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Pitfalls in anaesthesia for multiply injured patients
Injury, 14,81-88
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Printed in Great Britain
Symposium Paper Pitfalls in anaesthesia for multiply injured patients L. H. D. J.
Booij
Department of Anaesthesia University Hospital, St Radboud, Nijmegen, The Netherlands IN PROVIDING anaesthesia for the multiply injured patient the anaesthetist may find that he is faced with a variety of choices. Examples: Should he use positive end expiratory pressure (PEEP) ventilation, in patients with severe pulmonary contusion, increased intracranial pressure and haemorrhagic shock? Should he resuscitate these patients with crystalloids or with colloids? What measures should he take to prevent aspiration of gastric content? Such dilemmas may exist and depend on the type and combination of the injuries. Many injured patients may also have major systemic diseases which can influence the course of anaesthesia and should be recognized before deciding the best types of treatment. Quite often pre-existing conditions are unrecognized and then the choice of methods must rest on the nature of the injuries and the experience and skill of the anaesthetist. As most multiply injured patients need an operation immediately after admission, there can be no stabilization period before anaesthesia. This may mean that medical treatment has to begin during anaesthesia and decisions must be taken during this time about the further course of treatment. If anuria is present on admission, then stimulation of urine production should be undertaken during anaesthesia to prevent the development of renal impairment or failure, Antibiotic treatment often needs to be started at this time. The prognosis in multiply injured patients is often uncertain and victims with shock and acute respiratory failure after chest injury have
a high mortality and morbidity rate if proper treatment is not carried out (Wilson et al., 1977). It should also be realized that the mortality due to anaesthesia is doubled or even trebled in emergency operations compared with elective cases (Vacanti et al., 1970: Feigal and Blaisdell, 1979). Therefore, for example, with pre-existing cardiovascular disease we must carefully consider whether delay is possible to allow for adequate preparation of the patient for the stress of the operation and the anaesthetic. On the other hand, valuable time should not be lost by looking for irrelevant information. In view of possible underlying medical diseases, the absence of a history and the various choices available and the need to make quick decisions, these patients should be anaesthetized by experienced consultants and not by junior doctors. This is true for all the other people involved in treating multiply injured patients, as has recently been stressed by West et al. (1979). I would now like to discuss some of the pitfalls that can confront even the experienced anaesthetist when dealing with these cases.
IMPAIRED GAS EXCHANGE IN THE LUNGS in patients with multiple injuries, pulmonary gas exchange is often disturbed. This may arise from the injury itself or may be the result of treatment (Table I). In multiply injured patients the chest is often involved when pulmonary contusion, pneumothorax, haemathorax and fractures of the ribs may make gas exchange insufficient (Trinkle et al.,
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Table L Causes of impaired pulmonary gas exchange
Causes due to injury
Pulmonary contusion Pneumothorax Haemathorax Rib fractures Adult respiratory distress syndrome (ARDS) Causes due to treatment Pneumothorax Fluid overload Aspiration ARDS
1973). Many factors may combine to produce adult respiratory distress syndrome (ARDS). Treatment may provoke a pneumothorax or fluid overload and pulmonary contusion is important. Pulmonary contusion This is common after thoracic injury, and may not be associated with fractures of ribs or a pneumothorax. The chest X-ray may show no signs during the first few hours after injury and the first warning of pulmonary contusion may be disturbance in the arterial blood gases. Blood gas analysis may in fact be more accurate in determining the severity and extent of the contusion than the chest X-ray (Erickson et al., 1971). If the syndrome is not recognized, large volumes of crystalloids may be administered to maintain an adequate circulation but can reduce the pulmonary gas exchange by the exudation of fluid into the damaged lung tissue (Richardson et al., 1974). When pulmonary contusion is diagnosed, PEEP ventilation should be started but this may interfere with the development and treatment of increased intracranial pressure, when high pressures are used, At a safe therapeutic range of below 30 cmH20, recent studies show that PEEP does not interfere with intracrania[ pressure. Hypotension due to PEEP is more likely to occur when it must then be decreased (Frost, 1977). Artificial ventilation may provoke or increase pneumothorax but nevertheless pulmonary contusion should be treated by artificial PEEP ventilation, the prevention of fluid accumulation in lungs and the administration of cortico-steroids (Richardson et al., 1974). Careful monitoring and weighing the risks of the treatment should be the guide lines. Pneumothorax A pneumothorax can be present without any fractured ribs (Paredes and Hipona, 1975).
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When pneumothorax is recognized, an intercostal drain should be inserted immediately (McCoy and Ayim, 1976). Sometimes pneumothorax is not recognized or only develops as a result of artificial ventilation, especially when PEEP is being used with high pressures (Downs and Chapman, 1976), This was thought to be the case in particular when a patient coughs and strains or fights the ventilator. In a recent study, however, the incidence of pulmonary barotrauma was shown to be less than 1 per cent (Cullen and Caldera, 1979), but this study did not include injured patients. If a very small pneumothorax exists, artificial ventilation may force air into the cavity through ruptures of alveolar or bronchiolar walls. In other cases artificial ventilation may lead to the pleura and lung being punctured by the edges of broken ribs and this may lead to pneumothorax. This is rare when the patient is awake and breathing spontaneously as he experiences pain, but in the anaesthetized patient under nitrous oxide, an existing small pneumothorax will increase as nitrous oxide diffuses faster into cavities than other gases diffuse out. This may result in the rapid development of a tension pneumothorax and a reduction in the circulation. Even a very small pneumothorax should therefore be drained before the induction of anaesthesia or the start of artificial ventilation. If it is still uncertain whether a pneumothorax exists, nitrous oxide should be avoided and the patient carefully and continuously monitored. High frequency jet ventilation may prevent the development ofa bronchopleural fistula, as may occur with artificial PEEP ventilation in patients with pneumothorax. Ira tension pneumothorax develops, the patient becomes cyanotic, tachycardiac, hypotensive and subcutaneous emphysema develops and the airway pressure will increase. Immediate thoracic drainage with a large-bore chest tube or a wide needle is then needed. It is often forgotten that pneumothorax may result from the attempted insertion of a canula into the subclavian or internal jugular vein. C O N S E Q U E N C E S OF S H O C K TREATM E N T AND FLUID I N F U S I O N Many patients with multiple injuries are in haemorrhagic shock, Replacement of the circulatory volume is very important and in shock and multiple injuries there is an obligatory third space available due to increased vascular permeability (Ledgerwood and Lucas, 1974). As a
Booij: Pitfalls in Anaesthesia
result a large volume of fluid must be administered to maintain the circulation, and balanced polyvalent solutions like Ringer's are best. As most patients are already hyperglycaemic due to the stress of the injury, plain solutions should be used, as glucose only increases the hyperglycaemia and results in increased diuresis. Colloid solutions in these circumstances disappear into the third space. From the third day onwards, this fluid will be absorbed leading to overload and pulmonary insufficiency (Fulton and Jones, 1975). This will be more pronounced if renal function is impaired, either from pre-existing disease or due to the injury and resulting shock (Lucas et al., 1977). The mortality ofexsanguination is however higher than that of fluid overload. If there is damaged brain, fluids may also accumulate here resulting in increased ICP. The symptoms of this may be masked during anaesthesia. In a patient with a normal cardiovascular system, a decrease in the haematocrit leads to an increase in oxygen transport. It is only below a value of 0.20 that a decrease in oxygen transport occurs (Sunder-Plasmann et al., 1971). In the presence of shock, before stopping the major bleeding, infusion should be enough to maintain the haemodynamics with fluid. Blood or its components should only be administered when there is insufficient oxygen transport capacity. The anaesthetist may be faced with the problem of too few intravenous lines, which may be because they are either too narrow or too few or inserted in the wrong place. The patient with multiple injuries needs at least two large-bore intravenous lines and a central venous line. Lines for transfusion and for measuring arterial pressure should be inserted in the arm or neck, because sometimes in severe cases, clamping of the great vessels is needed and then lower limb lines are useless.
