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The postoperative period—some important complications
15 The postoperative period complications DOREEN
some important
A. JEWKES
THE POSTOPERATIVE PERIOD
The postoperative period covers the time when the patient is recovering from anaesthesia and the immediate effects of surgery, and when complications are most likely to arise. It may last a few hours or be prolonged for 2 or 3 days. It is a time when the patient must be watched closely, but the observations made, and their timing, differ from the monitoring required during surgery. For most cases, the sophisticated electronic equipment so useful in the operating theatre is not required and the necessary observations are best made by a well trained recovery room nurse. The reliance on electronic displays of physiological data, perhaps at a point somewhat r e m o t e from the patient, may result in vital signs being missed. There is as yet no computer printout that can display minor but critical changes in the patient's responsiveness. This departure from the practice in the operating theatre may not be adequate if the patient subsequently develops some of the serious complications which are discussed later in the chapter. More technology may then be of great help. For this reason, some of the facilities used in the operating theatre may be kept available. For example, an arterial line may be kept patent by infusing heparinized saline under pressure, and ECG leads are often left attached. After craniotomy, the patient usually regains consciousness in the first half hour, more quickly if he has been anaesthetized with isoflurane, rather more slowly if halothane has been used throughout the operation or if a total intravenous technique was employed. The patient lies in a 15-20 ~ head-up tilt to encourage venous drainage. He is given oxygen---4 l/rain by face mask for the first 3-4 hours to avoid possible hypoxia. The patient's temperature is recorded periodically, axiUary readings with a routine clinical thermometer being sufficient. Many patients will have become moderately hypothermic during the operation, perhaps as low as 34~ Gentle warming with blankets is desirable to avoid possible shivering which may contribute to hypoxia and lactic acidosis. Analgesia is usually given early to prevent restlessness, as this may lead to raised blood pressure, undesirable in post craniotomy patients. Codeine phosphate 0.75 mg/kg is given intramuscularly, usually with prochlorperazine Bailli~re's ClinicalAnaesthesiology--Vol. 1, No. 2, June 1987
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maleate (Stemetil) 12.5mg intramuscularly. Codeine is an adequate analgesic, does not cause pupillary changes, and decreases mobility of the intestine which may help to prevent vomiting. A fluid balance chart is started. The aim is to allow the patient about 2 litres of balanced electrolyte solution (Hartman's solution or equivalent) in 24 hours for the first 2-3 days. Oral fluids are restricted for 24 hours. Patients who have had a supratentorial craniotomy are allowed fluids after being fully awake for some hours, providing that they have discernible bowel sounds. Patients who have had a posterior fossa exploration must be carefully assessed to make sure that they have an adequate swallowing reflex as this may have been impaired temporarily by disturbance of the IXth nerve. All patients submitted to neurosurgery are on steroids (dexamethasone) and are usually given H-2 antagonists to avoid gastric or duodenal ulceration (Cimetidine 400rag once daily, usually in the evening, orally or intravenously). Bladder distension can cause restlessness and the patient must be examined for this at regular intervals. Many patients are likely to be sufficiently conscious and cooperative to micturate on demand even if diuresis ensues. If drowsiness persists or the patient is confused, catheterization may be unavoidable. Patients who have had previous anaesthetics or prolonged unconsciousness are likely to develop chest infections. These patients are often given prophylactic antibiotics and will require the attention of a physiotherapist soon after regaining consciousness. Physiotherapy must be gentle, avoiding violent coughing and the head-down position. Patients must be periodically assessed by a recovery room nurse for response to pain, verbal command, the ability to perform motor tasks (power of the hand-grip and flexion of the knee), the size and reaction of the pupils, and correct orientation in time and place. If no disturbing signs have developed over a period of 12 hours the immediate postoperative period can be considered to have passed uneventfully and the patient returned to the care of the general neurosurgical ward. The challenge of the postoperative period relates to the eventful recovery and the anticipation, early recognition and treatment of untoward events. The more important of these will now be considered along with some other aspects of intensive care. RAISED I N T R A C R A N I A L PRESSURE
In the first few hours after operation, the patient may show signs of raised intracranial pressure due either to bleeding, into a tumour cavity or subdurally, or to cerebral oedema. Oedema may have been present when a tumour was excised or biopsied, or may develop subsequently. It may also occur after surgery to a vascular lesion, either due to transient ischaemia or infarction. The usual presentation is for the level of consciousness to deteriorate subtly and for the patient to become gradually tess responsive to verbal command, or dysphasic. Limb weakness may appear in a patient previously without such a sign, or a previous hemiparesis may deepen. An unconscious
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patient may cease to respond to painful stimuli. The patient will often have obvious pupillary changes, usually the pupil on the operated side dilating and becoming fixed. Formal testing of tendon reflexes and plantar responses is of little help. A slow progressive deterioration may best be judged by inspection of the chart plotted by the recovery room nurse (Figure 1).
WARD DEPT
Operation date
9.11,86
Craniotomy for excision "of left parietal angioma
Level of Consciousness
RE Spon
Eye Opening
To sf To p Non{
Orier Best Verbal Response
Conf
InaPl I ncor Non( Obe~ Loca
Best Motor
Flex
Response
Exte Non~
P U P L S
Size: Reaction to Light
D = N = S = Yes No
dilat norr smal + --
Limb Power
Upper
(0-5) (M.R.C.)
Lower
M.R.C. MUSCLE POWER G
Figure 1. Chart plotted by recovery room nurse.
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Given the clinical deterioration described, it is essential to differentiate bleeding from oedema. In well equipped units this is done by means of a CAT scan. In the absence of this, the wound must be reopened if bleeding is a serious possibility. Before the patient is transferred to the radiology department, the anaesthetist has to decide whether the patient should be intubated and ventilated. In my opinion the patient who has become drowsy needs controlled lowering of PaCO2 as a rising PaCO2 will cause increased cerebral blood flow leading to a worsening of cerebral oedema or bleeding. Early ventilation of such patients appears to be much the safest policy, not least as it avoids the difficulties and dangers of emergency intubation in the middle of the x-ray procedure. Undoubtedly there is one potential hazard to intubation, the effect of the pressor response to laryngoscopy in a patient who could be bleeding (Stoelting, 1977). This can, however, be mitigated by thiopentone or one of the benzodiazepines, e.g. Diazemuls (diazepam) or midazolam, in addition to the usual suxamethonium to facilitate intubation. It is a good practice to insert a nasogastric tube at the same time. After diagnosis, the definitive treatments of bleeding and oedema are totally different. Bleeding will probably require prompt surgical intervention, to evacuate a cavity clot or subdural haematoma. Extradural haematomas are sometimes encountered when pin fixation has been used during the operation. This is a particular hazard of this technique in children. Cerebral oedema can be helped by continuing ventilation to maintain the PaCO2 at a low level, usually 3.3-4 kPa (25-30 mmHg). Cerebral blood flow is then prevented from increasing and compounding the problem. Control of oedema demands prompt administration of diuretics, usually mannito120% solution with a dose of 0.5 g/kg given over 30 minutes. Frusemide 40mg intravenously is also often used in addition. Urine output must be carefully monitored and bladder catheterization may be necessary. Large doses of dexamethasone are often given to reduce oedema, although there is little evidence that they are really useful. If the oedema is in the posterior fossa, rapid diagnosis is even more vital as treatment must be implemented before coning occurs. The presence of hydrocephalus preoperatively usually indicates that the tumour in the posterior fossa or region of the third ventricle has obstructed the ventricular outflow and compensation has failed. The surgeon will have prepared a burr hole, perhaps leaving a ventricular drain in situ. If so, this can be opened and left on drainage at a controlled rate. If not, a quickly reopened burr hole with placement of a catheter into a lateral ventricle can indeed be lifesaving. Oedema once treated will usually subside, but treatment may be needed for several days before the patient shows signs of awakening. Mechanical ventilation must be continued to maintain respiration and to maintain the reduction of PaCO2 to lower cerebral blood flow. The PaCO2 must be kept at about 4 kPa (30 mmHg) measured by capnography or repeated blood gas analysis. Patient compliance is achieved by the use of non-depolarizing relaxants such as pancuronium, vecuronium or atracurium. Sedation will be achieved by benzodiazepines, such as Diazemuls, or midazolam. If, at the
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intubation, a nasogastric tube was passed, this may be used to administer anticonvulsants and eventually for nutrition when the patient is again absorbing reliably from the intestinal tract. Recovery of the patient is shown by improvement in consciousness measured by response to commands. Relaxants are withdrawn and spontaneous respiration measured. A Wright's respirometer reading of tidal volume appropriate to the patient's size, checked by blood gas analysis indicates when ventilation may be discontinued. Blood gases must be checked with particular care if there is any additional complication such as chest infection.
