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The management of the patient with severe multiple injuries
THE MANAGEMENT OF THE PATIENT WITH SEVERE MULTIPLE INJURIES
A Symposium given at the Spring Meeting of the British Association of Oral Surgeons at Oxford, April z97~ J. W. LLOYD, F.F.A.R.C.S., P. R. W. MONAHAN,F.R.C.S., M. BRIG6S, M.B., B.S., F.R.C.S., G. HIGGINS, B.Sc., and D. GWYN~ WILLIAMS, M.B., B.Ch., M.R.C.P. Radcliffe Infirmary, Oxford IMMEDIATE RESUSCITATION
J. W. Lloyd--Nuffield Department of Anaesthetics As AN anaesthetist and therefore as one who should be amongst the first to arrive on the scene, I am privileged to speak first. In recent years, anaesthetists have shown an increasing trend to move out of the operating theatre into the field of resuscitation. With their emphasis on respiratory physiology and the complicated electronic equipment so necessary for monitoring, they are now becoming one of the many specialties with contributions to make towards the management of that most exacting but, nevertheless, rewarding 'Cinderella of the surgical f i e l d ' u the Accident Service. The management of trauma involves many disciplines. The need for one man to co-ordinate the efforts of a team and assume clinical responsibility for the whole patient cannot be too strongly emphasised. In Oxford, we recognise the Accident Surgeon as that man. It is expedient to reduce the immediate care of the acutely injured patient to three basic requirements: firstly, oxygen; secondly, blood; and thirdly, a pump to circulate it. A survey carried out in the Radcliffe Infirmary in I965-66 showed that 82 per cent of chest injuries had associated head injuries and in these patients the airway may be seriously impeded whether d u e to unconsciousness or to respiratory obstruction by blood, mucous or foreign bodies. Interference with the mechanism of respiration as occurs in many aspects of chest injuries might also be classified under the heading respiratory obstruction. It is seen in its most severe form when the integrity of the rib framework is lost as in the 'floating segment' of the crushed chest. Paradoxical respiration or movement of the chest wall in reverse of normal occurs, and unless intubation and positive pressure ventilation are instituted at once, the patient will almost certainly die of asphyxia. Pneumothorax and haemothorax by compressing the lung may also impair ventilation. We consider that art endotracheal tube in an unconscious person is obligatory in order to secure the airway and allow a route for added oxygen. Further damage to the brain and vital centres may be minimised if this is performed at an early stage. Unfortunately this is not always possible, and the damage may be irreversible when the patient is first seen, particularly if much time has elapsed between the injury and arrival in hospital. The choice between an endotracheal tube and tracheotomy has aroused much controversy in recent years. A tracheotomy performed when one first thinks about it is a life-saving procedure, but now that there is a tendency to leave endotracheal tubes in place for longer periods F 73
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the place of the tracheotomy is in some jeopardy. The present position can be summarised: (a) A tracheotomy requires an anaesthetic which may be an added complicating factor in an already seriously injured person. The passage of an endotracheal tube is relatively simple and should be accomplished by most casualty officers. (b) An cndotracheal tube is cxtremcly uncomfortable in a conscious person and is difficult to manage from a nursing aspect. Tracheotomy has none of these disadvantages, but it will almost certainly become infected with a Ps. pyocyaneus. (It has recently been said that if the pyocyaneus does not appear within three days in a patient who has had prophylactic antibiotic(s), tracheotomy and intermittent positive pressure respiration, there is something wrong with the technique.) (c) Stenosis of the trachea appears to be slightly more common in long-term tracheotomy than in long-term intubation. (d) Necrosis of the tracheal mucous membrane has occurred in certain patients due to polymerisation of some tubes. In Oxford we have found it valuable to adopt the following policy: (I) Emergency tracheotomies are never performed. An endotracheal tube is always passed in the first instance. (2) I f the patient remains sufficiently unconscious as not to object to the endotracheal tube, it is left in situ for an indefinite period. I f the patient objects to the tube but still needs tracheal intubation, as in the case of a severe chest injury, a tracheotomy is performed. The second requirement is blood, and it is also convenient to consider the heart or pump in this section. Regardless of the claims of the Medical Press, the best replacement for blood is blood. Many of these injuries are multiple, and patients may need large amounts of blood--up to two and a half times their own blood volume. Hartmann's solution is useful while the blood is being crossmatched, and I to 2 litres may be given within half an hour or so of serious injury. A patient in 'cold hypotension' will need blood immediately, and in these cases uncross-matched group 0 rhesus negative blood should be transfused. Whilst this is being done ABO cross-matching is taking place and blood should be ready in half an hour's time. In the meantime, a full cross-match is being completed. As this takes about 2 hours, it means that there should be no delay in blood availability and that each batch of blood is progressively more cross-matched. The central venous pressure (C.V.P.) has probably become the most satisfactory guide to the adequacy of volume replacement, but it should be evaluated along with the blood pressure. We have adopted the following regime: the patient is transfused until either the C.V.P. reaches 13 cm of water or the blood pressure returns to normal. If the C.V.P. pressure reaches 13 cm and the blood pressure is still low, it is reasonable to assume that there is a myocardial deficit and in these cases we have used isoprenaline to improve the cardiac output. If the blood pressure returns to normal before the C.V.P. reaches 13 cm of water, we feel that it is safe to assume that there is a volume deficit and transfusion is continued.
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Irreversible shock is often associated with a delay in restoring blood volume. This, together with the outpouring of catechol amines by the patient himself, leads to a progressive vasoconstriction. Tissue hypoxia and metabolic acidosis complete the vicious circle. Once the condition has developed, it is essential to establish adequate tissue perfusion. To this end it may become necessary to produce vasodilation which can be accomplished by the use of alpha-blocking drugs such as phenoxybenzamine. EARLY ASSESSMENT OF T H E P A T I E N T P. R. W. Monahan--Accident Service
The initial assessment of the multi-injured patient should be performed as quickly aspossible so that treatment which may be life-saving, can be instituted without delay. A diagnosis of the injuries sustained may be difficult for a variety of reasons. For example, a patient in acute shock or unconscious from a head injury will be unable to give a history. Injury to dissimilar organs can give similar signs and symptoms, and trauma to one area may mask the presence of an associated injury. A history of the accident and the patient's clinical condition at the time and subsequently should be obtained from the ambulance crew or witnesses. Resuscitation is the first priority. The pulse rate, blood pressure, pupillary size and reaction as well as the state of consciousness is recorded at frequent intervals. It should be remembered that when the clinical signs of shock are present, the blood volume is likely to be depleted by 2o-3o per cent. After taking blood for haemoglobin estimation, grouping and cross-matching, an intravenous infusion is started. A systematic examination is then made of the front and back of the patient. Particular attention is paid to the extent and site of contusions and soft tissue swelling, as these signs indicate the site of maximum impact and the degree of blood loss into the tissues. The spine is carefully examined for evidence of a fracture or dislocation and a decision made as to its stability. T h e abdomen is examined for signs of organ or viscus injury and a note is made of the degree of distension, the site of any pain on pressure and the other signs of peritonism. Perineal and scrotal contusion is an important sign of urethral injury. The spleen is the most commonly damaged organ in closed abdominal injuries with the liver second in frequency. Pelvic fractures are a notorious source of blood loss and thus the pelvis is carefully examined. Fractures of the anterior arch are associated with bladder and urethral injury, whereas the more severe fracture dislocation is associated with a rupture of the diaphragm in about 8 per cent of cases. Head and musculoskeletal injuries are the most frequent of all injuries. Fractures and dislocations are simple and compound in type. The initial problem with fractures is that vital structures lying close to the bony injury such as muscles, blood vessels and nerves may be damaged if the fracture is not immobilised at once. Similarly a simple closed fracture may become compound by the bone ends penetrating the skin. Thus splintage of a limb must be performed at once. Major vessel injury may be suggested by the picture of profound hypovolaemic shock, though it is not unusual for the initial signs to be minimal and for a sudden profuse secondary haemorrhage to occur. In all patients multiple-injured with
