postoperative care of the neurosurgical patient · postoperative care of the neurosurgical patient...

Br.J. Anaesth. (1976), 48, 797

POSTOPERATIVE CARE OF THE NEUROSURGICAL PATIENT

J. BARKER

The anaesthetist can make an important contributionto the care of surgical patients after operation,particularly in the field of neurosurgery wherecomplications can have such a catastrophic effect.This account will discuss the period immediatelyafter operation and also events and some rationale ofcare in later management when the anaesthetist willcontinue to play an important role.

In this Institute all major cases, includingcraniotomies and head injuries, are transferred tothe neurosurgical intensive care unit (ICU). Theanaesthetic recovery room receives spinal cases,shunts and patients who have had investigativeprocedures requiring general anaesthesia, but some ofthe latter, who are considered "high risk" neuro-surgical cases or have complications in other systems,are transferred directly to the ICU. Such a unit,having efficient monitoring and highly trainedpersonnel including the anaesthetist with his expertisein respiratory problems, can help to ensure smoother,quicker and more complete recovery of patients.

Much of the research in the "high risk" neuro-surgical patient has been carried out during theoperative procedure and in this issue Greenbaum(1976) and Horton (1976) have discussed the adverseeffects of both techniques and anaesthetic agents onintracranial pressure (ICP) and cerebral perfusionpressure. Yet in many ways the patient is in a bettersituation during the operation than after operation,being adequately ventilated and oxygenated, de-compressed intracranially and having, in most cases,a well-controlled arterial pressure, heart rate andrhythm. With the availability of an ICU, the combinedskills of surgeon, anaesthetist and nursing staff canimprove care after operation and ensure, wherepossible, the smooth recovery of the patient.

In broad terms, after operation the neurosurgicalanaesthetist is particularly concerned with levelof consciousness, intracranial pressure, respiratoryproblems, changes in the cardiovascular systemincluding arterial pressure, control of temperature,fluid balance, nutrition and prevention of infection.

J. BARKER, M.B.3 CH.B., F.F.A.R.C.S., D.A., Institute of Neuro-logical Sciences, Southern General Hospital, GlasgowG51 4TF.

LEVEL OF CONSCIOUSNESS

Teasdale (1976) has described in this symposium ascale of assessment of coma. Following operation thishas proved to be a simple useful guide in the day-to-day management of the patient. In his assessment theclinician must be aware of the contribution made byanaesthesia, which can be considerable. This maycause confusion of neurological assessment when, forexample, a ganglion-blocking drug has been givenduring operation causing fixed dilated pupils forseveral hours. The addition of anaesthesia to depth ofcoma may not always be undesirable, though at onetime it was the aim to keep anaesthesia as light aspossible in neurosurgical procedures. Several authorshave written recently about techniques of metabolicdepression and barbiturate protection (Yatsu et al.,1972; Smith et al., 1974), particularly in intracranialvascular operations, which led Larson and colleagues(1974) to comment that the desire for rapid emergencefrom anaesthesia may become a secondary consider-ation. C.n.s. metabolic depression should probably bethe aim in neuroanaesthesia, even if it means only agood effect on rCBF and therefore ICP. It is par-ticularly important at this time when there is lessconcern about having patients as awake as possibleat the end of the operation and when surgeons are notaverse to the idea of ventilating patients in the periodfollowing surgery.

INTRACRANIAL PRESSURE

It has already been suggested that patients may farebetter during operation than in the period immediatelyafter surgery, and this is particularly noticeable insituations where no decompressive procedure hasbeen carried out, for example biopsy of tumour orsome investigative procedures under general anaes-thesia. Leech, Barker and Fitch (1974) and Jergensenand Misfeldt (1975) have demonstrated increases inICP in neurosurgical operations at the termination ofanaesthesia and have commented that the danger maybe greater in these patients who have had no surgicaldecompression. A knowledge of ICP can be of greatvalue in management after surgery of these cases andin situations where drugs have been administered andcontrolled ventilation instituted.

798 BRITISH JOURNAL OF ANAESTHESIA

Nowadays it is common to monitor ICP, andTurner and McDowall (1976) have described varioustechniques in this symposium. Lundberg (1960) hasemphasized the importance of immediate diagnosisand treatment which is possible with ventricular fluidpressure (VFP) monitoring and is, in some cases,lifesaving. There is, of course, the danger of infectionwhich limits monitoring time, but G. M. Teasdale(personal communication, 1976) has recently madeuse of a closed system which includes an Omayareservoir through which a small butterfly needle canbe inserted at any time when VFP monitoring isrequired. A similar needle can be inserted into anartery, thus allowing calculation of cerebral perfusionpressure (that is, mean arterial pressure minus meanICP).

