Post traumatic hydrocephalus (PTH) is a relatively rare condition.(2,9,10, 12,13) Only a few series have been reported in the English literature,mainly in the form of case reports.(2,9,10,12,13) Dilatation of the ventricles with normal intracranial pressure after severe head injury is common due to loss of brain volume (hydrocephalus en vacuo) and is inconsequential in the long run. On the other hand, PTH is a distinct entity where ventricular dilatation is associated with raised intracranial pressure that needs to be relieved to prevent further intracranial pressure effects.(2) Authors report an analysis of severe head injury patients admitted in the Neuro-intensive care unit (NICU) over a period of two years to determine the incidence, causative factors, clinical course and outcome of PTH in these patients.

MATERIALS AND METHODS

The case records of 891 patients with severe head injury, who were admitted at the National Neurosurgical Centre at Khoula Hospital, Oman between March 1998 to March 2000, were retrospectively analysed. Records were scrutinised to analyse the type of injury, Glasgow coma scale (GCS) at admission, CT scan findings, clinical course, onset of PTH, the neurosurgical modalities employed and the outcome. The out-patient records were also evaluated for the long term follow-up results.

ANALYSIS

Among the 891 patients admitted with severe head injury, 22 patients developed PTH, thus giving an incidence of 2.4%. While 4 patients were less than 15 years old, 13 patients (59.09%) were in the age group of 15-40 years and 5 patients were more than 40 years of age. All the patients were involved in high speed road traffic accidents. There were 20 males and 2 females. These patients were admitted with a GCS of 8 or less. They were all electively paralysed, intubated and ventilated at admission. The pupillary responses were normal and the vital signs were stable in the normal range.

The initial CT scans showed intraventricular haemorrhage in 12 patients (54.54%); diffuse contusions in 2 cases (9.09%), traumatic SAH in 4 cases (18.8%), and significant localised intracranial haematomas in 4 cases (18.8%). Among the latter group two of the patients with thin subdural haematomas were treated conservatively, and only 2 patients with extra dural haematomas underwent surgery. Usually patients were weaned off the ventilator between the 3rd to 9th post-trauma day.

While PTH in 21 of our 22 patients developed between the 3rd to 8th week, in one case it presented on the 10th post-trauma day. Patients commonly presented with deterioration in the level of consciousness, or failure to maintain progressive clinical improvement. The repeat CT scan done in these patients confirmed the diagnosis of post-traumatic hydrocephalus. Diagnostic lumbar puncture (LP) was done in these patients as per the protocol, which revealed an initial pressure of more than 180 cms of H2O in all 22 patients. Among these 22 patients, 9 (40.9%) underwent medium pressure Codman Medos ventriculo-peritoneal (VP) shunts as a primary procedure, 4 patients underwent VP shunt after an initial external ventricular drain (EVD) insertion to clear the blood stained CSF. Five patients with intraventricular haemorrhage had an initial Omayya reservoir inserted followed by a medium pressure VP shunt insertion. Among the 4 patients with traumatic subarachnoid haemorrhage, 2 of the patients underwent repeated LP's and improved; one had a thecoperitoneal shunt performed and one patient did not improve after repeated LP and the relatives refused further treatment.

Of the 22 patients, 10 patients (45.45%) showed a good clinical improvement, 4 patients showed a moderate to minimal improvement. Seven patients (31.81%) showed no improvement and one patient died due to ventriculitis.

DISCUSSION

PTH although relatively rare, is a treatable condition. While the incidence of PTH is not well documented some series report an incidence of between 2-8%.(2,7,9,10,12,13) One in twenty patients with severe head injury may develop significant post-traumatic hydrocephalus. In some patients, the initial brain damage may preclude significant improvement. Most of these cases may be due to cerebral atrophy with secondary ventriculomegaly. If only CT findings of ventriculomegaly are taken into account, then an incidence of 30-86% has been reported. Hence, it is important to distinguish between PTH and cerebral atrophy as the latter usually do not respond to neurosurgical procedures.(2,9)

PTH may present with various clinical syndromes including obtundation, failure to improve and a tetrad of symptoms including psychomotor retardation, memory loss, gait ataxia and incontinence.(1,15) Sometimes, the patient may be too injured to demonstrate clinical signs and symptoms of PTH, or may present with atypical symptoms.(1) According to Groswasser, et al when a patient is in a state of prolonged coma or when there is an arrest in the clinical progress in conscious cranio-cerebral injured patients, communicating hydrocephalus should be suspected.(7)

