|LETTERS TO EDITOR
|Year : 2015 | Volume
| Issue : 3 | Page : 201-202
Acute onset of intracranial subdural haematoma 2 days after spinal anaesthesia
Sanjeev Kumar1, Mukund Prasad2, Ravinder Kumar2
1 Department of Anaesthesia, Paras HMRI Hospital, Patna, Bihar, India
2 Department of Neurosurgery, Paras HMRI Hospital, Patna, Bihar, India
|Date of Web Publication||12-Mar-2015|
Saheed Marg, Road No. B3, Mourya Vihar, Transport Nagar, Patna - 800 026, Bihar
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kumar S, Prasad M, Kumar R. Acute onset of intracranial subdural haematoma 2 days after spinal anaesthesia. Indian J Anaesth 2015;59:201-2
|How to cite this URL:|
Kumar S, Prasad M, Kumar R. Acute onset of intracranial subdural haematoma 2 days after spinal anaesthesia. Indian J Anaesth [serial online] 2015 [cited 2021 Jun 19];59:201-2. Available from: https://www.ijaweb.org/text.asp?2015/59/3/201/153050
Spinal anaesthesia (SA) is widely used for surgeries but serious complication such as intracranial subdural haemorrhage (ICSH) can rarely occur.  The incidence of ICSH after SA has been reported to be 1 in 500, 000.  During literature review, 35 cases were identified, and most had a chronic course and associated with post-dural puncture headache (PDPH).  We report a case of acute onset of ICSH 2 days after SA with no history of trauma.
The 21-year-old young male presented with fistula in ano, and was scheduled for an elective surgery in our hospital. Patient belonged to American Society of Anaesthesiologists physical status 1 with no comorbid conditions. He had no history of any pre-existing brain pathology.
The anaesthetic procedure was completed with ease in a single attempt with lumbar puncture at the L 2/3 level using 25-gauge Quincke's needle; there was free flow of clear cerebrospinal fluid (CSF) and 0.5% heavy bupivacaine was injected. T 12 level of block was achieved, and surgery completed uneventfully. On 2 nd post-operative day patient suddenly developed severe headache, and 2 h later he developed generalised tonic clonic seizure and became unconscious. Patient was immediately intubated and administered intravenous phenytoin and mannitol as advised by neurologist. Computed tomography (CT) scan was obtained, which showed right subdural haematoma (SDH) with midline shift of 1.3 cm [Figure 1]. Patient was shifted to operation theatre where craniotomy with evacuation of haematoma was done. Post-craniotomy, patient was shifted to neuro-intensive care unit and after 48 h of ventilator support, was extubated. On the third post-operative day, non-contrast CT was done, which showed complete resolution of SDH [Figure 2]. Post-operatively during his stay in hospital patient remained apathetic and aphasic for which psychiatrist opinion was taken, and he advised thyroid function tests. He was found to be hypothyroid and hence he was put on the tablet thyroxine 100 μg once daily. On 7 th post-operative day, sutures were removed, and wound was found to be healthy. On discharge, patient was conscious with left residual hemiparesis. He was discharged on Ryle's tube feed and indwelling Foley's catheter. Fifteen days later, his left residual hemiparesis resolved and his Glasgow coma scale became 15. Sixty days later patient came back to our hospital for duraplasty, which was done, and he was discharged after 3 days.
|Figure 2: Computed tomography scan after evacuation of right acute subdural haematoma|
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Very few data exist about the consequences of SA-induced ICSH. As symptomatology frequently mimic PDPH, a number of them are frequently missed.  According to the literature, its prevalence ranges between 1/500,000 and 1/1,000,000. , A Swedish retrospective study published in 2004 and covering a decade (1990-1999) mentions 127 cases of neurological complications following SA, of whom the risk was assessed to be 1/20,000-1/30,000, among which two cases of SA-ICSH were reported. 
A French study reported 4 such cases of SA-ICSH over a period of 9 years in a medium size centre. 
The physiopathogenic mechanisms of SA-ICSH are poorly understood. A leak of CSF at the level of arachnoid tear probably induces a lowering of intraspinal and intracranial pressure. The resulting dynamic alteration of CSF flow leads to a relative ventricular collapse and a rostrocaudal movement of central nervous system. As a consequence sensitive meningeal structures or meningeal pain sensors, cranial nerve and bridging-veins that link the encephalon to the meninges and drain into the dural sinuses are stretched.  Electron microscopic data on human bridging veins show thin walls of variable thickness, circumferential arrangement of collagen fibres and lack of the outer reinforcement by arachnoids trabecules. All these render the subdural portion of the vein more fragile than its subarachnoid portion. These features explain the laceration of veins and the subdural location of resulting haematomas, which can evolve in various ways, acute or chronic. Cerebral SDH is a serious complication of SA that must be kept in mind and may mimic PDPH. History of lumbar puncture, prolonged non-postural PDPH and development of neurological symptoms should be regarded as a warning sign of an intracranial haematoma and initiate immediate diagnosis and treatment of the same.
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[Figure 1], [Figure 2]