Another useful measurement in the period follow-ing surgery is ventricular pressure response (VPR),which Miller and Garibi (1972) studied in patients byinducing small changes in volume in the lateralventricle. They added 1 ml of saline or withdrew 1 mlof c.s.f, in some cases obtaining an early warning ofthe stage at which small increases in volume causelarge increases in ICP. They were thus able to get ameasure of brain tightness or elastance (inversecompliance). Leech and Miller (1974a) have shownthat mannitol significantly reduces both VFP andVPR in primates with intracranial hypertension, thereduction of VPR being greater than that of VFP.Similarly, the reduction of VPR was more markedthan VFP reduction 24 h after the start of steroidtherapy. Their results suggest that both forms oftherapy can reduce VFP and make the intracranialcontents less susceptible to steep increases in pressurewith the addition of volume to the cranium. Mannitol,in fact, having a double action in reducing brainwater volume and periventricular elastance, providesa more satisfactory method than hyperventilation inprotecting the brain against the dangers of increasedICP. These authors also showed that hyperventilationhad less effect on elastance, although VFP is reducedwith hypocapnia. Furthermore, Rowed and colleagues(1975) suggested that any beneficial effect of hypo-capnia on ICP is likely to be only temporary.

PROBLEMS OF VENTILATION

In all patients with brain damage it is essential to havea good airway and this is particularly important in theperiod after operation. The patient may still beanaesthetized to a degree which will allow him toretain an endotracheal tube without respiratory

depression. Blood-gases should be checked at the endof operation when spontaneous respiration has beenestablished, and if hypoxia or hypercapnia is presentthen artificial ventilation may be established. Theuse of depressant drugs during operation can result inarterial hypoxaemia as a result of alveolar under-ventilation. These drugs can also result in the patientdepending on a hypoxic drive with the danger offurther respiratory depression by oxygen therapy(Leigh, 1975). Another important factor afterprolonged neurosurgical operations is diffusionhypoxia, which could conceivably last for a longerperiod than is usually expected. If there is a need toincrease the arterial tension of oxygen (Pa02), then itmay be necessary to commence artificial ventilationwhich will allow easier control of inspired oxygen.However, every effort should be made to avoid thedangers of oxygen toxicity which may result from theuse of high percentages of oxygen (Winter and Smith,1972).

There are certain operations following which it maybe desirable for the patient to retain his endotrachealtube for other reasons. This is the case with recon-structive cranio-facial operations when a tracheostomyhas not been performed electively. In posterior fossaexplorations, the lower cranial nerves may betraumatized, particularly in dissection of angletumours, making it necessary to have the airwayprotected for a period by retention of the endotrachealtube or tracheostomy. In these cases, a nasogastrictube should also be passed in order to aspirate stomachcontents during the first critical 24-h period; it canlater be used for nutrition or for the administration ofantacids. A useful monitor in these cases is theimpedance pneumograph, which will give a warningsignal if the patient stops breathing or if a ventilatorceases to function. An output can be taken from themonitor and displayed as a pattern of ventilation inspontaneously breathing patients, and this can becorrelated with other measurements, for exampleVFP (North and Jennett, 1974).

Artificial ventilation may be necessary in patientswith brain damage for other reasons, which includeimpairment of lung function, pulmonary oedema,multiple injuries, status epilepticus and apnoea.

Impairment of lung function may itself be a conse-quence of brain damage, and a decrease in PaOa,an increase in minute volume and a reduction inPapoj, are frequent accompaniments, often despitetracheostomy and care of the airway. The patient whohas suffered a head injury may have surgery forcraniotomy or for other reasons and is likely to have

