Clinical Surgery in General - part 2 pdf

TRAUMA Z and blood vessels. As the head moves because of an accel- erating or decelerating force, the skull, and then the brain, moves in the direction of the force. Consequently, strains develop in the brain tissue and small blood vessels opposite the impact point, producing the contusional changes previously described. Additionally, the brain continues to move until it impacts against the opposite side of the skull or its base, thus injuring it in two places, most severely at the site furthest from the impact; this is a contra coup injury (French = counterblow). Acute intracranial haematoma 1. Most extradural haematomas (EDHs) develop in the temporoparietal area following a tear in the middle meningeal artery. Much less commonly, they result from torn venous sinuses within the neurocranium. Compared to a venous cause, an arterially produced extradural haematoma develops quickly, producing a rapid rise in intracranial pressure. 2. The 'classic' presentation (Fig. 2.8) occurs in only one-fifth of patients. Some may be unconscious from the time of the impact, others do not lose consciousness at the time but later develop neurological features. Most commonly there is a deterioration of consciousness, pupil-size changes or a focal weakness. Acute intradural haematoma (IDH) 1. This incorporates both subdural (SDH) and intracerebral (ICH) haematomas, which frequently coexist, and are 3-4 times more common than extradural haematomas. Subdural haematomas usually develop in the temporal lobe and may be bilateral. Following application of an inertial force, some of the bridging veins tear and blood collects in the subdural space. Occasionally, a subdural haematoma develops without an accompanying intracerebral haematoma. Solitary intracerebral haematomas rarely develop in the frontal lobes. 2. Small intracerebral haematomas may result from inertial forces, and increase in volume over time. Depending on their location, they may cause localizing signs or a rise in the intracranial pressure, with deterioration in the patient's clinical state. 3. The forces needed to produce an intracerebral haematoma are greater than those needed to produce an extradural haematoma, so an intracerebral haematoma is usually associated with cerebral contusion and cortical lacerations. Consequently, the patient commonly loses consciousness immediately and may also exhibit focal signs such as contralateral hemiparesis (Greek parienai - to relax), unilateral pupil dilatation or focal fits. With a solitary subdural haematoma, an initial lucid period may be followed by deteriorating neurological state. This develops more slowly than following an extradural haematoma because the bleeding is venous rather than arterial. Tears of only a few bridging veins, in the presence of brain atrophy with enlargement of the intracranial space, may delay development of symptoms for several days. Subarachnoid haemorrhage (SAH) This occasionally follows a head injury. The patient often develops severe headaches and photophobia, but other signs of meningism can occur. Do not test for neck stiffness until cervical spine injury has been ruled out clinically and radiologically (see Ch. 1). SPINAL INJURIES In the UK, 10-15 people per million of the population suffer spinal injuries each year (Table 2.8). The commonest site is the cervical spine (55%), mainly because most people are injured following a road traffic accident (48%). Table 2.8 Site Cervical Thoracic Lumbar Multiple Sites of spinal injuries Blunt trauma (%) 55 35 10 10 Penetrating trauma (%) 24 56 20 • Transient loss of consciousness at the time of the injury from a momentary disruption of the reticular formation. • Patient then regains consciousness for several hours, the lucid period. • Localizing signs develop with neurological deficits, headache and eventually unconsciousness from the developing EDH, which causes the ICP to rise. Fig. 2.8 Classic history of an extradural haematoma (EDH). 37 EMERGENCY Primary neurological damage 1. This results directly from the initial insult, usually from blunt trauma, producing abnormal movement in the vertebral column. Severe trauma may lead to ligamental rupture and vertebral fractures, reducing the space around the spinal canal and allowing bone and soft tissue to impinge directly on the cord. The potential space around the spinal cord may already be small, increasing the chance of neurological damage. 2. Less commonly, penetrating trauma, as by stabbing, causes primary spinal damage. Much more extensive areas of destruction and oedema result when the spinal cord is subjected to a large force such as a gunshot. Secondary neurological damage 1. The three common causes of damage following the initial injury are mechanical disturbance of the back, hypoxia and poor spinal perfusion. These effects are additive. 2. Hypoxia can result from any of the causes mentioned above, but significant spinal injury alone can cause it (Table 2.9). The underlying problem is usually a lack of respiratory muscle power following a high spinal lesion. Lesions above T12 denervate the intercostal muscles. Injuries above the level of C5 also block the phrenic nerve, paralysing the diaphragm. 