433

INTRACRANIAL-PRESSURE CHANGESFOLLOWING HEAD INJURY

I. H. JOHNSTON J. A. JOHNSTONI.H.J OHNSTON J.A. JOHNSTON

BRYAN JENNETTUniversity Department of Neurosurgery,

Institute of Neurological Sciences, Glasgow

Summary Simultaneous continuous monitoringof ventricular-fluid pressure (V.F.P.)

and systemic arterial pressure (S.A.P.) was carried outin 32 patients following a severe head injury. Normal,moderately elevated, and high pressure groups wererecognised. All groups showed a high mortality,particularly the high-pressure group, of whom halfshowed evidence of less serious brain damage immedi-ately after injury and then deteriorated. The responseof S.A.P. to raised V.F.P. was variable, and high V.F.P.levels could be sustained without alteration in S.A.P.Mannitol and surgical decompression were variablein their effects on raised V.F.P. Aspiration of ventricularcerebrospinal fluid was very effective in cases not

responding to other measures. Clinical evidence ofraised intracranial pressure is unreliable after severehead injury, and management can be much more

securely based if intracranial pressure is directly andcontinuously measured.

Introduction

A VARIETY of mechanisms may contribute to the

neurological dysfunction which follows head injury.Such mechanisms include primary brain damage,cerebral swelling, and intracranial hsematoma forma-tion. In any given patient more than one of these factorsis frequently important, and these may or may notproduce a significant alteration in intracranial pressure.

Raised intracranial pressure may have importantconsequences such as the production of brain shiftsand possible impairment of the cerebral circulation.Intracranial pressure can now be reduced by severalmeasures besides surgical intervention, but unfor-

tunately the clinical signs usually indicative of risingintracranial pressure may be unreliable or even

misleading in the context of severe head injury. Amethod of directly monitoring intracranial pressurein such situations has obvious value. Several studieshave established the feasiblity of continuous monitor-ing of ventricular-fluid pressure (V.F.P.) using an

indwelling catheter in the lateral ventricle. 1 ,2 2 Anreliminarv sttiftv of the usf of the method in a sfnes

of head injuries has also been reported.3The aim of the present study has

been to extend the scope of these initialobservations by continuous monitoringof V.F.P. and also of systemic arterialpressure (s.A.P.) with particular atten-tion to three points: (1) to define thedifferences between those patients whodevelop a significant elevation of intra-cranial pressure following head injuryfrom those who do not, and to correlatethis information with the clinical and

pathological findings; (2) to study thesignificance of alterations in perfusionpressure with a view to correlating thesewith alterations in the cerebral circula-tion ; and (3) to seek a better under-

standing of the relative efficacy of themethods for controlling raised intra-cranial pressure.

Methods

Measurements were made on 32 patients(aged 1-68 years) admitted to a neurosur-gical unit following severe head injury overa period of 18 months. The method usedis based on that described by Lundberg.2A polyethylene catheter (8 Fr.) is insertedinto the right lateral ventricle via a standardfrontal burr-hole. The catheter is con-

nected to a diaphragm transducer and thepressure continuously recorded on a two-channel paper-chart recorder. The secondchannel is used for continuous measure-ment of the S.A.P. using a cannula in theradial or brachial artery connected to a

similar transducer. Calibration is carriedout against a 100 mm. column of mercuryonce or twice daily. Recording is started assoon as possible after injury and continuedfor a period of days (usually 4-5 days)according to the demands of the clinical

Fig. 1-Typical pressure patterns following a head injury.A, normal V.F.P. (max. mean v.F.P. < 20 mm. Hg), showing mean and maximum

and minimum values.B, high V.F.P. (max. mean V.F.P. > 40 mm. Hg).

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MAXIMUM MEAN V.F.P. LEVELS AND MORTALITY IN 32 PATIENTSWITH SEVERE HEAD INJURY

situation. Daily specimens of cerebrospinal fluid (c.s.F.) aresubmitted to the laboratory for bacteriological examination;no case of infection has occurred.

ResultsPressure Patterns

Wide variations in pressure occurred in some

patients over the period of recording, and the variouswave forms described by Lundberg 2 were observedas well as variations due to measures aimed at reducingintracranial pressure. Allowing for the intermittentnature of the pressure rises it was possible to recognisethree groups according to the maximum pressuresreached, excluding transient elevations due to cough-ing, movement, or other external factors (see accom-panying table). The three groups are as follows:those with relatively normal pressure (<20 mm. Hg),those with a moderate elevation of pressure (20-40 mm. Hg), and those with pronounced elevationsof pressure (>40 mm. Hg). Examples of the pressurepatterns in these groups are shown in fig. 1.

