Journal ofNeurology, Neurosurgery, and Psychiatry, 1978, 41, 834-839

Chronic subdural haematoma: a review of 114 cases

MALCOLM M. CAMERON

From the Department of Neurological Surgery, Salford Royal Hospital, Salford

S U M M A R Y One hundred and fourteen consecutive adult patients treated surgically for chronicsubdural haematoma are described and their clinical features presented in detail. The diagnosticinvestigations are evaluated and a regime of surgical management is described. The three mainmodes of clinical presentation and the diagnostic role of carotid angiography are emphasised. Itis suggested that the neurological state at the time of operation has no bearing on the prognosisand that, in particular, patients presenting in coma have a much better prognosis than might beexpected. The average follow-up period was two years and the longest 11 years.

The most widely accepted views on the aetiologyand evolution of chronic subdural haematomahave been well summarised recently (Araki, 1974;Sato and Suzuki, 1975). Aspects of the epidemi-ology, histology, and pathophysiology of thesehaematomas have been reported in several papers(Putnam and Cushing, 1925; Weir, 1971; Broder-sen and Gjerris, 1975; Fogelholm and Waltimo,1975). However, with the exception of two com-munications (McKissock et al., 1960; Loew andKivelitz, 1976), relatively little attention has beenpaid to the clinical presentation, diagnosticinvestigations, and prognosis.

Patients and methods

A 25 year retrospective review revealed 114 adultpatients shown at operation to have chronic sub-dural haematomas. Initially an attempt was madeto classify patients into either subacute or chronicgroups according to their histories. Those patientswith a history of symptoms or an interval fromknown head injury of less than three weeks wereconsidered subacute and those longer than threeweeks, chronic. Tables 1 and 2 show various dataof these two groups. However, in some patients thelength of history was uncertain, and in others norelevant history could be obtained, and it provedunhelpful, in terms of clinical presentation andprognosis, to attempt to maintain the separation.Therefore, it was decided that the finding at opera-tion of a black fluid surface collection over one or

Address for reprint requests: Department of Neurological SurgerySalford Royal Hospital, Chapel Street, Salford M60 9EP.Accepted 30 March 1978

Table 1 Some features of 114 patients with subduralhaematoma

Total patient group Subacute Chronic % of(114) (44) (70) total

Male 26 56 72Female 18 14 28Average age 56 56 -

History of head injury 32 40 63Fluctuation in symptoms or signs 7 21 24In coma by the time of surgery 12 3 13Bilateral haematomas evacuated 1 12 11

Table 2 Most comnmon clinical findings in 114patients with subdural haematoma

Clinicalfinding Subacute Chronic % oftotal

Hemiparesis (45 patients) 40ipsilateral to haematoma 11 7 16contralateral to haematoma 10 17 24

Personality or intellectual change 11 23 30Papilloedema (23 patients) 20

with headache and vomiting 1 6 6with hemiparesis 2 7 8with coma 4 3 6

Coma (15 patients) 12 3 13Unilateral pupillary dilatation 5 1 5Headache (48 patients)

with other neurological findings 38alone 5

both hemispheres would define that patient as achronic subdural haematoma case. The agedistribution of the patients is shown in Fig. 1.

AETIOLOGYA direct head injury was identified in 63% ofpatients (Table 3). Of the remaining 42 patients,six were known epileptics, four were documentedalcoholics, and two were receiving anticoagulant

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Chronic subdural haematoma: a review of 114 cases

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10

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10 20 30 40 50 60 70 80Age (yr)

Fig. 1 Age distribution of 114 patients with chronicsubdural haematoma. The youngest patient was16 years and the oldest 79 years.

Table 3 Probable precipitating factors

Precipitating factors CasesNumber %

Direct head injury 72 63Fall to the sitting position 3 2Epilepsy 6 5Alcoholism 4 3Anticoagulant therapy 2 2Severe sneezing 1 1Severe coughing 1 1Strain at heavy lifting 1 1Shunted hydrocephalus I INone identified 23 20

therapy. A fall to the sitting position, perhapsproducing indirect cerebral trauma, coincided withthe onset of symptoms in a further three patientsand, similarly, severe bouts of coughing and sneez-ing appeared to be precipitating factors in anothertwo patients. One further patient had had aventriculoatrial shunt inserted previously fornormal pressure hydrocephalus. No causative or

precipitating factors could be identified in theremaining 20% of patients.