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injury to the aorta, heart and pericardium, the front and back of the chest should be carefully auscultated for murmurs, the synchronous nature of the radial and femoral pulses assessed and the level and pulsation of the jugular venous pressure noted. Finally, shock may be intensified by burns, whether due to petrol, flame or friction and accurate assessment of their extent in relation to the total body surface area is vitally important in estimating the amount of fluid replacement that will be required. After this initial examination and whilst resuscitation is proceeding, the patient can be moved to the X-ray unit where only those X-rays that are immediately required are performed. Head injuries may require films of the cervical spine as well as routine skull films, due to the increased incidence of associated injury to the neck. A chest X-ray is taken to look for rib fractures, the presence of a haemo- or pneumothorax, to assess the size of the heart and mediastinum and the height of the diaphragm. A plain X-ray of the abdomen may show injury to the lumbar spine, pelvis and lower ribs. It may also reveal the presence of peritoneal and retroperitoneal blood by obliteration of the psoas and may outline the size of various organs. X-rays of the limbs are taken to determine the site of fracture, displacement and type, and whether it is transverse, oblique or cornminuted. Further investigations may be required; for example, an intravenous pyelogram for renal tract injuries, arteri0grams for vascular trauma and intracerebral injuries. Spinal injuries are treated by bed rest on fracture boards, and for the more severe by traction with the patient lying on a Stryker bed so that regular turning can be performed. In some patients a decompression laminectomy and spinal fusion may be indicated. The more minor abdominal injuries such as contusions and retroperitoneal haematomata may only require intravenous fluid replacement and nasogastric suction; whereas, for more major injuries a laparotomy is performed and a ruptured spleen removed, a tear of the liver, bladder or viscus repaired, etc. Urethral injuries are treated initially by closed bladder drainage via a supra-pubic catheter and at a later stage surgical reconstruction of the urethra is performed. In the treatment of musculoskeletal injuries, skin wounds are carefully cleaned and tattooing must be avoided by thorough skin toilet. Neat skin apposition must be obtained, especially in facial wounds. Muscles, tendons and nerves may be repaired if the site of rupture and the degree of contamination is no bar to primary repair. A thorough wound toilet and debridement of compound injuries is performed to prevent the occurrence of gas gangrene and tetanus in devitalised necrotic muscle or bone sepsis leading to the complication of osteomyelitis. Limb fractures are reduced into good alignment, care being taken to secure normal rotation at the fracture site, and the affected part immobilised in either a splint or plaster cast. The period of immobilisation required depends on the time taken for union to occur as assessed by clinical and radiological examination; upper limb fractures may require 6-8 weeks and major lower limb fractures 3-4 months. Open reduction and fixation is performed for a variety of reasons and the criteria for its use must be strict, as a failed case due, for example, to infection is a disaster. Thus in the management of the 'multipleinjured' patient assessment and resuscitation must be carried out carefully and quickly, and a knowledge of the great variety of injuries that may occur is essential.
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T H E EARLY M A N A G E M E N T OF HEAD INJURIES
M. Briggs--Department of Neurological Surgery The early management of patients with head injuries involves three basic principles, namely, general resuscitation, early establishment of baselines of observation and, in a relatively few cases, surgical intervention. The damaged brain, be it damaged by concussion, contusion or laceration, does not tolerate hypoxia as well as the normal uninjured brain, so that a relatively minor head injury may appear, or indeed become, more severe if this condition is present. Some degree of cerebral hypoxia is commonly present in patients with head injury at the time they are first seen in the Accident Service recovery room. For example, it is not uncommon for an unconscious patient to develop airway obstruction from inhaled blood or vomit, particularly if he had been previously transported in the supine position. Other conditions such as flail chest, severe lung contusion or pneumothorax will all lead to impaired ventilatory function, a lowered arterial oxygen tension and cerebral hypoxia. Likewise, severe blood loss will lead to peripheral circulatory failure and inadequate perfusion of cerebral tissues. Even in the presence of an unobstructed airway, normal chest wall and lungs, cerebral hypoxia may occur if insufficient blood, or blood with impaired oxygen carrying capacity, is reaching the brain. From these observations it can be seen that adequate blood replacement, the establishment of an unobstructed airway and maintenance of good ventilation are of supreme importance in the management of patients with head injury. The treatment of individual injuries can, and usually should, wait until the two priorities (of blood replacement and oxygenation) have been dealt with. For example, it has been shown that definitive surgery to a compound depressed skull fracture can be left up to 18 hours without increasing the morbidity, providing the wound has been covered with a sterile dressing and prophylactic antibiotics given. General anaesthetics should be avoided as far as possible in the acute stage. In emergency conditions, the induction may be associated with periods of relative hypoxia and transient elevation of intracranial pressure (I.C.P.), during endotracheal intubation. The use of volatile anaesthetic agents, such as halothane, may cause a dangerous rise in I.C.P., and the reaction of the injured brain to routine drugs can be capricious and unpredictable. The second principle in the early management of the head-injured patient is that of careful observation. Observation is intended t o p rovide a guide to further treatment, particularly as to whether the brain is being compressed by an intracranial haematoma which needs surgical evacuation. In this event, the most consistent feature is a progressive lowering of responsiveness. In the classical picture of an extradural haemorrhage the patient has been concussed, but by the time he is seen in hospital he is fully conscious and alert, the so-called 'lucid interval.' As the haematoma develops he becomes less responsive at a rate proportional to the severity of the bleeding, until, untreated, he is completely unresponsive to any form of stimulation. With some extradural haematomata and with the majority of acute subdural haematomas the lucid interval is fleeting and relative. With the increasing size of the haematoma, changes in the neurological status may be observed. For example, a clot situated over the motor area may cause weakness of the contralateral face and arm; over the speech area,
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aphasia, and so on. As the pressure above the tentorium rises, herniation of the temporal lobe occurs through the tentorial hiatus, distorting the occulomotor nerve in the process. This leads to the typical pupillary signs of progressive dilatation and loss of reaction of light, on the side of the clot. The other changes involve the vital signs of pulse, blood pressure and respiration. As the intracranial pressure rises, so too does the arterial tension. This results in an increased vagal activity and a slowing of the pulse rate. Compression of the brain stem by the tentorial hernia causes progressive respiratory embarrassment. Therefore the careful observation of head injuries must include frequent assessment of the level of responsiveness, estimation of pupil size and its reaction to light and measurement of pulse, blood pressure and respiratory rate. Baseline observations of these parameters should be established as soon as possible so that the progressive changes associated with an enlarging intracranial haematoma may be noticed early and prompt surgical treatment carried out. Morphine and its derivatives, atropine and sedatives are best avoided because they interfere with pupillary observations and hinder the assessment of the level of responsiveness. When indicated by the progressive change in observations, the operation for release of an extradural haematoma must be carried out without delay. The situation has been described as the one true surgical emergency. The result of failure to recognise this fact is demonstrated by an overall mortality for extradural haematomata of 5o per cent in this country at large. Frequently with a rapidly developing clot there is not time for the patient to be transferred to a specialised neurosurgical unit and, therefore, the simple procedure of burr hole and craniectomy for the evacuation of such a clot should be within the scope of any surgeon working in a hospital which admits accident cases. So much for the initial resuscitation and observations designed to detect cerebral compression. A further feature which must be watched for and protected against, both in the immediate and later stages in the care of patients with head injury, is that of infection. The majority of superficial infections should be preventable by adequate primary treatment of scalp lacerations. Likewise a large proportion of brain abscesses, which may follow penetrating brain injuries, can be avoided by adequate wound toilet. However, the complication of meningitis may be less easy to guard against. It is known to be associated with certain types and combinations of injuries, and awareness of this fact should lead to a more adequate prophylaxis and early treatment of this potentially lethal complication. The presence of a C.S.F. leak, be it rhinorrhoea or otorrhoea, is evidence of a fistula between the subarachnoid space and the exterior. The risks of meningitis developing in this situation are very high and, therefore, all patients with such a leak should be given adequate antibiotic prophylactic as soon as the complication is recognised. In this service we use benzylpenicillin 6oo mg 6 hourly and sulphadiazine 2 g stat. followed by I g 4 hourly. This prophylaxis must be maintained for the duration of the leak which, if prolonged, will require surgical closure of the fistula. The association between meningitis and fractures involving the frontal or ethmoidal sinuses or of the maxilla have been noted by many authors, and with this complication in mind it is stressed that patients with such injuries must be watched closely. It has similarly been noted that immediate post-traumatic pneumocephalus, which carries an equally high risk of meningitis is frequently associated with fractures of the facial bones; indeed, in a recent survey, as many as 5° per cent