In the normal-pressure group (group I) 5 out of 9patients died. All 9 had been rendered immediatelyunconscious at the time of injury and showed theclinical syndrome commonly ascribed to primarybrain-stem injury, although in those coming to

necropsy no definite brain-stem damage was found.Group 11, with moderate pressure elevations, showed

Fig. 4-Comparison of the effects of (A) mannitol and (B)ventricular C.S.F. aspiration on V.F.P. in a patient, aged15 years, 5 days after head injury.

a variety of clinical pictures, some cases being clinicallyindistinguishable from those in group I and othersfrom those in group III; of 11 cases in this group6 died. Only 1 of the 12 patients in the high-pressuregroup (group III) has made a satisfactory recovery;3 remain in coma and the rest have died. Of thisgroup, 6 were recorded as having talked at some timeafter their injury and before their clinical deterioration,and only 1 of these had an intracranial haematoma.Preliminary neuropathological studies in this groupsuggest a relatively high incidence of cerebralinfarction.

Relation of V.F.P. to S.A.P.Perfusion pressure has been defined as the difference

between the mean S.A.P. and the mean intracranial

pressure.4 Opinions may vary as to the exact validityof this definition, but there is no doubt that the

relationship between V.F.P. and s.A.P. is of criticalsignificance. Since rising intracranial pressure mayevoke a rise in s.A.P. the effect of a given level ofintracranial pressure on perfusion pressure can be

judged only if these two parameters are measuredsimultaneously. In fact we have found that thesetwo pressures are very inconstantly related to eachother. In some cases an increase in v.F.P. has beenassociated with an increase in s.A.P., in others withno alteration in s.A.P., and in yet others with a fallin s.A.P. Indeed all three such situations have beenseen in one patient over a period of twenty minutes(fig. 2). Failure of S.A.P. to respond to a prolongedelevation of V.F.P. is shown in fig. 3. 3 cases hadperiods of a zero or negative perfusion pressure (bythe above definition); and 2 of these deterioratedrapidly and died after such an episode, while the 3rd,who showed a presumed failure of perfusion for aperiod of 45 minutes (fig. 3), remains unconscioussome three months after injury. In addition a situation

Fig. 3-Failure of S.A.P. to rise with prolonged elevation ofV.F.P. in a patient, aged 15 years, 5 days after head injury.

435

of vasomotor paralysis as described by Langfitt et al.5following experimental head injury in animals hasbeen seen in patients in whom the intracranial pressurepassively follows the S.A.P.Methods of ControlThe methods studied include osmotic diuretic

agents, hyperventilation, withdrawal of ventricular

c.s.F., and surgical decompression. As might be

expected no single method proved uniformly effective,and it was only by continuous monitoring of V.F.P.that the worth of a particular method in an individualcase could be assessed. In certain situations mannitolwas extremly effective, but in other situations, par-ticularly with prolonged and pronounced elevationsof V.F.P., it had no significant effect (fig. 4A). Therebound effect following mannitol was not obvious,but repeated doses tended to become progressivelyless effective. Both withdrawal of ventricular c.s.F.

and hyperventilation proved very effective in loweringraised intracranial pressure (fig. 4B). In one case

repeated aspiration of c.s.F. was the only effectivemeans of controlling the raised pressure. Indeedwhen the pressure is considerably raised there maybe a striking difference in the efficacy of c.s.F. drainageand of mannitol during episodes of high pressure.The effect of bony decompression was sometimesshortlived, and the v.F.P. could return to extremelyhigh levels despite the removal of a large bone-flap.

Discussion

Classification of severe head injuries into distinct

groups, as a means of delineating different types ofbrain damage, as a basis for prognosis, and as a guideto management, has not been satisfactorily achieved.

Certain patients following severe head injury showthe clinical syndrome classically ascribed to primarybrain-stem injury, the salient features of whichinclude immediate and deep unconsciousness, decere-brate rigidity, abnormalities of respiratory rhythm,and disturbances of autonomic function. Some

patients with this syndrome have been found, in thepresent study, to have a relatively normal intracranialpressure over a prolonged period of recording (up to10 days after injury). On the other hand, some patientswith an apparently identical neurological picture mayhave quite pronounced elevation of intracranial

pressure. It is well established that secondary brain-stem lesions with corresponding physical signs mayoccur as a sequel to raised intracranial pressure 6;but in some of our patients with the classical pictureand raised intracranial pressure there has been no

temporal sequence which would allow the assumptionthat the brain-stem damage was secondary, and theseparticular cases would therefore fall into the categoryof primary brain-stem injury. Thus to describe a

particular case as having a primary brain-stem injuryis no reliable guide to the presence or absence ofraised intracranial pressure, or to methods of

management likely to be appropriate.The concept of a primary brain-stem lesion has

developed from a correlation between clinical observa-tions and early animal experiments 7 and accordswith the more recently understood connection betweenthe brain-stem reticular system and the maintenanceof consciousness. 9 The nature and situation of the

