for 12–24 hours. Advanced age (>60 years old), severe mechanism of trauma, headache and vomiting, drug or alcohol intoxication or seizure activity are some factors that warrant CT scanning and admission into hospital.

Management of moderate head injury (GCS 9–13)

Approximately 10% of head-injured patients presenting to the emergency department will have a moderate injury. These patients frequently have been involved in a motor vehicle accident and a large proportion suffer from intracranial haematoma (EDH or SDH). Clinical presentation is varied but includes confusion, headache, somnolence, amnesia, seizures and vomiting. Focal neurological signs may also be present. All of these patients should undergo CT scanning and admission into hospital (under a neurosurgical bedcard) for close observation and serial examination. A repeat CT scan may be indicated to investigate changes in neurological status or to assess for progression of known lesions.

Management of severe head injury (GCS 3–8)

One in 10 patients will be classified as having a severe head injury on presentation to the emergency department. These patients require a structured approach, described above, incorporating the ATLS™ principles of primary and secondary surveys with simultaneous resuscitation, management and frequent reassessment. Outcome following severe head injury is relatively poor, with less than half of adult patients surviving and of these, a significant proportion experiencing severe neurological deficits.

Management of specific complications

The treatment of head injuries can lead to a number of potentially dangerous complications that clinicians must be aware of (Box 13.5).

Box 13.5

Complications of head injury

Open and depressed skull fractures

Intracranial haemorrhage and cerebral compression

CSF leak, meningitis and intracranial abscess

Posttraumatic epilepsy and post-concussion syndrome

Facial injuries: airway, fractures

Compound or depressed fracture of the skull. The main aim in treating open fractures (in the absence of significant underlying brain injury) is to prevent infection. Debridement and closure of scalp wounds should be performed as soon as practicable. The amount of skin excised is determined by skin mobility, as well as the extent of damage to skin, but wounds of the scalp heal well, so tissue can usually be preserved. Debridement of imbedded foreign material and identification of underlying skull and cerebral damage is very important in minimising complications. In addition to infection risk, depressed fractures are also associated with a higher risk of early posttraumatic seizures; anticonvulsant therapy may therefore be indicated in the emergency department.

Depressed fractures are elevated if the depression is significant (i.e. if the depressed segment is at a deeper level than the adjacent inner table of the skull). This is done through an adjacent burr hole. Only completely detached fragments of bone are removed and with caution to avoid further damage to the underlying dura. All depressed fractures should be evaluated with CT scanning to exclude underlying intracerebral haematoma or contusion.

Intracranial haemorrhage. EDH: Current thinking (ATLS™) regarding the emergency management of EDH recommends that patients be transferred to a facility with neurosurgical services. In patients who are rapidly deteriorating due to expansion of the haematoma or, where neurosurgical facilities are a considerable distance away, an emergency burr hole may be life-saving. The procedure is not without risk, however, and should not be attempted without consultation with a neurosurgeon. The burr hole itself may cause direct trauma to the brain or contribute to intracranial haemorrhage. Furthermore, a well-positioned burr hole may only partially evacuate the haematoma.

SDH: These result from slower, venous bleeding. Early neurosurgical consultation is necessary and most patients undergo formal surgical evacuation in theatre.

Intracerebral haemorrhage, forming a localised haematoma in the brain, is uncommon. The early signs are of a focal expanding lesion. Operative decompression may be indicated when there is a local intracerebral lesion seen on CT scan.

CSF leak, meningitis and intracranial abscess (Fig 13.15). In most cases with CSF rhinorrhoea or otorrhoea, the leak will close spontaneously. CSF rhinorrhoea is detected by noting a thin nasal discharge, which must be distinguished from the discharge of allergic rhinitis. Beta-2-transferrin is found almost only in CSF and its presence in fluid assay confirms the diagnosis of CSF leak. Blowing the nose or sitting up should be avoided so that chances of retrograde CSF flow are minimised. There is no current evidence to support the routine use of prophylactic antibiotics. Rhinorrhoea is more likely to cease spontaneously than otorrhoea.

