Journal of

Neurology

J Neurol (1987) 234 : 254-256

© Springer-Verlag 1987

Successful treatment of acute subdural haematoma associated
with severe bleeding disorder
P. Verlooy x, B. J. M. Lamers 2, G.J. de Haan 1, and L. A. Noach 3
Departments of 1Neurology, 2Neurosurgery, and 3Internal Medicine, Academic Medical Centre, Meibergdreef 9, 1105 AZ-Amsterdam,
The Netherlands

Summary. A 76-year-old man suffering from myelofibrosis with
thrombocytopenia sustained an acute subdural haematoma
with severe neurological deficit. He was treated initially by
bedrest and dexamethasone. Craniotomy was contraindicated
because his bleeding time exceeded 20 min in spite of multiple
infusions of platelet concentrate. After 3 weeks his condition
deteriorated with increase of the fluid collection shown by CT.
Partial drainage of the haematoma by subdural puncture with
a 22-gauge spinal needle resulted in complete recovery from
the neurological deficit and complete resorption of the effusion. The case shows that it is possible to avoid craniotomy in
the acute phase of a subdural haematoma in patients with
bleeding disorders and that it may be advantageous to use
needle evacuation instead of burr-hole drainage in the chronic
phase.

Key words: Subdural haematoma - Thrombocytopenia

Introduction
When severe neurological deficit exists in patients with subdural haematoma, craniotomy is the treatment of choice during the first 2 or 3 weeks after injury, because most clots are
solid and cannot be satisfactorily evacuated through burrholes [3, 7, 12]. Slow continuous external drainage of the subdural collection through a burr-hole or twist-drill opening is
suitable from 3 weeks after the injury, when the subdural collection has liquefied [8]. Unfortunately these methods are not
feasible in the presence of a bleeding disorder which cannot be
improved by replacement therapy [4, 13, 14]. Since bleeding
disorders (particularly iatrogenic thrombocytopenia caused by
cytostatic or radiation treatment) have become common nowadays, a search for safer treatment of subdural haematoma is
important. There are a few reports of successful non-surgical
treatment of acute (defined as those presenting in the first 3
days after injury) and chronic (from 2 or 3 weeks after injury)
subdural haematoma with severe neurological deficit [1, 2,
111 .
Successful results have also been reported from a relatively
atraumatic and simple bedside technique for partial evacuation of chronic subdural haematoma by needle trephination
[9]. With this method the cranium is perforated after shaving
and surgical preparation with twisting movements of an 18- or
Offprint requests to: P. Verlooy, Onze Lieve Vrouwe Gasthuis, Department of Neurology, 1e Oosterparkstraat 179, 1091 HA Amsterdam, The Netherlands

22-gauge spinal needle. Once the skull is penetrated, the perforating needle is removed, a fresh needle inserted into the
subdural space and the haematoma slowly aspirated. The following case illustrates that successful management of a subdural haematoma in the presence of a severe uncorrectable
haemostatic disorder is possible by a combination of non-surgical treatment in the first 3 weeks and subdural puncture in
the chronic phase.

Case report
A 76-year-old man, with myelofibrosis, anaemia and thrombocytopenia, who was being treated with 250 mg pyridoxine
daily and regular blood transfusions, was admitted with
haematuria and renal colic. Intravenous pyelography showed
obstruction of the left proximal ureter probably due to uric
acid stones or blood clots. Treatment consisted of allopurinol
and intravenous hydration. On the 24th hospital day he fell
out of bed without apparent injury to his head. There was no
loss of consciousness. A minimal right hemiparesis was present. Speech was fluent and dysnomic with moderate impairment of comprehension but sparing of repetition. A C T scan
showed a left-sided 15-mm-thick frontopartietal subdural
haematoma without midline shift. The platelet count was less
than 10 x 109/1 with normal parameters for plasma coagulation (activated partial thromboplastin time 39 s; prothrombin
time 12.8s, control 12.4s). Bleeding time was not investigated.
The patient was treated with bedrest and 8 units of platelet
concentrate every 8h. •
On the 2nd day his condition was complicated by epileptic
seizures of the right arm and leg, which were treated with
intravenous phenytoin and later clonazepam, but seizure activity continued intermittently until the 8th day. There was
severe progression of the dysphasia and the hemiparesis became complete. This was accompanied by an increase in volume of the hyperdense fluid collection on CT scan. In spite of
the platelet transfusions, the bleeding time exceeded 20 min,
so that craniotomy would have been dangerous. Platelet
counts varied from 16 to 34 x 109/1 during treatment. From
the 8th day 5 mg dexamethasone was given twice daily. From
then on there were no more focal seizures and both dysphasia
and hemiparesis improved, although marked neurological deficit persisted. After the 16th day the symptoms increased
again and the patient became drowsy.
From the 18th day the left pupil was sometimes 2ram
larger than the right. The fluid collection on CT scan was in-