POSTOPERATIVE CARE OF THE NEUROSURGICAL PATIENT 799

special respiratory problems in the period aftersurgery. Denny-Brown and Russell (1941) haveshown in head injuries that inhalation of secretions orvomitus occurs at the time of the injury because thelarynx becomes incompetent and swallowing reflexesare interrupted. The inhalation of gastric contents cancause a severe inflammatory response in the alveolarmembrane (Mendelson, 1946) and the presence ofirritant material below the laryngeal inlet can resultin an increase in airway resistance because of reflexbronchial narrowing. Brackett (1971) demonstratedgeneralized patchy areas of atelectasis which may havebeen the result of depressed ciliary activity. Thesecases can benefit from a period of artificial ventilation.So, also, may cases of pulmonary oedema which canoccur as a pathophysiological haemodynamic responseto increased intracranial pressure. Ducker (1968)found that increased ICP was the only commonaetiological factor in 11 young patients with pulmon-ary oedema. Permanent relief occurred in one patientby the reduction of ICP, which may indicate that VFPmonitoring is of value in these cases as a therapeuticas well as a prognostic guide. An increase in endexpiratory pressure (PEEP) will increase intra-alveolar pressure which is likely to oppose the passageof fluid from the capillaries into the alveoli andthereby improve the transfer of oxygen (Russell,Morgan and Lumley, 1971). However, a study byEsteban and colleagues (1973) showed that the effectof PEEP in the management of pulmonary oedemawas variable and that it was not easy to predict whichpatients would benefit. There could also be an adverseeffect on cardiac output.

One-third of all head injuries have multipleinjuries (Lewin, 1966) and the combined head andchest injury is becoming increasingly common. Eachof these carries a high risk when occurring separately.A combination of the two is particularly lethal andartificial ventilation will be urgently required. Othermajor injuries accompanying head injury, such asthose in the upper abdomen or major limb or pelvicfractures causing immobilization, are likely to benefitfrom a period of artificial ventilation.

Status epilepticus can be a major complication in theperiod after operation and if the control of thisrequires the administration of depressant drugs, thenartificial ventilation can sometimes be of value in themanagement of these cases.

Finally there is the vexed question of brain death.The clinician is not infrequently faced with a patientwho has suffered severe brain damage and has become

apnoeic. With the use of ventilators, such a patientmay be kept alive for a period causing great distress torelatives and affecting adversely the morale of the staffof an intensive care unit. Death is generally defined ascessation of cardiovascular activity, but, in an attemptto lessen suffering to the relatives of patients,Mohandas and Chou (1971) have discussed theconcept of brain death based on the integrity of thec.n.s. Having excluded depressant drugs and hypo-thermia as factors causing or contributing to the coma,this applies to patients who have no spontaneousrespiration or motor responses above the spinal cordand in whom the pupils are fixed in the absence ofevidence of 2nd or 3rd nerve lesions. Spinal reflexesmay persist even when the brain stem is autolysed.Artificial ventilation and other supportive measuresshould then be continued for only 12 h. E.e.g. ex-amination is not essential in the determination ofbrain death (Editorial, 1974). The patient is takenoff mechanical ventilation for a period of 5 mincommencing with a normal PaCOi and having oxygenadministered by diffusion (6 litre/min by trachealcatheter). If no spontaneous respiration occurs, thenit is recommended that the ventilator be switchedoff. However, a further period of artificial ventilationfor 12 h may be commenced followed by a final testof apnoea.

In recent years there have been accounts of the useof controlled hyperventilation as a specific therapeuticmeasure, but this area of use is controversial. Spon-taneous hyperventilation in brain damage may be theresult of hypoxia, a central neurological non-chemicalventilatory drive or a secondary compensatingmechanism to restore normal intracerebral pH.Hyperventilation itself can cause an increase in c.s.f.lactic acid concentration (Domonkos and Huszak,1959), and this is likely to be associated with a lowc.s.f. bicarbonate. However, Gordon and Rossanda(1968) concluded from their studies in patients withsevere head injuries that low c.s.f. pH was caused, notby chronic hypocapnia, but by alterations in brainmetabolism. They suggested, therefore, that thisacidosis should be corrected by the use of controlledhyperventilation. C.s.f. pH was used as a guide to thedegree of intracerebral acidosis, and these workershave demonstrated a reduction of acidosis, though notconsistently, in both lumbar and ventricular samplesin ventilated patients. While it is difficult to obtaincontrolled studies to assess this form of therapy,Gordon (1971) has reported clinical evidence of amortality rate significantly lower in patients treatedin this manner.