Figure 13.15 Complications of basal skull fracture

A: anterior fossa fracture with posterior conjunctival haemorrhage, CSF rhinorrhoea and epistaxis; B: middle fossa fractures with bleeding and CSF leak from the ear

The onset of meningitis should be suspected in the patient who develops fever and toxicity, with headache, restlessness, photophobia, vomiting and meningism. Lumbar puncture is indicated under these circumstances to obtain fluid for culture of organisms and antibiotic sensitivity. Empirical antibiotics should be commenced.

Intracranial abscess may be extradural, subdural or intracerebral. It should be suspected in the patient with meningitis who is unresponsive to treatment. Evidence of a space-occupying lesion is sought on CT scan. Abscess may arise from reversal of flow in CSF leak, an infected scalp wound in association with compound fracture or as an embolic phenomenon from sepsis elsewhere in the body.

Post-concussion syndrome (PCS). The duration of symptoms in concussion have been arbitrarily defined as less than six hours. When symptoms following the initial concussion persist for weeks, months or even years later, this is termed PCS. Headaches and dizziness are the most common symptoms experienced. Emotional disturbance and cognitive deficits may also be associated with PCS.

Le Fort classification

René Le Fort was a French army surgeon whose experiments with facial fractures in cadaveric skulls were published in 1901, giving rise to the Le Fort classification of midface fractures. Although some consider this classification to be an oversimplification, it is still used widely today (Table 13.6 and Fig 13.17). All Le Fort fractures involve a fracture of the pterygoid plates. Combinations of fractures frequently occur.

Figure 13.17 Le Fort classification of fractures of the maxilla

I: the infraorbital rim remains stable as the maxilla is rocked; II: only the medial section of the infraorbital rim moves — associated infraorbital nerve damage is common; III: the whole of the infraorbital rim moves with the maxilla

Source: Department of Radiology, University of Washington

Le Fort I: horizontal fracture of the maxilla immediately above the teeth and hard palate.

Le Fort II: pyramidal fracture that extends from the nasal bridge, inferior orbital floor, through the maxillary processes and across the pterygomaxillary fissure to involve the pterygoid plates.

Le Fort III: transverse fractures that are positioned at a high (suprazygomatic) level. These fractures extend from the nasal bridge and cribriform plate, to the medial wall of the orbit and into the zygomaticofacial suture.

Mandibular fractures

Mandibular fractures are described according to the anatomical site of damage, which may include the condylar process, body, angle, ramus, coronoid process or alveolar process.

Chemical injury

The most severe ocular injuries result from strong alkalis and acids. Alkalis such as powdered lime (used in cement) and sodium hydroxide (the basis of most industrial and domestic bleaches) readily penetrate the ocular tissues causing cell death and destruction of stromal ground substance. There is immediate sloughing of the corneal and conjunctival epithelium and in severe injuries damage occurs to blood vessels, leading to ischaemic necrosis. Death of corneal stem cells located at the limbus (junction of cornea and sclera) may result in progressive corneal ulceration and perforation. Subsequent scarring of the corneal and conjunctival surfaces can result in permanent visual loss and problems such as chronic dry eye syndrome. In contrast to alkalis, strong acids denature and coagulate protein, forming a barrier to further penetration. The damage tends to be more superficial, so the underlying stroma and important cellular elements may be spared. Solvents such as petrol or irritants such as capsicum spray cause painful injuries but rarely result in any long-term sequelae. The effects of other chemical classes on the eye are less predictable but information is usually available through the local poisons advisory service. Many industrial and domestic chemicals are supplied with labels or information sheets providing details of ocular toxicity and suggested first aid measures.

