INTRACRANIAL-PRESSURE CHANGES FOLLOWING HEAD INJURY

433

securely based if intracranial continuously measured.

INTRACRANIAL-PRESSURE CHANGES FOLLOWING HEAD INJURY J. A. JOHNSTON

I. H. JOHNSTON I.H. OHNSTON

J.A.

J

BRYAN

JOHNSTON

University Department of Neurosurgery, Institute of Neurological Sciences, Glasgow

Simultaneous continuous monitoring of ventricular-fluid pressure (V.F.P.) and systemic arterial pressure (S.A.P.) was carried out in 32 patients following a severe head injury. Normal, moderately elevated, and high pressure groups were recognised. All groups showed a high mortality, particularly the high-pressure group, of whom half showed evidence of less serious brain damage immediately after injury and then deteriorated. The response of 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 variable in their effects on raised V.F.P. Aspiration of ventricular cerebrospinal fluid was very effective in cases not responding to other measures. Clinical evidence of raised intracranial pressure is unreliable after severe head injury, and management can be much more

Sum ary

directly and

Introduction of mechanisms may contribute to the neurological dysfunction which follows head injury. Such mechanisms include primary brain damage, cerebral swelling, and intracranial hsematoma formation. In any given patient more than one of these factors is frequently important, and these may or may not produce a significant alteration in intracranial pressure. Raised intracranial pressure may have important consequences such as the production of brain shifts and possible impairment of the cerebral circulation. Intracranial pressure can now be reduced by several measures besides surgical intervention, but unfortunately the clinical signs usually indicative of rising intracranial pressure may be unreliable or even misleading in the context of severe head injury. A method of directly monitoring intracranial pressure in such situations has obvious value. Several studies have established the feasiblity of continuous monitoring of ventricular-fluid pressure (V.F.P.) using an indwelling catheter in the lateral ventricle. 1 ,22 A

A

JENNETT

pressure is

VARIETY

nreliminarv sttiftv of the

of head

usf

of the method in

injuries

has also been

a

sfnes

reported.3

The aim of the present study has been to extend the scope of these initial observations by continuous monitoring of V.F.P. and also of systemic arterial pressure (s.A.P.) with particular attention to three points: (1) to define the differences between those patients who develop a significant elevation of intracranial pressure following head injury from those who do not, and to correlate this information with the clinical and pathological findings; (2) to study the significance of alterations in perfusion pressure with a view to correlating these with alterations in the cerebral circulation ; and (3) to seek a better understanding of the relative efficacy of the methods for controlling raised intracranial pressure. Methods Measurements were made on 32 patients (aged 1-68 years) admitted to a neurosurgical unit following severe head injury over a period of 18 months. The method used is based on that described by Lundberg.2 A polyethylene catheter (8 Fr.) is inserted into the right lateral ventricle via a standard frontal burr-hole. The catheter is connected to a diaphragm transducer and the pressure continuously recorded on a twochannel paper-chart recorder. The second channel is used for continuous measurement of the S.A.P. using a cannula in the radial or brachial artery connected to a similar transducer. Calibration is carried out against a 100 mm. column of mercury Fig. 1-Typical

A, normal

V.F.P.

pressure patterns

(max.mean

v.F.P. <

20

following

mm.

V.F.P.

(max.

mean V.F.P. >

40

mm.

head injury.

Hg), showing

and minimum values.

B, high

a

Hg).

mean

and maximum

daily. Recording is started as possible after injury and continued for a period of days (usually 4-5 days) according to the demands of the clinical once or soon as

twice

434 MAXIMUM MEAN V.F.P. LEVELS AND MORTALITY IN WITH SEVERE HEAD INJURY

32 PATIENTS

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

Wide variations in pressure occurred in some over the period of recording, and the various wave forms described by Lundberg 2 were observed as well as variations due to measures aimed at reducing intracranial pressure. Allowing for the intermittent nature of the pressure rises it was possible to recognise three groups according to the maximum pressures reached, excluding transient elevations due to coughing, movement, or other external factors (see accompanying table). The three groups are as follows: mm. Hg), those with relatively normal pressure (<20 those with a moderate elevation of pressure (2040 mm. Hg), and those with pronounced elevations mm. Hg). Examples of the pressure of pressure (>40 patterns in these groups are shown in fig. 1. In the normal-pressure group (group I) 5 out of 9 patients died. All 9 had been rendered immediately unconscious at the time of injury and showed the clinical syndrome commonly ascribed to primary brain-stem injury, although in those coming to necropsy no definite brain-stem damage was found. Group 11, with moderate pressure elevations, showed

patients

Fig. 4-Comparison of the effects of (A) mannitol and (B) ventricular C.S.F. aspiration on V.F.P. in a patient, aged 15 years, 5 days after head injury.

