| Article Access Statistics|
| Viewed||11019 |
| Printed||207 |
| Emailed||5 |
| PDF Downloaded||191 |
| Comments ||[Add] |
| Cited by others ||10 |
Click on image for details.
|Year : 2002 | Volume
| Issue : 4 | Page : 508-10
Subarachnoid hemorrhage and intracereebral hematoma following lumboperitoneal shunt for pseudotumor cerebri : a rare complication.
Suri A, Pandey P, Mehta VS
Department of Neurosurgery, All India Institute of Medical Sciences, C.N. Center, New Delhi - 110029, India.
Department of Neurosurgery, All India Institute of Medical Sciences, C.N. Center, New Delhi - 110029, India.
Placement of lumboperitoneal (LP) shunt as a surgical treatment for benign intracranial hypertension (BIH) is generally a safe procedure, with complications like mechanical failure, overdrainage and infections. Subarachnoid hemorrhage and intracerebral hematoma were seen after lumboperitoneal shunt in a patient having BIH. These complications were the cause of the patient's deterioration. After removal of the hematoma and performing a decompressive procedure, patient's neurological condition improved. The clinical features, investigations and clinical course are described and the literature reviewed.
|How to cite this article:|
Suri A, Pandey P, Mehta V S. Subarachnoid hemorrhage and intracereebral hematoma following lumboperitoneal shunt for pseudotumor cerebri : a rare complication. Neurol India 2002;50:508
|How to cite this URL:|
Suri A, Pandey P, Mehta V S. Subarachnoid hemorrhage and intracereebral hematoma following lumboperitoneal shunt for pseudotumor cerebri : a rare complication. Neurol India [serial online] 2002 [cited 2019 Aug 22];50:508. Available from: http://www.neurologyindia.com/text.asp?2002/50/4/508/1325
Pseudotumor cerebri (PTC) or benign intracranial hypertension (BIH) is a clinical entity characterized by elevated intracranial pressure unrelated to hydrocephalus, tumor, brain edema or any other structural entity. Typical symptoms include headache, transient or permanent obscuration of vision, diplopia, and typically has a protracted course. Management of this disorder is both medical and surgical. The two main surgical procedures performed are lumboperitoneal (LP) shunt and optic nerve sheath fenestration (ONSF).,, LP shunt has been shown to be an effective and relatively safe method of treatment of BIH., We here described a rare complication of LP shunt done for BIH not mentioned earlier in the medical literature.
A 42 year old, obese female (body weight=73kg.) presented with history of headache and progressive visual deterioration of 8 years duration. She was not on steroids, oral contraceptive or any other drugs like
tetracycline or nitrofurantoin. There was no history suggestive of deficiency or excess of vitamin A, or associated endocrinological disorders. Clinical examination revealed visual acuity of 6/9 in both eyes, and bilateral papilledema; visual field examination was within normal limits. The examination of the motor and sensory systems was normal. Ophthalmological referral ruled out other causes of 'disc edema' like drusen. Cerebrospinal fluid (CSF) was under moderately high pressure and its examination was within normal limits. CT scan and MRI of the brain were normal [Figure 1a] and [Figure b]. Since the imaging studies were non-contributory and no other causative lesion for increased intracranial pressure could be found, a diagnosis of BIH was made after exclusion of all other causative factors. Patient was on medical therapy for seven years consisting of acetazolamide and furosemide, but for the last one year, had increasing headache and visual blurring.
A lumboperitoneal shunt with a distal slit valve was inserted. Clear CSF under moderately high pressure emanated. CSF cytology and biochemistry were normal and culture was sterile. Intraoperative and immediate postoperative periods were uneventful. Eight hours after surgery, she had three episodes of left focal motor seizures. CT scan revealed evidence of subarachnoid hemorrhage and a small hematoma in right parietal region. Platelet counts and coagulation profile were normal (bleeding time-3min.15sec., clotting time -4min. 20sec., platelet count -2,75,000/cu.mm., prothrombin time index -100%) cerebral digital subtraction angiogram was normal there was no evidence of aneurysm, arteriovenous malformation or venous sinus thrombosis. Forty hours after the surgery, she deteriorated and was found to be unresponsive to commands. She had rapidly worsened to decerebrating posture with bilateral pupils dilated and sluggishly reacting to light. CT scan revealed diffuse subarachnoid hemorrhage and a large hematoma in right frontal lobe causing mass effect and midline shift [Figure 2a] and [figure 2b]. The lumboperitoneal shunt was removed. Bilateral osteoplastic frontotemporal flap craniotomy was performed; the right frontal hematoma was evacuated and a wide duraplasty was done. Bone flaps were replaced but not secured, with the intention to decompress the cranial cavity. She had a stormy postoperative course consisting of chest infection, prolonged intubation and tracheostomy. At the time of discharge from the hospital, she was alert, oriented, and continent with no motor or sensory deficits; visual acuity was the same as before surgery, bone flaps on both sides were full and headache had subsided.
Histopathological analysis of the blood clot revealed a few cells resembling foam cells, which were not considered to be significant. No other explanation for the subarachnoid hemorrhage and intracerebral hematoma could be found and it was attributed to the placement of the lumboperitoneal shunt. Plain and contrast CT scans of the head after four weeks revealed thin bilateral frontotemporal subdural effusions with normal ventricles and cisterns. CSF examination was normal and there was no evidence of abnormal cells. Follow-up examination would aim at regular neurological and opthalmological examination to prevent recurrence of symptoms.