C O N S E Q U E N C E S OF I N T U B A T I O N In severely injured patients endotracheal intubation is indicated either for anaesthesia or for articial ventilation in the prevention or treatment of aspiration or ARDS. In most cases requiring intubation, muscle relaxation is necessary and succinylcholine is commonly used for this. This drug, however, causes fasciculation of the muscle, it leads to increase in intraocular and intracranial pressure and may displace a fracture. The increase in intra-abdominal pressure may lead to regurgitation and aspiration of stomach contents. Immediately after injury, an increase in potassium release can occur and the resulting muscular paralysis may start internal bleeding
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again by release of the tamponade effect and this may result in sudden death of the patient (Kopriva et aI., 1971). This is especially the case with blunt abdominal injury. For intubation, the head and neck must be extended and if there has been a cervical injury, this may lead to vertebral dislocation which can cause neurological complications. In multiple injuries the trachea may also be damaged and if there are fractures of the first three ribs, the bronchi or aorta may be ruptured (Chesterman and Satsangi, 1966; Paredes and Hipona, 1975). In patients with laryngeal injuries or transection of the trachea, both anaesthetist and surgeon must be aware of the dangers ofintubation. The tube may follow a false route and result in loss of the airway, and even if the trachea is intact it may follow a false passage due to fracture of the thyroid cartilage and the cricoid, lntubation should then be done with the help of a fibreoptic bronchoscope under local anaesthesia or a primary tracheostomy should be established (Sofferman, 1981). If the patient is breathing satisfactorily, intubation is not needed primarily even when there is emphysema. Such emphysema may be mediastinal, or the air may enter the pleura leaving a pneumothorax (Metson, 1953). In a blunt neck injury there may be oedema of the trachea without other injury to the airway and this too may make intubation difficult and a tracheostomy should again be considered. Trouble with intubation may also occur in cases of facial injuries and laceration of the soft tissues or fractures of the orofacial skeleton. In all these conditions tracheostomy should be considered primarily. Whenever prolonged ventilation is anticipated, simple nasogastric intubation is sometimes considered but in my opinion this should be avoided to start with. Sometimes a crash intubation is requested to prevent aspiration and avoid periods of hypoxia, and intubation then has to be done as quickly as possible. In fractures of the base of the skull, nasal tubes may lead to microorganisms gaining access to the brain and meninges. When primary tracheostomy is considered, it must be remembered that aspiration pneumonitis is more common than after a simple endotracheal tube, which is thought to be due to impairment of the laryngeal muscles, and so tracheostomy should be avoided if possible.
Aspiration In elective surgery, silent regurgitation takes place in about l0 per cent of cases while in
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emergencies the incidence is 25 per cent (Stewardson and Nijhuis, 1977). Whether a Mendelson syndrome (Mendelson, 1946) develops on aspiration depends on the pH and quantity of the stomach contents that have been aspirated. In animal models it has been shown that when the volume aspirated is about 50 ml and the pH is below 2.5, it is almost certain that the syndrome will develop (Stewardson and Nijhuis, 1977). In patients it has been proven that if the pH is between 1.8 and 2.5 the mortality is 25 per cent, and with a pH below 1.8 it is 100 per cent (Wynne and Modell, 1977). In obese patients the incidence of aspiration is increased (Wilson et al., 1981). In injury, the pain, fear, release of catecholamine and the possible administration of drugs delay gastric emptying and therefore increase the risk of aspiration (Zaricznyj et al., 1977). It has been suggested that cimetidine might be given intravenously to injured patients to decrease the risk of Mendelson's syndrome but this drug does not increase the pH of the gastric content already present, but only increases the pH of newly produced gastric fluid. It takes 45 minutes to have an effect (Stoelting, 1978; Dobb et al., 1979) and thus it can have no effect in injured patients when immediate operation is needed. In the past, the administration of antacids has been advocated but aspiration of antacids is likely to be as dangerous as the aspiration of gastric fluid (Gibbs et al., 1979). The most reliable measures to prevent aspiration are to intubate while the patient is awake or to do a crash induction with cricoid pressure. The treatment of Mendelson's syndrome consists of bronchial suction without lavage to prevent the spread of the fluid, PEEP ventilation, corticosteroids if administered immediately, and antibiotics. It is also possible to have aspiration at the end of the anaesthesia when the tube is removed. Therefore patients should only be extubated when laryngeal reflexes have been reestablished. Increase in intracranial pressure Head injury occurs in many multiply injured patients and the resulting cerebral oedema or haemorrhage can cause increased intracranial pressure. It is well known that hypoxia, hypercapnia and some anaesthetics increase the intracranial pressure even further. Nitrous oxide can also increase intracranial pressure (Phirman and Shapiro, 1977). Because the permeability of cerebral vessel is increased, fluid tends to
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accumulate in the oedematous tissue, leading to a further increase in intracranial pressure. Colloidal fluids can also penetrate in these circumstances into the tissues so that fluid resuscitation should be carried out with the possibility of cerebral oedema or bleeding being borne in mind. If not absolutely indicated, there should be no massive infusion of fluids, but if there is such a need, blood, plasma, albumin or high molecular weight dextran is better than the use of low molecular weight dextran, gelatin or crystalloids. One must also determine during the anaesthetic whether a patient is developing a subdural or extradural haematoma and the signs of these conditions may be masked by a general anaesthetic. Warning signs are an unexpected increase in arterial pressure, bradycardia or change in the pupil size, and the anaesthetist should be continuously alert to detect an increased intracranial pressure due to haemorrhage or oedema in the multiply injured patient. It should be remembered also that pain can increase intracranial pressure (Lassen and Christensen, 1976). C O N S E Q U E N C E S OF M A S S I V E BLOOD TRANSFUSION The effects of massive infusion of blood or fluid can precipitate electrolyte imbalance, pulmonary oedema, transfusion reactions and disseminated intravascu[ar coagulopathy. Blood transfusion can be called massive if more than 8 units or the equivalent of one or one and a half times the patient's estimated blood volume are given in an adult (Miller, 1973). Because a decrease in the haematocrit will optimize the oxygen transport in healthy patients, one can usually begin by infusing 2 litres of Ringer's solution before blood is given, unless there is exsanguination. This makes the use of uncross-matched blood in most cases unnecessary. Hypothermia This may develop due to the infusion of large amounts of cold blood or other fluid and can be limited by warming the blood beforehand and using warm blankets on the patient himself. Profound hypothermia induces postoperative shivering, which leads to increased oxygen consumption which may reduce the oxygen delivery to the tissues. As most patients are ventilated after operation, shivering and increased oxygen consumption can be prevented by using muscle relaxants and sedation.
Booij: Pitfalls in Anaesthesia
Hyperkalaemia This occurs when the blood is old, as normal fresh blood contains 3 mmol/l, but after 7 days of storage it increases to 12 mmol/l and after 21 days to 32 mmol/l (Bunker, 1966). Although it is dangerous, hyperkalaemia has been reported to be rare (Schweizer and Howland, 1962). In multiple injuries, shifts ofelectrolytes take place and these can lead to hypokalaemia, so that potassium levels must be estimated frequently and blind administration of potassium given up.