variety of clinical pictures, some cases being clinically indistinguishable from those in group I and others a

from those in group III; of 11 cases in this group 6 died. Only 1 of the 12 patients in the high-pressure group (group III) has made a satisfactory recovery; 3 remain in coma and the rest have died. Of this group, 6 were recorded as having talked at some time after their injury and before their clinical deterioration, and only 1 of these had an intracranial haematoma. Preliminary neuropathological studies in this group suggest a relatively high incidence of cerebral

infarction.

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

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 validity of this definition, but there is no doubt that the relationship between V.F.P. and s.A.P. is of critical significance. Since rising intracranial pressure may evoke a rise in s.A.P. the effect of a given level of intracranial pressure on perfusion pressure can be judged only if these two parameters are measured simultaneously. In fact we have found that these two pressures are very inconstantly related to each other. In some cases an increase in v.F.P. has been associated with an increase in s.A.P., in others with no alteration in s.A.P., and in yet others with a fall in s.A.P. Indeed all three such situations have been seen in one patient over a period of twenty minutes (fig. 2). Failure of S.A.P. to respond to a prolonged elevation of V.F.P. is shown in fig. 3. 3 cases had periods of a zero or negative perfusion pressure (by the above definition); and 2 of these deteriorated rapidly and died after such an episode, while the 3rd, who showed a presumed failure of perfusion for a period of 45 minutes (fig. 3), remains unconscious some three months after injury. In addition a situation

435 vasomotor paralysis as described by Langfitt et al.5 following experimental head injury in animals has been seen in patients in whom the intracranial pressure

of

passively follows

the

S.A.P.

Methods of Control The 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 individual case could be assessed. In certain situations mannitol was extremly effective, but in other situations, particularly with prolonged and pronounced elevations of V.F.P., it had no significant effect (fig. 4A). The rebound effect following mannitol was not obvious, but repeated doses tended to become progressively less effective. Both withdrawal of ventricular c.s.F. and hyperventilation proved very effective in lowering raised intracranial pressure (fig. 4B). In one case repeated aspiration of c.s.F. was the only effective means of controlling the raised pressure. Indeed when the pressure is considerably raised there may be a striking difference in the efficacy of c.s.F. drainage and of mannitol during episodes of high pressure. The effect of bony decompression was sometimes shortlived, and the v.F.P. could return to extremely high 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 of brain damage, as a basis for prognosis, and as a guide to management, has not been satisfactorily achieved. Certain patients following severe head injury show

the clinical syndrome classically ascribed to primary brain-stem injury, the salient features of which include immediate and deep unconsciousness, decerebrate rigidity, abnormalities of respiratory rhythm, Some and disturbances of autonomic function. patients with this syndrome have been found, in the present study, to have a relatively normal intracranial pressure over a prolonged period of recording (up to 10 days after injury). On the other hand, some patients with an apparently identical neurological picture may have quite pronounced elevation of intracranial pressure. It is well established that secondary brainstem lesions with corresponding physical signs may occur as a sequel to raised intracranial pressure 6; but in some of our patients with the classical picture and raised intracranial pressure there has been no temporal sequence which would allow the assumption that the brain-stem damage was secondary, and these particular cases would therefore fall into the category of primary brain-stem injury. Thus to describe a particular case as having a primary brain-stem injury is no reliable guide to the presence or absence of raised 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 observations and early animal experiments 7and accords with the more recently understood connection between the brain-stem reticular system and the maintenance of consciousness.9 The nature and situation of the