CONVULSIONS Convulsions greatly increase postoperative morbidity. The increased muscular activity and loss of consciousness cause the airway to become obstructed. An obstructed airway promotes hypoxia at a time of increased oxygen consumption, and hypercarbia during a period of increased carbon dioxide production. This combination raises the arterial blood pressure and increases cerebral blood flow, threatening the patient with the danger of rebleeding. Metabolic acidosis increases potassium concentration in the extracellular fluid of the brain and will lead to localized hyperkalaemia and further impairment of cerebral autoregulation. Fits considerably increase the difficulty of assessment of the postoperative patient. The resulting unconsciousness removes one of the most sensitive signs of recovery. Occasionally, fits are due to other complications such as rebleeding, and diagnosis of this may be delayed. Epileptic fits are often not obvious. The first sign may just be less responsiveness from a patient whose consciousness was gradually returning. This may be accompanied by involuntary twitching of the facial muscles or upper or lower limbs usually on one side. This may or may not progress to a generalized convulsion. Minor fits may be even less obvious and it may require experience to distinguish them from the shivering of a cold patient, clonus from muscular spasticity, or halothane 'shakes'. However, the clinical significance of minor manifestations is the same as a major convulsion and must be treated just as seriously. Patients who are maintained on a ventilator and who are receiving muscle relaxants may of course also fit and these represent a special problem. The degree of relaxation induced in these circumstances is usually not profound and some evidence of twitching or shaking will be seen, though it could be overlooked by an inexperienced attendant. In this situation it is helpful to have the use of a portable E E G machine or a,cerebral function analysing monitor. If these are not available, the diagnosis will remain in doubt. In this situation, it is best to continue to observe extremely closely as fits are often repeated. If signs appear which suggest a second fit, then the patient should be treated without further delay. If an experienced observer suspects the possibility of fits then this is probably what is happening.
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There is considerable controversy concerning the prophylactic use of anticonvulsants. Some studies (Richardson and Uttley, 1980) have shown higher rates of epilepsy in those patients who are operated on without anticonvulsant therapy compared to those patients who have received anticonvulsants. Another recent study, however, failed to show any significant effect on t h e incidence of postoperative epilepsy in a group of patients pretreated with phenytoin and carbamazepine (Shaw et al, 1983). It is probably true to say that the majority of neurosurgeons favour the use of preoperative anticonvulsants, but the issue is still being debated. Since epilepsy usually occurs during the first 24 hours after an operation, anticonvulsants must be used preoperatively in doses high enough to achieve adequate plasma levels before surgery (Foy et al, 1981; Gurusinghe et al, 1986). Plasma levels should be checked preoperatively in high risk cases. Drugs most commonly used are phenytoin, sodium valproate and carbamazepine. Phenytoin acts by stabilizing all neuronal membranes. It prevents the sodium influx which occurs during depolarization. It also limits intracellular calcium accumulation necessary for transmitter release (Sohn and Ferendelli, 1978). Intestinal absorption of phenytoin is slow, variable and incomplete. Peak plasma concentration occurs any time between 2 and 12 hours. The relationship between dose and plasma level is not linear, and it is therefore essential to measure plasma levels. The therapeutic range for plasma phenytoin is 10-20 gg/1. Crystal formation may occur when it is injected intramuscularly, causing unreliable absorption (Dam and Olsen 1966; Wilensky and Lowden, 1973). Intravenous injection is widely used but is not without danger. Too rapid injection may be associated with hypotension and depression of the sinoatrial node of the heart. This may be so severe as to produce cardiac arrest, which seems characteristically difficult to reverse, sometimes with a fatal outcome. In the rather critical postoperative state, phenytoin is not entirely satisfactory and new anticonvulsants seem more predictable, as therapeutic serum levels are more quickly and reliably achieved. Sodium valproate (Carraz et al, 1964) is a newer alternative to phenytoin which has distinct advantages. It rapidly achieves therapeutic plasma concentrations, usually about 1M hours after oral administration with a biological half-life of 8--15 hours (Schobbers, 1983). An injectable preparation exists but is not yet freely available. The antiepileptogenic action of sodium valproate is not completely known. The metabolites of sodium valproate may also be pharmacologically active, accounting for the long-lasting anticonvulsant activity. The drug should, however, be avoided in patients with known liver disease. Carbamazepine is also used as an anticonvulsant and seems particularly well tolerated by children. No injectable form is available. It has been shown to have a depressant effect on the nucleus ventralis of the thalamus, which has been implicated in the generalization of epileptic discharges (Richens and Rimmer, 1985). It is a point to note that both phenytoin and carbamazepine are hepatic enzyme inducers and that their use may modify the metabolism of other drugs. Sodium valproate does not have this property.
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M A N A G E M E N T OF P O S T - C R A N I O T O M Y SEIZURES
Management of any convulsion must be swift and effective. To achieve this an intravenous drug must be used. There are several alternatives. Diazemuls is probably the most widely used agent. It is administered as a bolus via the intravenous line, 10 mg initially. It may be repeated if necessary, although alternatives should be considered if response is not immediate. Barbiturates have been used for longer than any of the currently used agents and are very effective. They are general depressants of nerve conduction, acting at the neuronal synapse. In the postoperative situation, sodium thiopentone is sure to be readily available. The initial dose is 5 mg/kg which should stop the fit. An intravenous infusion may be necessary to maintain control of fitting in a difficult case and intubation and ventilation may be advisable. Chlormethiazole is a very effective anticonvulsant and regarded as the treatment of choice in our unit (Brodrick et al, 1984). It is a strong sedative, but there is no action on the autonomic nervous system, and it causes little change in blood pressure or cardiac output although the pulse tends to rise. In large doses, respiratory depression may be produced. The drug is given as an 0.8% solution in 5% dextrose. Initial control is obtained with a dose of 50-200 ml in the first hour, or it may be used after control has been obtained from diazepam or thiopentone (Gurusinghe et al, 1986). Subsequent maintenance may require a dose of 30-60 ml per hour. Roughly 50% of patients on chlormethiazole infusion at this dose require intubation, and some need mechanical ventilation. Fits may be controlled but respiration is often depressed and as the patient's state is often unstable, nasal intubation is a wise precaution. If intubation is carried out, a nasogastric tube may also be passed to permit the administration of oral anticonvulsants if unconsciousness is prolonged. In practice, chlormethiazole infusion is continued for 12-16 hours, at which time the plasma level of oral anticonvulsants is checked. If there have been no further fits, and oral anticonvulsants are present in the plasma at therapeutic levels, chlormethiazole is slowly withdrawn over 6-8 hours. Abrupt withdrawal may precipitate further convulsions. As chlormethiazole must be given in dilute solution, large doses could lead to overloading of the circulation. Care must therefore be taken to restrict appropriately other intravenous fluids. If necessary, guidance may be obtained from measuring central venous pressure (CVP). A CVP line is used for this in our unit if chlormethiazole is continued beyond 12 hours. If the patient is ventilated, muscle relaxants may be used in conjunction with chlormethiazole. Vecuronium, pancuronium and atracurium are now the relaxants of choice. However, 50% of patients on chlormethiazole do not require intubation and ventilation, their blood gases remaining in the normal range using a Guedel airway with humidified air enriched by oxygen at 41/min. If at all possible, a portable E C G or cerebral function analysing monitor should be used for assessing whether or not the fits have passed, or noting the return of epileptogenic activity.
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P O S T O P E R A T I V E C O N T R O L OF B L O O D PRESSURE AND C E R E B R O V A S C U L A R SPASM
In the postoperative period, the blood pressure should be the same as the preoperative value or slightly lower. Low blood pressure is likely to be due to hypovolaemia and needs treatment. Hypotension induced in the operating theatre is always reversed before dural closure to check that all possible bleeding points have been dealt with. Deliberately maintained low blood pressure (in normotensive subjects) has no place in postoperative management. Low blood pressure will be detected during the routine postoperative observations. The level requiring treatment depends to some extent on the condition which required surgery. A low blood pressure in someone who has undergone a debulking procedure (e.g. tumour removal) is less of a cause for concern than in a patient who has undergone surgery for a vascular lesion such as clipping of an aneurysm. A patient with a normal systolic pressure of 120 mmHg is unlikely to require active treatment unless the systolic blood pressure falls to about 90mmHg. The exception to this rule is the patient who develops some neurological symptoms or signs after regaining consciousness, for example dysphasia or limb weakness. The possibility that such dysfunction is due to hypotension must be considered and treatment instituted. Treatment is by cautious blood volume expansion. If there was significant blood loss during surgery then blood replacement is indicated. Otherwise other agents such as Haemaccel (polygeline) or PPF (purified protein fraction) can be used. The majority of patients, however, will spontaneously correct a deficit in the first few hours after surgery. Hypertension in the postoperative period is of more concern than hypotension as it may precipitate intracranial bleeding. Hypertension is of two types, pre-existing hypertension in a chronically hypertensive patient and acute hypertension developing, for instance, after a subarachnoid haemorrhage and in the postoperative period. Pre-existing hypertension requires treatment with drug therapy before surgery to bring the diastolic blood pressure down to high normal levels, preferably of the order of 100mmHg. This is usually achieved by oral administration of [3-blockers and by the use of diuretics, methyl dopa and calcium antagonists such as nifedipine. During surgery, control of blood pressure will have been achieved by an infusion of [3-adrenergic blocking agents in combination with volatile anaesthetic agents and muscle relaxants. Tubocurarine potentiates the ganglion blocking effect of halothane. Sodium nitroprusside may have been used. Postoperatively, it may be convenient to continue the infusion of the B-blocking agent. A satisfactory response is usually obtained with labetalol 100 mg in 100 ml of normal saline, administered through a paediatric drip set, or if available, an infusion pump. The blood pressure responds rapidly to changes in infusion rate and the rate eventually chosen is that which maintains the systolic blood pressure at slightly less than that regularly recorded preoperatively.