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Fig. 1. CT scan on 23rd day after injury showing a 45-mm, mainly hypodense subdural haematoma with severe compression of the left ventricle
Fig. 2. CT scan on 27th day after injury (2 days after puncture) showing a decreased subdural fluid collection and air in the punctured area
Fig. 3. CT scan 5 months after injury

creased again with a mixed hyper- and hypodense appearance.
Mannitol was given daily. On the 25th day the patient opened
his eyes only after he was called loudly, uttering some unintelligible sounds. The right hemiparesis was complete. There was
markedly increased displacement of the ventricular system on
CT scan, by a collection of largely hypodense fluid (Fig. 1).
Because of the progressive neurological deficit and impairment of consciousness, evacuation of the haematoma was required. Since the effusion on CT scan was considered to be
liquefied, a percutaneous subdural puncture was performed
with a 22-gauge spinal needle [9]. The platelet count was 20 ×
109/1 but the puncture was performed with a simultaneous
platelet transfusion.
Forty millilitres of dark liquefied haematoma, initially
under pressure, was aspirated. Neither complete evacuation
nor extensive irrigation of the subdural space was attempted.
Dexamethasone and mannitol were stopped. Full consciousness was regained almost immediately and the paresis subsided in a few weeks. A C T scan 2 days after the puncture confirmed a marked reduction of the effusion (Fig. 2). No complications were observed. After 3 months only a pronation sign
of the right hand and minimal paresis of the right leg were present. A CT scan after 5 months revealed only a very small
hypodense zone (Fig. 3). After 7 months the patient had to be
readmitted because of severe haematological complications of
the myelofibrosis and died within a few days. On post-mortem
examination a small well-organized membrane consisting or
several layers and containing some fluid was seen, covering
the left parietal-temporal lobes, adherent to the cortex cerebri
but not to the dura.

pair neomembrane formation, which possibly could decrease
subsequent enlargement of the subdural haematoma [6]. In
Our case steroids seemed efficacious initially but did not prevent subsequent enlargement of the subdural fluid collection.
Ther osmotic pressure theory has led to the use of osmotic
agents, as reported by Bender and Christoff [2] and Suzuki
and Takaku [11]. The only clinical trial comparing the effect of
mannitol treatment and surgical intervention in chronic subdural
haematoma was discontinued after the first seven patients did
not respond to mannitol [5]. In our case mannitol was given
for only a few days, without clear benefit.
The changes in density of the subdural fluid collection on
CT scan during its evolution accord with the findings of Scotti
et al. [10]. During the acute phase there was no clear correlation between the size of the subdural fluid collection and the
neurological deficit, but the seizure activity may have worsened
the symptoms temporarily. In the subacute and chronic phase
the neurological deficit correlated with the size of the fluid
collection on CT scan. Though evacuation could only be partial and irrigation was not performed, almost complete resorption eventually took place, as in the five cases of Negr6n et al.
[91.
Needle puncture, being less traumatic than burr-hole
trephination, is possibly advantageous in patients with severe
bleeding disorder, but of course a much larger series would be
necessary to prove this point.

Discussion

References

The severely prolonged bleeding time could not be improved
by platelet transfusions probably because of sequestration of
platelets by the enlarged spleen. Therefore neurosurgical intervention (burr-holes or craniotomy) during the first 3 weeks
had to be avoided despite the severe neurological deficit. The
therapeutic effect of steroids in the treatment of subdural
haematoma has not been proven by means of a controlled
clinical trial but Bender and Christoff [2] reported good resuits. There is some experimental evidence that steroids im-

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Acknowledgements. The authors thank H.v. Crevel for constructive
remarks. T. C. T. M. Bots performed the autopsy.

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Received January, 30, 1986 /
Received in revised form September 15, 1986 /
Accepted September 29, 1986