SYMPTOMS AND SIGNSNinety-two per cent of patients fell into threegroups of symptomatology: hemiparesis, per-

sonality or intellectual change, and the featuresof raised intracranial pressure (Table 2). Some ofthese patients showed evidence of more than onegroup of symptoms but the majority signalled withonly one element. The remaining 8% of patientspresented either in coma with no reliable history,or with headache alone. Many patients had beenmistakenly diagnosed as having cerebrovasculardisease, psychiatric disorder, or brain tumour, andthose patients with a known history of head injury

were not diagnosed any sooner than those withoutthis alerting signal. The 13 patients who hadbilateral haematomas had an average duration ofsymptoms of 63 days (compared with 45 days forall 114 patients), and an average age of 63 years(compared with 56 years).

Hemiparesis was the most common abnormalneurological sign and it was contralateral to thehaematoma in 60% of patients, whereas unilateralpupillary dilatation (seen in six patients) wasalways on the side of the haematoma. Personalityor intellectual change was a more common pre-sentation than were the features of raised intra-cranial pressure. Twenty-three patients showedpapilloedema but only seven of these had theclassical triad of headache, vomiting, andpapilloedema.

Fifteen patients were in coma (no verbalresponse and no better than a flexion response inthe limbs to painful stimuli) by the time of opera-tion. They had an average age of 61 years, and 14of them had an average duration of symptoms ofonly 16 days. The remaining patient, a 35 year oldfemale with bilateral haematomas, had an un-usually long history of five months after a fallfrom a motor cycle. Twelve patients in this comagroup had had a head injury, and in four casesconsciousness had been lost for longer than twohours.

Six patients had a fracture on plain skull radio-graphs, and in each of them the haematoma wascontralateral to the fracture. Of these patients,three presented with headache and dysphasia, onewith headache and third nerve palsy, one withpersonality disturbance, and one with coma. Threeof these patients had lost consciousness at the timeof their head injury and two of them died afteroperation.

Less than half of all patients (43%) experiencedheadache and in 5% of patients it was the onlysymptom.

INVESTIGATIONSEighty-two per cent of patients had plain skullradiographs available for review and six skullfractures were found. Ten patients had radioactivetechnetium brain scans, and three of these ex-aminations were falsely negative. Forty-three percent of patients had been investigated by lumbarpuncture before admission to the NeurosurgicalDepartment, and review of this group showed nocorrelation between the CSF protein content ormanometry and the symptoms or signs of raisedintracranial pressure. No patient appeared todeteriorate within 12 hours of lumbar puncture.Computed tomography (CT) was available for only

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the last three patients in this series. In two of themunilateral hypodense haematomas were found. Theother showed no abnormality, but repeat CT a

week later showed bilateral hypodense collections.One hundred and two patients were examined

by bilateral carotid angiography and the correctdiagnosis was revealed in all but one. Of the 12patients who did not have angiography, six hadextreme clinical states and were submitted directlyto surgery, four had clearly positive technetiumscans, one had air encephalography, and one

ventriculography. The films in these last twopatients were mistakenly interpreted as showingfrontal tumour, and the subdural haematomaswere found at craniotomy.

TREATMENT

One hundred and twelve patients had similarsurgical management. Two burrholes were madeover each haematoma, and complete evacuationwas aided by saline irrigation. If the brain failedto achieve satisfactory spontaneous re-expansion,isotonic saline was injected by lumbar puncturewith the dura still open. This was considerednecessary in 40% of patients, and the volume ofsaline injected ranged from 40 to 350 ml. Twopatients had elective craniotomy for presumedfrontal tumour after air contrast examination.Three patients required burrhole reopening forevacuation of further haematoma.

Results

Table 4 shows the results of surgical treatmentassessed by patient review in the outpatient clinicand by spouse interview. The average follow-upperiod was two years and the longest 11 years.Detailed psychometric testing was not performed.One hundred and nine patients (96%) were alive

at the average follow-up time of two years. Onehundred and one of these patients had made a

complete recovery within six weeks of surgery, 83of them doing so within one week. The remainingeight survivors (7%) were unimproved by evacua-tion of their haematomas (Table 5), and the fivepatients who died are shown in Table 6. No patientremained in a deteriorated state after operation.