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Some patients do not respond readily and further drugs may be needed. The first choice is hydralazine, which has a different action, being thought to affect the intracellular mobilization of calcium and to some extent calcium movement. It is given as repeated intravenous boluses of 10-20 mg. Maintenance of control is usually possible with intramuscular injections of similar quantities, as it is rapidly and reliably absorbed. When the patient returns to the ward, oral treatment will be reinstituted. Acute hypertension appearing for the first time postoperatively is not rare and usually but not always requires prompt treatment if intracranial bleeding is to be avoided. Possible causes of raised postoperative blood pressure should be considered, as their elimination may be all the treatment that is required. The first thing to consider is pain. Pain must be avoided and the favoured analgesic is codeine phosphate 0.75 mg/kg by intramuscular injection. An alternative analgesic is meptazinol 2 mg/kg of body weight. If given intravenously while the patient is receiving oxygen by face mask at 41/min, it produces good sedation and pain relief in most patients without significant impairment of respiration and with the patient rousable for periodic neurological assessment. Restlessness due to acute discomfort may also raise blood pressure. The most common cause is an unrecognized full bladder.
HYPERTENSION AS A SIGN OF CEREBRAL VASCULAR SPASM
The most difficult problem relates to the hypertension associated with intracranial vascular spasm which requires entirely different treatment. This condition is seen almost exclusively after intracranial aneurysm surgery. It can occur at almost any time in the postoperative period and is accompanied by physical signs of decreasing conscious level or limb paresis. It must be actively treated or it will result in cerebral infarction. As the spasm develops, the rising blood pressure appears to be the patient's attempt to maintain cerebral blood flow. Systolic blood pressure should not be lowered in these patients as it will reduce cerebral perfusion. On the contrary, it may need to be boosted by the infusion of colloid plasma expanders, particularly low molecular weight dextran, or the infusion of inotropic drugs such as metaraminol or dopamine. Blood pressure should be maintained at the level at which the patient again becomes alert or at which paresis is relieved. This may be a blood pressure well above the patient's normal level and may approach 200mmHg systolic. This should be achieved fairly rapidly, certainly within 30 minutes. A constant infusion of metaraminol 100 mg in 500 ml of Hartman's solution is given at increasing rate until symptoms are relieved. An intra-arterial cannula with continuous display of blood pressure is highly desirable. A patient with severe cerebral vasospasm may require intubation and ventilation until again able to maintain an airway. The optimum PaCO2 is again rather low at 4 kPa (30 mmHg). This level is chosen not for its effect on cerebral blood flow so much as the fact that it is easier to control mechanical ventilation at this level. A nasogastric tube may also be passed which can be
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used subsequently for nutrition if the patient's state takes time to resolve. Chest physiotherapy must be carried out. The assessment of such patients is essentially clinical. However, if facilities are available~ the progress of vasospasm may be monitored by repeated assessments of cerebral blood flow using radioactive xenon clearance measurements. If the vasospasm is in the territory of the middle cerebral artery, useful information may also be obtained by measuring somatosensory evoked potentials as a measure of central conduction time. The affected hemisphere can be compared with the normal side (Symon et al, 1979). Vascular spasm may not subside for up to 10 days, and treatment and monitoring must continue. Tolerance to metaraminol may develop after several days. Dopamine must then be substituted until the patient's catecholamine resources have been restored. Dopamine infusion may also be necessary temporarily when weaning the patient from metaraminol. A useful preparation is dopamine 400 mg in 250 ml normal saline infused at up to I ml per minute according to response (10-20 ~tg/kg/min). Calcium antagonists have been suggested as arteriolar relaxants. In theory, nimopidine crosses the blood-brain barrier and should be useful in treating severe vasospasm. However, no large scale experience has yet been reported to confirm that it has a place in the treatment of this condition (Boullin, 1985). P O S T O P E R A T I V E FLUID B A L A N C E AND SOME A B N O R M A L I T I E S
In proposing guidelines for postoperative fluid balance in the neurosurgical patient several aspects require consideration. Areas of brain which have been adjacent to a tumour may have impaired perfusion in the early postoperative period and are prone to develop oedema. The pressure of cerebrospinal fluid will be low immediately postoperatively, but may rise rapidly in some patients, in particular in those with preoperative hydrocephalus for posterior fossa or third ventricular tumours. Arterial blood pressure, and therefore cerebral perfusion pressure, may be sensitive to fluid balance to some extent in these patients. These considerations suggest that the best policy is to keep the patient slightly fluid-restricted postoperatively, certainly not fluid-overloaded. A satisfactory rule for these patients in temperate climates is to provide 30 ml/kg of water per 24 hours. This is well tolerated in the form of balanced electrolyte solution (Hartman's solution or equivalent). This seems preferable to dextrose solutions which may aggravate a tendency to hyperglycaemia produced by steroid therapy (Prockop, 1981). However, in calculating postoperative fluid requirements it is necessary to assess fluid losses from therapeutic manoeuvres, particularly mannitol infusion or the administration of frusemide. If the blood pressure is maintained at a satisfactory level, this loss should not be replaced immediately but restoration allowed to occur naturally, perhaps over several days. If loss is excessive, cautious addition to the daily allowance is permitted.
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Facilities for rapid assessment of plasma electrolytes are highly desirable and measurement should be obtained in any patient in whom unusual gains or losses have been noted. Estimates of blood glucose are essential if the patient has any tendency to preoperative diabetes, long-standing or steroid-induced. Hyperglycaemia stimulates diuresis and increases anaerobic respiration in poorly perfused regions of the brain. This results in local lactic acid accumulation which may damage cell membranes and release adenosine, prostaglandins and leukotrienes (Lewis and Maestro, 1979). After aneurysm surgery, some units routinely administer Rheomacrodex (dextran 40 intravenous infusion) 500 ml of 10% solution to reduce blood viscosity and prevent sludging in small vessels, while also expanding intravascular volume. This is usually given after a little delay, perhaps about 4 hours, to reduce the incidence of early postoperative bleeding.
Postoperative diabetes insipidus Postoperative diabetes insipidus (DI) is commonly seen in the recovery room. It is usually a complication of surgery in the subfrontal region for pituitary tumour, carniopharyngioma, meningioma or metastases. It may also occur after head injury. DI is suspected when a litre of urine is passed in 4 hours, the patient not previously having a fluid overload. The antidiuretic hormone in man is arginine vasopressin, synthesized in the paraventricular and supraoptic nuclei of the hypothalamus. It appears as neurosecretory granules, which pass from the cells in which they are formed along axons to the posterior pituitary where they are stored. Some of the axons of the vasopressogenic neurones terminate elsewhere for instance in the median eminence, brain stem and floor of the 3rd ventricle. The importance of this is that antidiuretic hormone secretion may occur or be restored even after destruction of the posterior pituitary gland. Release of vasopressin into the systemic circulation is mainly determined by plasma osmolality. Changes are detected by receptors in the anterior hypothalamus. Vasopressin secretion is suppressed by plasma osmolalities of less than 280 mosmol/kg to allow maximum water diuresis. Above this threshold, plasma vasopressin concentration increases in direct proportion to plasma osmolality. The first is normally experienced at plasma osmolalities of about 298mosmol/kg. The combination of the osmotic threshold for stimulating vasopressin release and thirst maintain osmolality at 280-295 mosmol/kg in health. Disturbance in the region of the posterior pituitary causes DI when 80% of neurones synthesizing vasopressin are destroyed or temporarily nonfunctional (Robertson et al, 1982). In the postoperative period, a urine flow of 15-20 ml/min maintained for an hour is highly likely to be due to DI. It is vital to exclude brisk but usually less persistent diuresis induced by therapy. When spontaneous urine output reaches 1 litre/hour it is routine in our unit to administer synthetic vasopressin (deamino-D-arginine vasopressin) 0.5 gg intramuscularly repeated as needed. We allow all but unconscious patients to cope with fluid loss by drinking. Fluid balance is best left to the
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patient. Intravenous infusions are avoided as far as possible as they may override normal controls and promote unnecessary diuresis. A patient having DI should be checked twice daily for fluid balance, plasma osmolality and plasma electrolytes. Treatment can cause water intoxication, though this usually only occurs if the patient has an intravenous infusion. Alternatively, concomitant sodium retention may produce hypernatraemia which can be life-threatening. Unconscious patients (with active bowel sounds) are given fluid by nasogastric tube. They must be closely monitored by frequent laboratory studies (initially four-hourly) until their treatment and clinical state are stable. They will then require an intake equal to urine volume and other obvious losses, with an additional litre per day for insensible loss and sweating. If the state remains for several days, these patients tend to become dehydrated and require 'topping up' from time to time as indicated by the periodic laboratory results. Treatment for DI has to be continued for as long as necessary. It may persist for hours, days, weeks or months. At some stage, the route of treatment may be varied for convenience. Subcutaneous injection is effective and intranasal administration satisfactory in cooperative patients. It is usually only necessary to give ADH substitute once or twice daily. The syndrome of inappropriate antidiuresis The syndrome of inappropriate antidiuresis is commonly seen in intracranial pathological conditions, particularly in patients having a long period of intensive care (Zerbe et al, 1980). It can be associated with intracranial haemorrhage, head injury, brain tumours, hydrocephalus, meningitis and many other disorders. Biochemical diagnosis is made on the basis of hyponatraemia with low plasma osmolality, urine osmolality greater than plasma osmolality and persistent sodium excretion. Other factors are the absence of hypotension and hypovolaemia and oedema formation with normal renal and adrenal function. Clinically, cerebral symptoms of confusion, nausea and irritability may develop with a plasma sodium of less than 120 mmol/1 (120 mEq/1). If untreated, fits, coma and hemiparesis can occur, particularly if the plasma sodium falls to 110 ml/1 (110 mEq/1). Management requires treatment of the underlying cause if possible, followed by treatment of the symptoms of hyponatraemia. Restriction of fluid intake to 500-1000 ml/24 hours is usually effective. There are no rapidly acting drugs available to block the antidiuretic effect of vasopressin.