lesions in this type of injury have not, however, beendefinitely established. The pathological studies ofStrich 10,11 have demonstrated a diffuse lesion of thesubcortical white matter; on the basis of a burr-holein one case, and the absence of post-mortem signs ofincreased pressure in others, she has suggested thatthis type of lesion is not associated with raised intra-cranial pressure. Using the present method we arehoping to identify with greater certainty those caseswhere intracranial pressure does remain normal aftersevere head injury and to correlate the clinical and

pathological findings in this important group.On the other hand it is clear that, excluding those

patients who develop a space-occupying haematoma,some do develop a pronounced and progressive risein intracranial pressure, and in our experience the

majority of these have succumbed within the first fewdays after injury (see table). In the present study suchcases had a relatively less severe neurological deficitat the time of initial examination, in that they madesome verbal response, only to undergo subsequentclinical deterioration associated with uncontrolledintracranial hypertension.

In such situations of raised pressure the level of

perfusion pressure is probably of greater significancethan the level of intracranial pressure alone. The

early studies of Cushing 12 established a relationshipbetween rising intracranial pressure and S.A.P. whichhas been widely accepted and which may be regardedas a mechanism helping to maintain an adequateperfusion pressure. The present results, however,confirm the views of other workers that the relation-

ship between intracranial pressure and S.A.P. is veryvariable.13,14Whether or not a certain level of intracranial

pressure will threaten the cerebral circulation dependson what is happening to the s.A.P. at the same time.The effect of alterations in perfusion pressure on thecerebral circulation is probably the most importantfactor in determining the degree of secondary braindamage caused by raised intracranial pressure followinghead injury. Previous studies have shown that raisedintracranial pressure may produce a fall in cerebralblood-flow 15,16; more recently Greenfield and Tin-dall,14 measuring intemal-carotid-artery flow, showeda reduction to 25% of the original level when intra-cranial pressure levels reached 70 mm. Hg. In additionLundberg et aU? ,18 have shown a fall in cerebralblood-flow associated with the plateau waves ofincreased intracranial pressure together with a subse-quent increase in cerebral blood-volume during suchwaves.

The precise relationship between perfusion pressure,rather than intracranial pressure, and the cerebralcirculation has not yet been investigated clinically.Experimental studies in this Institute have shown that,once the perfusion pressure falls below 30-40 mm. Hgthere is a serious reduction in cerebral blood-flow, 19Pathological studies in rhesus monkeys have shownwidespread neuronal necrosis following episodes of lowperfusion pressure due to arterial hypotension.2O In

patients selective involvement of the boundary zonesbetween major arterial territories has followed such

episodes of low perfusion pressure,21 and similarlesions have been identified in some of the cases in

436

group in in the present study.22 Further clinical and

neuropathological studies are being directed towardsthe significance of this relationship, both after headinjury and in other patients with raised intracranialpressure in whom perfusion pressure has beenmonitored.

In dealing clinically with raised intracranial pressureor falling perfusion pressure following head injurythere is no doubt that continuous monitoring of bothV.F.P. and s.A.P. provides the most sensitive guide tothe effectiveness of the therapeutic measures employed.When the intracranial pressure/volume curve entersthe steeply rising phase 23 immediate measures aimedat reducing the volume of one of the components of theintracranial compartment may be called for. In thissituation mannitol may fail to prove effective. With-drawal of ventricular c.s., seems likely to be themost useful method, although induced hypocapniaproduced by controlled hyperventilation may also bevaluable.Thus a regimen centred on the combined use of

controlled hyperventilation, mannitol, and ventriculardrainage, in conjunction with continuous monitoringof V.F.P. and s.A.P. may reduce the high mortality andmorbidity of those patients with head injuries whoshow a progressive rise in intracranial pressure in theabsence of any surgically correctable expanding lesion.The value of c.s.F. aspiration in an acutely developingpressure situation is a cogent argument for a method of

monitoring which involves ventricular catheterisationrather than sensors placed on the surface of the brain.

1. H. J. and J. A. J. held research fellowships financed by theNational Fund for Research into Crippling Diseases. Mr. J. O.Rowan, regional department of clinical physics and bio-engineer-ing, Glasgow, gave invaluable advice in the development of themethod. The consultants of the Division of Neurosurgery (Mr.J. S. Robertson, Mr. A. Paterson, Mr. J. W. Turner, and Mr.John Russell) kindly agreed to the inclusion in this report ofpatients under their care.

Requests for reprints should be addressed to B. J., UniversityDepartment of Neurosurgery, Institute of Neurological Sciences,Killearn Hospital, Glasgow.

REFERENCES1. Guillaume, J., Janny, P. Presse mid. 1951, 59, 953.2. Lundberg, N. Acta psychiat. neurol. scand. 1960, 36, suppl. 149.