lesions in this type of injury have not, however, been definitely established. The pathological studies of Strich 10,11 have demonstrated a diffuse lesion of the subcortical white matter; on the basis of a burr-hole in one case, and the absence of post-mortem signs of increased pressure in others, she has suggested that this type of lesion is not associated with raised intracranial pressure. Using the present method we are hoping to identify with greater certainty those cases where intracranial pressure does remain normal after severe head injury and to correlate the clinical and pathological findings in this important group. On the other hand it is clear that, excluding those who develop a space-occupying haematoma, do develop a pronounced and progressive rise in intracranial pressure, and in our experience the majority of these have succumbed within the first few days after injury (see table). In the present study such cases had a relatively less severe neurological deficit at the time of initial examination, in that they made some verbal response, only to undergo subsequent clinical deterioration associated with uncontrolled intracranial hypertension. In such situations of raised pressure the level of perfusion pressure is probably of greater significance than the level of intracranial pressure alone. The early studies of Cushing 12 established a relationship between rising intracranial pressure and S.A.P. which has been widely accepted and which may be regarded as a mechanism helping to maintain an adequate perfusion pressure. The present results, however, confirm the views of other workers that the relationship between intracranial pressure and S.A.P. is very variable.13,14 Whether or not a certain level of intracranial pressure will threaten the cerebral circulation depends on what is happening to the s.A.P. at the same time. The effect of alterations in perfusion pressure on the cerebral circulation is probably the most important factor in determining the degree of secondary brain damage caused by raised intracranial pressure following head injury. Previous studies have shown that raised intracranial pressure may produce a fall in cerebral blood-flow 15,16; more recently Greenfield and Tindall,14 measuring intemal-carotid-artery flow, showed a reduction to 25% of the original level when intracranial pressure levels reached 70 mm. Hg. In addition Lundberg et aU? ,18 have shown a fall in cerebral blood-flow associated with the plateau waves of increased intracranial pressure together with a subsequent increase in cerebral blood-volume during such

patients some

waves.

The precise relationship between perfusion pressure, rather than intracranial pressure, and the cerebral circulation has not yet been investigated clinically. Experimental studies in this Institute have shown that, once the perfusion pressure falls below 30-40 mm. Hg there is a serious reduction in cerebral blood-flow, 19 Pathological studies in rhesus monkeys have shown widespread neuronal necrosis following episodes of low perfusion pressure due to arterial hypotension.2O In patients selective involvement of the boundary zones between major arterial territories has followed such episodes of low perfusion pressure,21 and similar lesions have been identified in some of the cases in

436 in in the present study.22 Further clinical and neuropathological studies are being directed towards the significance of this relationship, both after head injury and in other patients with raised intracranial pressure in whom perfusion pressure has been

THE FIST AS AN EXTERNAL CARDIAC PACEMAKER

group

JOHN B. WILD JOHN D. GROVER

monitored. In dealing

clinically with raised intracranial pressure or falling perfusion pressure following head injury there is no doubt that continuous monitoring of both V.F.P. and s.A.P. provides the most sensitive guide to the effectiveness of the therapeutic measures employed. When the intracranial pressure/volume curve enters the steeply rising phase 23 immediate measures aimed at reducing the volume of one of the components of the intracranial compartment may be called for. In this situation mannitol may fail to prove effective. Withdrawal of ventricular c.s., seems likely to be the most useful method, although induced hypocapnia produced by controlled hyperventilation may also be

Permanente

Summary

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

In

three patients asystole the hearts

regimen centred on the combined use of hyperventilation, mannitol, and ventricular drainage, in conjunction with continuous monitoring of V.F.P. and s.A.P. may reduce the high mortality and morbidity of those patients with head injuries who show a progressive rise in intracranial pressure in the absence of any surgically correctable expanding lesion. The value of c.s.F. aspiration in an acutely developing pressure situation is

a

cogent argument for

a

method of

monitoring which involves ventricular catheterisation rather than sensors placed on the surface of the brain. 1. H. J. and J. A. J. held research fellowships financed by the National Fund for Research into Crippling Diseases. Mr. J. O. Rowan, regional department of clinical physics and bio-engineering, Glasgow, gave invaluable advice in the development of the method. 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 of patients under their care. Requests for reprints should be addressed to B. J., University Department of Neurosurgery, Institute of Neurological Sciences, Killearn Hospital, Glasgow. REFERENCES 1. 2. 3. 4. 5.

6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Guillaume, J., Janny, P. Presse mid. 1951, 59, 953. Lundberg, N. Acta psychiat. neurol. scand. 1960, 36, suppl. Lundberg, N., Troupp, H., Lorin, N. J. Neurosurg. 1965, 22,

149. 581.