INDICATIONS FOR TRACHEOSTOMY With the availability and diligence of physiotherapists, there are fewer indications for preoperative or postoperative tracheostomy. Nasotracheal tubes are now routinely left in situ for up to 3 weeks. However, in posterior fossa tumours causing paresis or partial loss of function of the glosso-
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pharyngeal or vagus nerves, and thus respectively loss of gag and cough reflexes, tracheostomy is often preferable to a long intubation. Recovery of these nerves may take many weeks but usually occurs sooner or later. Respiratory failure caused by brain stem haematoma or tumour is likewise commonly an indication for tracheostomy as the problem even with effective treatment is likely to remain for a considerable time. A patient who has been intubated for more than a day or two may have some difficulty in swallowing after decannulation and will usually inhale fluids. Oral fluids should not be given until laryngeal function has returned as demonstrated by the ability of the patient to speak in a normal voice. Treatment of postoperative chest infections can be aided by inserting a mini-tracheostomy. This allows secretions to be aspirated during physiotherapy, and is of great assistance if the patient has a weak cough or is greatly debilitated. Patients with chest complications whose blood gas analysis shows a PaO2 of 10 kPa or less usually require full intubation and ventilation.
POSTOPERATIVE PATIENT CARE SUMMARIZED
A patient in the recovery ward needs a dedicated, individual nurse to make routine observations. It is a great advantage if the nurse is known in advance and has made a preoperative visit to see the patient. Initially, postoperative observations will be required each 15 minutes for at least 2 hours and after that each 30 minutes until the patient returns to the general ward. The medical staff depend very heavily on these observations. Pulse rate
A slow pulse rate is usually due to persisting ]3-blockade from the time of surgery, or occurs when atropine given after surgery has been metabolized. Classically, a slow pulse is said to be a sign of raised intracranial pressure, but in the postoperative period this is rarely seen. Raised intracranial pressure is detected by other signs. A raised pulse rate is usually due to minor cardiovascular disease. However, rarely it may be neurogenic, particularly appearing after exploration of the posterior fossa for brain stem tumour. Blood pressure
Low or falling blood pressure usually indicates hypovolaemia or slight over-sedation, following the use of routine analgesics, even codeine phosphate. Raised blood pressure may be due to poorly controlled chronic hypertension reasserting itself or due to pain or restlessness from physical discomfort or tachycardia. The most difficult cause to identify with certainty is cerebral vascular spasm, which requires different treatment from other causes.
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Respiration Respiratory rate, depth and character of respiration should be noted. Slow respiration is usually caused by over-sedation. It can be associated with raised intracranial pressure from oedema or bleeding, but other signs will be present. Respiration becoming shallQwer with a tracheal tug is usually due to recurarization. It must be promptly treated by the anaesthetist. Rapid respiration is rarely seen and has no particular neurosurgical significance, except in the severely head-inj ured patient when it may require intubation and ventilation to gain control. Pulmonary embolism, spontaneous pneumothorax or lobar collapse are always possibilities.
Temperature Low temperature is caused by failure to prevent hypothermia during the operation. Heat loss from large wounds is unavoidable. High temperature and hyperpyrexia is due to hypothalamic disturbance and is usually seen in children. It demands immediate treatment by aspirin suppositories and tepid sponging.
Neurological observations The observation chart (Figure 1) lists the observations the recovery room nurse should make. The system of charting allows instant assessment by the anaesthetist of progression of the various aspects of the patient's neurological functioning. Gradual or sudden improvement or deterioration is evident on simple inspection. The importance of these observations lie in their sensitivity in pointing to important complications, requiring intervention, particularly postoperative intracranial bleeding, cerebral oedema and cerebral arterial spasm.
Fluid balance chart Charting of fluid intake is important for long-term assessment of the patient's fluid balance. Urine output observation is important for the early detection of diabetes insipidus.
Equipment Basic postoperative neurosurgical patient care requires minimal sophisticated equipment. The conscientious and experienced nurse, a good chart, a standard sphygmomanometer and a thermometer can take care of 90% of the observations required. With the onset of complications, additional equipment may be required, basically a ventilator and an ECG monitor. Infusion pumps are helpful and should be available. A portable EEG or cerebral function monitor is rarely required, but should be obtainable.
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REFERENCES Boullin D (1985) Prevention of spasm--strategy. In Crockard HA, Hoff J & Hayward R (eds) Neurosurgery. The Scientific Basis of Clinical Practice, (chapter 14). Brodrick PM, Bromley L & Jewkes D (1984) The use of chlormethiazole to control postcraniotomy epilepsy. British Journal of Anaesthesia 56: 1312. Carraz G, Fau R, Chateau R et al (1964) Communication apropos des premiers essais cliniques sur l'activit6 anti-dpileptique de l'acide N-dipropylac6tique (sel de Na+). Annales MedicoPsychologiques 122: 577-585. Dam M & Olsen V (1966) Intramuscular administration of phenytoin. Neurology 16: 288-292. Foy PM, Copeland GP & Shaw MDM (1981) The incidence of post-operative seizures. Acta Neurochirurgica 55: 253-264. Gurusinghe NT, Symon L, Jewkes D & Brodrick P (1986) Chlormethiazole in the management of post-craniotomy seizures. Acta Psychiatrica Scandinavica 73(supplement 329): 189-193. Lewis DM & Maestro RD (1979) Free radicals in medicine and biology. Acta Physiologica Scandinavica Supplement 429: 9-168. Prockop LD (1981) Hyperglycaemia effects on the nervous system. In Rose FC (ed.) Metabolic Disorders of the Nervous System, pp 77-98. London: Pitman. Richardson AE & Uttley D (1980) Prevention of post-operative epilepsy. Lancet h 650. Richens A & Rimmer E (1985) Pathogenesis of neuropharmacology of epilepsy. In Crockard HA, Hoff J & Hayward R (eds) Neurosurgery, The Scientific Basis of Surgical Practice (chapter 29) pp 486. Robertson GL, Aycinena P & Zerbe RL (1982) Neurogenic disorders of osmoregulation. American Journal of Medicine 72: 339-353. Schobbers I (1983) Valproic acid: pharmakinetic aspects. British Journal of Clinical Practice (supplement 2). Shaw MDM, Toy P & Chadwick D (1983) The effectiveness of prophylactic anticonvulsants in neurosurgery. Acta Neurochirurgica 69: 253-258. Sohn and Ferendelli (1978) Inhibition of Ca ++ transport into rat brain synaptosomes of diphenylhydantoin. Journal of Pharmacology and Experimental Therapeutics 185: 272-275. Stoelting RR (1977) Circulatory changes during direct laryngoscopy and tracheal intubation. Anesthesiology 43: 381. Symon L, Hargadine J, Zarirki M & Branston N (1979) Central conduction time as an index of ischaemia in subarachnoid haemorrhage. Journal of Neurological Sciences 44: 95. Wilensky AJ & Lowden JA (1973) Inadequate serum levels after intramuscular administration of diphenylhydantoin. Neurology 23: 318-324. Zerbe R, Stropes L & Robertson GL (1980) Vasopressin function in the syndrome of inappropriate antidiuretics. Annual Review of Medicine 31: 315-322.