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of patients with this complication had facial fractures in addition to their head injury. Obviously then, patients with such fractures should be watched closely, firstly to detect the presence of any intracranial air, secondly to confirm the presence of a C.S.F. leak and thirdly to diagnose meningitis early, should this complication develop. Patients who require surgical intervention form only a small proportion of those admitted with head injuries; being about 5 per cent of 2000 patients in this service. The indications for surgery in the acute stage are, the existence of a compressing intracranial haematoma, the signs of which we have already considered, and the presence of a compound depressed skull fracture. At a later stage surgery may be indicated for the treatment of subacute and chronic haematomata, the repair of C.S.F. fistulae, and the elvation of some closed depressed skull fractures. In the short time allowed we have only been able to consider the principles involved in the early care of a patient with a head injury. However, attention to these principles must be the basis of management of such casualties who are presenting themselves in ever-increasing numbers; for instance in I96o 818 patients with head injury were admitted under the Accident Service whereas ro years later the annual figure rose to I9O8. BIOCHEMICAL SEQUELAE TO SEVERE HEAD AND FACE T R A U M A G. Higgins--Principal Biochemist The serious biochemical effects seen in patients who have suffered multiple injuries, ruptured kidneys, spleen, liver, intestine, etc., are well known, but the biochemical upset which can occur in patients i n whom the injury is confined to the head is not so widely recognised. A review of our cases several years ago showed that many of the patients who survived the immediate effects of head injury, died some days or weeks later of what could only be described as biochemical deaths. It was apparent that deaths following head injury could be divided into several groups. The first group of patients were those who died of the immediate effects of the injury--in these cases the biochemical tests showed little abnormality. The second group comprised those who survived, perhaps for several months or years, and who showed no evidence of any biochemical upset at all; these were mainly young persons whose constitution enabled them to resist the adverse biochemical effects. Of the remaining cases who developed biochemical abnormalities, some, who had no injury to the renal system, subsequently developed renal impairment and died of uraemia; others developed hypernatraemia and hyperchloraemia. The elderly patient frequently developed hyponatraemia and hypochloraemia and died of a condition similar to Addison's disease. For many years it has been known that trauma to any part of the body may cause generalised changes in the biochemistry of the body. When these follow head injuries the effects may be very serious. It has been shown that in experimental animals, trauma to the head affected cells of the lung and renal tract. Quickly following the head injury, the lung cells showed pulmonary oedema causing impairment of the gaseous interchange. This may be an explanation, if the same effect occurs in humans, of the carbon dioxide retention and oxygen
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lack that many patients suffer and of the lung infection which develops in so many unconscious patients with head injuries. With the introduction of rapid methods for the determination of the body electrolytes, it was seen that trauma could cause retention of sodium, with loss of potassium. This could result in increased cellular osmotic pressure and impairment of the function of the cell. Simpler methods of estimating plasma hormones led to the recognition that the injury caused a state of stress which led to the outpouring of increased amounts of the adrenal hormones. In contrast to this, the immobilisation due to the injury could lead to the suppression of the androgenic hormones which, in its turn, leads to loss of muscle and tissue nitrogen as well as to a loss of muscle tone. It will be understood that, in view of possibilities, many undesirable metabolic states can be superimposed upon the actual traumatic damage resulting from the injury. In our review of the morbidity of severe trauma, it was apparent that when these abnormal biochemical states became established they were often very difficult to correct and also that these conditions were frequently made worse by the treatment given to the patient. In the early days of treatment of severe head injury victims difficulty was often experienced in feeding the patient or in giving him adequate fluid intake. The sequence of events was progressive dehydration of the patient, loss of cellular water, increased cellular osmotic pressure and impairment of cellular function. Renal insufficiency developed and the nitrogen load arising from the breakdown of damaged tissue soon led to uraemia and renal failure. When the importance of proper hydration was realised, many surgeons prescribed more than adequate fluid intake. In many cases no harm was done, but in some elderly patients hyponatraemia developed. This complication may be due to the washing out of body electrolytes, but can occur when there is failure of the adrenal and pituitary glands to respond to extreme stress and the kidney loses sodium. Although this is usually a complication in the older patient, it has been seen in teenagers, in whom it can be so severe as to induce mental impairment. The other condition of hypernatraemia and hyperchloraemia is more complex. There is some evidence that cerebral factors may play a part in the regulation of ionic concentration, and injury to the brain may upset this mechanism. The condition is often associated with a lung infection which itself may lead to dehydration and thus increased salt concentration. In some cases the overenthusiastic administration of intravenous saline solution may induce the condition. These toxic biochemical states following injury, which may be partly the metabolic effects of such injury and partly man-made, are probably easier to prevent than cure. Two approaches to these problems have been made. The first was to design a diet which was capable of giving adequate calories, salts, protein, etc., to maintain life and yet could be administered through a naso-gastric tube. Intensive monitoring of the patient was started until it was certain that he or she was in a normal biochemical balance: this included daily or twice-daily estimation of blood electrolytes, blood gases, blood constituents and urinary studies when indicated. These evaluations influenced the daily adjustment of intake of salts, protein and calories so that a normal balance could be maintained; thus more or less fluid salts, protein, etc., could be added as indicated by the results of the investigations. Whereas in the past many patients with multiple injuries have died because of these upsets, it is now the exception rather than the rule. It should be emphasised
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that these efforts do not bring about improvement alone; recovery ultimately depends upon the ability of the patient to overcome the crisis. M E D I C A L ASPECTS OF A C U T E T R A U M A