3. Inadequate spinal perfusion results either from general hypovolaemia or failure of the spinal cord to regulate its own blood supply following injury. A fall in mean arterial pressure therefore produces a reduced spinal perfusion. Conversely, if the pressure is increased too far it may produce a spinal haemorrhagic infarct. Secondary damage leads to interstitial and intracellular Table 2.9 Respiratory failure in spinal injury Tetraplegic Intercostal paralysis Phrenic nerve palsy Inability to expectorate V/Q mismatch Paraplegic Intercostal paralysis oedema, further aggravating the deficient spinal perfusion. As this oedema spreads, compressing neurons, it produces an ascending clinical deterioration. In cases of high spinal injury this process can lead to secondary respiratory deterioration. Partial spinal cord injury Anterior spinal cord injury results from direct compression or obstruction of the anterior spinal artery. It affects the spinothalamic and corticospinal tracts (Fig. 2.9), resulting in loss of coarse touch, pain and temperature sensation, and flaccid weakness. This type of injury is associated with fractures or dislocations in the vertebral column. Central spinal cord injury usually occurs in elderly patients with cervical spondylosis. Following a vascular event the corticospinal tracts are damaged, resulting in flaccid weakness. Because of the anatomical arrangement in the centre of the cord, the upper limbs are more affected than the lower. Sacral fibres in the spinothalamic tract are positioned laterally to corresponding fibres from other regions of the body (Fig. 2.9). It follows that anterior and central injuries, which primarily affect the midline of the spinal Fig. 2.9 Cross-section of the spinal cord demonstrating the longitudinal tracts. (With permission from Driscoll P, Gwinnutt C, Jimmerson C, Goodall O. In: Trauma resuscitation: the team approach, Macmillan Press Ltd). 38 2 TRAUMA Z cord, may not affect the sacral fibres. This 'sacral sparing' produces sensory loss below a certain level on the trunk, with retention of pinprick appreciation over the sacral and perineal area. Lateral spinal cord injury (Brown-Sequard syndrome) is the result of penetrating trauma. All sensory and motor function is lost on the side of the wound at the level of the lesion. Below this level there is contralateral loss of pain and temperature sensation with ipsilateral loss of muscle power and tone. Posterior spinal cord injury is a rare condition, resulting in loss of vibration sensation and proprioception. Spinal shock 1. This totally functionless condition occasionally occurs following spinal injury. The features are generalized flaccid paralysis, diaphragmatic breathing, priap- ism, gastric dilatation and autonomic dysfunction associated with neurogenic shock. The English neurologist C.E. Beevor (1854-1908) described movement of the umbilicus when the abdomen is stroked, resulting from paralysis of the lower rectus abdominis muscle. 2. This state can last for days or weeks, but areas of the cord are still capable of a full recovery. Permanent damage results in spasticity once the flaccid state resolves. Upper motor neuron reflexes return below the level of the lesion following complete transection of the cord, producing exaggerated responses to stimuli; however, sensation is lost. 3. During this stage there is risk of pressure sores, deep venous thrombosis, pulmonary emboli and acute peptic ulceration with either haematemesis or, occasionally, perforation. FRACTURES 1. Fracture occurs in normal bone as a result of trauma. The type of fracture depends on the direction of the viol- ence. A twisting injury causes a spiral or oblique fracture, a direct blow usually causes a transverse fracture, axial compression frequently results in a comminuted (Latin minuere - to make small) or burst fracture. 2. Stress fractures occur when the underlying bone is normal. It is the repetitive application of an abnormal load that causes the bone to fracture. The load alone is not sufficient to cause the fracture but rather the cumulative effect of repeated loading. It is most frequently seen in individuals undertaking increased amounts of unaccus- tomed exercise, such as the 'march' metatarsal fracture in army recruits and dancers. 3. Pathological fractures occur when the underlying bone is weak, perhaps from metastatic cancer or metabolic bone disease; as a result it gives way under minimal trauma. Fracture repair 1. When a fracture occurs, not only is the bone broken but the encircling tissues are also damaged. The bone ends are surrounded by a haematoma including these injured tissues. Within hours an aseptic inflammatory response develops, comprising polymorphonuclear leu- cocytes, lymphocytes, macrophages and blood vessels, followed later by fibroblasts. Within this organized fracture haematoma, bone develops either directly or following the formation of cartilage with endochondral ossification. At the same time osteoclasts resorb the necrotic bone ends. The initial bone that is laid down (callus) consists of immature woven bone, which is gradu- ally converted to stable lamellar (Latin lamina - a thin plate) bone with consolidation of the fracture. Resorption occurs within the bone trabeculae as recanalizing haversian systems (described by the English physician C. Havers 1650-1702) bridge the bone ends. 2. There are two types of callus. Primary callus results from proliferation of committed osteoprogenitor cells in periosteum and bone marrow. They produce directly membranous bone, a once-only phenomenon limited in duration. The second callus is inductive or external callus, derived from the surrounding tissues, formed by pluri- potential cells. A variety of factors, including mechanical and humoral factors, may induce these mesenchymal cells to differentiate to cartilage or bone. 3. The mediators for callus formation are not fully understood. Probably the fracture ends emit osteogenic substances, such as bone morphogenetic protein, into the surrounding haematoma. This is in addition to mediators such as IL-1 and growth factors released from the fracture haematoma. Angiogenic factors probably play an important role in the vascularization of the fracture haematoma. 