some important
A. JEWKES
THE POSTOPERATIVE PERIOD
The postoperative period covers the time when the patient is recovering from anaesthesia and the immediate effects of surgery, and when complications are most likely to arise. It may last a few hours or be prolonged for 2 or 3 days. It is a time when the patient must be watched closely, but the observations made, and their timing, differ from the monitoring required during surgery. For most cases, the sophisticated electronic equipment so useful in the operating theatre is not required and the necessary observations are best made by a well trained recovery room nurse. The reliance on electronic displays of physiological data, perhaps at a point somewhat r e m o t e from the patient, may result in vital signs being missed. There is as yet no computer printout that can display minor but critical changes in the patient's responsiveness. This departure from the practice in the operating theatre may not be adequate if the patient subsequently develops some of the serious complications which are discussed later in the chapter. More technology may then be of great help. For this reason, some of the facilities used in the operating theatre may be kept available. For example, an arterial line may be kept patent by infusing heparinized saline under pressure, and ECG leads are often left attached. After craniotomy, the patient usually regains consciousness in the first half hour, more quickly if he has been anaesthetized with isoflurane, rather more slowly if halothane has been used throughout the operation or if a total intravenous technique was employed. The patient lies in a 15-20 ~ head-up tilt to encourage venous drainage. He is given oxygen---4 l/rain by face mask for the first 3-4 hours to avoid possible hypoxia. The patient's temperature is recorded periodically, axiUary readings with a routine clinical thermometer being sufficient. Many patients will have become moderately hypothermic during the operation, perhaps as low as 34~ Gentle warming with blankets is desirable to avoid possible shivering which may contribute to hypoxia and lactic acidosis. Analgesia is usually given early to prevent restlessness, as this may lead to raised blood pressure, undesirable in post craniotomy patients. Codeine phosphate 0.75 mg/kg is given intramuscularly, usually with prochlorperazine Bailli~re's ClinicalAnaesthesiology--Vol. 1, No. 2, June 1987
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maleate (Stemetil) 12.5mg intramuscularly. Codeine is an adequate analgesic, does not cause pupillary changes, and decreases mobility of the intestine which may help to prevent vomiting. A fluid balance chart is started. The aim is to allow the patient about 2 litres of balanced electrolyte solution (Hartman's solution or equivalent) in 24 hours for the first 2-3 days. Oral fluids are restricted for 24 hours. Patients who have had a supratentorial craniotomy are allowed fluids after being fully awake for some hours, providing that they have discernible bowel sounds. Patients who have had a posterior fossa exploration must be carefully assessed to make sure that they have an adequate swallowing reflex as this may have been impaired temporarily by disturbance of the IXth nerve. All patients submitted to neurosurgery are on steroids (dexamethasone) and are usually given H-2 antagonists to avoid gastric or duodenal ulceration (Cimetidine 400rag once daily, usually in the evening, orally or intravenously). Bladder distension can cause restlessness and the patient must be examined for this at regular intervals. Many patients are likely to be sufficiently conscious and cooperative to micturate on demand even if diuresis ensues. If drowsiness persists or the patient is confused, catheterization may be unavoidable. Patients who have had previous anaesthetics or prolonged unconsciousness are likely to develop chest infections. These patients are often given prophylactic antibiotics and will require the attention of a physiotherapist soon after regaining consciousness. Physiotherapy must be gentle, avoiding violent coughing and the head-down position. Patients must be periodically assessed by a recovery room nurse for response to pain, verbal command, the ability to perform motor tasks (power of the hand-grip and flexion of the knee), the size and reaction of the pupils, and correct orientation in time and place. If no disturbing signs have developed over a period of 12 hours the immediate postoperative period can be considered to have passed uneventfully and the patient returned to the care of the general neurosurgical ward. The challenge of the postoperative period relates to the eventful recovery and the anticipation, early recognition and treatment of untoward events. The more important of these will now be considered along with some other aspects of intensive care. RAISED I N T R A C R A N I A L PRESSURE
In the first few hours after operation, the patient may show signs of raised intracranial pressure due either to bleeding, into a tumour cavity or subdurally, or to cerebral oedema. Oedema may have been present when a tumour was excised or biopsied, or may develop subsequently. It may also occur after surgery to a vascular lesion, either due to transient ischaemia or infarction. The usual presentation is for the level of consciousness to deteriorate subtly and for the patient to become gradually tess responsive to verbal command, or dysphasic. Limb weakness may appear in a patient previously without such a sign, or a previous hemiparesis may deepen. An unconscious
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patient may cease to respond to painful stimuli. The patient will often have obvious pupillary changes, usually the pupil on the operated side dilating and becoming fixed. Formal testing of tendon reflexes and plantar responses is of little help. A slow progressive deterioration may best be judged by inspection of the chart plotted by the recovery room nurse (Figure 1).
WARD DEPT
Operation date
9.11,86
Craniotomy for excision "of left parietal angioma
Level of Consciousness
RE Spon
Eye Opening
To sf To p Non{
Orier Best Verbal Response
Conf
InaPl I ncor Non( Obe~ Loca
Best Motor
Flex
Response
Exte Non~
P U P L S
Size: Reaction to Light
D = N = S = Yes No
dilat norr smal + --
Limb Power
Upper
(0-5) (M.R.C.)
Lower
M.R.C. MUSCLE POWER G
Figure 1. Chart plotted by recovery room nurse.
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Given the clinical deterioration described, it is essential to differentiate bleeding from oedema. In well equipped units this is done by means of a CAT scan. In the absence of this, the wound must be reopened if bleeding is a serious possibility. Before the patient is transferred to the radiology department, the anaesthetist has to decide whether the patient should be intubated and ventilated. In my opinion the patient who has become drowsy needs controlled lowering of PaCO2 as a rising PaCO2 will cause increased cerebral blood flow leading to a worsening of cerebral oedema or bleeding. Early ventilation of such patients appears to be much the safest policy, not least as it avoids the difficulties and dangers of emergency intubation in the middle of the x-ray procedure. Undoubtedly there is one potential hazard to intubation, the effect of the pressor response to laryngoscopy in a patient who could be bleeding (Stoelting, 1977). This can, however, be mitigated by thiopentone or one of the benzodiazepines, e.g. Diazemuls (diazepam) or midazolam, in addition to the usual suxamethonium to facilitate intubation. It is a good practice to insert a nasogastric tube at the same time. After diagnosis, the definitive treatments of bleeding and oedema are totally different. Bleeding will probably require prompt surgical intervention, to evacuate a cavity clot or subdural haematoma. Extradural haematomas are sometimes encountered when pin fixation has been used during the operation. This is a particular hazard of this technique in children. Cerebral oedema can be helped by continuing ventilation to maintain the PaCO2 at a low level, usually 3.3-4 kPa (25-30 mmHg). Cerebral blood flow is then prevented from increasing and compounding the problem. Control of oedema demands prompt administration of diuretics, usually mannito120% solution with a dose of 0.5 g/kg given over 30 minutes. Frusemide 40mg intravenously is also often used in addition. Urine output must be carefully monitored and bladder catheterization may be necessary. Large doses of dexamethasone are often given to reduce oedema, although there is little evidence that they are really useful. If the oedema is in the posterior fossa, rapid diagnosis is even more vital as treatment must be implemented before coning occurs. The presence of hydrocephalus preoperatively usually indicates that the tumour in the posterior fossa or region of the third ventricle has obstructed the ventricular outflow and compensation has failed. The surgeon will have prepared a burr hole, perhaps leaving a ventricular drain in situ. If so, this can be opened and left on drainage at a controlled rate. If not, a quickly reopened burr hole with placement of a catheter into a lateral ventricle can indeed be lifesaving. Oedema once treated will usually subside, but treatment may be needed for several days before the patient shows signs of awakening. Mechanical ventilation must be continued to maintain respiration and to maintain the reduction of PaCO2 to lower cerebral blood flow. The PaCO2 must be kept at about 4 kPa (30 mmHg) measured by capnography or repeated blood gas analysis. Patient compliance is achieved by the use of non-depolarizing relaxants such as pancuronium, vecuronium or atracurium. Sedation will be achieved by benzodiazepines, such as Diazemuls, or midazolam. If, at the
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intubation, a nasogastric tube was passed, this may be used to administer anticonvulsants and eventually for nutrition when the patient is again absorbing reliably from the intestinal tract. Recovery of the patient is shown by improvement in consciousness measured by response to commands. Relaxants are withdrawn and spontaneous respiration measured. A Wright's respirometer reading of tidal volume appropriate to the patient's size, checked by blood gas analysis indicates when ventilation may be discontinued. Blood gases must be checked with particular care if there is any additional complication such as chest infection.
