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THE TIGHT BRAIN

MERLIN MARSHALLM.B. Cantab., F.F.A. R.C.S.

ANÆSTHETIST

NEWCASTLE GENERAL HOSPITAL, NEWCASTLE UPON TYNE, 4

DURING the past few years various techniques designedto reduce brain bulk and tension have been introducedinto neurosurgical practice. The efficacy of these tech-niques varies greatly in different circumstances. In this

paper I discuss the underlying physiological mechanismsand then suggest the limitations and advantages ofinduced hypotension, induced hypothermia, over-

ventilation, and the infusion of hypertonic solutions.The cerebrospinal-fluid pressure and the intracranial

venous pressure can be reduced to atmospheric, or evensubatmospheric, by putting the patient in a head-upposition and by ensuring quiet unobstructed respiration.With the newer techniques, however, it is possible toreduce the bulk of the brain and to soften its consistence.The bulk and consistence of the brain depend upon:

(1) the mass of cellular elements present, which cannotreadily be altered; and (2) the amount of tissue fluid

present. The latter is partly under our control.

Formation of Tissue Fluid

Tissue fluid is normally formed as a transudate fromthe arteriolar end of the capillaries and most of it isreabsorbed at the venous end. Its formation is a simplefunction of the differences in hydrostatic and osmoticpressures on each side of the capillary wall.For example, if the hydrostatic pressure of the blood in the

arteriolar end of the capillary is 32 mm. Hg and the osmotic’pressure of the non-diffusible plasma-proteins is 25 mm. Hg,there is a resultant filtration pressure of 32 - 25 =7 7 mm. Hgtending to push fluid out through the capillary wall. At thevenous end of the capillary, the hydrostatic pressure of theblood is, say, 12 mm. Hg, the osmotic pressure of the plasma-proteins-slightly higher than at the arteriolar end because ofloss of the water that has diffused out-is, say, 27 mm. Hg.There will, therefore, be a negative pressure here of 27—12==15 mm. Hg tending to withdraw water from the tissue spacesinto the capillary.Obviously, increased hydrostatic pressure within the

capillary will increase tissue-fluid formation and hinderits reabsorption; and increases in the osmotic pressureof the blood will hinder its formation and encourage its

reabsorption. If the hydrostatic pressure along the wholelength of the capillary is greater than the osmotic

pressure of the plasma-proteins, fluid will be lost fromthe whole length of the capillary and none will bereabsorbed.

Normally the osmotic pressure of the non-diffusibletissue constituents is so small compared with that of theplasma-proteins that it can be ignored. If, however, as aresult of injury, cell contents leak into the tissue fluid, andif, as further response to injury, the capillaries becomemore permeable and allow plasma-proteins to leak out,the resulting tissue fluid will have a high protein content.This protein will, by its osmotic effect, encourage thediffusion of water out through the capillary wall andgreatly impede its return. This is the process by whichinflammatory oedema is formed.

Factors Influencing Capillary Hydrostatic PressureThe capillaries are protected from the full force of the

arterial blood-pressure by the narrow bore of the musculararterioles. After overcoming the arteriolar resistance, thehydrostatic pressure of the blood in the arteriolar end of

the capillary is about 30 mm. Hg (Landis 1930). If thearteriole were to relax, however, the capillary would besubjected to a much greater pressure. By the time theblood has overcome the resistance of the capillary itselfand reached the venous end its pressure has dropped tosome 12 mm. Hg. This residual pressure is the " vis a

tergo " that impels the blood into the veins. Even though

the pressure in the large veins is subatmospheric, thepressure in the venous end of the capillary is still about12 mm. Hg. Basically, therefore, the blood-pressure inthe capillary is controlled by the systemic arterial blood-pressure and the arteriolar resistance or tone. If the

pressure in the veins is raised, the pressure at the venousend of the capillary will rise until it is still some 12 mm.Hg higher than that in the veins. If the veins are com-

pletely obstructed, the venous capillary pressure will riseuntil it equals that at the arteriolar end when blood flowwill cease (though fluid is still diffusing out of the

capillary).Effect of HypotensionThe capillary blood-pressure (and, therefore, the filtra-.

tion pressure) is dependent ultimately upon the systemicblood-pressure. Increase in the systemic blood-pressurewill tend to increase tissue-fluid formation and thereforeto increase brain bulk and tenseness. Lowering the blood-pressure will shrink and soften the brain.