4. Movement of the fragments increases the fracture exudate. Rigid fixation minimizes the granulation tissue and external callus and may retard the release of mor- phogens and growth factors from the bone ends. Reaming of the intramedullary canal may cause addi- tional bone damage. Weight bearing stimulates growth factors and prostaglandins, which act as biochemical mediators. PERIPHERAL NERVE INJURY 1. Blunt trauma to a nerve may produce a temporary block in the conduction of impulses, leaving the axonal transport system intact. The axon distal to the injury survives and complete functional recovery can be expected; 39 EMERGENCY this is neuropraxia (Greek a - not + prassein = to act). More severe trauma will interrupt axonal transport and cause wallerian (Augustus Waller 1816-1870) degeneration: the distal axon dies, the myelin sheath disintegrates and the Schwann cells turn into scavenging macrophages which remove the debris. The cell body then embarks on a pre- programmed regenerative response which is usually known as chromatolysis, as it involves the disappearance of the Nissl's granules which are the rough endoplasmic reti- culum of the normal cell. An entirely new set of ribosomes appears, dedicated to the task of reconstruction. By their efforts, axon sprouts emerge from the axon proximal to the lesion and grow distally. Injury of this severity is known as axonotmesis (Greek tmesis = a cutting apart). It eventually produces a good functional result because the endoneurial tubes are intact and the regenerating axons are therefore guaranteed to reach the correct end organs. 2. Laceration or extreme traction producing neuro- tmesis also leads to wallerian distal degeneration and proximal chromatolysis - loosening of the chromatin of cell nuclei, followed by either cell death or axonal regen- eration. In this case, however, the final functional result is bound to be much worse than in any injury that leaves the endoneurial tubes intact. Not only do the axon sprouts have to traverse a gap filled with organizing repair tissue, but each one needs to grow down its original conduit at a rate of approximately 1 mm per day. Axons failing to enter the distal stump may form a tender neuroma, often producing troublesome symptoms. Progress can be monitored clinically using the sign described by the French neurologist Jules Tinel (1879-1952). These are electric feel- ings in the territory of the nerve produced by light per- cussion over regenerating axon tips, whether in the distal portion of the nerve or in a neuroma. 3. Motor axons are capable of producing collateral sprouts once they enter muscle, leading to abnormally large motor units with relatively good return of strength. Sensory axons often fail to reinnervate the specialized receptors forming the basis for the sense of touch and this, together with the mismatching of axons with conduits, invariably results in poor sensory recovery except in the very young. The functional result in the hand is poor. Compartment syndrome This specific type of neurovascular compromise can occur as part of any extremity injury. Although commonly caused by fractures and soft tissue injuries, the presence of a fracture is not essential. It is a progressive condition in which the elevated tissue pressure within a confined myofascial compartment exceeds capillary pressure, leading to vascular compromise of the muscles and nerves. It can result from a variety of causes, categorized as either expansive or compressive. External compression of compartment • Constricting dressing or cast • Closing fascial defects • Third degree, full thickness, burns. Expansion of compartment contents • Haemorrhage and oedema following fractures or soft tissue injuries • Haemorrhage following coagulopathy or vascular laceration • Postischaemic swelling. The four compartments of the lower leg are the most commonly involved areas, but it can occur in the shoulder, arm, forearm, hand, buttock, thigh or abdomen (following trauma or surgery). Key points • Continuously monitor at-risk sites in order to detect and correct impeding compartment syndrome (Table 2.10). • Increasing pain, exacerbated by passive flexion and extension, is a reliable combination signalling compartment syndrome. 1. Detect the condition in the early, potentially reversible stage or muscle may infarct, giving rise to rhabdomyolysis, hypovolaemia, hyperkalaemia, hyper- phosphataemia, high levels of uric acid, metabolic acidosis, renal failure and death. Locally fibrotic contractures may develop. 