Table 4 Results of surgical treatment

Result CasesNumber %

Complete recoverywithin seven days of surgery 83 73within six weeks of surgery 101 89

Unimproved at average interval of three monthsfrom surgery 8 7

Survived in a deteriorated state 0 0

Died 5 4

Malcolm M. Cameron

Table 5 Details of the eight unimproved survivors

Sex Age History Clinical Clinicalfeatures at three(yr) of trauma presentation months from surgery

F 30 Yes Dysphasia and Dysphasiaheadache

M 43 Yes Progressive Hemiparesishemiparesis

M 44 Yes Progressive Personality disorderhemiparesis

M 55 Yes Coma Severe personality disorderM 66 Yes Hemiparesis Personality disorderF 68 Yes Progressive Hemiparesis

hemiparesisM 70 Yes Dementia DementiaM 71 Yes Dysphasia and Dysphasia

diplopia

COMPLICATIONS OF OPERATIONOne burrhole became infected, resulting in a sub-dural abscess, but there was a good recovery atthree months, and one 34 year old male requiredCSF shunting for communicating hydrocephalus10 years after haematoma evacuation.

All of the six known epileptics in this series hadan increase in fit frequency after operation. Oneother patient developed early postoperative seizuresconfined to the first week, and two further patientsdeveloped generalised seizures at one and 10 yearsrespectively. Another four patients, not previouslyknown to be epileptic, experienced preoperativeseizures after the onset of their symptoms but noneof them had epilepsy after operation. Thus, 13patients (11%) experienced generalised seizures atsome stage. None of these patients died.

Discussion

Putnam and Cushing (1925) were the first to drawattention to the difficulty of diagnosis in chronicsubdural haematoma, and they emphasised thevarying symptomatology. The present review

Table 6 Details of the five patients who died

Sex Age History Clinical Findings at Post-(yr) oftrauma presentation necropsy operative

day ofdeath

F 52 No Personality Internal 1change capsule

haemorrhageM 67 Yes Raised intra- Myocardial 8

cranial pressure infarctionF 69 No Personality Massive 9

change pulmonaryembolus

F 70 Yes Raised intra- Massive 0*

cranial pressure pulmonaryembolus

M 71 Yes Hemiparesis Acute 4pulmonaryoedema

*The pulmonary embolus on day 0 occurred in theatre as the haema-toma was being evacuated.

Chronic subdural haematoma: a review of 114 cases

shows that 92% of patients had an approximatelyequal incidence of three modes of presentation:hemiparesis, personality or intellectual change, andthe features of raised intracranial pressure.Fluctuation in the conscious level or other neuro-logical signs was not a prominent feature in thisseries and was seen in only 24% of patients.

Bilateral carotid angiography under generalanaesthesia provided the correct diagnosis in allbut one of the 102 patients so examined (Figs. 2and 3). The exception was early in the series, and

the films were of poor quality. Ten patients hadtechnetium brain scans and falsely negative resultswere seen in three in whom subsequent carotidangiography revealed subdural haematomas. Thenumber of patients who showed falsely positivetechnetium scans and who were submitted to burr-hole exploration with negative results is notknown. Of the three patients in this seriesexamined by CT, two showed unilateral hypodensecollections and the other initially showed no abnor-mality. This inability of CT to show certain sub-

Fig. 2 Right carotid angiogram, venousphase, showing deep surface collectionand midline venous shift. Positivepressure lumbar puncture was requiredat surgery.

Fig. 3 Left carotid angiogram showing asurface collection and no significantmidline arterial shift. Right carotidangiography showed a similar sizedhaematoma on the right. Positivepressure lumbar puncture was notrequired at surgery.

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dural haematomas was first reported by Ambrose(1973) and further discussed by Scotti et al. (1977).A variety of different treatments for chronic

subdural haematoma have been advocated.Craniotomy and membranectomy were considerednecessary by Robinson (1955), while Svien andGelety (1964) suggested that burrhole evacuationof the liquid haematoma alone was superior tocraniotomy. Tabaddor and Shulman (1977) com-pared these two surgical treatments with twist-drillcraniostomy and closed-system drainage in a totalof 71 patients, and demonstrated the last methodto produce the best results. Non-surgical treatmentwith bedrest and mannitol therapy was advocatedby Bender and Christoff (1974) and by Suzuki(1974) but debated by Gjerris and Schmidt (1974).