First aid

Immediate and copious irrigation of the eye with tap water or a similar aqueous-based neutral fluid at the scene of the chemical injury is the only effective treatment. All other measures after this are essentially supportive towards healing and regeneration of the ocular tissues. Once the patient has presented to hospital, further irrigation using normal saline or a commercial eye irrigation fluid for a period of 20–30 minutes is recommended to remove any residual chemical. Lay the patient on a trolley and direct a stream of irrigating fluid at the inner canthus while the patient blinks frequently or if possible keeps their eye open. This step may be facilitated by an initial drop of single-use, non-preserved topical anaesthetic. Following irrigation, the pH of the tear film can be tested using litmus paper, to ensure that a neutral pH has been reached. The eyelids should be everted and the conjunctival fornices inspected for any residual particulate matter. This is especially important with powdered lime injuries, where residual particles will continue to cause injury if left undetected.

Clinical assessment

The diagnosis is usually easily made on history with the hallmark features of delayed onset, bilateral symptoms and exposure to a source of UV radiation. Sunburn involving the face may be an accompanying feature. Blepharospasm and tearing will usually make examination difficult and can be temporarily relieved by a drop of topical anesthetic. Test and record vision and examine the eye carefully for alternative causes of symptoms such as foreign bodies. Slit lamp examination typically reveals conjunctival hyperaemia and corneal epithelial changes that, when severe, may have the appearance of ground glass. Fluorescein usually stains the corneal and conjunctival epithelium with a punctate (point-like) pattern.

Treatment plan

Treatment is supportive, as the superficial epithelial changes will resolve usually over one to two days. Chloramphenicol ointment is often prescribed, but there is no evidence to support the need for antibiotic prophylaxis. Any simple lubricating drop or ointment would be as effective. Topical cycloplegic drops, such as homatropine 2%, twice daily may provide some improvement in discomfort and photophobia in severe cases. Simple oral analgesics can be prescribed but they are unlikely to prove effective against the pain. Never prescribe topical anaesthetic drops, as the effect of such drops will rapidly diminish with each subsequent dose and they will have a toxic effect on the corneal epithelium, resulting in ulceration and impaired healing.

Clinical assessment

Sometimes globe rupture or perforation is obvious even to the inexperienced eye. Collapse of the globe, a foreign body such as a nail or staple protruding from the cornea or scleral surface or the prolapse of black uveal tissue through a gaping scleral or corneal wound are obvious signs. If the globe rupture is posterior, poor vision, extensive subconjunctival haemorrhage, distorted pupil, hyphaema and the loss of the red reflex are important clues. If the penetrating object is small and travelling at high speed, the injury may not be so obvious. Small holes in the sclera or cornea may self-seal so that the architecture of the globe and its visual function can be relatively well maintained. Corneal wounds can be inspected thoroughly with the aid of a slit lamp. The presence of iris adherent to the inner surface of the corneal wound or a shallowing of the anterior chamber depth should alert the clinician to the presence of full-thickness penetration. Injury to the lens will result in a localised opacification and holes in the iris can be detected by looking for a red reflex or transillumination through the defect while shining a small beam through the pupil.

As mentioned previously, an attempt should be made to test and record visual acuity in each eye, even with severe injuries. A Snellen chart designed for use at three metres is usually the best option, particularly for patients examined in a bed or on a trolley. If this is not practical due to pain, severe blepharospasm or altered conscious state, simply asking the patient to detect a penlight beam or hand motions is still useful clinical information.

First aid

Once an open eye injury is suspected, no further examination should be attempted. Further pressure on the eye or eyelids should be avoided by covering the injured eye with a commercial plastic eye-shield. Alternatively, a makeshift shield can be constructed from the cut end of a disposable foam drinking cup or a cone made from a circle of cardboard. The edges of the shield should rest against the bony margins of the orbit and be fixed in place with tape until the patient is in the operating theatre. No attempt should be made to remove any intraocular foreign body, nor should any type of eye drop or ointment be used in the eye. Keep the patient fasted and establish intravenous access. Provide a parenteral antiemetic, such as prochlorperazine 12.5 mg IV, to prevent vomiting. If the injury is very painful, a small dose of opiate analgesic can be given but this should be delayed until the antiemetic has had an opportunity to work. Vomiting will raise central venous pressure and thereby raise intraocular pressure with the potential to extrude intraocular contents.