Impaired oxygenation of tissues In blood stored for 5 days in citrate dextrose solution (ACD), the 2,3-diphosphoglycerate (2,3- DPG) content falls, leading to an increased affinity of haemoglobin for oxygen. After 14 days of storage at 4 °C the average loss of 2,3-DPG is 70 per cent in ACD, 80 per cent in ACDadenine and 45 per cent in citrate phosphate dextrose (CPD) solution, with which the 2,3-DPG level is better maintained. For sufficient oxygen to be supplied to the tissues therefore the tissue oxygen level must be lower. It would take between 24 and 48 hours before the 2,3-DPG concentration returns to normal, so that hypoxaemia is a greater hazard during this period after massive blood transfusion (Waiters and Nott, 1977).
Acidosis The addition of ACD solution decreases the pH of fresh blood to 7-0 and in the following 21 days it falls further to 6-5 as a result of continued glycolysis and cellular metabolism. The Pco_, increases from 20 to 28 kPa (Howland and Schweizer, 1962). When massive transfusion is needed, the patient is often already acidotic and when blood is given, this will increase. The empirical administration of sodium bicarbonate is not, however, indicated (Miller et al., 1971). Blood gas analysis should always be performed instead, to determine the need for correction of the acidosis. Hypocalcaemia and the effects of citrate Depending on the total amount and the speed of transfusion, hypocalcaemia may develop (Kahn et al., 1979) and though it has no effect on coagulation it can reduce myocardial contractility, especially when hypoxia, hypercapnia, acidosis and anaesthetic drugs have already depressed myocardial function. Calcium only needs to be given when myocardial depression becomes apparent from hypotension and ECG changes.
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Decrease in calcium content does not depend on whether ACD or CPD blood is used (Drop and Scheideger, 1979). Citrate intoxication is very rare and it only occurs in patients with disturbed liver function and hypothermia. Citrate is metabolised in muscles, liver and kidney where the rate is limited by the enzyme aconitase. For each mmol of citrate, 3 mmol of bicarbonate are produced. Immediately after operation this may result in metabolic alkalosis, especially if any existing metabolic acidosis has been corrected by bicarbonate. Therefore blind administration of bicarbonate without doing the blood gases must be avoided.
Microaggregates and pulmonary microemboli Stored whole blood contains microaggregates which can cause microemboli, though these can be prevented by the use of microfilters with a mesh size of 40 to 20/tm. These filters can allow about l0 units ofblood to be given but they also reduce the platelet concentration so that fresh blood containing platelets should never be given through a micropore blood filter. When packed cells are used there is no need for a filter because the content of microaggregates is minimal, unless glucose or Ringer's has been added to the packed cells. Coagulation disorders In stored blood there is a fall in platelets, Factors V, VIII and IX. Coagulation disorders are to be expected when more than 10 units of blood are used. The concentration of platelets, thromboplastin time and fibrinogen concentration should then be measured. Replacement is by administration of 2 units of fresh blood or 4 units of fresh frozen plasma and 6 donor units of platelets. Hypocalcaemia has never been proven to be the origin of coagulation disorders in massive transfusions but in patients with extensive injuries, disseminated intravascular coagulation (DIC) may develop (Attar, 1969). In the past this paradox between bleeding and thrombosis used to be treated by giving heparin, but nowadays packed platelets and fresh blood are used, together with treating the precipitating cause such as hypovolaemia. A rough indication for coagulation disorders can be obtained by determining the clotting time of blood in a glass tube, which allows blood to clot normally in 6 minutes.
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CONSEQUENCES OF DRUG ADMINISTRATION Most drugs used in anaesthesia are very potent and have many side effects. Anaesthetic agents, whether administered by intravenous injection or inhalation, generally cause cardiovascular changes due to myocardial depression and/or peripheral vasodilatation. Decreased cardiac output, hypotension and tacbycardia or bradycardia can all be seen. Because of peripheral vasoconstriction and the resulting increase in central concentration of drugs in injured patients, lower doses are usually necessary, and the impaired cardiovascular function may make the cardiovascular depressant effect more obvious. The use ofhalothane or enflurane with barbiturates in such a patient can leave him without any arterial blood pressure. In our hospital we induce anaesthesia in the injured patient with minimal amounts of the least cardiovascular depressing agent i.e. gamma hydroxybutyric acid, etomidate or diazepam supplemented with fentanyl. For muscle relaxation succinylcholine, pancuronium and Org-NC45 are most appropriate. Only after enough fluid has been infused, are droperidol and other adjuvants given. In most emergency cases, ketamine-diazepam anaesthesia is allowed. There is frequently no urine production in patients with multiple injuries because of the reduced arterial pressure and insufficient renal perfusion or because of the hormonal regulating mechanism. (ADH, angiotensin, renin). The patient really needs to be considered as having no renal function, which means that several drugs which depend on renal excretion for elimination last longer and have higher plasma concentrations, which may prolong their action. Incremental doses of such drugs at normally used intervals can result in accumulation. A common example is the longer duration of action of non-depolarizing muscle relaxants in renal failure (Miller et al., 1973; Geha et al., 1976; Booij et al., 1982). Such prolonged action has been noted with the anuria of injury and shock. This is not only due to impaired renal function, but also to acidosis, hypothermia and shifts in electrolytes (Crul-Sluyter and Crul., 1974; Miller et al., 1978). Dextrans and gelatins are commonly used in shock as plasma expanders but both are usually excreted in the kidneys, and in anuria they remain longer in the body. Dextrans also increase the viscosity of the urine which may lead to tubular obstruction and further renal
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damage. In our unit, therefore, gelatin (Haemaeel) is used as a colloidal fluid. In some cases digitalization is required and anuria and abnormal potassium levels may then interfere. When antibiotics are needed it must be remembered that they can further impair renal function and in renal failure they may accumulate in the body and sometimes have ototoxic effects. CONSEQUENCES OF TECHNICAL PROCEDURES Multiply injured patients, not only for direct treatment purposes but also for monitoring their vital functions, need a number of indwelling catheters or cannulas, which may lead to complications. Haemothorax or pneumothorax can result from subclavian or internal jugular cannulas (Brown and Wallace, 1976; Linos et al., 1980). They may also take the wrong course or form loops (Malatinsky et al., 1976). Cannulas can obstruct cerebral blood flow resulting in increased ICP or they can break. This is a real hazard in accident cases because checking ofthe cannula may only take place after the operation. Testing for a free back-flow ofblood and observing oscillation in pressure synchronous with ventilation is helpful in preventing such complications. Insertion of arterial lines can also give complications, especially when arterial thrombosis develops. Because the rate of'urine production is a good index of the adequacy of replacement of hypovolaemia, a urethral catheter is obligatory. In fracture of the pelvis a false route can easily be obtained while inserting such a catheter and in these cases suprapubic percutaneous puncture of the bladder should be performed. Because in such a case the patient must be prepared in a hurry, burns due to iodine or electrodes are a risk. P O S T - R E S U S C I T A T I O N DISORDERS A syndrome may develop some days after the primary care of the multiply injured patient in the form of post-resuscitation hypertension (Ledgerwood and Lucas, 1974). Due to the injury and the subsequent operation, sequestration of fluids and electrolytes in the interstitial spaces may take place: the third space is filled up. This cannot be prevented by primary restriction of fluid administration because these fluids are needed to maintain an adequate circulation. The sequestration of these fluids results From poor perFusion and cellular ischaemia and cannot be helped, but after 2 to 3 days when the vessels are recovered reabsorption of the fluid
Booij: Pitfalls in Anaesthesia
from the third space takes place. This can lead to vascular overload and hypertension which are more pronounced when the renal function is still impaired, though the vascular overload can lead to polyuria some days after resuscitation. When patients are resuscitated with human serum albumin, the renal excretion of excess fluid is impaired, leading to a longer period of hypertension (Siegel et al., 1973). Depending on the degree of overload, pulmonary congestion can take place leading to a second phase of respiratory failure, and encephalopathy can also follow. The treatment of post-resuscitation hypertension consists of fluid restriction, stopping colloids, the giving of diuretics and finally vasodilators. Respiratory failure must be anticipated by instituting artificial ventilation, and the combination of simultaneous support of the lungs and the kidneys provides the best chance of survival (Lucas et al., 1977). Digitalization before fluid mobilization may improve the circulation. After discussing some of the features of multiply injured patients, it can be concluded that anaesthesia in these victims is full of pitfalls. Because anaesthetic management of these patients must take into account many factors, including pre-existing disease and medication, concomitant injuries outside the range of planned operations, the condition at the time of operation, the lesions found and the facilities available as well as the foreseen postoperative complications, no single method of anaesthesia can be described. The choice of anaesthesia in emergency accident surgery is seldom easy or straightforward, and the way in which each individual patient should be treated can only be determined by the skilful experienced anaesthetist.