CONVULSIONS Convulsions greatly increase postoperative morbidity. The increased muscular activity and loss of consciousness cause the airway to become obstructed. An obstructed airway promotes hypoxia at a time of increased oxygen consumption, and hypercarbia during a period of increased carbon dioxide production. This combination raises the arterial blood pressure and increases cerebral blood flow, threatening the patient with the danger of rebleeding. Metabolic acidosis increases potassium concentration in the extracellular fluid of the brain and will lead to localized hyperkalaemia and further impairment of cerebral autoregulation. Fits considerably increase the difficulty of assessment of the postoperative patient. The resulting unconsciousness removes one of the most sensitive signs of recovery. Occasionally, fits are due to other complications such as rebleeding, and diagnosis of this may be delayed. Epileptic fits are often not obvious. The first sign may just be less responsiveness from a patient whose consciousness was gradually returning. This may be accompanied by involuntary twitching of the facial muscles or upper or lower limbs usually on one side. This may or may not progress to a generalized convulsion. Minor fits may be even less obvious and it may require experience to distinguish them from the shivering of a cold patient, clonus from muscular spasticity, or halothane 'shakes'. However, the clinical significance of minor manifestations is the same as a major convulsion and must be treated just as seriously. Patients who are maintained on a ventilator and who are receiving muscle relaxants may of course also fit and these represent a special problem. The degree of relaxation induced in these circumstances is usually not profound and some evidence of twitching or shaking will be seen, though it could be overlooked by an inexperienced attendant. In this situation it is helpful to have the use of a portable E E G machine or a,cerebral function analysing monitor. If these are not available, the diagnosis will remain in doubt. In this situation, it is best to continue to observe extremely closely as fits are often repeated. If signs appear which suggest a second fit, then the patient should be treated without further delay. If an experienced observer suspects the possibility of fits then this is probably what is happening.
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There is considerable controversy concerning the prophylactic use of anticonvulsants. Some studies (Richardson and Uttley, 1980) have shown higher rates of epilepsy in those patients who are operated on without anticonvulsant therapy compared to those patients who have received anticonvulsants. Another recent study, however, failed to show any significant effect on t h e incidence of postoperative epilepsy in a group of patients pretreated with phenytoin and carbamazepine (Shaw et al, 1983). It is probably true to say that the majority of neurosurgeons favour the use of preoperative anticonvulsants, but the issue is still being debated. Since epilepsy usually occurs during the first 24 hours after an operation, anticonvulsants must be used preoperatively in doses high enough to achieve adequate plasma levels before surgery (Foy et al, 1981; Gurusinghe et al, 1986). Plasma levels should be checked preoperatively in high risk cases. Drugs most commonly used are phenytoin, sodium valproate and carbamazepine. Phenytoin acts by stabilizing all neuronal membranes. It prevents the sodium influx which occurs during depolarization. It also limits intracellular calcium accumulation necessary for transmitter release (Sohn and Ferendelli, 1978). Intestinal absorption of phenytoin is slow, variable and incomplete. Peak plasma concentration occurs any time between 2 and 12 hours. The relationship between dose and plasma level is not linear, and it is therefore essential to measure plasma levels. The therapeutic range for plasma phenytoin is 10-20 gg/1. Crystal formation may occur when it is injected intramuscularly, causing unreliable absorption (Dam and Olsen 1966; Wilensky and Lowden, 1973). Intravenous injection is widely used but is not without danger. Too rapid injection may be associated with hypotension and depression of the sinoatrial node of the heart. This may be so severe as to produce cardiac arrest, which seems characteristically difficult to reverse, sometimes with a fatal outcome. In the rather critical postoperative state, phenytoin is not entirely satisfactory and new anticonvulsants seem more predictable, as therapeutic serum levels are more quickly and reliably achieved. Sodium valproate (Carraz et al, 1964) is a newer alternative to phenytoin which has distinct advantages. It rapidly achieves therapeutic plasma concentrations, usually about 1M hours after oral administration with a biological half-life of 8--15 hours (Schobbers, 1983). An injectable preparation exists but is not yet freely available. The antiepileptogenic action of sodium valproate is not completely known. The metabolites of sodium valproate may also be pharmacologically active, accounting for the long-lasting anticonvulsant activity. The drug should, however, be avoided in patients with known liver disease. Carbamazepine is also used as an anticonvulsant and seems particularly well tolerated by children. No injectable form is available. It has been shown to have a depressant effect on the nucleus ventralis of the thalamus, which has been implicated in the generalization of epileptic discharges (Richens and Rimmer, 1985). It is a point to note that both phenytoin and carbamazepine are hepatic enzyme inducers and that their use may modify the metabolism of other drugs. Sodium valproate does not have this property.
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M A N A G E M E N T OF P O S T - C R A N I O T O M Y SEIZURES
Management of any convulsion must be swift and effective. To achieve this an intravenous drug must be used. There are several alternatives. Diazemuls is probably the most widely used agent. It is administered as a bolus via the intravenous line, 10 mg initially. It may be repeated if necessary, although alternatives should be considered if response is not immediate. Barbiturates have been used for longer than any of the currently used agents and are very effective. They are general depressants of nerve conduction, acting at the neuronal synapse. In the postoperative situation, sodium thiopentone is sure to be readily available. The initial dose is 5 mg/kg which should stop the fit. An intravenous infusion may be necessary to maintain control of fitting in a difficult case and intubation and ventilation may be advisable. Chlormethiazole is a very effective anticonvulsant and regarded as the treatment of choice in our unit (Brodrick et al, 1984). It is a strong sedative, but there is no action on the autonomic nervous system, and it causes little change in blood pressure or cardiac output although the pulse tends to rise. In large doses, respiratory depression may be produced. The drug is given as an 0.8% solution in 5% dextrose. Initial control is obtained with a dose of 50-200 ml in the first hour, or it may be used after control has been obtained from diazepam or thiopentone (Gurusinghe et al, 1986). Subsequent maintenance may require a dose of 30-60 ml per hour. Roughly 50% of patients on chlormethiazole infusion at this dose require intubation, and some need mechanical ventilation. Fits may be controlled but respiration is often depressed and as the patient's state is often unstable, nasal intubation is a wise precaution. If intubation is carried out, a nasogastric tube may also be passed to permit the administration of oral anticonvulsants if unconsciousness is prolonged. In practice, chlormethiazole infusion is continued for 12-16 hours, at which time the plasma level of oral anticonvulsants is checked. If there have been no further fits, and oral anticonvulsants are present in the plasma at therapeutic levels, chlormethiazole is slowly withdrawn over 6-8 hours. Abrupt withdrawal may precipitate further convulsions. As chlormethiazole must be given in dilute solution, large doses could lead to overloading of the circulation. Care must therefore be taken to restrict appropriately other intravenous fluids. If necessary, guidance may be obtained from measuring central venous pressure (CVP). A CVP line is used for this in our unit if chlormethiazole is continued beyond 12 hours. If the patient is ventilated, muscle relaxants may be used in conjunction with chlormethiazole. Vecuronium, pancuronium and atracurium are now the relaxants of choice. However, 50% of patients on chlormethiazole do not require intubation and ventilation, their blood gases remaining in the normal range using a Guedel airway with humidified air enriched by oxygen at 41/min. If at all possible, a portable E C G or cerebral function analysing monitor should be used for assessing whether or not the fits have passed, or noting the return of epileptogenic activity.
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P O S T O P E R A T I V E C O N T R O L OF B L O O D PRESSURE AND C E R E B R O V A S C U L A R SPASM
In the postoperative period, the blood pressure should be the same as the preoperative value or slightly lower. Low blood pressure is likely to be due to hypovolaemia and needs treatment. Hypotension induced in the operating theatre is always reversed before dural closure to check that all possible bleeding points have been dealt with. Deliberately maintained low blood pressure (in normotensive subjects) has no place in postoperative management. Low blood pressure will be detected during the routine postoperative observations. The level requiring treatment depends to some extent on the condition which required surgery. A low blood pressure in someone who has undergone a debulking procedure (e.g. tumour removal) is less of a cause for concern than in a patient who has undergone surgery for a vascular lesion such as clipping of an aneurysm. A patient with a normal systolic pressure of 120 mmHg is unlikely to require active treatment unless the systolic blood pressure falls to about 90mmHg. The exception to this rule is the patient who develops some neurological symptoms or signs after regaining consciousness, for example dysphasia or limb weakness. The possibility that such dysfunction is due to hypotension must be considered and treatment instituted. Treatment is by cautious blood volume expansion. If there was significant blood loss during surgery then blood replacement is indicated. Otherwise other agents such as Haemaccel (polygeline) or PPF (purified protein fraction) can be used. The majority of patients, however, will spontaneously correct a deficit in the first few hours after surgery. Hypertension in the postoperative period is of more concern than hypotension as it may precipitate intracranial bleeding. Hypertension is of two types, pre-existing hypertension in a chronically hypertensive patient and acute hypertension developing, for instance, after a subarachnoid haemorrhage and in the postoperative period. Pre-existing hypertension requires treatment with drug therapy before surgery to bring the diastolic blood pressure down to high normal levels, preferably of the order of 100mmHg. This is usually achieved by oral administration of [3-blockers and by the use of diuretics, methyl dopa and calcium antagonists such as nifedipine. During surgery, control of blood pressure will have been achieved by an infusion of [3-adrenergic blocking agents in combination with volatile anaesthetic agents and muscle relaxants. Tubocurarine potentiates the ganglion blocking effect of halothane. Sodium nitroprusside may have been used. Postoperatively, it may be convenient to continue the infusion of the B-blocking agent. A satisfactory response is usually obtained with labetalol 100 mg in 100 ml of normal saline, administered through a paediatric drip set, or if available, an infusion pump. The blood pressure responds rapidly to changes in infusion rate and the rate eventually chosen is that which maintains the systolic blood pressure at slightly less than that regularly recorded preoperatively.