D. Gwyn Williams--Department of Clinical Medicine Among the many effects of trauma on the body, there are a considerable number which involve the physician. His assistance may necessarily be required at the time of actual admission, and, in fact, he is more likely to be called at a later date when some complication has arisen, either due to the trauma itself or to surgical treatment. The most important medical complication of acute injury is renal failure due to acute tubular necrosis. This occurs from the loss of body fluids, which may be blood (deficient due to injury or surgery), plasma (lost as the result of burns) or gastrointestinal secretions (usually lost post-operatively). Such deprivation of body fluid produces renal ischaemia, leading to renal tubular damage and eventually to acute tubular necrosis. From first to last in this succession of events there is concomitant oliguria and uraemia, but the significance of these phenomena varies with the acutal stage in the chain of events. Initially, the kidneys work very well, and the oliguria is physiological, i.e. an attempt to conserve fluid (stage I oliguria). When acute tubular necrosis has developed, there is a gross derangement of renal function, with a clear-cut state o f renal failure (stage I I I oliguria). Somewhere in this progression of events, there is a metamorphosis of physiological interpathological oliguria corresponding to a state in which some renal tubules are damaged and some are not (stage I I oliguria). The recognition of stages I and I I in this march of events is of practical importance, as the oliguria of these stages is reversible. However, at the bedside, the three stages of oliguria are indistinguishable, uraemia accompanying each one. They can most easily and quickly be recognised in one of two ways. Firstly, by measuring the concentration of urea in the urine, and comparing this with the concentration of blood urea. Normally, urine urea is 14 times more concentrated than the blood urea, whereas in acute tubular necrosis the urine concentration of urea is equal to that of blood, or greater by a factor of only two or three. In stage H oliguria, although the concentration of urine urea is less than normal, it is still appreciably more concentrated than the blood urea. Secondly, one can measure the urine osmolarity and compare this with the plasma osmolarity. In the face of fluid loss the urine osmolarity should be much higher than that o f the plasma, but in acute tubular necrosis the urine osmolarity will be much diminished, and in stage I I oliguria the osmolarity of the urine will be less than in stage I, but greater than in stage I I L The oliguria having been noted, and the correct diagnosis having been made, the correct treatment can now be given. I f the oliguria is that of stage I, then the appropriate fluid should be given to the patient quickly and in adequate quantity. Speed in repairing the hypovolaemia is vital, and this is precisely the sort of case in which measuring the central venous pressure provides an ideal way of monitoring the intravenous infusion of fluids, so that large amounts can be given rapidly. In stage II, there are two methods of treatment which are often complementary. Just as in stage I, rapid administration of the correct fluid is vital,
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In addition, it has been found empirically, and there is some theoretical justification for this, that the use of diuretics at this stage can induce a diuresis and avert the impeding acute tubular necrosis. One is, of course, interested in a rapid effect, and the ideal diuretic in this situation would be frusemide given intravenously, or manitol, also given intravenously. The latter has the advantage of providing increased intravascular volume, and also of raising the blood pressure. There is, of course, no reason why both diuretics should not be used at the time. It is worth noting, in his context, that the use of intravenous ethacrynic acid should be avoided, because if the patient remains oliguric without a diuresis being obtained then the ethacrynic acid may produce deafness. If treatment of stage I or stage I I oliguria fails, or if the patient has already developed acute tubular necrosis, then a situation now exists of absolute renal damage. If the patient is depleted of body fluid, then the correct replacement should be given, but of course the patient will not be able to deal with an excess load, and heart failure and pulmonary oedema become a danger if too much fluid is given. Again, measuring the central venous pressure while giving intravenous fluid would be a sensible precaution. If there is no indication for dialysis, then conservative measures should be used at first. These comprise restriction of protein (to 4 ° g a day), sodium, potassium and fluid, and, at the same time, providing as many calories as possible by means of a high-calorie carbohydrate liquid concentrate in order to keep the breakdown of body protein to a minimum, so lessening the rise in blood urea. In mild cases, these conservative measures buy sufficient time for natural healing to occur with eventual recovery of the kidneys, and without gross uraemia occurring. Particular attention must be paid during the diuretic phase of recovery to the correct balance of sodium, potassium and water. In severe cases of acute tubular necrosis, and in those in whom conservative measures are inadequate, a dialysis becomes imperative. Practice varies from centre to centre but, in general, the following are the indications for dialysis: (i) A blood urea greater than 200 mg per cent. (2) Serum potassium 6 m Eq/litre or greater. (3) A patient overloaded with fluid through careless or overenthusiastic treatment. (4) Clinical deterioration, not due to other causes, irrespective of the biochemical values noted above. Peritoneal dialysis is the method to be preferred, as it is more economical of time, staff and materials, and is a less drastic procedure as far as the physiology of the body is concerned. However, in some cases--notably those who are catabolising rapidly or those with abdominal injuries which inhibit peritoneal dialysis-haemodialysis must be used. Nowadays the prognosis of acute tubular necrosis following trauma is relatively good, as the measures outlined above for correcting the maleffects of renal failure are usually successful. Indeed, spontaneous recovery is the rule if acute tubular necrosis is the only lesion affecting the kidneys. In conclusion, with respect to renal failure, it is worth remembering two guidelines which will prevent a considerable amount of morbidity and mortality. The first is to watch very carefully the patients' urine output from the time of admission. It is all too easy to forget this rather mundane body function during the drama of the acute injury and its treatment. The importance of this observation lies
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in the fact that correct treatment during the early stages of oliguria can prevent a progression to acute tubular necrosis. Secondly, if the oliguria is irreversible and there is a rise in blood urea, then the time to notify the physicians is as soon as this fact is recognised and not to wait until a blood urea of several hundred milligrams per cent is reached. The second most common complication in injured and immobilised patients is, of course, pulmonary embolus. This is usually an easy diagnosis with its well-recognised signs and symptoms. However, it can sometimes present in other subtle ways, such as shock without pain, breathlessness alone, cardiac failure, or syncope. Treatment of pulmonary embolus begins first and foremost with its prophylaxis. Whenever possible, patients should be activity mobilised; if not the whole body, then all parts which Call be. I f there is ally immobilisation, again whether of the whole or of a part, there is good evidence that prophylaxis with anticoagulants providing, of course, that there is no contra-indication to their use, is effective in preventing deep vein thromboses and pulmonary emboli. Once the pulmonary embolus has occurred, prophylaxis should be instituted if it has not already been done. In severe cases aggressive curative measures are worth trying. The only proven method of cure at present is surgery. In recent years a new drug, streptokinase, has been marketed. Its action is to dissolve blood clot by fibrinolysis, and there have been some striking anecdotal experiences of its use in pulmonary embolus, but its efficacy has still to be proven in a controlled trial. As far as the acutely injured or recent surgical patient is concerned, its use involves the obvious danger of haemorrhage. Fat embolism presents mainly with disturbance of file central nervous system, the cardiorespiratory system or as oliguria. Its exact cause is still not understood, and it is therefore no surprise that its treatment is vague and unsatisfactory. The following measures have been described: (I) Use of heparin and clofibrate, which have been shown to reduce lipaemia. (2) The use of phenoxybenzamine to dilate blood vessels. (3) Hypofilermia, because this reduces viscosity of fat, and it is thought therefore to reduce emboli from fractured bones. No controlled trials of these various measures have been performed, and it remains a moot point whether any of them are really effective. The physician can be called in to see various metabolic disturbances such as jaundice which can occur through shock alone or hypotension reducing the arterial blood supply to the liver with consequent hepatocellular damage. It can also arise through file use of drugs, particularly anaesthetic agents. Hyperglycaemia can occur following head injury. It is transient and does not need treatment, but it must be differentiated from diabetes mellitus which may be precipitated by the stress of the acute trauma. Following head injury, there may be hypernatraemia as a manifestation of diabetes insipidus. This may be permanent or temporary, and if severe enough it merits replacement therapy. Hyponatraemia can occur as a result of excessive and inappropriate A D H secretion following head injury. The resulting water retention leads to a low serum sodium, and this should be treated by restriction of water intake. Thrombocytopenia can, of course, follow treatment with various drugs,
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but it is also a complication of massive blood transfusion, which the acutely injured patient is likely to receive. If the thrombocytopenia is severe enough, with bleeding, then a platelet transfusion should be given. Rashes of all sorts, sizes and descriptions can occur, nearly always as a result of the drugs administered. Apart from the obvious causes of shock already mentioned, two other conditions should be borne in mind. The first of these is septicaemia, the second is myocardial infarction. There is no reason why this latter disease should not strike the victim of acute trauma lying in his bed, as easily as if he were listening to a talk on the medical aspects of trauma.