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Crul-Sluyter E. J. and Crul J. F. (1974) Acidosis and neuromuscular blockade. Acta Anaesthesiol. &'and. 18, 224. Cullen D. J. and Caldera D. L. (1979) The incidence of ventilator-induced pulmonary barotrauma in critically ill patients. Anesthesiology 50, 185. Dobb G., Jordan M. J. and Williams J. G. (1979) Cimetidine in the prevention of the pulmonary acid aspiration (Mendelson's) syndrome. Br. J. Anaesth. 51,967. Downs J. B. and Chapman R. L. (1976) Treatment of bronchopleural fistula during continuous positive pressure ventilation. Chest 63, 363. Drop L. J. and Scheidegger D. (1979) Haemodynamic consequences ofcitrate infusion in the anaesthetized dog: comparison between two citrate solution and the influence of beta blockade. Br. J. Anaesth. 51, 513. Erickson D. R., Shinozuki T., Beekman E. et al. (1971 ) Relationship of arterial blood gases and pulmonary radiographs to the degree of pulmonary damage in experimental pulmonary contusion. J. Trauma 11, 689. Feigal D. W. and Blaisdell F. W. (1979) The estimation of surgical risk. Med. Clin. North Am. 63, 1131. Frost E. A. M. (1977) Effects of positive endexpiratory pressure on intracranial pressure and compliance in brain-injured patients. J. Neurosurg. 47, 195. Fulton R. L. and Jones C. E. (1979) The cause of posttraumatic pulmonary insufficiency in man. Surg. Gynecol. Obstet. 140, 179. Geha D. G., Blitt C. D. and Moon B. J. (1976) Prolonged neuromuscular blockade with pancuronium in the presence of acute renal failure: a case report. .4nesth. Analg. (Cleve.) 55, 343. Gibbs C. P., Schwarz D. J., Wynne J. W. et al. (1979) Antacid pulmonary aspiration in the dog. Anesthesiology 51,380. Howland W. S. and Schweizer O. (1962) Increased carbon dioxide tension as a factor in the activity ofbank blood. Surg Gynecol. Obstet. 115,599. Kopriva C., Ratliff J., Fletcher J. R. et al. (1971) Serum potassium changes after succinylcholine in patients with acute massive muscle trauma..4nesthesiolog.v 34, 246. Lassen N. A. and Christensen M. S. (1976) Physiology of cerebral blood flow. Br. J..4naesth. 48, 719. Ledgerwood A. M. and Lucas C. E. (1974) Post resuscitation hypertension. Etiology, morbidity and treatment..4rch. Surg. 108, 531. Linos D. A., Mucha P. jun. and van Heerden J. A. (1980) Subclavian vein, a golden route. Mayo Clin. Proc. 55, 315. Lucas C. E., Ledgerwood A. M., Shies M. R. et al. (1977) The renal factor in the post-traumatic "fluid overload" syndrome. J. Trauma 17,667. Malatinsk~, J., Kadlic T., M~ijek M. et al. (1976) Misplacement and loop formation of central venous catheters..4cta Anesthesiol. Scand. 20, 237. McCoy J. A. and Ayim E. (1976) The management of acute thoracic injuries..4naesthesia 31,532.
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Mendelson C. L. (1946) The aspiration of stomach contents into the lung during obstetric anaesthesia. Am. J. Obstet. Gynecol. 52, 191. Metson B. F. (1953) Subcutaneous rupture of the trachea. Arch. Otolaryngol. 57, 182. Miller R. D. (1973) Complications of massive blood transfusion. Anesthesiology 39, 82. Miller R. D., Tong M. J. and Robbins T. O. (1971) Effects of massive transfusion of blood on acid-base balance. JAMA 216, 1762. Miller R. D., Stevens W. C. and Way W. L. (1973) The effect of renal failure and hyperkalemia on the duration of pancuronium neuromuscular blockade in man. Anesth. Analg. (Cleve.) 52, 661. Miller R. D., Agoston S., van der Pol F. et al. (1978) Hypothermia and the pharmacokinetics and pharmacodynamics of pancuronium in the cat. J. Pharmacol. Exp. Ther. 207,532. Paredes S. and Hipona F. A. (1975) The radiologic evaluation of patients with chest trauma: respiratory system. Med. Clin. North Am. 59, 37. Phirman J. R. and Shapiro H. M. (1977) Modification of nitrous-oxide-induced intracranial hypertension by prior induction of anesthesia. Anesthesiology 46, 150. Richardson J. D., Franz J. L., Grover F. L. et al. (1974) Pulmonary contusion and haemorrhage-crystalloid versus colloid replacement. J. Surg. Res. 16, 330. Schweizer O. and Howland W. S. (1962) Potassium levels, acid-base balance and massive blood transfusion. Anesthesiology 23, 735. Siegel D. C., Cochin A., Geocaris T. et al. (1973) Effects of saline and colloid resuscitation on renal function. Ann. Surg.177, 51. Sofferman R. A. (1981) Management of laryngotracheal trauma. Am. J. Surg. 141,412.
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Stewardson R. H. and Nyhuis L. M. (1977) Pulmonary aspiration. An update. Arch. Surg. 112, 1192. Stoelting R. K. (1978) Gastric fluid pH in patients receiving cimetidine. Anesth. Analg. (Cleve.) 57, 675. Sunder-Plasmann L., Kloevekorn W. P. and Messmer K. (1971) Blutviskosit~it und H~imodynamik bei Anwendung kolloidaler Volumenersatzmittel. Anaesthesist 20, 172. Trinkle J. K., Fuman R, W., Hinshaw M. A. et al. (1973) Pulmonary contusion. Ann. Thorac. Surg. 16, 568. Vacanti C. J., van Houten R. J. and Hill R. C. (1970) A statistical analysis of the relationship of physical status to postoperative mortality in 68 388 cases. Anaesth. Analg. (Cleve.) 49, 564. Waiters F. J. and Nott M. R. (1977) The hazards of anaesthesia in the injured patient. Br. J. Anaesth. 49, 707. West J. G., Trunkey D. D. and Lira R. C. (1979) System of trauma care. A study of two countries. Arch. Surg. 114, 455. Wilson R. F., Gibson D. B. and Antonenko D. (1977) Shock and acute respiratory failure after chest trauma. J. Trauma 17, 695. Wilson S. L., Mantena N. R. and Halverson J. D. (1981) Effects of atropine, glycopyrrolate and cimetidine on gastric secretion in morbidly obese patients. Anesth. Analg. (Clew.) 60, 37. Wynne J. W. and Modell J. H. (1977) Respiratory aspiration of stomach contents. Ann. Intern. Med. 87, 466. Zaricznyj B., Rockwood C. A., O'Donoghuem D. J. et al. (1977) Relationship between trauma to the extremities and stomach motility. J. Trauma 17,920.
Requestsfor reprints shouM be addressed to: Dr Leo H. D. J. Booij, Department of Anaesthesia, University Hospital. St Radboud. University of Nijmegen, The Netherlands.
