The Editor,
Sir,
We report the development of an intracranial subdural haematoma (ISH) in a 33-year old male patient who underwent an epidural procedure without evidence of dural puncture, after obtaining his written consent.
The patient presented for surgical excision of a gastrointestinal stromal tumour. He had no history of trauma, headaches or neurological disorders. His coagulation profile was normal. Preoperatively, a thoracic epidural catheter was placed uneventfully and the patient received general anaesthesia under intermittent positive pressure mechanical ventilation (IPPV). Postoperatively, the epidural catheter was used for 72-hour analgesia. Only once did the patient report a mild, diffuse headache which was relieved with paracetamol. After being discharged, he developed an intense, postural headache, and bilateral sixth cranial nerve palsy (esophoria). Amagnetic resonance imaging (MRI) revealed diffuse meningeal thickening with gadolinium enhancement, consistent with intracranial hypotension. The patient preferred conservative treatment over blood patch and his symptoms resolved completely. Twenty days later, he returned to hospital with a severe, persistent headache, not clearly postural, accompanied by nausea/vomiting. He gradually became drowsy and confused, and an urgent MRI revealed a large left ISH (Figure).
Figure
Cranial magnetic resonance imaging scan on the 45th postoperative day showing a 2.0 cm thick left-sided subacute subdural haematoma with 1.7 cm right midline shift.
The haematoma was surgically evacuated via parietal burr holes under local anaesthesia. The patient had a good outcome without neurological deficits.
Intracranial subdural haematoma is associated with cerebrospinal fluid (CSF) leakage and consequent intracranial hypotension; the stretching of bridging veins, along with a compensatory intracranial hyperaemia may lead to rupture of these fragile vessels during their intrasubdural course (1). Development of ISHs after neuraxial techniques is extremely rare, mainly reported in parturients (1). During labour, prolonged Valsalva manoeuvre may increase the CSF pressure and leakage through a dural hole (2). Similarly, IPPV may raise the intrathecal pressure via transmission of intrathoracic pressures through the intervertebral foramina.
In the present case, a pre-existing low CSF pressure (primary intracranial hypotension) could possibly explain the absence of obvious CSF outflow (3). Intracranial subdural haematoma development due to rupture of aneurysm/arteriovenous malformation seems unlikely; no vascular abnormalities were detected on the MRI, while such ruptures usually result in subarachnoid and intraparenchymal haemorrhage (4).
Although it seems reasonable that blood patching would prevent postdural puncture ISHs, they may still develop (5). Moreover, blood patch may produce intracranial hypertension in patients with undiagnosed ISH.
Warning signs of ISH are changes of postdural puncture headache characteristics; it becomes non-postural, more intense and resistant to analgesics (1). Further symptomatology includes nausea/vomiting, vision abnormalities, motor/sensory dysfunction, confusion/disorientation/drowsiness, seizures and coma (1). Diagnosis is based on computed tomography scan with contrast media or cerebral MRI (4). Regarding management, ISHs under 5 mm may resolve spontaneously (1), while large haematomas producing serious neurological symptoms require prompt evacuation.
In conclusion, after neuraxial techniques, the development of intense, worsening non-postural headache resistant to analgesics requires further investigation to exclude serious intracranial pathology.
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