A Symposium given at the Spring Meeting of the British Association of Oral Surgeons at Oxford, April z97~ J. W. LLOYD, F.F.A.R.C.S., P. R. W. MONAHAN,F.R.C.S., M. BRIG6S, M.B., B.S., F.R.C.S., G. HIGGINS, B.Sc., and D. GWYN~ WILLIAMS, M.B., B.Ch., M.R.C.P. Radcliffe Infirmary, Oxford IMMEDIATE RESUSCITATION
J. W. Lloyd--Nuffield Department of Anaesthetics As AN anaesthetist and therefore as one who should be amongst the first to arrive on the scene, I am privileged to speak first. In recent years, anaesthetists have shown an increasing trend to move out of the operating theatre into the field of resuscitation. With their emphasis on respiratory physiology and the complicated electronic equipment so necessary for monitoring, they are now becoming one of the many specialties with contributions to make towards the management of that most exacting but, nevertheless, rewarding 'Cinderella of the surgical f i e l d ' u the Accident Service. The management of trauma involves many disciplines. The need for one man to co-ordinate the efforts of a team and assume clinical responsibility for the whole patient cannot be too strongly emphasised. In Oxford, we recognise the Accident Surgeon as that man. It is expedient to reduce the immediate care of the acutely injured patient to three basic requirements: firstly, oxygen; secondly, blood; and thirdly, a pump to circulate it. A survey carried out in the Radcliffe Infirmary in I965-66 showed that 82 per cent of chest injuries had associated head injuries and in these patients the airway may be seriously impeded whether d u e to unconsciousness or to respiratory obstruction by blood, mucous or foreign bodies. Interference with the mechanism of respiration as occurs in many aspects of chest injuries might also be classified under the heading respiratory obstruction. It is seen in its most severe form when the integrity of the rib framework is lost as in the 'floating segment' of the crushed chest. Paradoxical respiration or movement of the chest wall in reverse of normal occurs, and unless intubation and positive pressure ventilation are instituted at once, the patient will almost certainly die of asphyxia. Pneumothorax and haemothorax by compressing the lung may also impair ventilation. We consider that art endotracheal tube in an unconscious person is obligatory in order to secure the airway and allow a route for added oxygen. Further damage to the brain and vital centres may be minimised if this is performed at an early stage. Unfortunately this is not always possible, and the damage may be irreversible when the patient is first seen, particularly if much time has elapsed between the injury and arrival in hospital. The choice between an endotracheal tube and tracheotomy has aroused much controversy in recent years. A tracheotomy performed when one first thinks about it is a life-saving procedure, but now that there is a tendency to leave endotracheal tubes in place for longer periods F 73
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the place of the tracheotomy is in some jeopardy. The present position can be summarised: (a) A tracheotomy requires an anaesthetic which may be an added complicating factor in an already seriously injured person. The passage of an endotracheal tube is relatively simple and should be accomplished by most casualty officers. (b) An cndotracheal tube is cxtremcly uncomfortable in a conscious person and is difficult to manage from a nursing aspect. Tracheotomy has none of these disadvantages, but it will almost certainly become infected with a Ps. pyocyaneus. (It has recently been said that if the pyocyaneus does not appear within three days in a patient who has had prophylactic antibiotic(s), tracheotomy and intermittent positive pressure respiration, there is something wrong with the technique.) (c) Stenosis of the trachea appears to be slightly more common in long-term tracheotomy than in long-term intubation. (d) Necrosis of the tracheal mucous membrane has occurred in certain patients due to polymerisation of some tubes. In Oxford we have found it valuable to adopt the following policy: (I) Emergency tracheotomies are never performed. An endotracheal tube is always passed in the first instance. (2) I f the patient remains sufficiently unconscious as not to object to the endotracheal tube, it is left in situ for an indefinite period. I f the patient objects to the tube but still needs tracheal intubation, as in the case of a severe chest injury, a tracheotomy is performed. The second requirement is blood, and it is also convenient to consider the heart or pump in this section. Regardless of the claims of the Medical Press, the best replacement for blood is blood. Many of these injuries are multiple, and patients may need large amounts of blood--up to two and a half times their own blood volume. Hartmann's solution is useful while the blood is being crossmatched, and I to 2 litres may be given within half an hour or so of serious injury. A patient in 'cold hypotension' will need blood immediately, and in these cases uncross-matched group 0 rhesus negative blood should be transfused. Whilst this is being done ABO cross-matching is taking place and blood should be ready in half an hour's time. In the meantime, a full cross-match is being completed. As this takes about 2 hours, it means that there should be no delay in blood availability and that each batch of blood is progressively more cross-matched. The central venous pressure (C.V.P.) has probably become the most satisfactory guide to the adequacy of volume replacement, but it should be evaluated along with the blood pressure. We have adopted the following regime: the patient is transfused until either the C.V.P. reaches 13 cm of water or the blood pressure returns to normal. If the C.V.P. pressure reaches 13 cm and the blood pressure is still low, it is reasonable to assume that there is a myocardial deficit and in these cases we have used isoprenaline to improve the cardiac output. If the blood pressure returns to normal before the C.V.P. reaches 13 cm of water, we feel that it is safe to assume that there is a volume deficit and transfusion is continued.
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Irreversible shock is often associated with a delay in restoring blood volume. This, together with the outpouring of catechol amines by the patient himself, leads to a progressive vasoconstriction. Tissue hypoxia and metabolic acidosis complete the vicious circle. Once the condition has developed, it is essential to establish adequate tissue perfusion. To this end it may become necessary to produce vasodilation which can be accomplished by the use of alpha-blocking drugs such as phenoxybenzamine. EARLY ASSESSMENT OF T H E P A T I E N T P. R. W. Monahan--Accident Service
The initial assessment of the multi-injured patient should be performed as quickly aspossible so that treatment which may be life-saving, can be instituted without delay. A diagnosis of the injuries sustained may be difficult for a variety of reasons. For example, a patient in acute shock or unconscious from a head injury will be unable to give a history. Injury to dissimilar organs can give similar signs and symptoms, and trauma to one area may mask the presence of an associated injury. A history of the accident and the patient's clinical condition at the time and subsequently should be obtained from the ambulance crew or witnesses. Resuscitation is the first priority. The pulse rate, blood pressure, pupillary size and reaction as well as the state of consciousness is recorded at frequent intervals. It should be remembered that when the clinical signs of shock are present, the blood volume is likely to be depleted by 2o-3o per cent. After taking blood for haemoglobin estimation, grouping and cross-matching, an intravenous infusion is started. A systematic examination is then made of the front and back of the patient. Particular attention is paid to the extent and site of contusions and soft tissue swelling, as these signs indicate the site of maximum impact and the degree of blood loss into the tissues. The spine is carefully examined for evidence of a fracture or dislocation and a decision made as to its stability. T h e abdomen is examined for signs of organ or viscus injury and a note is made of the degree of distension, the site of any pain on pressure and the other signs of peritonism. Perineal and scrotal contusion is an important sign of urethral injury. The spleen is the most commonly damaged organ in closed abdominal injuries with the liver second in frequency. Pelvic fractures are a notorious source of blood loss and thus the pelvis is carefully examined. Fractures of the anterior arch are associated with bladder and urethral injury, whereas the more severe fracture dislocation is associated with a rupture of the diaphragm in about 8 per cent of cases. Head and musculoskeletal injuries are the most frequent of all injuries. Fractures and dislocations are simple and compound in type. The initial problem with fractures is that vital structures lying close to the bony injury such as muscles, blood vessels and nerves may be damaged if the fracture is not immobilised at once. Similarly a simple closed fracture may become compound by the bone ends penetrating the skin. Thus splintage of a limb must be performed at once. Major vessel injury may be suggested by the picture of profound hypovolaemic shock, though it is not unusual for the initial signs to be minimal and for a sudden profuse secondary haemorrhage to occur. In all patients multiple-injured with