2. Detection should be clinical but the intracompart- mental pressure can be monitored when clinical assessment is difficult or if you are in doubt about the clinical Table 2.10 Features of impending or established compartment syndrome Early Pain in the limb Pain on passive movement of the distal joints Paraesthesia Loss of distal sensation Late Tension or swelling of the compartment Absent muscle power Very /ate Absent pulse pressure in the distal limb 40 2 TRAUMA 2 features. Examples of such cases are when the patient is unresponsive because of neurological injury or sedation, or has a nerve defect from other causes, or has a regional nerve block. Use it as an adjunct to, not a replacement for, clinical monitoring. 3. Absolute pressure values are unreliable because perfusion is dependent upon the difference between the arterial blood pressure and the compartmental pressure. A difference of less than 30 mmHg between diastolic blood pressure and compartment pressure is recommended as a threshold for releasing the tension by carrying out fasciotomy. A fall in the distal pulse pressure is a very late sign and indicates imminent tissue ischaemia. Pulse oximetry is not a reliable help in diagnosing or monitoring impaired perfusion secondary to raised compartment pressure. 4. Myoglobinuria and raised plasma myoglobin result not only from direct myocyte damage but also from polymorphonuclear neutrophil-mediated cell lysis and microvascular coagulation. Acute renal failure complicates severe crush injury as a result of hypovolaemia leading to prerenal failure, while the released myoglobin from damaged muscle cells precipitates and obstructs flow in the renal tubules. Myoglobin and macrophage-generated cytokines experi- mentally induce levels of potent vasoconstrictors such as platelet activating factor and endothelins, causing renal arteriole constriction, decreased glomerular filtration and renal ischaemia. A high concentration of myoglobinuria produces a red or smoky brown discoloration of the urine. Look for this when you catheterize the patient and check the urine regularly. CRUSH SYNDROME 1. Crush injuries occur in a variety of ways: for example, in patients becoming trapped under fallen masonry or in a car following a road traffic accident. The patient's own body weight may be sufficient to compress the tissue if the consciousness level is depressed for a con- siderable time. Severe beatings and epileptic seizures may also be responsible. 2. They present both local and systemic problems. The local injury may be complicated with compartment syndrome. Systemic concerns include intravascular volume depletion, electrolyte imbalance and renal injury from myoglobin. Until the limb is released there is little systemic effect; once reperfusion starts, plasma and blood leak into the previously crushed soft tissues as a result of the increased capillary membrane permeability and vessel damage. The effect depends upon the degree of tissue damage and in severe cases may produce hypovolaemia. Devitalized tissue is at high risk of secondary infection with a further systematic release of toxins. 3. Abnormal systemic blood markers of muscle infarc- tion include rising blood urea nitrogen, raised potassium, phosphate, uric acid and creatine kinase. Metabolic acidosis develops with an increased anion gap. Hypocalcaemia occurs although intracellular calcium is raised. The packed cell volume is raised but there is thrombocy topenia. Key point The sudden rise in serum potassium concentration may produce cardiac arrhythmias (and arrest) soon after the patient is released. FAT EMBOLISM SYNDROME 1. Ninety per cent of cases result from blunt trauma associated with long bone fractures. It has, however, also been reported following burns, decompression sickness and even liposuction! 2. The classical triad of respiratory failure, neurological dysfunction and petechial rash is not present in all cases; indeed the rash, though pathognomonic, is only present in 50% of cases. 3. As several organs can be affected, there is a wide range of possible clinical presentations, although dysp- noea is the commonest. The onset of symptoms is usually between 24 and 48 h postinjury. Pulmonary changes include ventilation-perfusion (V/Q) mismatch, impaired alveolar surfactant activity and segmental hypoper- fusion. Shadowing on chest X-ray is not dissimilar to ARDS. Neurological changes occur as a result of hypoxia and /or the humoral and cellular factors released from the bone. Effects on the heart may result in a fall in mechanical performance and arrhythmias. Renal damage can lead to lipiduria with tubular damage and ischaemic glomerular-tubular dysfunction. 4. Lipid globules are formed mainly from circulating plasma triglycerides, carried by very low density lipopro- teins (VLDLs). In trauma, this is commonly a result of the release into the circulation of lipid globules from damaged bone marrow adipocytes; however, it can also occur with increased peripheral mobilization of fatty acids and increased hepatic synthesis of triglycerides or reduced peripheral uptake of plasma VLDLs (Fig. 2.10). It gives rise to thromboembolism of the microvasculature, with lipid globules and fibrin-platelet thrombi. In addition, the local release of free fatty acids can cause a severe inflammatory reaction that initiates the SIRS chemical 41 2 EMERGENCY Fig. 2.10 The mechanism of interaction between raised plasma triglycerides and the pathogenesis of multiorgan system dysfunction in fat embolism. cascade, which is probably responsible for the high asso- ciation of fat emboli syndrome with both progressive anaemia and pyrexia (> 38.5° C). Key point • Diagnosis of fat embolism rests on identifying fat globules in body fluids, histological recognition, or pulmonary involvement with at least one other organ system dysfunction. 