In addition to correction of intracerebral acidosis,Gordon and Rossanda (1968) claim that reductionin ICP, improvement in oxygenation and betterperfusion of brain tissue are produced by the use ofcontrolled hyperventilation. Clinicians are aware thatartificial ventilation can be of use in patients withbrain damage who have respiratory insufficiency, butit must also be recognized that oxygenation may beadversely affected even in patients with normal lungs.Decrease in compliance (Howell and Beckett, 1957),increase in VD/VT ratio (Watson, 1962) and decreasein cardiac output (Cournand et al., 1948) have beenreported. Christensen (1976) found, in a study ofartificial hyperventilation in cerebral apoplexy, thatapproximately half the patients treated in this waydeveloped pathological x-ray findings in the lung bythe 2nd day. The institution of artificial ventilationmay do little to improve KA/£) inequalities or frankshunting in the lungs of patients following headinjury. In fact, Michenfelder, Fowler and Theye(1966) noted that hyperventilation and a very lowPaC02 increased pulmonary shunting and decreasedcardiac output. However, one advantage of artificialventilation may be better control of inspired oxygen,but this should not result in />aOa increasing abovenormal values. Rossanda and Gordon (1970) advisedthe use of high percentages of oxygen, but this can bedangerous to the respiratory system (Winter andSmith, 1972). Patients with neurological diseasesaffecting respiration can be ventilated for long periods,even years, without evidence of lung impairment, butthe use of high inspired oxygen can initiate respiratoryfailure. In a retrospective study of those patientswho had developed respiratory failure, Nash,Blennerhassett and Pontoppidan (1967) concludedthat oxygen was the most likely cause of this failureand not controlled ventilation.

Cerebral oxygenation may also suffer as a result ofsevere cerebral vasoconstriction which becomessignificant when Pncot reaches 20 mm Hg (Wolhnanet al., 1968). Below this value increases in cerebraltissue lactate/pyruvate ratio and increasing reductionof the NADH/NAD+ system may represent hypoxia(Granholm and Siesjo, 1969), but so long as the energycharge potential of the tissue is unaltered this hypoxiais most likely to be reversible (Granholm, 1971).Evidence that border line hypoxia exists at this degreeof hypocapnia is given by the reversal of high tissueand c.s.f. lactate by the inhalation of hyperbaricoxygen (Plum, Posner and Smith, 1968). If sodiumbicarbonate is infused to produce a metabolic alkalosisat PaCOi 20 mm Hg, rCBF will increase because of

tissue hypoxia resulting from a shift to the left of theoxygen dissociation curve (Wollman et al., 1968).Similar studies, also in man, at PaC02 30 mm Hgdemonstrated no alterations in rCBF. Other evidenceis given by the reversal of slow-wave activity in thee.e.g. which is produced by inhaling hyperbaricoxygen (Cohen, Reivich and Greenbaum, 1966).Granholm (1971) and Harp and Wolhnan (1973)emphasized that these observations apply to normalbrain and that patients with damaged cerebralcirculation resulting from arterio-sclerosis or intra-cranial disease of any kind cannot be expected totolerate such a degree of hyperventilation.

The rate of delivery of oxygen to cerebral tissue isan additional factor regulating oxygenation. It hasbeen postulated that hyperventilation will improveperfusion to ischaemic areas by an inverse stealphenomenon, but there is confusion in the literatureregarding this. In areas of canine brain made ischaemicby occlusion of the middle cerebral artery, Solowayand colleagues (1968) demonstrated a reduction in thesize of the infarct following the induction of hypo-capnia. In a subsequent similar investigation onmonkey brain (Soloway et al., 1970), the induction ofhypocapnia was delayed for 1 h and they were unableto reproduce these results. Lassen and Palvolgyi(1968) described increases in rCBF during hypocapniain patients with apoplexy and cerebral tumours.However, Brock, Hadjidimos and Schurmann (1969)demonstrated, in a patient with ischaemic braindamage, that hyperventilation can be harmful ifreactivity to carbon dioxide is still present in collateralvessels. In other studies on the effect of PaC02 onthe brain of the squirrel monkey made ischaemicfor 2 h by occlusion of the middle cerebral artery,Michenfelder and Sundt (1973) concluded thathypocapnia did not improve but rather aggravated themetabolic effects of ischaemia. There were furtherdecreases of energy reserve measured as decreasingATP values and increasing lactic acidosis.

Damaged brain may also have hyperaemic fociwhere perfusion is in excess of metabolic needs, andit has been postulated that loss of vasomotor control isa result of localized cerebral acidosis (Lassen, 1966).If this is partly a result of increased PaC0]!, thenhyperventilation may minimize the damage; at thesame time ICP will be decreased and this will helpto maintain adequate cerebral perfusion (Kjallquist,Siesjo and Zwetnow, 1969). However, this tissue acid-osis is likely to be metabolic; tissue metabolites willhave an overriding effect on CBF and hyperventila-tion will be of little use other than by decreasing ICP.