Diagnostic plan

A CT scan performed with fine axial and coronal sections through the orbits will provide useful information about the architecture of the globe, the presence of associated bony orbital fractures and retained foreign bodies within the eye or orbit. This is particularly important in patients with a history of striking metal against metal where small, high-velocity metal fragments may have penetrated the eye or orbit. Intraocular foreign bodies consisting of iron and copper are toxic to the intraocular tissues over time if left undetected.

Treatment plan

The next steps in management involve preparing the patient for surgery. Antibiotic prophylaxis is given in the form of broad-spectrum parenteral agents with good ocular penetration. An example is ceftriaxone 1 g IV combined with clindamycin 600 mg IV. Alternatively, a single agent such as gatifloxacin, (a fourth-generation fluoroquinolone) has broad-spectrum activity against both Gram-negative and Gram-positive organisms, with good ocular penetration. Tetanus prophylaxis should also be given. Surgery should be performed as soon as it is practical, given the constraints of fasting and transportation to a facility equipped to deal with ocular trauma. Delay in repair of open eye injuries increases the likelihood of infection and is associated with poorer outcome.

The principles of primary surgical repair are to remove any foreign objects, close the ocular wound and restore normal ocular anatomy as best as possible. Subsequent surgery may involve treatment of intraocular infection (endophthalmitis), removal of a cataract, reattachment of the retina, corneal grafting or removal of the eye (enucleation). The latter is usually reserved for cases where the eye is blind, painful and has a significant cosmetic deformity. Enucleation is sometimes necessary to avoid the rare condition of sympathetic ophthalmia where cell-mediated immune destruction of the injured eye may also involve the uninjured eye.

Clinical assessment

Ask about the possible mechanism or injury and details of safety measures in place. If a penetrating injury is suspected then proceed as detailed in the previous section. Test and record vision and make an initial inspection of the eye using a slit lamp. If you are confident that no penetration has occurred then instill a drop of single-use, non-preserved topical anaesthetic into the eye. This will facilitate your examination and allow vision to be tested if the patient has difficulty in opening their eye. Inspect the corneal and conjunctival surfaces of the eye, including the conjunctival surfaces of the upper and lower eyelids. The upper eyelid can be everted by first asking the patient to look down, grasping the upper eyelashes and applying gentle counter pressure to the upper eyelid crease. Practice is necessary to accomplish this manoeuvre reliably with minimal distress to the patient. Your examination will be enhanced by staining the tear film with fluorescein and examining the surfaces using the cobalt blue light. Fine linear abrasions or larger areas of epithelial loss on the corneal and conjunctival surfaces suggest a subtarsal foreign body until proven otherwise.

Treatment plan

The surgical aim is to remove the object and any associated rust while minimising damage to the ocular tissues. Foreign bodies only lightly embedded in the conjunctiva and cornea may be removed using a cotton bud or dislodged using the tip of a 25-gauge needle. This is best achieved with the aid of a slit lamp. The slit lamp provides a well-illuminated, magnified image of the foreign body and a stable platform for the patient’s head. When using a needle to remove foreign bodies it should be held parallel to the plane of the face to avoid inadvertent ocular penetration. The elbows of the surgeon should rest on the table of the slit lamp to reduce tremor and involuntary movement of the arm and hand. Anaesthesia is provided by two or three drops of topical anaesthetic (e.g. amethocaine or benoxinate) applied over a few minutes. The patient’s eyelids should be held open by the surgeon’s other hand or by an assistant.