Zwetnow, N. Scand. J. Lab. clin. Invest. 1968, suppl. 102. Langfitt, T. W., Weinstein, J. O., Kassell, N. F. Neurology, Minneap. 1965, 15, 622. Johnson, R. T., Yates, P. O. Acta radiol. 1956, 46, 242. Sherrington, C. S. J. Physiol., Lond. 1898, 22, 319. Walshe, F. M. R. Proc. R. Soc. Med. 1922, 15, 41. Moruzzi, G., Magoun, H. W. EEG clin. Neurophysiol. 1949, 1, 455. Strich, S. J. J. Neurol. Psychiat. 1956, 19, 163. Strich, S. J. Lancet, 1961, ii, 443. Cushing, H. Am. J. med. Sci. 1902, 124, 375. Browder, J., Meyers, R. Am. J. Surg. 1936, 31, 403. Greenfield, J. C., Tindall, G. T. J. clin. Invest. 1965, 44, 1343. Kety, S. S., Shenkin, H. A., Schmidt, C. F. ibid. 1948, 27, 493. Noell, W., Schneider, M. Arch. Psychiat. NervKrankh. 1948, 180, 713.

17. 18. 19.

20. 21. 22.

23.

Lundberg, N., Cronqvist, S., Kjallquist, A. Prog. Brain Res. 1968, 30, 70. Risberg, J., Lundberg, N., Ingvar, D. H. J. Neurosurg. 1969, 31, 303. Rowan, J. O., Harper, A. M., Miller, J. D., Tedeschi, G., Jennett, W. B. J. Neurol. Neurosurg. Psychiat. (in the press). Brierley, J. W., Brown, A. W., Excell, B. J., Meldrum, B. S Brain Res., 1969, 13, 68. Adams, J. H., Brierley, J. R., Connor, R. C. R., Treip, C. S Brain, 1966, 89, 235. Adams, J. H. in Symposium on the Pathology of Trauma. J. clin Path. suppl. (in the press). Langfitt, T. W. Clin. Neurosurg. 1969, 16, 436.

ventricular

responded

to con-

tinuous rhythmical chest-pounding—in one case for more than 40 minutes. Each blow on the chest was followed by ventricular depolarisation and systole. Metabolic acidosis did not develop, and no precautions were needed to prevent it. This method might be tried as the first line of treatment for asystole in hospitals; and outside hospitals it seems to have a better chance of success than cardiac massage as a first-aid measure for cardiac arrest. Introduction

valuable. Thus a controlled

with

METABOLIC acidosis is one of the obstacles to recovery from cardiac standstill.1 When adequate amounts of intravenous sodium bicarbonate cannot be given to patients with cardiac standstill, owing either to ventricular fibrillation or to electrical inactivity, they die of metabolic acidosis despite effective cardiac massage and artificial respiration. There is no accepted simple first-aid measure which an untrained person can apply to help a victim of prolonged ventricular asystole. In the unlikely event that adequate artificial respiration and circulation can be established within five minutes to prevent brain damage, the patient, if he is to survive, must reach medical facilities within twenty minutes, unless his own ventricular contractions take over and prevent irreversible acidosis. Our experience with several patients suggests that in fact a simple first-aid measure could sustain life in many cases. Case 1

Case-records

A 60-year-old woman developed Adams-Stokes attacks after fracture of epicardial pacemaker leads which had been placed in March, 1968, for the treatment of complete heart-block. Before a temporary transvenous pacemaker could be inserted, ventricular fibrillation developed and

successfully accomplished. Several stopped but responded immediately to chest-pounding, which was continued periodically for about thirty minutes while a temporary transvenous pacemaker was inserted. Each episode of chest-pounding would last several minutes until her ideoventricular rhythm was resumed (no intravenous sodium bicarbonate was given). Unfortunately, no tracings were recorded. Her heart is now functioning well with a permanent transvenous pacemaker.

D.c.

depolarisation

was

times thereafter her ventricles

Case 2 An 83-year-old woman developed complete atrioventricular block and cardiac standstill three days after an acute myocardial infarction. Heart-pounding by the nurse in charge, without massage, maintained an adequate output while we failed to place a transvenous pacemaker on the ward, took her to the X-ray department, and finally succeeded in placing a pacemaker which paced her ventricles. She responded normally after the procedures, but the next day cerebral symptoms developed and she died.