BIH is a condition with a wide variety of treatment options, both surgical and non-surgical. Initial medical treatment is with drugs such as acetazolamide, as was done in this case. The presence of visual deterioration or intractable headache is an indication for surgery. Two main surgical procedures for BIH are LP shunt and ONSF.,, A number of studies have confirmed both efficacy and complication rates of LP shunt.,, Placement of LP shunt has been regarded a safe procedure. The most common cause of revision of LP shunt in most large reviews of medical literature is shunt obstruction followed by secondary intracranial hypotension resulting in low-pressure headache due to excessive CSF drainage.,,,, Duther et al in 1996, in a study of LP shunts in 195 patients noted 47 complications (chronic subdural effusion -8, meningitis -10, mechanical failure -28 and Chiari malformation -1). Eggenberger et al studied the efficacy and safety of LP shunts in BIH in 27 procedures and showed no major complications apart from shunt obstruction. Several other series have been associated with sporadic incidence of minor complications like lumbar radiculopathy,,, shunt infection,, shunt migration,,, and acquired Chiari malformation (tonsillar herniation) and syringomyelia, Another study by Burgett et al did not reveal any major complications after LP shunt in BIH. Muthukumar et al reported one case of tension pneumocephalus complicating LP shunt placement. Miller et al reported one case of bilateral visual loss and simultagnosia after LP shunt for BIH. Murtagh and Lehman and Jones, reported acute subdural hematoma after LP shunting. Four cases of acute subdural hematoma after minor head trauma in patients with pre-existing LP shunts have been reported.,,
Development of subarachnoid hemorrhage and intracerebral hematoma following LP shunt has not been previously reported in literature. The potential pathogenesis is of overdrainage, but lack of any subdural effusion or blood is a pointer against this possibility. This points towards altered CSF dynamics leading to SAH and intracerebral hematoma due to variation in the differential pressures in various intracranial compartments.
|1.||Frederick HSklar : Pseudotumour cerebri : In : Neurosurgery. Rengachary SS, Wilkins RH (eds.). Mc Graw -Hill Co. . Vol.I, PartIV, 357-361. |
|2.||Burgett RA, Purin VA, Kawasaki A : Lumboperitoneal shunting in pseudotumor cerebri. Neurology 1997; 49 : 734-739 |
|3.||Eggenberger RE, Miller NR, Vitake S : Lumboperitoneal shunt for treatment of pseudotumor cerebri. Neurology 1996; 46 : 1524-1530 |
|4.||Sporr TC, McHenry JG : Long term effectiveness of optic nerve sheath fenestration for pseudotumor cerebri. Arch Ophthalmol 1993; 111 : 632-635 |
|5.||Angiari P, Corradini L, Corsi M et al : Pseudotumor cerebri. Lumboperitoneal shunt in long lasting cases. J Neurosurg Sci 1992; 36(3) : 145-149 |
|6.||Eisenberg HM, Davidson RI, Shillito J : Lumboperitoneal shunt- review of 34 cases. J Neurosurg 1971; 35 : 427-431 |
|7.||Duther R, Nuti C et al : Complications of lumboperitoneal shunts- a retrospective study of series of 195 patients( 214 procedures). Neurochirurgie 1996; 42 : 83-89. |
|8.||Rosenberg M, Smith C, Beck R et al : The efficacy of shunting procedures in pseudotumor cerebri. Neurosurgery 1989; 39 ( suppl.1) : 209. |
|9.||Selman WR, Spetzler RF, Wilson CB et al : Percutaneous lumboperitoneal shunt: review of 130 cases. Neurosurgery 1980; 6 : 255-257. |
|10.||Chumas PD Kulkarni AV, Drake JM : Lumboperitoneal shunting- a retrospective study in pediatric population. Neurosurgery 1993; 32 : 376-383. |
|11.||Fischer EG, Welch K, Shillito J : Syringomyelia following lumboperitoneal shunting for communicating hydrocephalus: report of three cases. J Neurosurg 1977; 47 : 96-100 |
|12.||Sullivan LP, Stears JC, Ringel SP : Resolution of syringomyelia and Chiari I malformation by ventriculoatrial shunting in a patient with pseudotumor cerebri and a lumboperitoneal shunt. Neurosurgery 1988; 22 : 744-747. |
|13.||Muthukumar N, Palaniappan P, Gajendran R : Tension pneumocephalus complicating lumboperitoneal shunt. J Indian Med Assoc 1996; 94 : 457-459. |
|14.||Miller NR : Bilateral visual loss and simultagnosia after lumboperitoneal shunt for pseudotumor cerebri. J Neuroophthalmol 1997; 17 : 36-38. |
|15.||Murtagh F, Lehman R : Peritoneal shunts in the management of hydrocephalus. JAMA 1967; 202 : 1010-1014. |
|16.||Jones RFC : Long term results in various treatments of hydrocephalus. J Neurosurg 1967; 26 : 313-315. |
|17.||Aoki N : Acute subdural hematoma of arterial origin in a patient with a lumboperitoneal shunt. Neurol Med Chir (Tokyo) 1987; 27 : 60-62. |
|18.||Aoki N, Mizutani H : Acute subdural hematoma due to minor head trauma in patients with a lumboperitoneal shunt. Surg Neurol 1988; 29 : 22-26. |
|19.||Aoki N : Lumboperitoneal shunt: clinical applications, complications and comparison with ventriculoperitoneal shunt. Neurosurgery 1990; 26 : 998-1003. |