Rust staining of the corneal stroma is difficult to remove with a needle and is best debrided using a small-tipped dental burr attached to a battery-powered motor. Centrally placed or deeply embedded corneal foreign bodies should be referred to a specialist for removal. Corneal foreign bodies in young children should be removed under general anaesthesia. Prophylactic topical antibiotic cover should be provided with chloramphenicol drops or ointment four times a day until the eye is healed. Applying a patch to the eye for the first 12 hours is traditional but there is no firm evidence to suggest that this improves comfort or recovery.

Clinical assessment

Test and record vision. Examine the direct and consensual pupil responses, looking carefully for evidence of an afferent pupillary defect. An afferent pupillary defect will be present in cases of optic nerve injury and retinal detachment. An efferent pupillary defect is usually the result of trauma to the iris sphincter muscle, which may result in a permanently dilated pupil (traumatic mydriasis). A hyphaema is often visible macroscopically as a collection of blood or clot in the anterior chamber. A small hyphaema consisting of circulating red blood cells in the anterior chamber fluid may only be visible with the aid of a slit lamp. Over time, a hyphaema will collect in the inferior portion of the anterior chamber due to the influence of gravity. Check for the presence of a red reflex. Any opacity in the ocular media, such as hyphaema, traumatic cataract or vitreous haemorrhage, will lead to a reduction or loss of the red reflex. An attempt should be made to examine the fundus with a direct ophthalmoscope. Blunt trauma often results in a visible whitening of the retina (commotio retinae) that may affect vision if it involves the macula region. Commotio retinae usually resolves spontaneously with recovery of vision. Retinal tears are more common in the peripheral zones and are difficult to detect with a direct ophthalmoscope. Clues to the presence of a retinal tear include symptoms of flashes (photopsia) or mobile spots (floaters) in the vision. Look for an accompanying orbital injury (see below).

Diagnostic plan

A CT scan performed with fine axial and coronal sections through the orbits will provide information about the integrity of the globe and detect the presence of any associated orbital fractures.

Treatment plan

Refer blunt globe injuries to an ophthalmologist for further assessment. Management is usually conservative, but retinal tears and retinal detachment will require surgical intervention. The management of hyphaema is bed rest and the avoidance of antiplatelet medications, to minimise the potential for secondary haemorrhage. The risk of secondary haemorrhage is greatest in the first week following injury. The decision to admit the patient to hospital will depend on the likelihood of compliance with treatment and the presence of pain or complications. The threshold for hospital admission should be lower with children, large hyphaemas and patients living in remote locations. Complications of hyphaema include secondary glaucoma and corneal blood staining. Anti-glaucoma medications are sometimes required and less commonly surgical intervention.

Clinical assessment

Test and record vision. Look for any associated injury to the globe. Check the direct and consensual pupil responses to assess the function of the optic nerve. Ask about diplopia and test the vertical, horizontal and oblique binocular movements. A restriction of upward gaze is typical of orbital floor fractures involving the inferior rectus muscle. Ocular movement may also be limited by orbital haemorrhage. Enophthalmos is usually not evident in the first few days following an orbital fracture but will become manifest over the next few weeks as haemorrhage and swelling subside. Subcutaneous air (emphysema) due to communication between the orbit and sinuses may be palpable in the periorbital tissues. Test sensation over the lip and gum.

Diagnostic plan

A CT scan performed with fine axial and coronal sections through the orbits will demonstrate the presence of an orbital fracture, any prolapse of orbital tissue and the likelihood of extraocular muscle entrapment. The latter should be suspected when the muscle is seen in close proximity to the fracture site. Blood in the maxillary sinus is a strong indicator of orbital floor fracture, even if the bony landmarks do not appear displaced. Associated fractures of the zygoma, maxilla and nasal bones may also be evident.