5. Search for fat globules in body fluids, such as sputum and urine, or lipid emboli in retinal vessels on fundoscopy; histological diagnosis requires demonstra- tion of intracellular and intravascular aggregation of lipid globules with Sudan black stain. PATHOPHYSIOLOGY OF WOUND HEALING Soft tissue injuries heal by a complex series of cellular events that lead to connective tissue formation and repair by scar formation. Three fundamental things must happen for wound healing to occur: (1) haemostasis must be achieved; (2) an inflammatory response must be mounted in order to defend against microbial infection as well as attracting and stimulating the cells needed for tissue repair; and (3) many different cells must proliferate and synthesize the proteins necessary for restoring integrity and strength to the damaged tissue. This is covered in more detail in Chapter 33. Wound healing therefore requires: • Haemostais • Inflammation • Cell proliferation and repair. Wound contracture When wounds with tissue loss are left to heal by secondary intention, contraction of granulation tissue reduces the size of the tissue defect. The cell responsible for this process is the myofibroblast, although the exact role of this cell is unresolved. Even though reducing the size of the tissue deficit is of benefit in wound healing, the distortion and scar formation produced by the process inhibit function in certain areas of the body (particularly on the face and around joints). PATHOPHYSIOLOGY OF BURNS Three risk factors for death after burn injury have been identified: age more than 60 years; burn surface area of more than 40%; and the presence of inhalational injury. Increased fluid losses due to uncontrolled evaporation are coupled with fluid shifts for the first 24-48 h after a major burn. Leakage of intravascular water, salt and protein occurs through the porous capillary bed into the interstitial space. This, in turn, results in loss of circulating plasma volume, haemoconcentration and hypovolaemia, the severity of which increases with the severity of the burn. In a burn over 15% of the total body surface area (TBSA), the capillary leak may be systemic, causing generalized oedema and a significant fall in blood volume. Shock associated with burn injuries The effect on the circulation is directly related to the size and severity of the burn wound. The body compensates for this loss of plasma with an increase in peripheral vascular resistance, and the patient will appear cool, pale and clammy; however, this compensation will only be effective in maintaining circulation for a period of time, depending on the severity of the burn and the 42 presence of other injuries. Ultimately, the patient will demonstrate signs of hypovolaemic shock as the cardiac output falls. During this time it is rarely possible to keep the circulating volume within normal limits. The end of the shock phase in the adequately resuscitated burn patient is usually marked by a diuresis. This occurs approximately 48 h after the burn and is usually associated with a fluid balance that is more like that of an uninjured individual. A burn of greater than 15% TBSA almost always requires intravenous fluid administration to expand the depleted vascular volume. However, shock can occur with a burn involving as little as 10% TBSA, as a result of complicating factors such as age, pre-existing disease and other major injuries. In these circumstances, a burn of 25-40% becomes a potentially lethal injury. Numerous fluid regimens have been calculated to assist in burn resuscitation: it is sensible to use the regimen favoured by your local burns department. Depth of burn and cause of burn The diagnosis of the depth of burn is not always easy. If doubtful, it should be reassessed at 24 h, using non- adherent dressings between examinations. Superficial burns Superficial burns are characterized by erythema, pain and the absence of blisters. Typical examples of superficial burns would be sunburn or simple flashburns. The epithelium remains intact so infection is not usually a problem and they generally do not require fluid replacement. Healing takes place over a few days and, with the exception of some pigmentation changes, no scarring occurs. Partial thickness burns Superficial partial thickness and deep partial thickness burns have been described. In the superficial variety the epidermis and the superficial dermis are burnt. They appear pink, moist and have fluid-filled, thin-walled blisters. They are associated with more swelling and are painfully sensitive, even to air current. Healing is by epithelialization from the pilosebaceous and sweat glands, as well as the wound edges. Therefore healing is often prolonged to 3-4 weeks. In deep partial thickness burns the reticular dermis is involved. The appearance is a mixture of red and white, with blistering also a feature. The capillary refill is often prolonged and two-point discrimination may well be diminished. Healing is from the few remaining epithelial appendages and can take up