3. Lundberg, N., Troupp, H., Lorin, N. J. Neurosurg. 1965, 22, 581.4. Zwetnow, N. Scand. J. Lab. clin. Invest. 1968, suppl. 102.5. Langfitt, T. W., Weinstein, J. O., Kassell, N. F. Neurology,

Minneap. 1965, 15, 622.6. Johnson, R. T., Yates, P. O. Acta radiol. 1956, 46, 242.7. Sherrington, C. S. J. Physiol., Lond. 1898, 22, 319.8. Walshe, F. M. R. Proc. R. Soc. Med. 1922, 15, 41.9. Moruzzi, G., Magoun, H. W. EEG clin. Neurophysiol. 1949, 1, 455.

10. Strich, S. J. J. Neurol. Psychiat. 1956, 19, 163.11. Strich, S. J. Lancet, 1961, ii, 443.12. Cushing, H. Am. J. med. Sci. 1902, 124, 375.13. Browder, J., Meyers, R. Am. J. Surg. 1936, 31, 403.14. Greenfield, J. C., Tindall, G. T. J. clin. Invest. 1965, 44, 1343.15. Kety, S. S., Shenkin, H. A., Schmidt, C. F. ibid. 1948, 27, 493.16. Noell, W., Schneider, M. Arch. Psychiat. NervKrankh. 1948, 180,

713.

17. Lundberg, N., Cronqvist, S., Kjallquist, A. Prog. Brain Res. 1968,30, 70.

18. Risberg, J., Lundberg, N., Ingvar, D. H. J. Neurosurg. 1969, 31, 303.19. Rowan, J. O., Harper, A. M., Miller, J. D., Tedeschi, G., Jennett,

W. B. J. Neurol. Neurosurg. Psychiat. (in the press).20. Brierley, J. W., Brown, A. W., Excell, B. J., Meldrum, B. S

Brain Res., 1969, 13, 68.21. Adams, J. H., Brierley, J. R., Connor, R. C. R., Treip, C. S

Brain, 1966, 89, 235.22. Adams, J. H. in Symposium on the Pathology of Trauma. J. clin

Path. suppl. (in the press).23. Langfitt, T. W. Clin. Neurosurg. 1969, 16, 436.

THE FIST AS AN EXTERNAL

CARDIAC PACEMAKER

JOHN B. WILDJOHN D. GROVER

Permanente Clinic, Portland, Oregon, U.S.A.

Summary In three patients with ventricularasystole the hearts responded to con-

tinuous rhythmical chest-pounding&mdash;in one case formore than 40 minutes. Each blow on the chest wasfollowed by ventricular depolarisation and systole.Metabolic acidosis did not develop, and no precautionswere needed to prevent it. This method might be triedas the first line of treatment for asystole in hospitals;and outside hospitals it seems to have a better chanceof success than cardiac massage as a first-aid measurefor cardiac arrest.

Introduction

METABOLIC acidosis is one of the obstacles to

recovery from cardiac standstill.1 When adequateamounts of intravenous sodium bicarbonate cannotbe given to patients with cardiac standstill, owingeither to ventricular fibrillation or to electricalinactivity, they die of metabolic acidosis despiteeffective cardiac massage and artificial respiration.There is no accepted simple first-aid measure whichan untrained person can apply to help a victim ofprolonged ventricular asystole. In the unlikely eventthat adequate artificial respiration and circulationcan be established within five minutes to preventbrain damage, the patient, if he is to survive, mustreach medical facilities within twenty minutes, unlesshis own ventricular contractions take over and preventirreversible acidosis.Our experience with several patients suggests that

in fact a simple first-aid measure could sustain lifein many cases.

Case 1 Case-records

A 60-year-old woman developed Adams-Stokes attacksafter fracture of epicardial pacemaker leads which hadbeen placed in March, 1968, for the treatment of completeheart-block. Before a temporary transvenous pacemakercould be inserted, ventricular fibrillation developed andD.c. depolarisation was successfully accomplished. Severaltimes thereafter her ventricles stopped but respondedimmediately to chest-pounding, which was continuedperiodically for about thirty minutes while a temporarytransvenous pacemaker was inserted. Each episode of

chest-pounding would last several minutes until herideoventricular rhythm was resumed (no intravenoussodium bicarbonate was given). Unfortunately, no tracingswere recorded. Her heart is now functioning well with apermanent transvenous pacemaker.

Case 2

An 83-year-old woman developed complete atrioven-tricular block and cardiac standstill three days after anacute myocardial infarction. Heart-pounding by the nursein charge, without massage, maintained an adequate out-put while we failed to place a transvenous pacemaker onthe ward, took her to the X-ray department, and finallysucceeded in placing a pacemaker which paced herventricles. She responded normally after the procedures,but the next day cerebral symptoms developed and shedied.