Treatment plan

Orbital injuries resulting in reduced vision, proptosis or a relative afferent pupil defect should be referred promptly so that measures can be taken to relieve pressure on the globe and optic nerve. This can be achieved relatively quickly by performing a lateral canthotomy. A canthotomy releases pressure on the orbital tissues by enlarging the palpebral opening. After infiltrating the skin of the lateral canthus with 2% lignocaine or similar local anaesthetic agent, the lateral canthus can be cut horizontally using scissors. This incision cuts through the skin, orbicularis muscle and the centre of the lateral canthal tendon. Bleeding from the incision can be minimised by first compressing the area with a vascular clamp prior to making the incision. Intravenous mannitol may also be effective in reducing orbital pressure. Parenteral antibiotics covering upper respiratory organisms may be given as prophylaxis in cases of orbital fracture. Repair of orbital fracture is indicated in the presence of restricted eye movement or if the fracture is large and enophthalmos is likely to develop overtime. Ideally this should be performed in the first two weeks following injury before fibrosis and permanent restriction of eye movement occurs. A subperiosteal approach is used to identify the fracture site and after releasing any orbital tissues the defect is closed using a synthetic implant.

Clinical assessment

The laceration must be inspected to see if it is superficial (i.e. involving skin and or the obicularis muscle) or full thickness. Always suspect an injury to the lacrimal canaliculus if the eyelid margin is involved medial to the lacrimal punctum. Failure to repair the canaliculus, particularly on the lower eyelid, will result in a watery eye (epiphora). Ask the patient to look up and note the function of the levator tendon. If the levator tendon is damaged, it will need to be explored and repaired to avoid a permanent ptosis. These cases are best referred to an experienced plastic or ophthalmic surgeon.

Treatment plan

Superficial lacerations involving the skin and orbicularis can be closed simply with interrupted sutures using 6/0 silk or nylon. Full thickness lacerations require both deep closure with an absorbable suture such as 6/0 polyglactin and superficial closure with 6/0 silk or nylon. Care is needed when reforming the eyelid margin to avoid a notch, which will result in an obvious cosmetic deformity and, on the lower lid, constant leakage of the tear film through the gap. Opposing the two edges of the eyelid margin is best achieved using a vertical mattress suture of 6/0 silk through the middle or ‘grey line’ of the eyelid margin. The ends of the suture should be left long, folded forward over the skin of the eyelid and tied within the knot of a superficial skin suture. This will avoid suture ends rubbing against the globe. Deep sutures should be placed anterior to the tarsal surface, again to avoid rubbing against the eye. Due to the natural tension across the eyelid, the silk sutures should be left for 14 days in cases of full-thickness laceration.

Initial assessment

Investigations

A posteroanterior chest X-ray is performed in the upright position to better display effusions and pneumothorax. Other features to be sought are fractures, collapse or contusion of the lung, diaphragmatic hernia and mediastinal widening. Chest X-rays should precede intubation and controlled ventilation, apart from extreme emergencies. CT scanning of the chest is also indicated, especially when there is a significant mechanism of injury or when injury to lung parenchyma, mediastinum or great vessels is suspected. Haemoglobin and serial blood gas estimations are necessary in most patients. A baseline ECG should be performed and may be abnormal if cardiac injury has occurred. Echocardiography can be used to provide diagnostic information on valvular function, ejection fraction, left ventricular systolic function, right atrial pressures and can also assess the pericardial space for effusions. Angiography may be indicated when mediastinal widening suggests the possibility of mediastinal injury, such as a ruptured thoracic aorta with temporary tamponade.

Definitive care

General management

The patient with major thoracic trauma should be managed at a facility that offers cardiothoracic surgical services. Immediate measures to establish a clear airway, assist ventilation and treat circulatory failure are instituted. Endotracheal intubation and ventilation are indicated in most patients with severe chest injuries, associated head injury and altered consciousness, airway obstruction because of facial or neck injuries, sucking chest wounds, flail chest and associated severe shock. Failure to respond to adequate resuscitation also suggests the possibility of massive haemothorax, tension pneumothorax, cardiac injury or cardiac tamponade. Immediate thoracotomy is indicated in patients with a penetrating chest wound that has possibly involved the heart (traversing the mediastinum) and is associated with cardiopulmonary arrest or with shock that has not responded rapidly to blood transfusion. Immediate thoracotomy is rarely required or of benefit in blunt chest injuries. Thoracotomy may be indicated at a somewhat later stage for significant and continuing haemothorax or for large air leaks preventing re-expansion of the lung. An intrapleural chest tube (intercostal catheter) is required for flail chest and in patients with haemothorax or pneumothorax or tension pneumothorax.