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Some patients do not respond readily and further drugs may be needed. The first choice is hydralazine, which has a different action, being thought to affect the intracellular mobilization of calcium and to some extent calcium movement. It is given as repeated intravenous boluses of 10-20 mg. Maintenance of control is usually possible with intramuscular injections of similar quantities, as it is rapidly and reliably absorbed. When the patient returns to the ward, oral treatment will be reinstituted. Acute hypertension appearing for the first time postoperatively is not rare and usually but not always requires prompt treatment if intracranial bleeding is to be avoided. Possible causes of raised postoperative blood pressure should be considered, as their elimination may be all the treatment that is required. The first thing to consider is pain. Pain must be avoided and the favoured analgesic is codeine phosphate 0.75 mg/kg by intramuscular injection. An alternative analgesic is meptazinol 2 mg/kg of body weight. If given intravenously while the patient is receiving oxygen by face mask at 41/min, it produces good sedation and pain relief in most patients without significant impairment of respiration and with the patient rousable for periodic neurological assessment. Restlessness due to acute discomfort may also raise blood pressure. The most common cause is an unrecognized full bladder.
HYPERTENSION AS A SIGN OF CEREBRAL VASCULAR SPASM
The most difficult problem relates to the hypertension associated with intracranial vascular spasm which requires entirely different treatment. This condition is seen almost exclusively after intracranial aneurysm surgery. It can occur at almost any time in the postoperative period and is accompanied by physical signs of decreasing conscious level or limb paresis. It must be actively treated or it will result in cerebral infarction. As the spasm develops, the rising blood pressure appears to be the patient's attempt to maintain cerebral blood flow. Systolic blood pressure should not be lowered in these patients as it will reduce cerebral perfusion. On the contrary, it may need to be boosted by the infusion of colloid plasma expanders, particularly low molecular weight dextran, or the infusion of inotropic drugs such as metaraminol or dopamine. Blood pressure should be maintained at the level at which the patient again becomes alert or at which paresis is relieved. This may be a blood pressure well above the patient's normal level and may approach 200mmHg systolic. This should be achieved fairly rapidly, certainly within 30 minutes. A constant infusion of metaraminol 100 mg in 500 ml of Hartman's solution is given at increasing rate until symptoms are relieved. An intra-arterial cannula with continuous display of blood pressure is highly desirable. A patient with severe cerebral vasospasm may require intubation and ventilation until again able to maintain an airway. The optimum PaCO2 is again rather low at 4 kPa (30 mmHg). This level is chosen not for its effect on cerebral blood flow so much as the fact that it is easier to control mechanical ventilation at this level. A nasogastric tube may also be passed which can be
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D.A. JEWKES
used subsequently for nutrition if the patient's state takes time to resolve. Chest physiotherapy must be carried out. The assessment of such patients is essentially clinical. However, if facilities are available~ the progress of vasospasm may be monitored by repeated assessments of cerebral blood flow using radioactive xenon clearance measurements. If the vasospasm is in the territory of the middle cerebral artery, useful information may also be obtained by measuring somatosensory evoked potentials as a measure of central conduction time. The affected hemisphere can be compared with the normal side (Symon et al, 1979). Vascular spasm may not subside for up to 10 days, and treatment and monitoring must continue. Tolerance to metaraminol may develop after several days. Dopamine must then be substituted until the patient's catecholamine resources have been restored. Dopamine infusion may also be necessary temporarily when weaning the patient from metaraminol. A useful preparation is dopamine 400 mg in 250 ml normal saline infused at up to I ml per minute according to response (10-20 ~tg/kg/min). Calcium antagonists have been suggested as arteriolar relaxants. In theory, nimopidine crosses the blood-brain barrier and should be useful in treating severe vasospasm. However, no large scale experience has yet been reported to confirm that it has a place in the treatment of this condition (Boullin, 1985). P O S T O P E R A T I V E FLUID B A L A N C E AND SOME A B N O R M A L I T I E S
In proposing guidelines for postoperative fluid balance in the neurosurgical patient several aspects require consideration. Areas of brain which have been adjacent to a tumour may have impaired perfusion in the early postoperative period and are prone to develop oedema. The pressure of cerebrospinal fluid will be low immediately postoperatively, but may rise rapidly in some patients, in particular in those with preoperative hydrocephalus for posterior fossa or third ventricular tumours. Arterial blood pressure, and therefore cerebral perfusion pressure, may be sensitive to fluid balance to some extent in these patients. These considerations suggest that the best policy is to keep the patient slightly fluid-restricted postoperatively, certainly not fluid-overloaded. A satisfactory rule for these patients in temperate climates is to provide 30 ml/kg of water per 24 hours. This is well tolerated in the form of balanced electrolyte solution (Hartman's solution or equivalent). This seems preferable to dextrose solutions which may aggravate a tendency to hyperglycaemia produced by steroid therapy (Prockop, 1981). However, in calculating postoperative fluid requirements it is necessary to assess fluid losses from therapeutic manoeuvres, particularly mannitol infusion or the administration of frusemide. If the blood pressure is maintained at a satisfactory level, this loss should not be replaced immediately but restoration allowed to occur naturally, perhaps over several days. If loss is excessive, cautious addition to the daily allowance is permitted.
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Facilities for rapid assessment of plasma electrolytes are highly desirable and measurement should be obtained in any patient in whom unusual gains or losses have been noted. Estimates of blood glucose are essential if the patient has any tendency to preoperative diabetes, long-standing or steroid-induced. Hyperglycaemia stimulates diuresis and increases anaerobic respiration in poorly perfused regions of the brain. This results in local lactic acid accumulation which may damage cell membranes and release adenosine, prostaglandins and leukotrienes (Lewis and Maestro, 1979). After aneurysm surgery, some units routinely administer Rheomacrodex (dextran 40 intravenous infusion) 500 ml of 10% solution to reduce blood viscosity and prevent sludging in small vessels, while also expanding intravascular volume. This is usually given after a little delay, perhaps about 4 hours, to reduce the incidence of early postoperative bleeding.
Postoperative diabetes insipidus Postoperative diabetes insipidus (DI) is commonly seen in the recovery room. It is usually a complication of surgery in the subfrontal region for pituitary tumour, carniopharyngioma, meningioma or metastases. It may also occur after head injury. DI is suspected when a litre of urine is passed in 4 hours, the patient not previously having a fluid overload. The antidiuretic hormone in man is arginine vasopressin, synthesized in the paraventricular and supraoptic nuclei of the hypothalamus. It appears as neurosecretory granules, which pass from the cells in which they are formed along axons to the posterior pituitary where they are stored. Some of the axons of the vasopressogenic neurones terminate elsewhere for instance in the median eminence, brain stem and floor of the 3rd ventricle. The importance of this is that antidiuretic hormone secretion may occur or be restored even after destruction of the posterior pituitary gland. Release of vasopressin into the systemic circulation is mainly determined by plasma osmolality. Changes are detected by receptors in the anterior hypothalamus. Vasopressin secretion is suppressed by plasma osmolalities of less than 280 mosmol/kg to allow maximum water diuresis. Above this threshold, plasma vasopressin concentration increases in direct proportion to plasma osmolality. The first is normally experienced at plasma osmolalities of about 298mosmol/kg. The combination of the osmotic threshold for stimulating vasopressin release and thirst maintain osmolality at 280-295 mosmol/kg in health. Disturbance in the region of the posterior pituitary causes DI when 80% of neurones synthesizing vasopressin are destroyed or temporarily nonfunctional (Robertson et al, 1982). In the postoperative period, a urine flow of 15-20 ml/min maintained for an hour is highly likely to be due to DI. It is vital to exclude brisk but usually less persistent diuresis induced by therapy. When spontaneous urine output reaches 1 litre/hour it is routine in our unit to administer synthetic vasopressin (deamino-D-arginine vasopressin) 0.5 gg intramuscularly repeated as needed. We allow all but unconscious patients to cope with fluid loss by drinking. Fluid balance is best left to the
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patient. Intravenous infusions are avoided as far as possible as they may override normal controls and promote unnecessary diuresis. A patient having DI should be checked twice daily for fluid balance, plasma osmolality and plasma electrolytes. Treatment can cause water intoxication, though this usually only occurs if the patient has an intravenous infusion. Alternatively, concomitant sodium retention may produce hypernatraemia which can be life-threatening. Unconscious patients (with active bowel sounds) are given fluid by nasogastric tube. They must be closely monitored by frequent laboratory studies (initially four-hourly) until their treatment and clinical state are stable. They will then require an intake equal to urine volume and other obvious losses, with an additional litre per day for insensible loss and sweating. If the state remains for several days, these patients tend to become dehydrated and require 'topping up' from time to time as indicated by the periodic laboratory results. Treatment for DI has to be continued for as long as necessary. It may persist for hours, days, weeks or months. At some stage, the route of treatment may be varied for convenience. Subcutaneous injection is effective and intranasal administration satisfactory in cooperative patients. It is usually only necessary to give ADH substitute once or twice daily. The syndrome of inappropriate antidiuresis The syndrome of inappropriate antidiuresis is commonly seen in intracranial pathological conditions, particularly in patients having a long period of intensive care (Zerbe et al, 1980). It can be associated with intracranial haemorrhage, head injury, brain tumours, hydrocephalus, meningitis and many other disorders. Biochemical diagnosis is made on the basis of hyponatraemia with low plasma osmolality, urine osmolality greater than plasma osmolality and persistent sodium excretion. Other factors are the absence of hypotension and hypovolaemia and oedema formation with normal renal and adrenal function. Clinically, cerebral symptoms of confusion, nausea and irritability may develop with a plasma sodium of less than 120 mmol/1 (120 mEq/1). If untreated, fits, coma and hemiparesis can occur, particularly if the plasma sodium falls to 110 ml/1 (110 mEq/1). Management requires treatment of the underlying cause if possible, followed by treatment of the symptoms of hyponatraemia. Restriction of fluid intake to 500-1000 ml/24 hours is usually effective. There are no rapidly acting drugs available to block the antidiuretic effect of vasopressin.