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injury to the aorta, heart and pericardium, the front and back of the chest should be carefully auscultated for murmurs, the synchronous nature of the radial and femoral pulses assessed and the level and pulsation of the jugular venous pressure noted. Finally, shock may be intensified by burns, whether due to petrol, flame or friction and accurate assessment of their extent in relation to the total body surface area is vitally important in estimating the amount of fluid replacement that will be required. After this initial examination and whilst resuscitation is proceeding, the patient can be moved to the X-ray unit where only those X-rays that are immediately required are performed. Head injuries may require films of the cervical spine as well as routine skull films, due to the increased incidence of associated injury to the neck. A chest X-ray is taken to look for rib fractures, the presence of a haemo- or pneumothorax, to assess the size of the heart and mediastinum and the height of the diaphragm. A plain X-ray of the abdomen may show injury to the lumbar spine, pelvis and lower ribs. It may also reveal the presence of peritoneal and retroperitoneal blood by obliteration of the psoas and may outline the size of various organs. X-rays of the limbs are taken to determine the site of fracture, displacement and type, and whether it is transverse, oblique or cornminuted. Further investigations may be required; for example, an intravenous pyelogram for renal tract injuries, arteri0grams for vascular trauma and intracerebral injuries. Spinal injuries are treated by bed rest on fracture boards, and for the more severe by traction with the patient lying on a Stryker bed so that regular turning can be performed. In some patients a decompression laminectomy and spinal fusion may be indicated. The more minor abdominal injuries such as contusions and retroperitoneal haematomata may only require intravenous fluid replacement and nasogastric suction; whereas, for more major injuries a laparotomy is performed and a ruptured spleen removed, a tear of the liver, bladder or viscus repaired, etc. Urethral injuries are treated initially by closed bladder drainage via a supra-pubic catheter and at a later stage surgical reconstruction of the urethra is performed. In the treatment of musculoskeletal injuries, skin wounds are carefully cleaned and tattooing must be avoided by thorough skin toilet. Neat skin apposition must be obtained, especially in facial wounds. Muscles, tendons and nerves may be repaired if the site of rupture and the degree of contamination is no bar to primary repair. A thorough wound toilet and debridement of compound injuries is performed to prevent the occurrence of gas gangrene and tetanus in devitalised necrotic muscle or bone sepsis leading to the complication of osteomyelitis. Limb fractures are reduced into good alignment, care being taken to secure normal rotation at the fracture site, and the affected part immobilised in either a splint or plaster cast. The period of immobilisation required depends on the time taken for union to occur as assessed by clinical and radiological examination; upper limb fractures may require 6-8 weeks and major lower limb fractures 3-4 months. Open reduction and fixation is performed for a variety of reasons and the criteria for its use must be strict, as a failed case due, for example, to infection is a disaster. Thus in the management of the 'multipleinjured' patient assessment and resuscitation must be carried out carefully and quickly, and a knowledge of the great variety of injuries that may occur is essential.
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T H E EARLY M A N A G E M E N T OF HEAD INJURIES
M. Briggs--Department of Neurological Surgery The early management of patients with head injuries involves three basic principles, namely, general resuscitation, early establishment of baselines of observation and, in a relatively few cases, surgical intervention. The damaged brain, be it damaged by concussion, contusion or laceration, does not tolerate hypoxia as well as the normal uninjured brain, so that a relatively minor head injury may appear, or indeed become, more severe if this condition is present. Some degree of cerebral hypoxia is commonly present in patients with head injury at the time they are first seen in the Accident Service recovery room. For example, it is not uncommon for an unconscious patient to develop airway obstruction from inhaled blood or vomit, particularly if he had been previously transported in the supine position. Other conditions such as flail chest, severe lung contusion or pneumothorax will all lead to impaired ventilatory function, a lowered arterial oxygen tension and cerebral hypoxia. Likewise, severe blood loss will lead to peripheral circulatory failure and inadequate perfusion of cerebral tissues. Even in the presence of an unobstructed airway, normal chest wall and lungs, cerebral hypoxia may occur if insufficient blood, or blood with impaired oxygen carrying capacity, is reaching the brain. From these observations it can be seen that adequate blood replacement, the establishment of an unobstructed airway and maintenance of good ventilation are of supreme importance in the management of patients with head injury. The treatment of individual injuries can, and usually should, wait until the two priorities (of blood replacement and oxygenation) have been dealt with. For example, it has been shown that definitive surgery to a compound depressed skull fracture can be left up to 18 hours without increasing the morbidity, providing the wound has been covered with a sterile dressing and prophylactic antibiotics given. General anaesthetics should be avoided as far as possible in the acute stage. In emergency conditions, the induction may be associated with periods of relative hypoxia and transient elevation of intracranial pressure (I.C.P.), during endotracheal intubation. The use of volatile anaesthetic agents, such as halothane, may cause a dangerous rise in I.C.P., and the reaction of the injured brain to routine drugs can be capricious and unpredictable. The second principle in the early management of the head-injured patient is that of careful observation. Observation is intended t o p rovide a guide to further treatment, particularly as to whether the brain is being compressed by an intracranial haematoma which needs surgical evacuation. In this event, the most consistent feature is a progressive lowering of responsiveness. In the classical picture of an extradural haemorrhage the patient has been concussed, but by the time he is seen in hospital he is fully conscious and alert, the so-called 'lucid interval.' As the haematoma develops he becomes less responsive at a rate proportional to the severity of the bleeding, until, untreated, he is completely unresponsive to any form of stimulation. With some extradural haematomata and with the majority of acute subdural haematomas the lucid interval is fleeting and relative. With the increasing size of the haematoma, changes in the neurological status may be observed. For example, a clot situated over the motor area may cause weakness of the contralateral face and arm; over the speech area,
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aphasia, and so on. As the pressure above the tentorium rises, herniation of the temporal lobe occurs through the tentorial hiatus, distorting the occulomotor nerve in the process. This leads to the typical pupillary signs of progressive dilatation and loss of reaction of light, on the side of the clot. The other changes involve the vital signs of pulse, blood pressure and respiration. As the intracranial pressure rises, so too does the arterial tension. This results in an increased vagal activity and a slowing of the pulse rate. Compression of the brain stem by the tentorial hernia causes progressive respiratory embarrassment. Therefore the careful observation of head injuries must include frequent assessment of the level of responsiveness, estimation of pupil size and its reaction to light and measurement of pulse, blood pressure and respiratory rate. Baseline observations of these parameters should be established as soon as possible so that the progressive changes associated with an enlarging intracranial haematoma may be noticed early and prompt surgical treatment carried out. Morphine and its derivatives, atropine and sedatives are best avoided because they interfere with pupillary observations and hinder the assessment of the level of responsiveness. When indicated by the progressive change in observations, the operation for release of an extradural haematoma must be carried out without delay. The situation has been described as the one true surgical emergency. The result of failure to recognise this fact is demonstrated by an overall mortality for extradural haematomata of 5o per cent in this country at large. Frequently with a rapidly developing clot there is not time for the patient to be transferred to a specialised neurosurgical unit and, therefore, the simple procedure of burr hole and craniectomy for the evacuation of such a clot should be within the scope of any surgeon working in a hospital which admits accident cases. So much for the initial resuscitation and observations designed to detect cerebral compression. A further feature which must be watched for and protected against, both in the immediate and later stages in the care of patients with head injury, is that of infection. The majority of superficial infections should be preventable by adequate primary treatment of scalp lacerations. Likewise a large proportion of brain abscesses, which may follow penetrating brain injuries, can be avoided by adequate wound toilet. However, the complication of meningitis may be less easy to guard against. It is known to be associated with certain types and combinations of injuries, and awareness of this fact should lead to a more adequate prophylaxis and early treatment of this potentially lethal complication. The presence of a C.S.F. leak, be it rhinorrhoea or otorrhoea, is evidence of a fistula between the subarachnoid space and the exterior. The risks of meningitis developing in this situation are very high and, therefore, all patients with such a leak should be given adequate antibiotic prophylactic as soon as the complication is recognised. In this service we use benzylpenicillin 6oo mg 6 hourly and sulphadiazine 2 g stat. followed by I g 4 hourly. This prophylaxis must be maintained for the duration of the leak which, if prolonged, will require surgical closure of the fistula. The association between meningitis and fractures involving the frontal or ethmoidal sinuses or of the maxilla have been noted by many authors, and with this complication in mind it is stressed that patients with such injuries must be watched closely. It has similarly been noted that immediate post-traumatic pneumocephalus, which carries an equally high risk of meningitis is frequently associated with fractures of the facial bones; indeed, in a recent survey, as many as 5° per cent