to 6 weeks. It results in poor quality skin and marked pigmentation change (either hyper- or hypopigmentation). Hypertrophic scar formation may be a problem, as can wound contraction. Infection may complicate the recovery of any partial thickness burn because the epithelium has been breached. This may take the form of locally delayed wound healing or sytemically-induced multiorgan failure (MOF). Deep dermal burns can result from scalds, contact burns, chemical burns and flame burns. Full thickness burns Full thickness burns involve the destruction of both the epidermis and dermis. They appear white, leathery and have no sensation to pinprick. The diagnosis between deep dermal and full thickness burns can be difficult, as they commonly lie adjacent to each other within the same wound. They can only heal naturally by epithelialization from the wound edge, leaving a contracted, poor quality scar. In the acute situation, circumferential full thickness burns around limbs and the chest can act as tourniquets, impeding the distal circulation and respiration, respect- ively. Urgent escharotomy may be required in these situations so discuss the possibility early with the local burns centre (see Ch. 24). Simplistically, the depth of a burn is a product of the injurious temperature and the contact time. Thus the arm of an alert individual exposed to a hot flame, and quickly removed, will cause damage similar to that in a comatose patient lying against a warm radiator. The young and elderly are similarly immobile and prone to deep burns from relatively innocuous hazards (e.g. hot bathwater). Patients with peripheral neuropathies (e.g. diabetics) may also present with unexpectedly severe contact burns. Chemical injury, such as that due to hydrofluoric acid or strong bases, can give rise to full thickness burns requiring specialist treatment. A high index of suspicion is appropriate when dealing with electrical burns because current flows preferentially through the deep structures, and extensive tissue damage may not be evident on early superficial inspection. Patients with full thickness burns may require blood transfusion, as red cell haemolysis occurs with direct thermal injury; indeed there is generalized fragility of the entire red cell population leading to reduced cell lifespan. Toxic shock syndrome Toxin-producing strains of staphylococcal or streptococ- cal bacteria can colonize wounds. A marked cytokine 43 TRAUMA 2 1 EMERGENCY response is stimulated, leading to a severe systemic illness typified by: • Pyrexia (usually >39° C) • Vomiting and /or diarrhoea • Rash (erythematous, maculopapular) • Malaise, dizziness, peripheral shutdown or frank shock. It can occur even with relatively small, superficial burns and is more common in children. Treatment is with oxygen, intravenous fluids and antibiotics. Response of the respiratory system to inhalational injury The upper airway may receive thermal burns, and tissue swelling can develop very rapidly in these vascular tissues. Injury to the mouth and oropharynx in particular can cause acute respiratory obstruction. Oedema from these injuries may also involve the vocal cords. Dramatic changes in the patient's ability to maintain the airway have been observed over a short period of time following this type of injury. The lungs themselves are rarely injured from 'burning'. Usually laryngeal spasm occurs from the heat of the inspired gases, thereby protecting the lower airway and lungs from exposure; however, steam, with a heat capacity approximately 4000 times that of dry air, can carry heat to the lower airways, resulting in significant distal thermal injury. Smoke inhalational injury secondary to confinement in a house fire may be associated with a wide variety of concomitant chemical injuries; for example, plastic furniture and textiles will release hydrogen chloride. Not only does this cause irritation to the eyes and throat but it also causes severe pulmonary oedema. Phosgene, produced from the burning of polyvinyl chloride, is also associated with the development of significant pulmonary oedema. Burning mattresses can produce nitrogen dioxide. As fires can produce such a wide variety of chemicals, the resultant pulmonary damage may be multifactorial. This may result in necrosis of respiratory epithelium, inactivation of the respiratory cilia, and destruction of type II pneumocytes and alveolar macrophages. This leads to a decrease in lung compliance, which is seen as an increase in the work of breathing and an impairment of diffusion through the alveolar membrane. In view of the very large surface area of the lung, fluid requirements for resuscitation may increase by as much as 50% of the calculated values if a severe inhalation injury has been sustained. The severity of the injury will not be related to the TBSA burn size, but rather to the length of time and intensity of exposure to the inhalation. Accurate information from the prehospital care providers relative to these conditions is vital in planning the patient's care and anticipating respiratory complications. Carbon monoxide poisoning Systemic absorption of inhaled toxins may also occur. Carbon monoxide (CO) is reported to be the leading toxi- cological cause of death. Burning any carbon-containing material can release CO, a byproduct of incomplete com- bustion. The mechanisms of CO toxicity are multiple. CO