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Printed in Great Britain
Symposium Paper Pitfalls in anaesthesia for multiply injured patients L. H. D. J.
Booij
Department of Anaesthesia University Hospital, St Radboud, Nijmegen, The Netherlands IN PROVIDING anaesthesia for the multiply injured patient the anaesthetist may find that he is faced with a variety of choices. Examples: Should he use positive end expiratory pressure (PEEP) ventilation, in patients with severe pulmonary contusion, increased intracranial pressure and haemorrhagic shock? Should he resuscitate these patients with crystalloids or with colloids? What measures should he take to prevent aspiration of gastric content? Such dilemmas may exist and depend on the type and combination of the injuries. Many injured patients may also have major systemic diseases which can influence the course of anaesthesia and should be recognized before deciding the best types of treatment. Quite often pre-existing conditions are unrecognized and then the choice of methods must rest on the nature of the injuries and the experience and skill of the anaesthetist. As most multiply injured patients need an operation immediately after admission, there can be no stabilization period before anaesthesia. This may mean that medical treatment has to begin during anaesthesia and decisions must be taken during this time about the further course of treatment. If anuria is present on admission, then stimulation of urine production should be undertaken during anaesthesia to prevent the development of renal impairment or failure, Antibiotic treatment often needs to be started at this time. The prognosis in multiply injured patients is often uncertain and victims with shock and acute respiratory failure after chest injury have
a high mortality and morbidity rate if proper treatment is not carried out (Wilson et al., 1977). It should also be realized that the mortality due to anaesthesia is doubled or even trebled in emergency operations compared with elective cases (Vacanti et al., 1970: Feigal and Blaisdell, 1979). Therefore, for example, with pre-existing cardiovascular disease we must carefully consider whether delay is possible to allow for adequate preparation of the patient for the stress of the operation and the anaesthetic. On the other hand, valuable time should not be lost by looking for irrelevant information. In view of possible underlying medical diseases, the absence of a history and the various choices available and the need to make quick decisions, these patients should be anaesthetized by experienced consultants and not by junior doctors. This is true for all the other people involved in treating multiply injured patients, as has recently been stressed by West et al. (1979). I would now like to discuss some of the pitfalls that can confront even the experienced anaesthetist when dealing with these cases.
IMPAIRED GAS EXCHANGE IN THE LUNGS in patients with multiple injuries, pulmonary gas exchange is often disturbed. This may arise from the injury itself or may be the result of treatment (Table I). In multiply injured patients the chest is often involved when pulmonary contusion, pneumothorax, haemathorax and fractures of the ribs may make gas exchange insufficient (Trinkle et al.,
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Table L Causes of impaired pulmonary gas exchange
Causes due to injury
Pulmonary contusion Pneumothorax Haemathorax Rib fractures Adult respiratory distress syndrome (ARDS) Causes due to treatment Pneumothorax Fluid overload Aspiration ARDS
1973). Many factors may combine to produce adult respiratory distress syndrome (ARDS). Treatment may provoke a pneumothorax or fluid overload and pulmonary contusion is important. Pulmonary contusion This is common after thoracic injury, and may not be associated with fractures of ribs or a pneumothorax. The chest X-ray may show no signs during the first few hours after injury and the first warning of pulmonary contusion may be disturbance in the arterial blood gases. Blood gas analysis may in fact be more accurate in determining the severity and extent of the contusion than the chest X-ray (Erickson et al., 1971). If the syndrome is not recognized, large volumes of crystalloids may be administered to maintain an adequate circulation but can reduce the pulmonary gas exchange by the exudation of fluid into the damaged lung tissue (Richardson et al., 1974). When pulmonary contusion is diagnosed, PEEP ventilation should be started but this may interfere with the development and treatment of increased intracranial pressure, when high pressures are used, At a safe therapeutic range of below 30 cmH20, recent studies show that PEEP does not interfere with intracrania[ pressure. Hypotension due to PEEP is more likely to occur when it must then be decreased (Frost, 1977). Artificial ventilation may provoke or increase pneumothorax but nevertheless pulmonary contusion should be treated by artificial PEEP ventilation, the prevention of fluid accumulation in lungs and the administration of cortico-steroids (Richardson et al., 1974). Careful monitoring and weighing the risks of the treatment should be the guide lines. Pneumothorax A pneumothorax can be present without any fractured ribs (Paredes and Hipona, 1975).
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When pneumothorax is recognized, an intercostal drain should be inserted immediately (McCoy and Ayim, 1976). Sometimes pneumothorax is not recognized or only develops as a result of artificial ventilation, especially when PEEP is being used with high pressures (Downs and Chapman, 1976), This was thought to be the case in particular when a patient coughs and strains or fights the ventilator. In a recent study, however, the incidence of pulmonary barotrauma was shown to be less than 1 per cent (Cullen and Caldera, 1979), but this study did not include injured patients. If a very small pneumothorax exists, artificial ventilation may force air into the cavity through ruptures of alveolar or bronchiolar walls. In other cases artificial ventilation may lead to the pleura and lung being punctured by the edges of broken ribs and this may lead to pneumothorax. This is rare when the patient is awake and breathing spontaneously as he experiences pain, but in the anaesthetized patient under nitrous oxide, an existing small pneumothorax will increase as nitrous oxide diffuses faster into cavities than other gases diffuse out. This may result in the rapid development of a tension pneumothorax and a reduction in the circulation. Even a very small pneumothorax should therefore be drained before the induction of anaesthesia or the start of artificial ventilation. If it is still uncertain whether a pneumothorax exists, nitrous oxide should be avoided and the patient carefully and continuously monitored. High frequency jet ventilation may prevent the development ofa bronchopleural fistula, as may occur with artificial PEEP ventilation in patients with pneumothorax. Ira tension pneumothorax develops, the patient becomes cyanotic, tachycardiac, hypotensive and subcutaneous emphysema develops and the airway pressure will increase. Immediate thoracic drainage with a large-bore chest tube or a wide needle is then needed. It is often forgotten that pneumothorax may result from the attempted insertion of a canula into the subclavian or internal jugular vein. C O N S E Q U E N C E S OF S H O C K TREATM E N T AND FLUID I N F U S I O N Many patients with multiple injuries are in haemorrhagic shock, Replacement of the circulatory volume is very important and in shock and multiple injuries there is an obligatory third space available due to increased vascular permeability (Ledgerwood and Lucas, 1974). As a
Booij: Pitfalls in Anaesthesia
result a large volume of fluid must be administered to maintain the circulation, and balanced polyvalent solutions like Ringer's are best. As most patients are already hyperglycaemic due to the stress of the injury, plain solutions should be used, as glucose only increases the hyperglycaemia and results in increased diuresis. Colloid solutions in these circumstances disappear into the third space. From the third day onwards, this fluid will be absorbed leading to overload and pulmonary insufficiency (Fulton and Jones, 1975). This will be more pronounced if renal function is impaired, either from pre-existing disease or due to the injury and resulting shock (Lucas et al., 1977). The mortality ofexsanguination is however higher than that of fluid overload. If there is damaged brain, fluids may also accumulate here resulting in increased ICP. The symptoms of this may be masked during anaesthesia. In a patient with a normal cardiovascular system, a decrease in the haematocrit leads to an increase in oxygen transport. It is only below a value of 0.20 that a decrease in oxygen transport occurs (Sunder-Plasmann et al., 1971). In the presence of shock, before stopping the major bleeding, infusion should be enough to maintain the haemodynamics with fluid. Blood or its components should only be administered when there is insufficient oxygen transport capacity. The anaesthetist may be faced with the problem of too few intravenous lines, which may be because they are either too narrow or too few or inserted in the wrong place. The patient with multiple injuries needs at least two large-bore intravenous lines and a central venous line. Lines for transfusion and for measuring arterial pressure should be inserted in the arm or neck, because sometimes in severe cases, clamping of the great vessels is needed and then lower limb lines are useless.