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of patients with this complication had facial fractures in addition to their head injury. Obviously then, patients with such fractures should be watched closely, firstly to detect the presence of any intracranial air, secondly to confirm the presence of a C.S.F. leak and thirdly to diagnose meningitis early, should this complication develop. Patients who require surgical intervention form only a small proportion of those admitted with head injuries; being about 5 per cent of 2000 patients in this service. The indications for surgery in the acute stage are, the existence of a compressing intracranial haematoma, the signs of which we have already considered, and the presence of a compound depressed skull fracture. At a later stage surgery may be indicated for the treatment of subacute and chronic haematomata, the repair of C.S.F. fistulae, and the elvation of some closed depressed skull fractures. In the short time allowed we have only been able to consider the principles involved in the early care of a patient with a head injury. However, attention to these principles must be the basis of management of such casualties who are presenting themselves in ever-increasing numbers; for instance in I96o 818 patients with head injury were admitted under the Accident Service whereas ro years later the annual figure rose to I9O8. BIOCHEMICAL SEQUELAE TO SEVERE HEAD AND FACE T R A U M A G. Higgins--Principal Biochemist The serious biochemical effects seen in patients who have suffered multiple injuries, ruptured kidneys, spleen, liver, intestine, etc., are well known, but the biochemical upset which can occur in patients i n whom the injury is confined to the head is not so widely recognised. A review of our cases several years ago showed that many of the patients who survived the immediate effects of head injury, died some days or weeks later of what could only be described as biochemical deaths. It was apparent that deaths following head injury could be divided into several groups. The first group of patients were those who died of the immediate effects of the injury--in these cases the biochemical tests showed little abnormality. The second group comprised those who survived, perhaps for several months or years, and who showed no evidence of any biochemical upset at all; these were mainly young persons whose constitution enabled them to resist the adverse biochemical effects. Of the remaining cases who developed biochemical abnormalities, some, who had no injury to the renal system, subsequently developed renal impairment and died of uraemia; others developed hypernatraemia and hyperchloraemia. The elderly patient frequently developed hyponatraemia and hypochloraemia and died of a condition similar to Addison's disease. For many years it has been known that trauma to any part of the body may cause generalised changes in the biochemistry of the body. When these follow head injuries the effects may be very serious. It has been shown that in experimental animals, trauma to the head affected cells of the lung and renal tract. Quickly following the head injury, the lung cells showed pulmonary oedema causing impairment of the gaseous interchange. This may be an explanation, if the same effect occurs in humans, of the carbon dioxide retention and oxygen
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lack that many patients suffer and of the lung infection which develops in so many unconscious patients with head injuries. With the introduction of rapid methods for the determination of the body electrolytes, it was seen that trauma could cause retention of sodium, with loss of potassium. This could result in increased cellular osmotic pressure and impairment of the function of the cell. Simpler methods of estimating plasma hormones led to the recognition that the injury caused a state of stress which led to the outpouring of increased amounts of the adrenal hormones. In contrast to this, the immobilisation due to the injury could lead to the suppression of the androgenic hormones which, in its turn, leads to loss of muscle and tissue nitrogen as well as to a loss of muscle tone. It will be understood that, in view of possibilities, many undesirable metabolic states can be superimposed upon the actual traumatic damage resulting from the injury. In our review of the morbidity of severe trauma, it was apparent that when these abnormal biochemical states became established they were often very difficult to correct and also that these conditions were frequently made worse by the treatment given to the patient. In the early days of treatment of severe head injury victims difficulty was often experienced in feeding the patient or in giving him adequate fluid intake. The sequence of events was progressive dehydration of the patient, loss of cellular water, increased cellular osmotic pressure and impairment of cellular function. Renal insufficiency developed and the nitrogen load arising from the breakdown of damaged tissue soon led to uraemia and renal failure. When the importance of proper hydration was realised, many surgeons prescribed more than adequate fluid intake. In many cases no harm was done, but in some elderly patients hyponatraemia developed. This complication may be due to the washing out of body electrolytes, but can occur when there is failure of the adrenal and pituitary glands to respond to extreme stress and the kidney loses sodium. Although this is usually a complication in the older patient, it has been seen in teenagers, in whom it can be so severe as to induce mental impairment. The other condition of hypernatraemia and hyperchloraemia is more complex. There is some evidence that cerebral factors may play a part in the regulation of ionic concentration, and injury to the brain may upset this mechanism. The condition is often associated with a lung infection which itself may lead to dehydration and thus increased salt concentration. In some cases the overenthusiastic administration of intravenous saline solution may induce the condition. These toxic biochemical states following injury, which may be partly the metabolic effects of such injury and partly man-made, are probably easier to prevent than cure. Two approaches to these problems have been made. The first was to design a diet which was capable of giving adequate calories, salts, protein, etc., to maintain life and yet could be administered through a naso-gastric tube. Intensive monitoring of the patient was started until it was certain that he or she was in a normal biochemical balance: this included daily or twice-daily estimation of blood electrolytes, blood gases, blood constituents and urinary studies when indicated. These evaluations influenced the daily adjustment of intake of salts, protein and calories so that a normal balance could be maintained; thus more or less fluid salts, protein, etc., could be added as indicated by the results of the investigations. Whereas in the past many patients with multiple injuries have died because of these upsets, it is now the exception rather than the rule. It should be emphasised
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that these efforts do not bring about improvement alone; recovery ultimately depends upon the ability of the patient to overcome the crisis. M E D I C A L ASPECTS OF A C U T E T R A U M A