Effects of OverventilationHigh arteriolar resistance reduces the filtration pressure

in the capillary. The argument here is the same as thatfollowed by Wood (1954) in discussing the protectiveeffect of a high pulmonary vascular resistance in pre-venting the formation of pulmonary oedema in patientswith mitral stenosis. Now, the tone of the cerebralarterioles is largely controlled by the pH and theC02 andO2 concentrations in the blood and tissue fluid perfusingthem. If the pH and theo2 concentration are raised andthe C02 tension lowered there will be an increase inarteriolar tone and resistance. This will reduce the

hydrostatic and filtration pressure in the capillary. This,in turn, results in a reduction in tissue-fluid formation,and a reduction in brain bulk and tenseness follows.Thus overventilation shrinks and softens the brain.

Conversely, asphyxia, by causing a relaxation of thearterioles, produces cerebral swelling and oedema.

If the patient is in a head-up position and the largerveins near the superior sagittal sinus are exposed, theycan be seen to empty and fill with each respiratory cycle.If the patient is being ventilated with a pump, they willfill during the positive-pressure phase of inflation andempty during the negative or low-positive phase ofexpiration. But they can also be seen to empty (i.e.,collapse completely) even though a positive pressure of5-10 cm. H2O is maintained during expiration. I suspect,therefore, that the hydrostatic pressure in an intracranialsinus will remain atmospheric or subatmospheric untilthe pressure in the chest, measured in centimetres ofwater, equals the height in centimetres of the sinus abovethe heart.The better conditions obtained by the use of pumps

that produce a negative pressure during expiration are,in my opinion, due to: (1) the greater tidal volume andmore efficient overventilation achieved with a negative-pressure phase; and (2) the reduction in venous-pressurewhich can sometimes, but only sometimes, be broughtabout by a negative phase, when positioning the patientis ineffective.

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Effects of Hypertonic InfusionsIf the osmotic pressure of the plasma is increased, water

will tend to pass from the extravascular into the vascularcompartment. This redistribution will increase the blood-volume and raise the blood-pressure; it will also reducethe osmolarity of the plasma. At the same time the osmo-larity of the tissue fluid will rise slightly and this processwill continue until a new equilibrium is reached. In

reaching this new equilibrium the increasing blood-

pressure, caused by an increasing blood-volume, will bepartly counteracting the effect of the increased plasmaosmolarity.For example, a 500 ml. infusion of triple-strength plasma

will withdraw from the extracellar compartment some 1000 ml.of water, thus becoming equivalent to an infusion of 1500 ml.Assuming a blood-volume of 6 litres, this will represent anincrease in the blood-volume of 25%

In intracranial surgery, this increase in blood-volumeand blood-pressure sometimes offsets the advantagesgained by hypertonic infusions.The brain receives about 1/7 of the cardiac output

(Kety and Schmidt 1945). Assuming a brain weight of1500 g. in a patient weighing 75 kg., this means that 1/50of the body is receiving 1/7 of the circulating blood. If theblood is made temporarily hypertonic we would thereforeexpect it to withdraw proportionately more fluid from thebrain than from parts less liberally supplied. This issufficient to explain the apparently selective action of

hypertonic infusions in relieving cerebral oedema andraised intracranial pressure without having to postulatepeculiarities of the blood-brain barrier.Hypothermia. Cooling patients to 30°-32° C does not seem as effectivein reducing brain bulk as overventilation or hypertonicinfusions-its main usefulness lies in protecting cellsfrom the effects of an inadequate blood-supply. Coolingwill, however, by reducing metabolism reduce the forma-tion of C02 and of acid metabolites and will, therefore,have an effect resembling that of overventilation.

Applications and Limitations of These TechniquesAll methods of reducing brain bulk depend eventually

upon their action on the exchange of fluid across thecerebral capillary wall. They must, therefore, be inter-dependent. Thus, for hypertonic infusions to producetheir best effect, ventilation must be adequate, and theblood-pressure and temperature must be normal. Buteach technique has concomitants which tend to nullifythe effects desired-for example:

1. Active cooling of a patient often raises the blood-pressure,and at lowered body temperatures breathing may be inadequate.

2. Hypertonic infusions raise the blood-pressure.3. Over ventilation can sometimes require so high an infla-

tion pressure that the venous pressure is unduly raised.4. Hypotension may cause serious tissue anoxia.