competes with oxygen for binding with haemoglobin, myoglobin and cellular cytochrome oxidase. In addition, off-loading of oxygen to the tissues is impaired by the leftward shift of the oxygen-dissociation curve induced by carboxyhaemoglobinaemia. The result is profound hypoxia both in the intra- and extracellular environ- ments. The areas most affected are those with a high metabolic rate: heart and brain. Fetal tissue is also at significant risk. Measured carboxyhaemoglobin levels do not neces- sarily correspond to clinical symptoms. The duration of the patient's exposure to CO is significant, as short expos- ures to a high concentration may give high carboxyhaemoglobin levels but not cause significant metabolic effects (usually acidosis with bicarbonate deficit). Carboxyhaemoglobin levels greater than 10% are significant and levels greater than 50% are generally lethal. Early treatment with high concentration oxygen is essential. Carbon monoxide intoxication is the biggest cause of death in people caught in house fires or other types of closed-space fires. Cyanide poisoning When the polyurethane foam in modern furniture burns, a thick black smoke is produced. This not only contains CO and the corrosive substances mentioned above but also cyanide gas. The latter is another metabolic poison which binds to mitochondrial cytochrome oxidase. This leads to inhibition of adenosine triphosphate (ATP) production, with rapid onset of profound cellular anoxia and death. Cyanide gas is difficult to measure but should be assumed to be present if the carbon monoxide level is greater than 10%. Severe metabolic acidosis and raised 44 2 TRAUMA 2 lactate levels found on arterial blood gas analysis provide further clues towards the diagnosis. TRAUMA SEVERITY SCORING Essentially two separate types of trauma score have been developed. One type is based on the anatomical injuries sustained by the patient, while the other makes use of physiological data taken from the patient at first contact. They have developed in an attempt to achieve two separate objectives: firstly, to predict the probability of survival of an individual patient; and, secondly, to compare outcomes between different hospitals, or the same hospi- tal over time. The Injury Severity Score (ISS) is an anatomical scoring system that gives an overall score for patients with multiple injuries. The body is divided into six regions. Within each region every injury is given an Abreviated Injury Scale (AIS) score. This is a predetermined score from 1 (minor) to 6 (unsurvivable). The three highest grading scores, which are found in separate regions, are squared and then added together to make the final score. An obvious deficiency in this model is that it does not take account of multiple injuries within one body region. More recent scores such as the New Injury Severity Score (NISS) have been developed in an attempt to take account of such inaccuracies. The Revised Trauma Score (RTS) is a physiological scoring system which attempts to predict outcome based on the first set of data obtained on the patient. The timing of first data recording and the effect of any treatment previously instigated will have a variable effect. None the less, it has been shown to correlate well with the probability of survival. It is calculated by combining three separately weighted scores based on the observed GCS, respiratory rate and systolic blood pressure. TRISS determines the probability of survival of a patient by combining the ISS and RTS along with weightings to take account of the patient's age and the mechanism of injury (i.e. blunt or penetrating). The weightings have been calculated from a large database of trauma victims and allow comparative audit to be carried out. ACKNOWLEDGEMENTS Thanks are due to Geraldine M c Mahon, Richard Cowie, Charles Galasko, Roop Kishen, Roderick Little, David Marsh, Mohamed Rady, Stewart Watson and David Whitby. Summary • Trauma is an important clinical and economic problem because it is a major cause of mortality and morbidity in all countries of the world. • In order to be effective in trauma care, the clinician needs a good understanding of the biomechanics of injury and how they relate to specific anatomical regions of the body. • The clinician also needs to be aware of both the physiological and pathophysiological response to trauma, as this has direct implications for optimum patient resuscitation. • These anatomical and physiological assessments can be used to quantify the severity of the trauma so that comparisons between treatment methods can be made. References Department of Health 1998 Our healthier nation - a contract for health. DoH, London Further reading Beal AL, Cerra FB 1994 Multiple organ failure syndrome in the 1990s. JAMA 271:226-233 Burgess AR, Eastridge BJ, Young JW et al 1990 Pelvic ring disruptions: effective classification system and treatment protocols. Journal of Trauma 30: 848-856 Colucciello S 1995 The treacherous and complex spectrum of maxillofacial trauma: etiologies, evaluation and emergency stabilisation. Emergency Medicine Reports 16: 59-70 Committee on Trauma 1997 Head trauma. In: Advanced trauma life support manual. American College of Surgeons, Chicago, pp 181-206 Committee on Trauma 1997 Biomechanics of injury. In: Advanced trauma life support manual. American College of Surgeons, Chicago, pp 345-366 Demling RH, Seigne P 2000 Metabolic management of patients with severe burns. World Journal of Surgery 24: 673-680 Foex BA 1999 Systemic responses to trauma. British Medical Bulletin 55: 726-743 Greenberg C, Sane D 1990 Coagulation problems in critical care medicine. Critical Care: State of the Art 11: 187-194 45 2 EMERGENCY Grundy D, Swain A 1997 ABC of spinal cord injury, 3rd edn. British Medical Journal, London Irving M, Stoner H 1987 Metabolism and nutrition in trauma. 