C O N S E Q U E N C E S OF I N T U B A T I O N In severely injured patients endotracheal intubation is indicated either for anaesthesia or for articial ventilation in the prevention or treatment of aspiration or ARDS. In most cases requiring intubation, muscle relaxation is necessary and succinylcholine is commonly used for this. This drug, however, causes fasciculation of the muscle, it leads to increase in intraocular and intracranial pressure and may displace a fracture. The increase in intra-abdominal pressure may lead to regurgitation and aspiration of stomach contents. Immediately after injury, an increase in potassium release can occur and the resulting muscular paralysis may start internal bleeding
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again by release of the tamponade effect and this may result in sudden death of the patient (Kopriva et aI., 1971). This is especially the case with blunt abdominal injury. For intubation, the head and neck must be extended and if there has been a cervical injury, this may lead to vertebral dislocation which can cause neurological complications. In multiple injuries the trachea may also be damaged and if there are fractures of the first three ribs, the bronchi or aorta may be ruptured (Chesterman and Satsangi, 1966; Paredes and Hipona, 1975). In patients with laryngeal injuries or transection of the trachea, both anaesthetist and surgeon must be aware of the dangers ofintubation. The tube may follow a false route and result in loss of the airway, and even if the trachea is intact it may follow a false passage due to fracture of the thyroid cartilage and the cricoid, lntubation should then be done with the help of a fibreoptic bronchoscope under local anaesthesia or a primary tracheostomy should be established (Sofferman, 1981). If the patient is breathing satisfactorily, intubation is not needed primarily even when there is emphysema. Such emphysema may be mediastinal, or the air may enter the pleura leaving a pneumothorax (Metson, 1953). In a blunt neck injury there may be oedema of the trachea without other injury to the airway and this too may make intubation difficult and a tracheostomy should again be considered. Trouble with intubation may also occur in cases of facial injuries and laceration of the soft tissues or fractures of the orofacial skeleton. In all these conditions tracheostomy should be considered primarily. Whenever prolonged ventilation is anticipated, simple nasogastric intubation is sometimes considered but in my opinion this should be avoided to start with. Sometimes a crash intubation is requested to prevent aspiration and avoid periods of hypoxia, and intubation then has to be done as quickly as possible. In fractures of the base of the skull, nasal tubes may lead to microorganisms gaining access to the brain and meninges. When primary tracheostomy is considered, it must be remembered that aspiration pneumonitis is more common than after a simple endotracheal tube, which is thought to be due to impairment of the laryngeal muscles, and so tracheostomy should be avoided if possible.
Aspiration In elective surgery, silent regurgitation takes place in about l0 per cent of cases while in
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emergencies the incidence is 25 per cent (Stewardson and Nijhuis, 1977). Whether a Mendelson syndrome (Mendelson, 1946) develops on aspiration depends on the pH and quantity of the stomach contents that have been aspirated. In animal models it has been shown that when the volume aspirated is about 50 ml and the pH is below 2.5, it is almost certain that the syndrome will develop (Stewardson and Nijhuis, 1977). In patients it has been proven that if the pH is between 1.8 and 2.5 the mortality is 25 per cent, and with a pH below 1.8 it is 100 per cent (Wynne and Modell, 1977). In obese patients the incidence of aspiration is increased (Wilson et al., 1981). In injury, the pain, fear, release of catecholamine and the possible administration of drugs delay gastric emptying and therefore increase the risk of aspiration (Zaricznyj et al., 1977). It has been suggested that cimetidine might be given intravenously to injured patients to decrease the risk of Mendelson's syndrome but this drug does not increase the pH of the gastric content already present, but only increases the pH of newly produced gastric fluid. It takes 45 minutes to have an effect (Stoelting, 1978; Dobb et al., 1979) and thus it can have no effect in injured patients when immediate operation is needed. In the past, the administration of antacids has been advocated but aspiration of antacids is likely to be as dangerous as the aspiration of gastric fluid (Gibbs et al., 1979). The most reliable measures to prevent aspiration are to intubate while the patient is awake or to do a crash induction with cricoid pressure. The treatment of Mendelson's syndrome consists of bronchial suction without lavage to prevent the spread of the fluid, PEEP ventilation, corticosteroids if administered immediately, and antibiotics. It is also possible to have aspiration at the end of the anaesthesia when the tube is removed. Therefore patients should only be extubated when laryngeal reflexes have been reestablished. Increase in intracranial pressure Head injury occurs in many multiply injured patients and the resulting cerebral oedema or haemorrhage can cause increased intracranial pressure. It is well known that hypoxia, hypercapnia and some anaesthetics increase the intracranial pressure even further. Nitrous oxide can also increase intracranial pressure (Phirman and Shapiro, 1977). Because the permeability of cerebral vessel is increased, fluid tends to
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accumulate in the oedematous tissue, leading to a further increase in intracranial pressure. Colloidal fluids can also penetrate in these circumstances into the tissues so that fluid resuscitation should be carried out with the possibility of cerebral oedema or bleeding being borne in mind. If not absolutely indicated, there should be no massive infusion of fluids, but if there is such a need, blood, plasma, albumin or high molecular weight dextran is better than the use of low molecular weight dextran, gelatin or crystalloids. One must also determine during the anaesthetic whether a patient is developing a subdural or extradural haematoma and the signs of these conditions may be masked by a general anaesthetic. Warning signs are an unexpected increase in arterial pressure, bradycardia or change in the pupil size, and the anaesthetist should be continuously alert to detect an increased intracranial pressure due to haemorrhage or oedema in the multiply injured patient. It should be remembered also that pain can increase intracranial pressure (Lassen and Christensen, 1976). C O N S E Q U E N C E S OF M A S S I V E BLOOD TRANSFUSION The effects of massive infusion of blood or fluid can precipitate electrolyte imbalance, pulmonary oedema, transfusion reactions and disseminated intravascu[ar coagulopathy. Blood transfusion can be called massive if more than 8 units or the equivalent of one or one and a half times the patient's estimated blood volume are given in an adult (Miller, 1973). Because a decrease in the haematocrit will optimize the oxygen transport in healthy patients, one can usually begin by infusing 2 litres of Ringer's solution before blood is given, unless there is exsanguination. This makes the use of uncross-matched blood in most cases unnecessary. Hypothermia This may develop due to the infusion of large amounts of cold blood or other fluid and can be limited by warming the blood beforehand and using warm blankets on the patient himself. Profound hypothermia induces postoperative shivering, which leads to increased oxygen consumption which may reduce the oxygen delivery to the tissues. As most patients are ventilated after operation, shivering and increased oxygen consumption can be prevented by using muscle relaxants and sedation.
Booij: Pitfalls in Anaesthesia
Hyperkalaemia This occurs when the blood is old, as normal fresh blood contains 3 mmol/l, but after 7 days of storage it increases to 12 mmol/l and after 21 days to 32 mmol/l (Bunker, 1966). Although it is dangerous, hyperkalaemia has been reported to be rare (Schweizer and Howland, 1962). In multiple injuries, shifts ofelectrolytes take place and these can lead to hypokalaemia, so that potassium levels must be estimated frequently and blind administration of potassium given up.
Impaired oxygenation of tissues In blood stored for 5 days in citrate dextrose solution (ACD), the 2,3-diphosphoglycerate (2,3- DPG) content falls, leading to an increased affinity of haemoglobin for oxygen. After 14 days of storage at 4 °C the average loss of 2,3-DPG is 70 per cent in ACD, 80 per cent in ACDadenine and 45 per cent in citrate phosphate dextrose (CPD) solution, with which the 2,3-DPG level is better maintained. For sufficient oxygen to be supplied to the tissues therefore the tissue oxygen level must be lower. It would take between 24 and 48 hours before the 2,3-DPG concentration returns to normal, so that hypoxaemia is a greater hazard during this period after massive blood transfusion (Waiters and Nott, 1977).