Factors Governing Choice of TechniqueOverventilation

In the operating-theatre, I think, overventilation pro-vides the surest and safest method of producing a smallsoft brain. But, as already suggested, there are difficultieswith this technique and it is not always successful. Letus consider two types of case. ,

Firstly, there is the middle-aged man with chronicbronchitis and emphysema. Because of his fixed chestand poor lung compliance, this type of patient may provedifficult to ventilate at all and overventilation may bepossible only with a very high inflation pressure and a long

inflation time. This high inflation pressure and inflation I

time may raise the central venous pressure sufficiently tocause engorgement of the intracranial veins and sinuses.Thus, attempts at over ventilation may make conditionsworse rather than better.There is another possible explanation for bad results

with overventilation in this type of patient. In them,spontaneous breathing is often inadequate and they becomeacclimatised to a lowered oxygen tension and a raised

CO2 tension. Though I have no definite proof, it is Ipossible that the intracranial vessels become insensitive as Ia result of these abnormal tensions and no longer respond Inormally to changes in tension. I

Secondly, there are those patients with large tumours iand very high intracranial pressures. The most vigorous I

overventilation may produce little or no effect. I canthink of two possible explanations for this though, again,I have no direct evidence to support them:

1. A cerebrospinal fluid pressure of 240 mm. H20 is equiva-lent to nearly 18 mm. Hg; this is considerably higher than thepressure normally found in the venous end of the capillary andmuch higher than that found in the intracranial sinuses ina head-up position. As the intracranial pressure rises, the jcirculation is impeded. The tissues become anoxic and CO, ’,accumulates. The arterioles dilate in response to these changesand so raise the capillary pressure, but the circulation remains

’

borderline, being only maintained by high CO2 tension andlow O2 tension. The vessels may then no longer respondnormally to changes in these tensions.

2. Large or active tumours are associated with new malformedblood-vessels, and these also may be unresponsive to changesin gas-tensions and pH.Hypertonic Infusions

Hypertonic infusions have long been part of thestandard treatment of patients with cerebral oedema orraised intracranial pressure, for which they are veryeffective. They are also effective when overventilationhas failed, and (if my previous suppositions are right) theysucceed because they do not depend for their effect uponalterations in vascular tone but solely upon alterations inosmolarity of the circulating blood. For reducing brainbulk it matters little what substances are used in the

hypertonic solution. The effect will be related to the

tonicity and quantity of the solutions given rather thanits constituents. But different solutions have different

side-effects, and it is a consideration of these that shoulddecide the choice of solution. For example, in a" shocked " patient with a head injury, hypertonic plasmaor dextran, which will expand the blood-volume for severalhours, would be better than urea. In a patient with a nor-mal blood-volume, or one in whom a diuresis is desired,urea would be better. In those with signs of cerebralirritation, as in hypertensive encephalopathy or eclampsia,a solution that has a sedative action, such as magnesiumsulphate, would be the natural choice.Hypotension

Induced hypotension to levels below 90-100 mm. Hgis now considered to be too dangerous to have manyjustifiable uses (Davison 1953). But to lower the blood-pressure intentionally to 100-120 mm. Hg is not onlyuseful but often necessary if good results are to beobtained. This applies whether using overventilation.hypothermia, or hypertonic infusions, and is another

example of the interdependence of all these mechanisms.HypothermiaThe effect of hypothermia on brain bulk is definite

but small when compared with the effects of overventila-

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don or hypertonic infusions. Its use, therefore, is confinedmainly to two types of case. First, those in which theblood-supply to the brain may be temporarily inadequate;and secondly, those in which such great difficulty is

expected that every possible aid must be used.Conclusions

By a mixture of observation and speculation, I haveattempted to coordinate and rationalise our use of newtechniques to reduce brain bulk and tension. If myarguments are correct, we should be able to predict moreoften which cases will benefit from emphasis upon aparticular technique and which will not. But most

important of all is the realisation that only by a combina-tion of techniques can the best results be obtained. Toalter only one or two factors out of four will often resultin disappointment.

REFERENCES

Davison, M. H. A. (1953) Anœsthesia, 8, 255.Kety, S. S., Schmidt, C. F. (1945) Amer. J. Physiol. 143, 53.Landis, E. M. (1930) Heart, 15, 209.Wood, P. (1954) Brit. med. J. i, 1051, 1113.

A NEW TECHNIQUE IN THE SURGERY OFMASSIVE GASTRODUODENAL BLEEDING

HAROLD BURGEM.B.E., F.R.C.S.