It seems that there is still considerable doubt aboutthe efficacy of controlled hyperventilation as a specifictherapeutic measure in brain damage. It would beinteresting to know if the induction of a respiratoryalkalosis to treat acute brain injury characterized by acerebral metabolic acidosis causes a continuous c.s.f.alkalosis or if the effect is only transient. Christensen(1974) found that the effect was only transient inpatients with cerebral apoplexy. C.s.f. pH adaptationoccurred within 2 days. Good brain oxygenationcannot always be guaranteed with controlled hyper-ventilation, even under ideal conditions, nor canimproved patterns of cerebral perfusion. Mostclinicians would agree that artificial ventilation can bea very useful measure in controlling ICP, especially inthe period soon after trauma (Crockard, Coppel andMorrow, 1973), but its value at a later stage remains indoubt. There are occasions when it is obligatory to useartificial ventilation, but in other circumstances theclinician must carefully weigh the advantages and thedisadvantages of the technique before embarking onthe procedure. As he watches abnormal patterns ofrespiration the anaesthetist, almost instinctively, hasthe desire to take over ventilation, but he must guardagainst over-enthusiasm and at all times consult withthe neurosurgeon. Even if artificial ventilation isconsidered advisable, the situation should be reviewedregularly lest either recovery or brain death make itunnecessary. Artificial ventilation is not necessarilyindicated merely because intubation or tracheostomyis performed to maintain a clear airway, nor shouldartificial ventilation be equated with extreme hyper-ventilation, which can only be harmful.

CHANGES IN CARDIOVASCULAR SYSTEM

It is important to avoid severe hypotension and tomaintain adequate brain perfusion in the periodfollowing surgery. Tindal (1971) included drugs,hypothalamic lesions, pituitary failure, dehydration,electrolyte imbalance, haematemesis from gastro-intestinal lesions and inadequate transfusion as causesof hypotension in a neurosurgical intensive care unit.Most of these are treatable, but patients who havepersistent hypotension, which may be accompanied byspontaneous irreversible hypothermia, have probablysustained severe hypothalamic damage and theprognosis is very poor.

Acute hypertension may also be dangerousby causing a "breakthrough" of autoregulation ofcerebral blood flow (Skinhej and Strandgaard, 1973),but in studies in baboons made chronically hyperten-sive, the mean arterial pressure was increased to a

much greater value before rCBF became pressurepassive (Strandgaard et al., 1975). These authorssuggested that adaptative changes occur in thecerebral circulation which may help to protect thebrain from further increases in arterial pressure.Hypertension can also cause an increase in brainelastance or stiflhess (Leech and Miller, 1974b) and iffocal oedema is already present, an increase in arterialpressure can increase its volume and extent (Klatzoet al., 1967).

It is not uncommon for the patient who has hadsurgery for the treatment of intracranial aneurysm tobecome very hypertensive in the period immediatelyafter operation and the anaesthetist may be asked tocontrol this. This is a confusing area because somesurgeons believe that the arterial pressure should bestimulated at this time to provide a good perfusionpressure. In this unit the surgeon will often settle for"taking the top off the pressure". Ganglion blockingdrugs and phenothiazines are unpredictable in actionand may be difficult to control, and because of this theauthor prefers to use i.v. Althesin and to instituteartificial ventilation. Control of arterial pressure isvery easy with this method and the condition of thepatient may be improved by the reduction in cerebralmetabolism and rCBF produced by drug-inducedsedation.

The electrocardiograph is a useful monitor in ICUbecause of the association between acute cerebraldamage and myocarditis (Connor, 1968). It is also wellknown that brain stem lesions can be associated withcardiac dysrhythmias, but Rossanda (1975) considersthat, in neurosurgical intensive care, there is nospecial need for sophisticated instrumentation tocorrect these.

CONTROL OF TEMPERATURE

The technique of induced hypothermia for neuro-surgical operations has declined over the past decade,and the tendency now is to prevent accidentaldecreases in temperature which may occur as acomplication of prolonged operations. This helps toavoid shivering after operation and increased oxygenuptake of muscle and brain. However, there maybe a limited and specialized use for hypothermia,especially in situations where main cerebral vesselsare temporarily clamped. In these cases artificialventilation should be continued into the periodfollowing surgery to ensure better control of shivering,acid-base status and cardiac dysrhythmia.

Other uses of hypothermia include the control ofbrain swelling and after cardiac arrest (Rosomoff,


1968). The technique in these cases should be limitedto less than 48 h as hypothermia per se can inducecerebral oedema and brain swelling if prolongedbeyond this time (Bloch, 1967).