In the present series 112 patients had burrholeevacuation as the treatment of choice. The remain-ing two patients had craniotomy for supposedfrontal tumour. The results in this series, comparedwith those in some other published series, areshown in Table 7.Apart from the three patients who were re-

turned to theatre for burrhole reopening andevacuation of further haematoma, none of the109 survivors deteriorated postoperatively. Atoperation it was considered necessary, in 40% ofpatients, to inject saline by lumbar puncture toencourage the brain to come up to the dura. Thismay have contributed to the absence of that post-operative condition often called the low pressurestate.There was no significant difference in the

average age of patients in each of the three maingroups of clinical presentation: hemiparesis, 56years; personality or intellectual change, 59 years;features of raised intracranial pressure, 54 years.The remaining 11 patients, who presented withheadache alone or in coma with no historyavailable, had an average age of 55 years.No prognostic criteria emerged from this review,

and the neurological state of the patient at thetime of surgery seemed to have no bearing on the

Table 7 Outcome from surgical treatment of patientswith chronic subdural haematoma in some publishedseries

Author Total Unimproved Deathsnumber or worseofcases

McKissock et al. (1960) 307 35 31Plum and Posner (1973) 73 * 14 'Fogelholm et al. (1975) 109 * 1Tabaddor and Shulman 71 18 15(1977)Present author (1978) 114 8 5

*Information not given in article quoted.

Malcolm M. Cameron

prognosis. Of the 15 patients in coma at the timeof surgery, one died, one was unimproved, and 13made complete recoveries. Twelve patients in thiscoma group had a history of head injury, and alleight unimproved survivors (average age 56 years)also had a history of head injury.

Conclusion

The outcome from surgical treatment by burrholeevacuation, for patients with chronic subduralhaematoma, is uninfluenced by their age, mode ofpresentation, or neurological state at the time ofsurgery. Surgical treatment by simple burrholeevacuation, plus positive pressure saline lumbarpuncture in some patients, can give a very highrate of complete recovery to normal life.

References

Ambrose, J. (1973). Computerised transverse axialscanning (tomography). Part 2. Clinical application.British Journal of Radiology, 46, 1023-1047.

Araki, C. (1974). Recent Progress in NeurologicalSurgery, p. 14. Excerpta Medica: Amsterdam.American Elsevier: New York.

Bender, M. B., and Christoff, N. (1974). Non-surgicaltreatment of subdural haematomas. Archives ofNeurology (Chicago), 31, 73-79.

Brodersen, P., and Gjerris, F. (1975). Regional cere-bral blood flow in patients with chronic subduralhaematomas. A cta Neurologica Scandinavica, 51,233-239.

Fogelholm, R., and Waltimo, 0. (1975). Epidemiologyof chronic subdural haematoma. A cta Neuro-chirurgica (Wien), 32, 247-250.

Fogelholm, R., Heiskanen, O., and Waltimo, 0. (1975).Chronic subdural haematoma in adults. Influenceof patients age on symptoms signs and thickness ofhaematoma. Journal of Neurosurgery, 42, 43-46.

Gjerris, F., and Schmidt, K. (1974). Chronic subduralhaematoma. Surgery or mannitol treatment. Journalof Neurology, 40, 639-642.

Loew, F., and Kivelitz, R. (1976). Subdural Haema-toma. In Handbook of Clinical Neurology. Vol. 24,part 2, p. 297. Edited by P. J. Vinken and G. W.Bruyn. North-Holland Publishing Company:Amsterdam.

McKissock, W., Richardson, A., and Bloom, W. H.(1960). Subdural haematoma. A review of 389 cases.Lancet, 1, 1365-1369.

Plum, F., and Posner, B. J. (1973). Diagnosis ofStupor and Coma. F. A. Davis Company:Philadelphia.

Putman, T. J., and Cushing, H. (1925). Chronic sub-dural haematoma. Its pathology, its relation topachymeningitis haemorrhagica and its surgicaltreatment. Archives of Surgery, 11, 329-393.

Robinson, R. G. (1955). The treatment of subacuteand chronic subdural haematomas. British MedicalJournal, 1, 21-22.

Chronic subdural haematoma: a review of 114 cases

Sato, S., and Suzuki, J. (1975). Ultrastructuralobservations of the capsule of chronic subduralhaematoma in various clinical states. Journal ofNeurosurgery, 43, 569-578.

Scotti, G., Terbrugge, K., Melancon, D., andBelanger, G. (1977). Evaluation of the age of sub-dural haematomas by computerised tomography.Journal of Neurosurgery, 47, 311-315.

Suzuki, J. (1974). Mannitol treatment of subduralhaematomas. Journal of Neurosurgery, 41, 785-786.

Svien, H. J., and Gelety, J. E. (1964). On the surgical

management of encapsulated subdural haematoma.A comparison of the results of membranectomy andsimple evacuation. Journal of Neurosurgery, 21,172-177.

Tabaddor, K., and Shulman, K. (1977). Definitivetreatment of chronic subdural haematoma by twist-drill craniostomy and closed-system drainage.Journal of Neurosurgery, 46, 220-226.

Weir, B. (1971). The osmolality of subdural haematomafluid. Journal of Neurosurgery, 34, 528-533.

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