INDICATIONS FOR TRACHEOSTOMY With the availability and diligence of physiotherapists, there are fewer indications for preoperative or postoperative tracheostomy. Nasotracheal tubes are now routinely left in situ for up to 3 weeks. However, in posterior fossa tumours causing paresis or partial loss of function of the glosso-
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pharyngeal or vagus nerves, and thus respectively loss of gag and cough reflexes, tracheostomy is often preferable to a long intubation. Recovery of these nerves may take many weeks but usually occurs sooner or later. Respiratory failure caused by brain stem haematoma or tumour is likewise commonly an indication for tracheostomy as the problem even with effective treatment is likely to remain for a considerable time. A patient who has been intubated for more than a day or two may have some difficulty in swallowing after decannulation and will usually inhale fluids. Oral fluids should not be given until laryngeal function has returned as demonstrated by the ability of the patient to speak in a normal voice. Treatment of postoperative chest infections can be aided by inserting a mini-tracheostomy. This allows secretions to be aspirated during physiotherapy, and is of great assistance if the patient has a weak cough or is greatly debilitated. Patients with chest complications whose blood gas analysis shows a PaO2 of 10 kPa or less usually require full intubation and ventilation.
POSTOPERATIVE PATIENT CARE SUMMARIZED
A patient in the recovery ward needs a dedicated, individual nurse to make routine observations. It is a great advantage if the nurse is known in advance and has made a preoperative visit to see the patient. Initially, postoperative observations will be required each 15 minutes for at least 2 hours and after that each 30 minutes until the patient returns to the general ward. The medical staff depend very heavily on these observations. Pulse rate
A slow pulse rate is usually due to persisting ]3-blockade from the time of surgery, or occurs when atropine given after surgery has been metabolized. Classically, a slow pulse is said to be a sign of raised intracranial pressure, but in the postoperative period this is rarely seen. Raised intracranial pressure is detected by other signs. A raised pulse rate is usually due to minor cardiovascular disease. However, rarely it may be neurogenic, particularly appearing after exploration of the posterior fossa for brain stem tumour. Blood pressure
Low or falling blood pressure usually indicates hypovolaemia or slight over-sedation, following the use of routine analgesics, even codeine phosphate. Raised blood pressure may be due to poorly controlled chronic hypertension reasserting itself or due to pain or restlessness from physical discomfort or tachycardia. The most difficult cause to identify with certainty is cerebral vascular spasm, which requires different treatment from other causes.
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Respiration Respiratory rate, depth and character of respiration should be noted. Slow respiration is usually caused by over-sedation. It can be associated with raised intracranial pressure from oedema or bleeding, but other signs will be present. Respiration becoming shallQwer with a tracheal tug is usually due to recurarization. It must be promptly treated by the anaesthetist. Rapid respiration is rarely seen and has no particular neurosurgical significance, except in the severely head-inj ured patient when it may require intubation and ventilation to gain control. Pulmonary embolism, spontaneous pneumothorax or lobar collapse are always possibilities.
Temperature Low temperature is caused by failure to prevent hypothermia during the operation. Heat loss from large wounds is unavoidable. High temperature and hyperpyrexia is due to hypothalamic disturbance and is usually seen in children. It demands immediate treatment by aspirin suppositories and tepid sponging.
Neurological observations The observation chart (Figure 1) lists the observations the recovery room nurse should make. The system of charting allows instant assessment by the anaesthetist of progression of the various aspects of the patient's neurological functioning. Gradual or sudden improvement or deterioration is evident on simple inspection. The importance of these observations lie in their sensitivity in pointing to important complications, requiring intervention, particularly postoperative intracranial bleeding, cerebral oedema and cerebral arterial spasm.
Fluid balance chart Charting of fluid intake is important for long-term assessment of the patient's fluid balance. Urine output observation is important for the early detection of diabetes insipidus.
Equipment Basic postoperative neurosurgical patient care requires minimal sophisticated equipment. The conscientious and experienced nurse, a good chart, a standard sphygmomanometer and a thermometer can take care of 90% of the observations required. With the onset of complications, additional equipment may be required, basically a ventilator and an ECG monitor. Infusion pumps are helpful and should be available. A portable EEG or cerebral function monitor is rarely required, but should be obtainable.
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REFERENCES Boullin D (1985) Prevention of spasm--strategy. In Crockard HA, Hoff J & Hayward R (eds) Neurosurgery. The Scientific Basis of Clinical Practice, (chapter 14). Brodrick PM, Bromley L & Jewkes D (1984) The use of chlormethiazole to control postcraniotomy epilepsy. British Journal of Anaesthesia 56: 1312. Carraz G, Fau R, Chateau R et al (1964) Communication apropos des premiers essais cliniques sur l'activit6 anti-dpileptique de l'acide N-dipropylac6tique (sel de Na+). Annales MedicoPsychologiques 122: 577-585. Dam M & Olsen V (1966) Intramuscular administration of phenytoin. Neurology 16: 288-292. Foy PM, Copeland GP & Shaw MDM (1981) The incidence of post-operative seizures. Acta Neurochirurgica 55: 253-264. Gurusinghe NT, Symon L, Jewkes D & Brodrick P (1986) Chlormethiazole in the management of post-craniotomy seizures. Acta Psychiatrica Scandinavica 73(supplement 329): 189-193. Lewis DM & Maestro RD (1979) Free radicals in medicine and biology. Acta Physiologica Scandinavica Supplement 429: 9-168. Prockop LD (1981) Hyperglycaemia effects on the nervous system. In Rose FC (ed.) Metabolic Disorders of the Nervous System, pp 77-98. London: Pitman. Richardson AE & Uttley D (1980) Prevention of post-operative epilepsy. Lancet h 650. Richens A & Rimmer E (1985) Pathogenesis of neuropharmacology of epilepsy. In Crockard HA, Hoff J & Hayward R (eds) Neurosurgery, The Scientific Basis of Surgical Practice (chapter 29) pp 486. Robertson GL, Aycinena P & Zerbe RL (1982) Neurogenic disorders of osmoregulation. American Journal of Medicine 72: 339-353. Schobbers I (1983) Valproic acid: pharmakinetic aspects. British Journal of Clinical Practice (supplement 2). Shaw MDM, Toy P & Chadwick D (1983) The effectiveness of prophylactic anticonvulsants in neurosurgery. Acta Neurochirurgica 69: 253-258. Sohn and Ferendelli (1978) Inhibition of Ca ++ transport into rat brain synaptosomes of diphenylhydantoin. Journal of Pharmacology and Experimental Therapeutics 185: 272-275. Stoelting RR (1977) Circulatory changes during direct laryngoscopy and tracheal intubation. Anesthesiology 43: 381. Symon L, Hargadine J, Zarirki M & Branston N (1979) Central conduction time as an index of ischaemia in subarachnoid haemorrhage. Journal of Neurological Sciences 44: 95. Wilensky AJ & Lowden JA (1973) Inadequate serum levels after intramuscular administration of diphenylhydantoin. Neurology 23: 318-324. Zerbe R, Stropes L & Robertson GL (1980) Vasopressin function in the syndrome of inappropriate antidiuretics. Annual Review of Medicine 31: 315-322.