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Year : 2001  |  Volume : 49  |  Issue : 2  |  Page : 178--81

Bilateral subdural effusion and subcutaneous swelling with normally functioning csf shunt.

S Mitra, D Ghosh, A Pathak, L Kumar 
 Departments of Paediatrics and Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, 160 012, India., India

Correspondence Address:
S Mitra
Departments of Paediatrics and Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, 160 012, India.


We report a child with hydrocephalus due to tuberculous meningitis who developed a subcutaneous fluid collection around the ventriculoperitoneal shunt tube entry point, after one month of shunting. On investigation, he had decompressed ventricles with bilateral fronto parietal subdural hygroma. Bifrontal burr hole drainage helped resolution of both subdural effusion and subcutaneous scalp swelling. This complication is unique and its pathogenesis has been postulated.

How to cite this article:
Mitra S, Ghosh D, Pathak A, Kumar L. Bilateral subdural effusion and subcutaneous swelling with normally functioning csf shunt. Neurol India 2001;49:178-81

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Mitra S, Ghosh D, Pathak A, Kumar L. Bilateral subdural effusion and subcutaneous swelling with normally functioning csf shunt. Neurol India [serial online] 2001 [cited 2022 Dec 8 ];49:178-81
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Full Text

  ::   IntroductionTop

CSF shunt surgery in hydrocephalus is fraught with various complications including peritubal fluid collection at subcutaneous, subgaleal, subdural or intracerebral planes. These occur in the immediate postoperative period, secondary to shunt malfunctioning. Subdural effusion occurs as a delayed complication when shunt is overdraining.

  ::   Case reportTop

S, 2 year old male child, was admitted with history of fever and refusal of feeds for 10 days prior to admission. He had left focal clonic seizures with secondary generalisation one day before admission.

Subsequently, he was noticed to have weakness of the left half of body. He was being treated with isonex (INH) and rifampicin with good compliance, for pulmonary tuberculosis. Examination revealed prominent occipito-frontal circumference (OFC) of 45 cm, submandibular and posterior cervical matted lymphadenopathy and mild hepatomegaly. He was conscious but irritable with inability to communicate verbally. He had bilateral optic atrophy with absent visual fixation. Extra-ocular movements were normal. There was left sided upper motor neurone (UMN) type VII cranial nerve palsy. Primitive reflexes were elicitable. He had choreiform movement of right upper limb and spastic quadriparesis (left > right) with brisk deep tendon reflexes and upgoing planters. Meningeal signs were present. A clinical diagnosis of tuberculous meningitis with hydrocephalus was made. CT scan of head showed dilated lateral and third ventricles with basal exudates [Figure 1]. Ventricular CSF was normal. The patient was started on 4 drug antitubercular therapy (INH + Rifampicin + Pyrazinamide + Streptomycin) along with steroid and phenytoin. A ventriculoperitoneal shunt was performed using MDR Chhabra shunt. Over the next one month, the patient improved with initiation of speech, significant return of left sided power and disappearance of choreiform movements.

One month later, he presented with inconsolable crying and appearance of a swelling over the right temporo-parietal region. There was regression of motor and language milestones. Examination revealed a soft cystic swelling in the right post-auricular region extending upto the site where burr hole was made for the shunt [Figure 2]. There was no sign of inflammation or increase of the swelling on crying. He had bilateral VI nerve palsy (left > right) and worsening of right hemiparesis with residual spasticity of the left side. A clinical diagnosis of shunt block with peritubal leak was made. Radiological investigations confirmed continuity of shunt tube from the ventricles to the abdomen. CT scan of head showed bilateral frontal subdural effusions with adequately drained ventricles [Figure 3]. Bifrontal burr holes and drainage of subdural fluid was done which came under pressure. The swelling gradually subsided. There was no recurrence of the scalp swelling till 6 months follow-up. The patient had a vocabulary of 20 words and improved ability to interact with parents and peers. There was mild residual spasticity of the right lower limb and optic atrophy. After the first 2 months of 4 drug antitubercular therapy, he was continued on INH and rifampicin which have been planned for a total duration of 12 months.