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BMJ 310: 1502 Useful links www.doh.gov.uk/HPSSS Department of Health 2002 Indicators of the nation's health 46 2 [...]... per-rectal bleeding presenting to the colorectal clinic may well have piles easily visible on examination, but must undergo further examination to exclude colonic cancer Remember resource and financial implications when planning investigations in this manner; inappropriate investigations need to be avoided in all the surgical specialities, especially when pursuing ill-defined abdominal pain (in general. .. pain (in general surgery) , vague back pain (in orthopaedic surgery) , 'cystitis' in young women (in gynaecology and urology), chronic rhinitis (in ear, nose and throat (ENT) surgery) , ill-defined and longstanding headaches (in neurosurgery) Never ignore these symptoms, but take a 53 4 PATIENT ASSESSMENT full history and examination to form a clinical impression of the likely cause and think carefully of... radiological investigation Do not forget that the required information can often be obtained from plain X-rays and simple contrast studies No radiological technique replaces clinical skills Do not base clinical decision making on imaging findings alone Key point Remember the maxim, 'treat the patient and not the X-ray' TYPES OF RADIOLOGICAL INVESTIGATION The wide range of imaging techniques available includes... Resonance Imaging 8: 2 6-3 0 Gould SWT, Agarwal T, Benoist S, Patel B, Gedroyc W, Darzi A 20 01 Resection of soft tissue sarcomas with intra-operative magnetic resonance guidance Journal of Magnetic Resonance Imaging 15(1): 11 4-1 19 Gould SWT, Agarwal T, Martin S, Gedroyc W, Darzi A 20 02 Image guided surgery for anal fistula in a 0.5T interventional MRI unit Journal of Magnetic Resonance Imaging 16: 26 7 -2 76 Moriarty... appropriate investigations Determine the limitations of commonly used investigations Consider appropriate sequences and timing of multiple investigations Highlight important principles of investigations most commonly used in clinical practice INTRODUCTION The use of investigations in surgical practice is no substitute for clinical skill An investigation is only worthwhile when it is requested in order... suspected of having abdominal injuries Fluoroscopic imaging Many common requests to the radiology department involve the use of X-ray screening These include all barium examinations, most interventional procedures (except those under ultrasound, CT or MRI guidance) and sinograms, cholangiograms, nephrostograms, etc Each screening room has an image intensifier that converts the X-ray image into a light... erect chest X-ray to detect free intraperitoneal gas, and CT scan of the brain to detect intracranial bleeding following trauma 2 Radiology is a valuable screening aid, as in population screening such as mammography, and also as part of protocol-based preoperative imaging such as a chest X-ray when preparing patients for major surgery Always prefer the simple, hence cheaper, investigation before the complex,... occur concurrently A combination of clinical and risk assessment for each individual patient should guide the investigations performed criminately investigating in the domain of another speciality Consult the anaesthetist ahead of planned surgery to reduce avoidable cancellations on the day of surgery Key point Key point Treat all patients on an individual basis when considering tests to exclude alternative... confirm a clinical impression prior to intervention There is an ever-expanding range of investigative modalities available and unwary surgeons who are clinically uncertain can easily find themselves overwhelmed with information if too many poorly considered investigations are requested Furthermore, many modern tests are expensive and the costs of any investigation must always be considered in today's financially... choosing another test to answer the same question if an investigation does not support a firm clinical diagnosis Discuss the test with the person who performed it to ensure that as much clinical information as possible has been passed on to the individual who is trying to give you a result An inadequate report may have been based on inadequate information given on the request form Combined clinical . ascending clinical deterioration. In cases of high spinal injury this process can lead to secondary respiratory deterioration. Partial spinal cord injury Anterior spinal cord injury . principles of investigations most commonly used in clinical practice. INTRODUCTION The use of investigations in surgical practice is no substitute for clinical skill. An investigation . implications when planning investigations in this manner; inappropriate investigations need to be avoided in all the surgical specialities, especially when pursuing ill-defined abdominal

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