SURGEON, WEST LONDON HOSPITAL, LONDON, W.6

THROUGHOUT the long history of the surgery of massivegastroduodenal haemorrhage, it has been known thatsometimes at operation the lesion cannot be found inspite of careful examination of the outer surface of thestomach or duodenum.For many years, the teaching was that in these circum-

stances the surgeon should perform a standard 70%gastric resection. By so doing it was hoped that the lesionwould be excised with the stomach. In more recent timessuch " blind gastrectomy " has not been favoured, for theulcer may be retained within the patient, in either thestomach or the duodenum, and may continue to bleed.During the past few years it has been customary to open

the stomach by a gastrotomy, and to inspect and palpatethe mucosal surface of the stomach and of the duodenum.Bohn (1949) pointed out that the thrombosed arterialbleeding point could sometimes be palpated as a smallseedling within the stomach. But to palpate, or to seeclearly, the whole extent of the gastric mucosa is not easyunless an enormous gastrotomy incision is made. Themucosa lies in folds and a small ulcer is easily hidden.Also the duodenum cannot be properly inspected withouta fairly extensive incision into it. In fact, while sometimesthe mucous membrane of the stomach and that of theduodenum must be inspected thoroughly, gastrotomyis a most unsatisfactory means of doing it.

I wish to record a technique which I have used andwhich I believe to be of great value in this type of case.Perhaps it is best described by reporting the managementof a case.

Case-reportThe patient was a man aged 47, who gave a fifteen-year

history of dyspepsia. He was admitted to hospital with severehmatemesis, and gave a recent history of pain one hour afterfood. He was treated initially on a medical regimen; butbleeding continued, and after transfusion of six pints of bloodthe abdomen was opened by an oblique incision across theepigastrium. Stomach and duodenum appeared normal. Thestomach in the region of the lesser curve was rubbed with agauze swab, as was the anterior surface of the duodenum. Thisprocedure is sometimes helpful, for it can often bring up a

whole mass of small petechial haemorrhages over an ulcerwhich can neither be seen nor felt. In this patient suchhaemorrhages did appear in the region of the mid-lesser curve,and their occurrence suggested that there was an impalpableulcer at this level. No such response was obtained from theduodenum. If gastrectomy was to be performed, it was necessaryto see the lesion, sothat the gastrec-tomy would includethe ulcer in theexcised part of thestomach.A cuffed ceso-

phageal tube was

inflated in the lower

oesophagus to oc-

clude the lumen.An incision 1 in.

long was made inthe anterior surfaceof the stomach nearto the pylorus. All

gastric contents werecarefully removed

by suction. A steri-lised standardYeoman’s sig-moidoscope, with

magnifying eye-piece, was insertedthrough the smallgastrotomy wound,and this site was

Sigmoidoscope inserted through gas-trotomy wound.

made airtight by a thin rubber tube placed around the stomach(see figure). The stomach was then inflated by bellowsuntil it was considerably distended, and gastroscopy wascarried out through the sigmoidoscope. The view through thewide Yeoman’s instrument was excellent, and it was enhancedby the use of the magnifying eyepiece.A shallow ulcer was seen in the region of the lesser curve,

and the thrombosed end of the bleeding artery in the centre eof the ulcer was seen as a small dark spot. A Billroth I gastrec-tomy was performed to excise the ulcer, and from thisoperation the patient made an uninterrupted recovery.

Comment

During this " operative gastroscopy " a wonderful viewwas obtained of the gastric cardia, and the typical rosetteappearance of its mucosal folds was evident. It was

interesting to see the cardia open and shut in response tochanges in the intragastric pressure.A sigmoidoscope gives an excellent view of the upper

reaches of the stomach, and any lesion near the cardiacannot fail to be seen.

Cystoscopy is an excellent examination because thebladder is fully distended. Full distension must be the

key to a satisfactory gastroscopy, and this is obtained inthe examination described here. Some surgeons haveused operative gastroscopy to locate a bleeding lesion, butthe stomach must be completely emptied of fluid, andsometimes of clot; and gastroscopy is a safe techniqueonly in the hands of the most experienced physicians andsurgeons.

SummaryGastric ulcers may not be palpable, and the position of

the lesion must be known accurately before gastrectomyis carried out.

Gastroscopy during the operation is usually difficult,and is a technique for only the most experienced.

Full distension of the stomach seems the key to asuccessful gastroscopy. The use of a sigmoidoscope,introduced through a small gastrotomy wound, is advo-