Preferential cerebral hypothermia may find apermanent place (Balcalzo and Wolfson, 1971). It hasbeen used successfully in cardiac surgery and coldsaline has been recommended for intracarotidperfusion immediately following cardiac arrest(Demian et al., 1970).

In this Institute two rooms are available in the ICUwhere the ambient temperature can be decreased to10 °C. This has proved to be a better method than theuse of fans to control hyperpyrexia in the neuro-surgical patient. These rooms are also useful if adecision is made to induce hypothermia in a patient.

FLUID BALANCE

There are problems of fluid and electrolyte balanceand nutrition which are peculiar to the neurosurgicalpatient. Periods of unconsciousness and extensiveneuroradiological investigations quickly lead todehydration, particularly in the small child. Barker(1973) showed that a patient who received multipleanaesthetics before the start of surgery was likely todevelop a metabolic keto-acidosis.

As in a general ICU, it is important regularly tocheck weight, fluid intake and output, urinary specificgravity and electrolyte concentrations, plasma electro-lytes, urea and haematocrit. In neurosurgical practicemeasurements of osmolality ratios are also veryimportant in the control of fluid and electrolytebalance which may tend towards hyperosmolality orhypoosmolality. Hyperosmolality tends to occur in theearly period after brain damage and may be related toa hypothalamic lesion. Over a 6-month period at thisInstitute, 4% of patients showed abnormalities offluid and electrolyte balance, and, of these, the greatmajority were combined hyponatraemia and hypo-chloraemia (Tindal, 1971). Boselli and Betto (1973)have studied the pattern of hypoosmolality andwarned of the dangers of early administration ofelectrolyte-free solution which is retained by thekidneys under the influence of inappropriate ADHsecretion, thus expanding both extra- and intra-cellular spaces. This can enhance brain oedema andcause an increase in intracranial pressure whichusually occurs a few days after the injury. Theseauthors advise that the only suitable method oftreating this condition is by mild restriction of water.Rossanda (1975) observed that a decrease in serumsodium was especially dangerous when associated

with a simultaneous increase of -PaC02. Artificialventilation, of course, can help to avoid nypercapniathough Sladen, Laver and Pontoppidan (1968) havewarned that this technique may itself cause waterretention and enhance the development of plasmahypotonicity. The treatment of these patients shouldtherefore include the administration of osmoticdehydrating agents, diuretics and steroids.

NUTRITION

Haider and colleagues (1975) observed that patientswith severe brain damage show a greater increase inmetabolism than that following general trauma, andthey suggested that in these cases hypercaloricnutrition in the period immediately after trauma canbe of substantial benefit. The policy of fluid restrictionmay be difficult to combine with high caloric intake ifonly the parenteral route is available. Rossanda (1975)suggested that 30-50% glucose may be given withvariable amounts of insulin. Single solutions forparenteral nutritional requirements have recentlybecome available providing calories, fluids, proteinsand vitamins. If the gastric route is available andabsorption is good, then this is the best method offeeding these important constituents. Elementalnutrition by this route eliminates the risk of sepsis,phlebitis or thrombosis and reduces the need forconstant monitoring by nursing staff.

PREVENTION OF INFECTION

The anaesthetist can help to avoid infection. Heshould be meticulous about setting up i.v. and arteriallines in order to avoid sepsis, and particular careshould be taken about the insertion of central venouslines which may be used for parenteral feeding.

Modern disposable endotracheal tubes are alladequately sterilized and should be kept so beforeintubation. They should not be made unsterile byplacing them on benches or by applying lubricationwith unsterile fingers. Throat packs are likely to causepain after operation (Conway, Miller and Sugden,1960), which may be followed by respiratory infection.

Renal damage is a real danger in the neurosurgicalenvironment as in all intensive care units. Condomsand closed drainage can be used in male patients toavoid catheterization, which may lead to ascendinginfection. Mannitol is frequently administered duringsurgery, and it is a good technique to empty thebladder manually in the male patient when themuscles of the abdominal wall are relaxed. Catheteriz-ation with closed drainage may be necessary in


females, and a bladder irrigation system using aurinary antiseptic can be used after operation.

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Product Licence No: 0029/5058

I^^^H^H ^g HB Trade MarkFluothanethe original halothane - purely from ICI

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postoperative care of the neurosurgical patient · postoperative care of the neurosurgical patient...

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