  ::   DiscussionTop

Hydrocephalus of some degree is nearly always present in cases of tuberculous meningitis (TBM) who survive more than 4-6 weeks.[1] The features of raised intracranial pressure with hydrocephalus in the present case warranted CSF diversion. The development of TBM while on INH and rifampicin for 10 months may indicate drug resistance or failure to diagnose TBM at onset. Pericerebral fluid collections have been described as shunt complications.[2] Subdural haematoma (SDH) related to overdrainage is common.[3],[4] Complications of overdrainage including subdural effusion (SDE) have been described in 7% cases[5] as long as 2 years after shunt operation.[4] Data on incidence of post shunt SDE or hygromas in children is lacking. Normal intraventricular pressure ranges from 30 to 155 mm H2O in sitting posture. On insertion of VP shunt, this drops to an average of 25 mm H2O in adults.[4] This low pressure causes the brain to sag away from the calvarium, opening up the subdural space. Vessels traversing the subdural space get stretched resulting in transudation of fluid from the intravascular compartment to the subdural space. This is the probable pathogenesis of SDE in such cases. This complication has been noted to occur commonly in adults, tall children and in patients with macrocephaly.[6] Untreated hydrocephalus leading to large ventricles with associated cortical atrophy can predispose to SDE.[7],[8] The present case was a small child with moderate hydrocephalus without either macrocephaly or cerebral atrophy. So, in all probability, overdrainage was the main operating factor in this case leading to SDE. The SDE followed the path of least resistance along the peritubal space and led to subgaleal and subcutaneous accumulation of fluid. Unlike cases in a previous series[4] where subdural fluid was haemorrhagic or xanthochromic in patients presenting earlier than 3 months, in the present case it was primarily a hygroma which was detected one month following shunt surgery.

Subcutaneous or subgaleal fluid accumulation after shunt surgery has been described mostly with malfunctioning shunt[2] and this is more likely to develop in early post-operative period. In a series of 201 cases of shunt malfunction,[9] fluid around the shunt tract appeared within a mean period of 11.5 days of shunt placement in 43 cases.[10] This is contrary to the present case where such fluid collection occurred one month later. Fluid accumulation like pseudomeningocele has also been described following craniectomy/craniotomy. Peri-shunt tube leakage of CSF from the ventricle to the subdural space and then to the skin is another cause of these extracerebral collections.

Clear-cut guidelines on the management of SDE complicating shunts are lacking. Various procedures like (a) repeated taps for 7-10 days followed by osteoplastic craniotomy with irrigation of subdural space (b) removal of membrane and obliteration of subdural space by injection of saline or (c) placement of a subdural drain have been recommended.[11] Simple burr hole drainage with shunt ligation followed by repeated post-operative subdural taps has also been tried.[12] Shunt occlusion/ligation raises the intraventricular pressure and thereby reducing the pressure difference between subdural intraventricular

spaces. Simultaneous ventricular drainage may be necessary while shunt is occluded, to avoid rise in ICP to dangerous levels. Another option is to convert the low-pressure valve to a high-pressure one. Following burr hole drainage, subdural fluid may reaccumulate owing to increased pressure gradient between intravascular compartment and subdural space. However, if the fluid is under pressure, simple drainage may actually suffice.[8] Anti-siphon devices though designed to prevent SDE or SDH are not always successful,[4] sometimes posing additional problems.[6] The shunt used in the present case had an anti-siphon device which failed to prevent SDE. The latest advance in this direction has been the use of Orbis-Sigma valve, the aim of which is to provide CSF drainage at or below the rate of CSF secretion.[13]

Subcutaneous swellings may occur in cases of overdissection of the skin or a large opening in the dura. Infants who have loose skin, patients with highpressure shunts and those with large ventricles and thin cortical mantle at the site of insertion are prone to develop this complication. Shunt block is the commonest factor associated with such fluid collection. Once subcutaneous fluid starts collecting, movement of the shunt tube further perpetuates it. Such swellings usually resolve with repeated subcutaneous aspiration or lumbar puncture, combined with compression bandage. Appearance of subcutaneous swelling after one month of shunt surgery along with development of bilateral subdural effusions, with a normally functioning shunt is a unique feature in the case described. Drainage of SDE helped in resolution of subcutaneous swelling. There was no need for shunt revision.

To conclude, subcutaneous fluid collections occurring as a complication of shunt surgery (after a few weeks) do not necessairly imply a blocked shunt. Such collections, as in the case described, may indicate development of SDE. Simple burr hole drainage of SDE take care of both the complications.

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