Insertion of an intercostal catheter (ICC)

The successful insertion of an ICC relies on two factors: understanding the anatomy of the intercostal space and utilising a safe method of insertion. The intercostal space is bounded by the ribs (one above and one below). It is important to appreciate that the neurovascular bundle lies under the cover of the rib above. This comprises the vein, artery and nerve (V-A-N) from superior to inferior, in the plane between the internal intercostal and transversus group of muscles. The chest tube is preferably inserted through the fifth intercostal space anterior to the mid-axillary line (Fig 13.21) and ‘just above the rib below’ to avoid the neurovascular structures. In obese patients or in women with large breasts, the anterior mid-clavicular second intercostal space approach may be preferred. The pleura should be entered with the spreading tips of a forceps rather than with uncontrolled thrusting of a trochar. The intercostal catheter (size 30Fr) is passed posterosuperiorly (towards apex) for evacuation of air in pneumothorax or inferiorly, to facilitate dependent drainage of a haemothorax.

Figure 13.21 Tube thoracotomy

A: the fourth intercostal space is exposed in the mid-axillary line; B: a tunnel is made with an artery forcep starting over the fifth rib and directed under the fourth rib; C: finger or artery forceps entry is made into the pleural space; D: a large tube is inserted in a posterosuperior direction and sutured to the skin; E: the intercostal tube is attached to underwater drainage

Management of specific types of chest injury

Tension pneumothorax. Sometimes tension pneumothorax occurs immediately because a rib fracture has produced a one-way flap valve leak from the pleural surface. It may also be secondary to positive pressure ventilation in patients in whom an initially simple pneumothorax has not been recognised. Thus it is prudent to insert an ICC in all patients with posttraumatic pneumothorax or subcutaneous emphysema who need early endotracheal intubation and positive pressure ventilation. A suspected tension pneumothorax should be relieved immediately by inserting a wide-bore needle into the second intercostal space of the affected side. The diagnosis is made on clinical grounds — there is no time for a chest X-ray. The needle is subsequently replaced by a formal ICC with underwater drainage. A cardiothoracic referral should be made and the patient considered for VATS (video-assisted thoracoscopic surgery) pleurodesis at a later stage.

Haemothorax. Stony dullness to percussion, decreased breath sounds on auscultation and decreased chest wall expansion are features that are consistent with a haemothorax. A massive haemothorax may even cause mediastinal shift and contralateral deviation of the trachea. The diagnosis is confirmed by chest X-ray. Shock is treated by appropriate blood transfusion. In most patients the insertion of a large ICC (minimum 32Fr) is the only additional treatment necessary as bleeding has usually already stopped. Thoracotomy may, however, be indicated when there has been immediate drainage of blood greater than 1500 mL or continued blood loss greater than 150–200 mL per hour. The source of bleeding is usually found to arise from intercostal vessels that have been damaged by fractured ribs.

Open pneumothorax (‘sucking chest wound’) is treated early by surgical debridement and closure of the chest wound with ICC insertion. A simple first aid measure is to place a sterile, adherent dressing onto the wound, taped only on three sides so that a flap valve mechanism is formed. This enables air to leak out from the chest during the expiratory phase of breathing but prevents the sucking of air into the chest cavity during inhalation.