Acidosis The addition of ACD solution decreases the pH of fresh blood to 7-0 and in the following 21 days it falls further to 6-5 as a result of continued glycolysis and cellular metabolism. The Pco_, increases from 20 to 28 kPa (Howland and Schweizer, 1962). When massive transfusion is needed, the patient is often already acidotic and when blood is given, this will increase. The empirical administration of sodium bicarbonate is not, however, indicated (Miller et al., 1971). Blood gas analysis should always be performed instead, to determine the need for correction of the acidosis. Hypocalcaemia and the effects of citrate Depending on the total amount and the speed of transfusion, hypocalcaemia may develop (Kahn et al., 1979) and though it has no effect on coagulation it can reduce myocardial contractility, especially when hypoxia, hypercapnia, acidosis and anaesthetic drugs have already depressed myocardial function. Calcium only needs to be given when myocardial depression becomes apparent from hypotension and ECG changes.
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Decrease in calcium content does not depend on whether ACD or CPD blood is used (Drop and Scheideger, 1979). Citrate intoxication is very rare and it only occurs in patients with disturbed liver function and hypothermia. Citrate is metabolised in muscles, liver and kidney where the rate is limited by the enzyme aconitase. For each mmol of citrate, 3 mmol of bicarbonate are produced. Immediately after operation this may result in metabolic alkalosis, especially if any existing metabolic acidosis has been corrected by bicarbonate. Therefore blind administration of bicarbonate without doing the blood gases must be avoided.
Microaggregates and pulmonary microemboli Stored whole blood contains microaggregates which can cause microemboli, though these can be prevented by the use of microfilters with a mesh size of 40 to 20/tm. These filters can allow about l0 units ofblood to be given but they also reduce the platelet concentration so that fresh blood containing platelets should never be given through a micropore blood filter. When packed cells are used there is no need for a filter because the content of microaggregates is minimal, unless glucose or Ringer's has been added to the packed cells. Coagulation disorders In stored blood there is a fall in platelets, Factors V, VIII and IX. Coagulation disorders are to be expected when more than 10 units of blood are used. The concentration of platelets, thromboplastin time and fibrinogen concentration should then be measured. Replacement is by administration of 2 units of fresh blood or 4 units of fresh frozen plasma and 6 donor units of platelets. Hypocalcaemia has never been proven to be the origin of coagulation disorders in massive transfusions but in patients with extensive injuries, disseminated intravascular coagulation (DIC) may develop (Attar, 1969). In the past this paradox between bleeding and thrombosis used to be treated by giving heparin, but nowadays packed platelets and fresh blood are used, together with treating the precipitating cause such as hypovolaemia. A rough indication for coagulation disorders can be obtained by determining the clotting time of blood in a glass tube, which allows blood to clot normally in 6 minutes.
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CONSEQUENCES OF DRUG ADMINISTRATION Most drugs used in anaesthesia are very potent and have many side effects. Anaesthetic agents, whether administered by intravenous injection or inhalation, generally cause cardiovascular changes due to myocardial depression and/or peripheral vasodilatation. Decreased cardiac output, hypotension and tacbycardia or bradycardia can all be seen. Because of peripheral vasoconstriction and the resulting increase in central concentration of drugs in injured patients, lower doses are usually necessary, and the impaired cardiovascular function may make the cardiovascular depressant effect more obvious. The use ofhalothane or enflurane with barbiturates in such a patient can leave him without any arterial blood pressure. In our hospital we induce anaesthesia in the injured patient with minimal amounts of the least cardiovascular depressing agent i.e. gamma hydroxybutyric acid, etomidate or diazepam supplemented with fentanyl. For muscle relaxation succinylcholine, pancuronium and Org-NC45 are most appropriate. Only after enough fluid has been infused, are droperidol and other adjuvants given. In most emergency cases, ketamine-diazepam anaesthesia is allowed. There is frequently no urine production in patients with multiple injuries because of the reduced arterial pressure and insufficient renal perfusion or because of the hormonal regulating mechanism. (ADH, angiotensin, renin). The patient really needs to be considered as having no renal function, which means that several drugs which depend on renal excretion for elimination last longer and have higher plasma concentrations, which may prolong their action. Incremental doses of such drugs at normally used intervals can result in accumulation. A common example is the longer duration of action of non-depolarizing muscle relaxants in renal failure (Miller et al., 1973; Geha et al., 1976; Booij et al., 1982). Such prolonged action has been noted with the anuria of injury and shock. This is not only due to impaired renal function, but also to acidosis, hypothermia and shifts in electrolytes (Crul-Sluyter and Crul., 1974; Miller et al., 1978). Dextrans and gelatins are commonly used in shock as plasma expanders but both are usually excreted in the kidneys, and in anuria they remain longer in the body. Dextrans also increase the viscosity of the urine which may lead to tubular obstruction and further renal
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damage. In our unit, therefore, gelatin (Haemaeel) is used as a colloidal fluid. In some cases digitalization is required and anuria and abnormal potassium levels may then interfere. When antibiotics are needed it must be remembered that they can further impair renal function and in renal failure they may accumulate in the body and sometimes have ototoxic effects. CONSEQUENCES OF TECHNICAL PROCEDURES Multiply injured patients, not only for direct treatment purposes but also for monitoring their vital functions, need a number of indwelling catheters or cannulas, which may lead to complications. Haemothorax or pneumothorax can result from subclavian or internal jugular cannulas (Brown and Wallace, 1976; Linos et al., 1980). They may also take the wrong course or form loops (Malatinsky et al., 1976). Cannulas can obstruct cerebral blood flow resulting in increased ICP or they can break. This is a real hazard in accident cases because checking ofthe cannula may only take place after the operation. Testing for a free back-flow ofblood and observing oscillation in pressure synchronous with ventilation is helpful in preventing such complications. Insertion of arterial lines can also give complications, especially when arterial thrombosis develops. Because the rate of'urine production is a good index of the adequacy of replacement of hypovolaemia, a urethral catheter is obligatory. In fracture of the pelvis a false route can easily be obtained while inserting such a catheter and in these cases suprapubic percutaneous puncture of the bladder should be performed. Because in such a case the patient must be prepared in a hurry, burns due to iodine or electrodes are a risk. P O S T - R E S U S C I T A T I O N DISORDERS A syndrome may develop some days after the primary care of the multiply injured patient in the form of post-resuscitation hypertension (Ledgerwood and Lucas, 1974). Due to the injury and the subsequent operation, sequestration of fluids and electrolytes in the interstitial spaces may take place: the third space is filled up. This cannot be prevented by primary restriction of fluid administration because these fluids are needed to maintain an adequate circulation. The sequestration of these fluids results From poor perFusion and cellular ischaemia and cannot be helped, but after 2 to 3 days when the vessels are recovered reabsorption of the fluid
Booij: Pitfalls in Anaesthesia
from the third space takes place. This can lead to vascular overload and hypertension which are more pronounced when the renal function is still impaired, though the vascular overload can lead to polyuria some days after resuscitation. When patients are resuscitated with human serum albumin, the renal excretion of excess fluid is impaired, leading to a longer period of hypertension (Siegel et al., 1973). Depending on the degree of overload, pulmonary congestion can take place leading to a second phase of respiratory failure, and encephalopathy can also follow. The treatment of post-resuscitation hypertension consists of fluid restriction, stopping colloids, the giving of diuretics and finally vasodilators. Respiratory failure must be anticipated by instituting artificial ventilation, and the combination of simultaneous support of the lungs and the kidneys provides the best chance of survival (Lucas et al., 1977). Digitalization before fluid mobilization may improve the circulation. After discussing some of the features of multiply injured patients, it can be concluded that anaesthesia in these victims is full of pitfalls. Because anaesthetic management of these patients must take into account many factors, including pre-existing disease and medication, concomitant injuries outside the range of planned operations, the condition at the time of operation, the lesions found and the facilities available as well as the foreseen postoperative complications, no single method of anaesthesia can be described. The choice of anaesthesia in emergency accident surgery is seldom easy or straightforward, and the way in which each individual patient should be treated can only be determined by the skilful experienced anaesthetist.
