Shunt site chronic calcified extradural hematoma: An avoidable complication.

Extradural hematoma (EDH) after ventriculoperitoneal (VP) shunt procedure is a rare, dangerous but easily avoidable and manageable complication. It is more common in children and young adults presumably due to relatively lax adhesion of dura to calvarium. We report a case of an 18-year-old male with acqueductal stenosis who underwent VP shunt procedure. Three months later, a computed tomography (CT) scan was done for the complaints of intractable headache and altered sensorium which showed chronic calcified EDH near shunt site. The ventricular catheter was in position and the ventricles were decompressed. After surgical decompression of EDH his symptoms improved. We discuss the factors leading to formation of EDH, with stress on proper technique to prevent or minimize such an avoidable complication.

Introduction

VP shunt causes sudden decompression of the brain that can lead to either subdural hematoma (SDH) or EDH formation. Formation of EDH is relatively rare in comparison to SDH. Very few cases of post-VP shunt EDH formation have been reported in the literature. We report this case to spread awareness of this relatively rare complication of a very common neurosurgical procedure, which, in some cases, can be avoided, and, in all cases, can be diagnosed and managed easily before it turns into a catastrophic complication.

Case Report

An 18-year-old male presented to us with headache and altered behavior of 15-days duration. On neurological examination, he was disoriented without any apparent cranial nerve deficit or sensory or motor deficit. CT scan brain revealed moderate obstructive hydrocephalus with triventricular dilatation due to aqueductal stenosis [Figure 1]. The patient underwent right-sided VP shunt procedure through right parietal burr hole using medium pressure Chabra slit and spring device. Post-operatively, he improved symptomatically and was discharged after 10 days without any fresh neurological deficit. The patient was on follow-up thereafter, and 3 months after he presented to us again with complaints of intractable headache and altered sensorium of 10-days duration. CT scan brain revealed a chronic calcified right parietal EDH near shunt site [Figure 2] with mass effect. A coagulation profile was done, which was normal. Because the patient was symptomatic, he was managed surgically with evacuation of extradural collection and post-operatively he improved symptomatically, and was discharged without any neurological deficit. He has been on regular follow-up for the past 3 months, and has no neurological deterioration.

Figure 1

Moderate obstructive hydrocephalus with dilatation of lateral and third ventricles with thinned out cortical mantle due to aqueductal stenosis

Figure 2

Chronic calcified right parietal EDH at shunt site with mass effect

Discussion

As the brain slackens after decreasing ventricular pressure by ventriculoperitoneal shunting, the subdural bridging veins are stretched and may get torn, causing SDH. Hence, formation of acute SDH after ventricular decompression is well known in neurosurgical practice. Formation of EDH, however, is a rare complication of VP shunt surgery, with most reported cases in children[1] and young adults. This is thought to be due to the firm attachment of the dura to the skull in older adults. It is reported to be more frequent in the frontal and parietal regions and in patients with long-standing hydrocephalus. EDH is much rarer after ventricular drainage because the dura is generally adherent to the inner surface of the skull.[1]

The principal mechanism for hematoma formation after ventricular decompression is sudden lowering of intra-cranial pressure, which results in a suction force on structures between the cortex and the inner table of the skull.[2] Tearing of cortical bridging veins leads to SDH and of meningeal vessels leads to formation of EDH. In case of EDH, detaching the collagenous fixation of the dura from the inner table of the skull may initially cause the dural and diploic veins to bleed into the epidural space. As the hematoma enlarges and the distance between the dura and the bony arterial channels increases, the dural arteries may also tear. Many authors thought that the traction exerted on the dura mater by the many vessels attached to the brain cause a displacement and make the vessels between the membrane and the skull to be torn. This is supported by the fact that most reported cases occur in children, in whom the dura is less tightly adhered to the skull than in adults. Craniocerebral disproportion may be responsible in some patients.[1] Other mechanical factors mentioned include bridging vein tearing and dural detachment because of brain parenchyma displacement induced by cerebrospinal fluid (CSF) drainage. A sudden lowering of intracranial pressure, due to cortex collapse, helps hematomas, increasing up to a catastrophic complication if not recognized and treated in time. In case of EDH directly adjoining the burr hole site of VP shunt, excessive coagulation of dura of the burr hole before dural incision may, in some cases, cause enough shrinkage to result in dural separation from the skull and EDH formation. This dural separation is further aided by rapid lowering of intracranial pressure. Once bleeding has begun by any mechanism, arterial bleeding into the resulting pocket creates a hydraulic “water press” effect, progressively stripping away the dura from the skull and widening the perimeter of the hematoma. Use of valve-regulated shunt systems has lowered the incidence of SDH and EDH after ventricular drainage. There are only 18 cases of epidural hematomas after valve-regulated shunt placement in the literature.[3] Most of these cases had acute hematomas, and only five of them had chronic calcified/ossified hematomas.[4] These patients were 15-35 years old. EDH contralateral to the VP shunt has been also described.[5] In all epidural hematomas, the incidence of chronic EDH is between 3.9% and 30%. Chronic EDH occurs more commonly in younger ages. A post-operative EDH usually causes symptoms during or immediately after surgery. However, the diagnosis may be delayed in a case with VP shunt insertion because of a reduction in CSF volume in the ventricles via a properly functioning shunt.[4] The most common initial symptom is a headache, and there may be seizures in delayed cases.[4] The hematomas were unrelated to the burr-hole sites in most of the EDH cases due to a ventriculoperitoneal shunt. Post-shunt EDH can be managed surgically and conservatively. The choice between a surgical or a non-surgical treatment of post-shunt EDH requires the evaluation of various factors: Volume, thickness, midline shift and amount of fresh blood present on CT scan, the age of the patient and the clinical picture. Huge acute or subacute collections in adults or in children with closed fontanelles usually require surgical treatment. In our case, because the patient was symptomatic with CT scan findings of mass effect and midline shift, we considered for surgical intervention and the patient was kept on a close follow-up post-operatively for any neurological deterioration.

Some precautions are recommended to minimize the bleeding complications after VP shunting: Minimal CSF spillage at the time of ventricular catheter insertion, meticulous surgical technique, use of high- or medium-pressure valves or differential pressure valves, slow return to upright position and close follow-up even including a postoperative CT scan.[6] An antisiphon device or a flow rate-limiting system may also decrease the chances of the occurrence of this complication.

Conclusions

Formation of EDH after VP shunt surgery is a rare but potentially dangerous complication. Although many theories exist, the common initial event seems to be the separation of dura mater from the inner table of the skull, which may be facilitated by lax adhesions between the two. Careful clinical monitoring in the postoperative follow-ups helps in early recognition and treatment of this catastrophic complication. Minimal intraoperative CSF spillage, good surgical technique and pressure-regulated shunt systems can help prevent the incidence of such a potentially life-threatening complication.