Cardiac tamponade. Cardiac tamponade occurs when fluid accumulates within the pericardial space and is evidenced by Beck’s triad: decreased arterial blood pressure (due to impaired ventricular filling and subsequent reduction in stroke volume and cardiac output); distended neck veins (from poor right ventricular diastolic filling); and muffled heart sounds (due to pericardial effusion). Although the triad is considered pathognomonic for acute cardiac tamponade, it is important to recognise that the distension of neck veins may not be present in the hypovolaemic patient. Treatment of cardiac tamponade is by pericardial aspiration performed through the left fourth intercostal space or from the epigastrium below the xiphoid. Penetrating cardiac injuries require prompt thoracotomy with decompression of the pericardium and repair of the myocardium if necessary.

Flail chest. A flail segment may be difficult to detect on admission. Paradoxical movement may only become apparent later with the development of atelectasis, especially when associated with lung contusion. Pulmonary contusion causes a reduction in lung compliance, with maximum reduction at about 24–48 hours after injury. The contused lung is sensitive to under- and over-fluid resuscitation and intravenous fluid administration must therefore be carefully managed. Multiple rib fractures that isolate a flail segment of chest wall are usually sited anterolaterally. There must be at least two fractures of the same rib for a segment to float and to move paradoxically. Involvement of a specialist pain service (for multimodality analgesia) and physiotherapist (for aggressive chest physiotherapy) should be organised as soon as possible. The patient should never be allowed to languish on the surgical ward with suboptimal analgesia — the outcome is predictable: these patients become tachypnoeic, diaphoretic and develop pneumonia. In addition, the increased work of breathing and metabolic demands may result in myocardial ischaemia or infarction in some patients with underlying cardiovascular disease. In some cases endotracheal intubation and positive- pressure mechanical ventilation may be indicated. Although operative fixation of the fractures is not routinely performed, thoracic surgeons may take the opportunity to perform rib stabilisation when the patient requires a thoracotomy for another reason (e.g. ongoing intrathoracic bleeding).

Pulmonary contusion. This condition usually follows severe blunt trauma or high-velocity missile wounds. Interstitial haemorrhage, oedema and atelectasis occur with a risk of secondary infection and progressive hypoxia. The subsequent release of inflammatory mediators may lead to the development of ARDS in a significant proportion of patients and this is potentially lethal. Intubation and mechanical ventilation is often required in patients with significant pulmonary contusion — especially in patients with pre-existing chronic airways disease. A high index of suspicion is required as clinical and radiological signs commonly do not appear until about 24 hours after injury; these patients should therefore be monitored closely with arterial blood gas analysis, ECG monitoring and chest X-ray. High-velocity missile wounds require operative debridement and pulmonary resections.

Blunt cardiac injury. The mechanism of the thoracic injury is important. Patients not wearing seatbelts and with clinical evidence of contact with the steering column are most likely to have a cardiac injury. Blunt cardiac injury may result in myocardial contusion, valvular disruption or rupture of the atria or ventricles. Patients often present with a fractured sternum and the following management is necessary: initial ECG followed by continuous cardiac monitoring (telemetry) for at least 24 hours (to exclude myocardial ischaemia/infarction and arrhythmias); serial cardiac enzyme estimations (biochemical evidence of myocardial injury); and echocardiography (to exclude pericardial tamponade or other cardiac injury).

Penetrating chest injuries. Damage to intercostal vessels, underlying heart, lungs and pleura, the diaphragm and abdominal structures are common. Mediastinal traversing wounds from bullets and other missiles require early or immediate thoracotomy, as will stab wounds associated with massive haemothorax. Structures potentially damaged include lung parenchyma, tracheobronchial tree, oesophagus, heart, great vessels (e.g. aortic disruption) and diaphragm (with possible secondary injury to subdiaphragmatic structures such as the liver or stomach). Stab wounds without progressive haemopneumothorax may only require local wound care combined with thoracocentesis, if the wound of entry is above the nipple line. Stab wounds between the nipple line and costal margin may also require a diagnostic laparotomy to identify or exclude intra-abdominal or diaphragmatic injury.