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Crul-Sluyter E. J. and Crul J. F. (1974) Acidosis and neuromuscular blockade. Acta Anaesthesiol. &'and. 18, 224. Cullen D. J. and Caldera D. L. (1979) The incidence of ventilator-induced pulmonary barotrauma in critically ill patients. Anesthesiology 50, 185. Dobb G., Jordan M. J. and Williams J. G. (1979) Cimetidine in the prevention of the pulmonary acid aspiration (Mendelson's) syndrome. Br. J. Anaesth. 51,967. Downs J. B. and Chapman R. L. (1976) Treatment of bronchopleural fistula during continuous positive pressure ventilation. Chest 63, 363. Drop L. J. and Scheidegger D. (1979) Haemodynamic consequences ofcitrate infusion in the anaesthetized dog: comparison between two citrate solution and the influence of beta blockade. Br. J. Anaesth. 51, 513. Erickson D. R., Shinozuki T., Beekman E. et al. (1971 ) Relationship of arterial blood gases and pulmonary radiographs to the degree of pulmonary damage in experimental pulmonary contusion. J. Trauma 11, 689. Feigal D. W. and Blaisdell F. W. (1979) The estimation of surgical risk. Med. Clin. North Am. 63, 1131. Frost E. A. M. (1977) Effects of positive endexpiratory pressure on intracranial pressure and compliance in brain-injured patients. J. Neurosurg. 47, 195. Fulton R. L. and Jones C. E. (1979) The cause of posttraumatic pulmonary insufficiency in man. Surg. Gynecol. Obstet. 140, 179. Geha D. G., Blitt C. D. and Moon B. J. (1976) Prolonged neuromuscular blockade with pancuronium in the presence of acute renal failure: a case report. .4nesth. Analg. (Cleve.) 55, 343. Gibbs C. P., Schwarz D. J., Wynne J. W. et al. (1979) Antacid pulmonary aspiration in the dog. Anesthesiology 51,380. Howland W. S. and Schweizer O. (1962) Increased carbon dioxide tension as a factor in the activity ofbank blood. Surg Gynecol. Obstet. 115,599. Kopriva C., Ratliff J., Fletcher J. R. et al. (1971) Serum potassium changes after succinylcholine in patients with acute massive muscle trauma..4nesthesiolog.v 34, 246. Lassen N. A. and Christensen M. S. (1976) Physiology of cerebral blood flow. Br. J..4naesth. 48, 719. Ledgerwood A. M. and Lucas C. E. (1974) Post resuscitation hypertension. Etiology, morbidity and treatment..4rch. Surg. 108, 531. Linos D. A., Mucha P. jun. and van Heerden J. A. (1980) Subclavian vein, a golden route. Mayo Clin. Proc. 55, 315. Lucas C. E., Ledgerwood A. M., Shies M. R. et al. (1977) The renal factor in the post-traumatic "fluid overload" syndrome. J. Trauma 17,667. Malatinsk~, J., Kadlic T., M~ijek M. et al. (1976) Misplacement and loop formation of central venous catheters..4cta Anesthesiol. Scand. 20, 237. McCoy J. A. and Ayim E. (1976) The management of acute thoracic injuries..4naesthesia 31,532.
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Mendelson C. L. (1946) The aspiration of stomach contents into the lung during obstetric anaesthesia. Am. J. Obstet. Gynecol. 52, 191. Metson B. F. (1953) Subcutaneous rupture of the trachea. Arch. Otolaryngol. 57, 182. Miller R. D. (1973) Complications of massive blood transfusion. Anesthesiology 39, 82. Miller R. D., Tong M. J. and Robbins T. O. (1971) Effects of massive transfusion of blood on acid-base balance. JAMA 216, 1762. Miller R. D., Stevens W. C. and Way W. L. (1973) The effect of renal failure and hyperkalemia on the duration of pancuronium neuromuscular blockade in man. Anesth. Analg. (Cleve.) 52, 661. Miller R. D., Agoston S., van der Pol F. et al. (1978) Hypothermia and the pharmacokinetics and pharmacodynamics of pancuronium in the cat. J. Pharmacol. Exp. Ther. 207,532. Paredes S. and Hipona F. A. (1975) The radiologic evaluation of patients with chest trauma: respiratory system. Med. Clin. North Am. 59, 37. Phirman J. R. and Shapiro H. M. (1977) Modification of nitrous-oxide-induced intracranial hypertension by prior induction of anesthesia. Anesthesiology 46, 150. Richardson J. D., Franz J. L., Grover F. L. et al. (1974) Pulmonary contusion and haemorrhage-crystalloid versus colloid replacement. J. Surg. Res. 16, 330. Schweizer O. and Howland W. S. (1962) Potassium levels, acid-base balance and massive blood transfusion. Anesthesiology 23, 735. Siegel D. C., Cochin A., Geocaris T. et al. (1973) Effects of saline and colloid resuscitation on renal function. Ann. Surg.177, 51. Sofferman R. A. (1981) Management of laryngotracheal trauma. Am. J. Surg. 141,412.
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Stewardson R. H. and Nyhuis L. M. (1977) Pulmonary aspiration. An update. Arch. Surg. 112, 1192. Stoelting R. K. (1978) Gastric fluid pH in patients receiving cimetidine. Anesth. Analg. (Cleve.) 57, 675. Sunder-Plasmann L., Kloevekorn W. P. and Messmer K. (1971) Blutviskosit~it und H~imodynamik bei Anwendung kolloidaler Volumenersatzmittel. Anaesthesist 20, 172. Trinkle J. K., Fuman R, W., Hinshaw M. A. et al. (1973) Pulmonary contusion. Ann. Thorac. Surg. 16, 568. Vacanti C. J., van Houten R. J. and Hill R. C. (1970) A statistical analysis of the relationship of physical status to postoperative mortality in 68 388 cases. Anaesth. Analg. (Cleve.) 49, 564. Waiters F. J. and Nott M. R. (1977) The hazards of anaesthesia in the injured patient. Br. J. Anaesth. 49, 707. West J. G., Trunkey D. D. and Lira R. C. (1979) System of trauma care. A study of two countries. Arch. Surg. 114, 455. Wilson R. F., Gibson D. B. and Antonenko D. (1977) Shock and acute respiratory failure after chest trauma. J. Trauma 17, 695. Wilson S. L., Mantena N. R. and Halverson J. D. (1981) Effects of atropine, glycopyrrolate and cimetidine on gastric secretion in morbidly obese patients. Anesth. Analg. (Clew.) 60, 37. Wynne J. W. and Modell J. H. (1977) Respiratory aspiration of stomach contents. Ann. Intern. Med. 87, 466. Zaricznyj B., Rockwood C. A., O'Donoghuem D. J. et al. (1977) Relationship between trauma to the extremities and stomach motility. J. Trauma 17,920.
Requestsfor reprints shouM be addressed to: Dr Leo H. D. J. Booij, Department of Anaesthesia, University Hospital. St Radboud. University of Nijmegen, The Netherlands.