D. Gwyn Williams--Department of Clinical Medicine Among the many effects of trauma on the body, there are a considerable number which involve the physician. His assistance may necessarily be required at the time of actual admission, and, in fact, he is more likely to be called at a later date when some complication has arisen, either due to the trauma itself or to surgical treatment. The most important medical complication of acute injury is renal failure due to acute tubular necrosis. This occurs from the loss of body fluids, which may be blood (deficient due to injury or surgery), plasma (lost as the result of burns) or gastrointestinal secretions (usually lost post-operatively). Such deprivation of body fluid produces renal ischaemia, leading to renal tubular damage and eventually to acute tubular necrosis. From first to last in this succession of events there is concomitant oliguria and uraemia, but the significance of these phenomena varies with the acutal stage in the chain of events. Initially, the kidneys work very well, and the oliguria is physiological, i.e. an attempt to conserve fluid (stage I oliguria). When acute tubular necrosis has developed, there is a gross derangement of renal function, with a clear-cut state o f renal failure (stage I I I oliguria). Somewhere in this progression of events, there is a metamorphosis of physiological interpathological oliguria corresponding to a state in which some renal tubules are damaged and some are not (stage I I oliguria). The recognition of stages I and I I in this march of events is of practical importance, as the oliguria of these stages is reversible. However, at the bedside, the three stages of oliguria are indistinguishable, uraemia accompanying each one. They can most easily and quickly be recognised in one of two ways. Firstly, by measuring the concentration of urea in the urine, and comparing this with the concentration of blood urea. Normally, urine urea is 14 times more concentrated than the blood urea, whereas in acute tubular necrosis the urine concentration of urea is equal to that of blood, or greater by a factor of only two or three. In stage H oliguria, although the concentration of urine urea is less than normal, it is still appreciably more concentrated than the blood urea. Secondly, one can measure the urine osmolarity and compare this with the plasma osmolarity. In the face of fluid loss the urine osmolarity should be much higher than that o f the plasma, but in acute tubular necrosis the urine osmolarity will be much diminished, and in stage I I oliguria the osmolarity of the urine will be less than in stage I, but greater than in stage I I L The oliguria having been noted, and the correct diagnosis having been made, the correct treatment can now be given. I f the oliguria is that of stage I, then the appropriate fluid should be given to the patient quickly and in adequate quantity. Speed in repairing the hypovolaemia is vital, and this is precisely the sort of case in which measuring the central venous pressure provides an ideal way of monitoring the intravenous infusion of fluids, so that large amounts can be given rapidly. In stage II, there are two methods of treatment which are often complementary. Just as in stage I, rapid administration of the correct fluid is vital,
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In addition, it has been found empirically, and there is some theoretical justification for this, that the use of diuretics at this stage can induce a diuresis and avert the impeding acute tubular necrosis. One is, of course, interested in a rapid effect, and the ideal diuretic in this situation would be frusemide given intravenously, or manitol, also given intravenously. The latter has the advantage of providing increased intravascular volume, and also of raising the blood pressure. There is, of course, no reason why both diuretics should not be used at the time. It is worth noting, in his context, that the use of intravenous ethacrynic acid should be avoided, because if the patient remains oliguric without a diuresis being obtained then the ethacrynic acid may produce deafness. If treatment of stage I or stage I I oliguria fails, or if the patient has already developed acute tubular necrosis, then a situation now exists of absolute renal damage. If the patient is depleted of body fluid, then the correct replacement should be given, but of course the patient will not be able to deal with an excess load, and heart failure and pulmonary oedema become a danger if too much fluid is given. Again, measuring the central venous pressure while giving intravenous fluid would be a sensible precaution. If there is no indication for dialysis, then conservative measures should be used at first. These comprise restriction of protein (to 4 ° g a day), sodium, potassium and fluid, and, at the same time, providing as many calories as possible by means of a high-calorie carbohydrate liquid concentrate in order to keep the breakdown of body protein to a minimum, so lessening the rise in blood urea. In mild cases, these conservative measures buy sufficient time for natural healing to occur with eventual recovery of the kidneys, and without gross uraemia occurring. Particular attention must be paid during the diuretic phase of recovery to the correct balance of sodium, potassium and water. In severe cases of acute tubular necrosis, and in those in whom conservative measures are inadequate, a dialysis becomes imperative. Practice varies from centre to centre but, in general, the following are the indications for dialysis: (i) A blood urea greater than 200 mg per cent. (2) Serum potassium 6 m Eq/litre or greater. (3) A patient overloaded with fluid through careless or overenthusiastic treatment. (4) Clinical deterioration, not due to other causes, irrespective of the biochemical values noted above. Peritoneal dialysis is the method to be preferred, as it is more economical of time, staff and materials, and is a less drastic procedure as far as the physiology of the body is concerned. However, in some cases--notably those who are catabolising rapidly or those with abdominal injuries which inhibit peritoneal dialysis-haemodialysis must be used. Nowadays the prognosis of acute tubular necrosis following trauma is relatively good, as the measures outlined above for correcting the maleffects of renal failure are usually successful. Indeed, spontaneous recovery is the rule if acute tubular necrosis is the only lesion affecting the kidneys. In conclusion, with respect to renal failure, it is worth remembering two guidelines which will prevent a considerable amount of morbidity and mortality. The first is to watch very carefully the patients' urine output from the time of admission. It is all too easy to forget this rather mundane body function during the drama of the acute injury and its treatment. The importance of this observation lies
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in the fact that correct treatment during the early stages of oliguria can prevent a progression to acute tubular necrosis. Secondly, if the oliguria is irreversible and there is a rise in blood urea, then the time to notify the physicians is as soon as this fact is recognised and not to wait until a blood urea of several hundred milligrams per cent is reached. The second most common complication in injured and immobilised patients is, of course, pulmonary embolus. This is usually an easy diagnosis with its well-recognised signs and symptoms. However, it can sometimes present in other subtle ways, such as shock without pain, breathlessness alone, cardiac failure, or syncope. Treatment of pulmonary embolus begins first and foremost with its prophylaxis. Whenever possible, patients should be activity mobilised; if not the whole body, then all parts which Call be. I f there is ally immobilisation, again whether of the whole or of a part, there is good evidence that prophylaxis with anticoagulants providing, of course, that there is no contra-indication to their use, is effective in preventing deep vein thromboses and pulmonary emboli. Once the pulmonary embolus has occurred, prophylaxis should be instituted if it has not already been done. In severe cases aggressive curative measures are worth trying. The only proven method of cure at present is surgery. In recent years a new drug, streptokinase, has been marketed. Its action is to dissolve blood clot by fibrinolysis, and there have been some striking anecdotal experiences of its use in pulmonary embolus, but its efficacy has still to be proven in a controlled trial. As far as the acutely injured or recent surgical patient is concerned, its use involves the obvious danger of haemorrhage. Fat embolism presents mainly with disturbance of file central nervous system, the cardiorespiratory system or as oliguria. Its exact cause is still not understood, and it is therefore no surprise that its treatment is vague and unsatisfactory. The following measures have been described: (I) Use of heparin and clofibrate, which have been shown to reduce lipaemia. (2) The use of phenoxybenzamine to dilate blood vessels. (3) Hypofilermia, because this reduces viscosity of fat, and it is thought therefore to reduce emboli from fractured bones. No controlled trials of these various measures have been performed, and it remains a moot point whether any of them are really effective. The physician can be called in to see various metabolic disturbances such as jaundice which can occur through shock alone or hypotension reducing the arterial blood supply to the liver with consequent hepatocellular damage. It can also arise through file use of drugs, particularly anaesthetic agents. Hyperglycaemia can occur following head injury. It is transient and does not need treatment, but it must be differentiated from diabetes mellitus which may be precipitated by the stress of the acute trauma. Following head injury, there may be hypernatraemia as a manifestation of diabetes insipidus. This may be permanent or temporary, and if severe enough it merits replacement therapy. Hyponatraemia can occur as a result of excessive and inappropriate A D H secretion following head injury. The resulting water retention leads to a low serum sodium, and this should be treated by restriction of water intake. Thrombocytopenia can, of course, follow treatment with various drugs,
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but it is also a complication of massive blood transfusion, which the acutely injured patient is likely to receive. If the thrombocytopenia is severe enough, with bleeding, then a platelet transfusion should be given. Rashes of all sorts, sizes and descriptions can occur, nearly always as a result of the drugs administered. Apart from the obvious causes of shock already mentioned, two other conditions should be borne in mind. The first of these is septicaemia, the second is myocardial infarction. There is no reason why this latter disease should not strike the victim of acute trauma lying in his bed, as easily as if he were listening to a talk on the medical aspects of trauma.