PTH is thought to arise from the blockage of the cerebrospinal fluid (CSF) flow around the cerebral convexities.1 SAH leads to communicating hydrocephalus due to block in the subarachnoid pathways or even subarachnoid granulation, either as an acute obstruction or as a late effect. Posterior fossa contusions and blood in the 4th ventricles may also manifest as acute obstructive hydrocephalus.(5,6) Rarely, some patients may present with hydrocephalus following a craniotomy since decompressive craniotomy is thought to lead to blockage around the cerebral convexities.(13)

PTH is rare among children and has mainly been published as case reports, except neonatal hydrocephalus secondary to birth trauma and IVH.(1,4) In view of its association with neurodevelopmental disability, PTH in infants is a very serious condition.4 Hydrocephalus in these children may induce further parenchymal injury due to high pressure. This ventricular enlargement if not treated in time means the cerebral damage may not be reversible by CSF diversion procedures.(4)

While PTH commonly occurs in the 1st year post- trauma, it has been occasionally described as early as within 7 hours post-trauma.(2,16) In our series one patient was diagnosed on the 10th post-trauma day and 21 patients between the 3rd to 8th week following severe head injury.

Clinical and radiological correlation remain the cornerstone for the diagnosis of PTH. Serial CT scans are the investigative modality of choice in these patients. Other modalities of investigation, advised by various authors, include overnight intracranial pressure recording, lumboventricular infusion testing, cisternography mainly to differentiate PTH from hydrocephalus en vacuo, although there is still considerable uncertainty about shunt prediction ability.(1) However, on lumbar computerised infusion test, a pattern of CSF circulation with low or normal resistance to the CSF outflow, increased brain compliance with very few vasogenic waves is characteristic of cerebral atrophy.(3) Beryel, et al have opined that when the lumbar CSF pressure is above 180 cms of water, PTH should be treated with a shunt unless a contraindication to the surgery exists.(1)

Gudeman, et al have reported that, radionucleide cisternography provided an additional means of determining those patients whose recovery was impaired by PTH and might therefore improve with shunting.(8)

Enlargement of the lateral ventricles as defined by the ventricle – brain ratio can be demonstrated in up to 72% of head injured patients.(11) Although Kishore, et al in their study had demonstrated a significant correlation between the ventricular size and the outcome, PTH was seen in only 13.7% of their patients with ventriculomegally.(10) Levin, et al in their study have also showed that dilatation of ventricles is directly related to the duration of the coma, and subsequent memory and intellectual deficits.(11)

Increased periventricular lucency, obliteration of cerebral cortical sulci, and enlargement of the temporal horns together with internal hydrocephalus on a CT scan indicate an active process and favours CSF shunting.(14)

Most series have demonstrated good recovery rates between 45-50% in patients with PTH following CSF shunting.(2,12) In our series 45% of the patients showed a good recovery and 18.8% showed moderate to minimal recovery following neurosurgical intervention.

Table 1 - Total head injury admissions between March 1998 - March 2000

Total Admissions (GCS)	No. of cases	Incidence of PTH
Mild head injury  (13-15)	2231	0%
Moderate head injury  (9-12)	1325	0%
Severe head injury  (8 or below)	891	2.4% (22 cases)

Table 2 - CT scan findings

CT scan findings	Incidence
Traumatic intraventricular haemorrhage	12 (54.54%)
Traumatic subarachnoid haemorrhage	4 (18.8%)
Diffuse contusions	2 (9.09%)
Localised intracranial haematomas	4 (18.8%)

Table 3 - Outcome following neurosurgical intervention

Neurosurgical intervention	No. of cases	Outcome
Ventriculo-peritoneal shunt	9	6 - good improvement 1 - moderate improvement 2 - no improvement
External ventricular drain followed by  VP shunt	4	2 - good improvement 1 - no improvement 1 - died due to ventriculitis
Omayya reservoir for drainage followed by VP shunt	5	1 - good improvement 1 - minimal improvement 3 - no improvement
Thecoperitoneal shunt	1	1 - good improvement
Repeat lumbar puncture	3	2 - moderate improvement 1 - no improvement

CONCLUSION

REFERENCES

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