This document describes a case series study of 32 patients with post-traumatic hydrocephalus conducted at a hospital in Hyderabad, India between 2004-2016. The study aimed to examine the incidence, risk factors, prognosis factors, and Glasgow Outcome Scale for these patients. Key findings included that decompressive craniectomy and delays in bone flap replacement increased the risk of developing post-traumatic hydrocephalus. Clinical improvement was observed in most patients after ventricular-peritoneal shunt placement treatment.

1. POST TRAUMATIC
HYDROCEPHALUS; A CASE
SERIES (INSTITUTIONAL EXPERIENCE)
DR . K .VAMSHI KRISHNA
M.ch (NEUROSURGERY)
NIZAMS INSTITUTE OF MEDICAL SCIENCES
HYDERABAD

2. INTRODUCTION
Post-traumatic hydrocephalus (PTH) is
a rare clinico- pathologic entity as a
result of sequelae of head injury.

3. Hydrocephalus following traumatic
brain injury (TBI) or post-traumatic
hydrocephalus (PTH) is not just a
ventricular enlargement but an active
and progressive disorder of
cerebrospinal fluid (CSF) accumulation
in the ventricular system, causing
compression of the brain parenchyma.

4. AIMS AND OBJECTIVES
To look at the Incidence, risk factors,
prognosis factors and Glasgow
outcome scale for post traumatic
hydrocephalus patients.

5. MATERIALS AND METHODS
 RETROSPECTIVE STUDY
 2004- 2016
 32 PATIENTS
 SURGICAL PROTOCOL
 FOLLOW UP

6. DEMOGRAPHIC PROFILE
 Data
 Mode of injury
 Time of injury
 Admission GCS
 CT findings
 Time of bone flap replacement
 Mode of management.

7. Outcome assessments were done
using Glasgow coma outcome (GCS)
scale.
Follow up data was obtained from
outpatient reviews and telephonic
interviews and death summaries.

8. GENDER
MALE 27
FEMALE 5

9. AGE GROUP
0
2
4
6
8
10
12
14
16
18
10-20(2) 20- 30(2) 30-40(16) 40-50(10) 50-60(1)
Series 1

10. 0
2
4
6
8
10
12
14
16
CEREBRAL
CONTUSION
SDH EDH DEP
FRACTURE
Series 1
Series 1

11. CLINICAL FEATURES
0
2
4
6
8
10
12
14
16
18
Series 1
Series 1

12. MANAGEMENT AT INTIAL TRAUMA
32
22
10

13. 22
16 BEFORE
CRANIOPLASTY
6
AFTER
CRANIOPLASTY

14. TIME PERIOD
0
2
4
6
8
10
12
14
3 MONTHS 3-6 MONTHS >6 MONTHS
Series 1
Series 1

15. 32
• TOTAL
• PATIENTS
22
• DECOMPRESSIVE CRANIECTOMY
• 11 MONTHS
10
• NON DECOMPRESSION
• 17 MONTHS

16. TREATMENT MODALITIES
VP SHUNT 18
TP SHUNT 10
LP

17.  Of the 32 patients Preoperative mean GCS was
10.37 standard deviation (3.80).
 Post shunt 19 patients had improvement IN GCS.
 Post Treatment 6 patients had shunt related
complications.

18. *P<0.001

19. 0
1
2
3
4
5
6
7
GR + GR - MD DEATH EXPIRED
DURING
FOLLOW
UP
Series 1
Series 1

20. DISCUSSION
The clinical entity of Post traumatic
hydrocephalus was first recognized in
1914 by Dandy and Blackfan who
described a case of hydrocephalus
developed in child after a severe fall.

21. The incidence of PTH in the World
literature is quite variable ranging from
0.7 to 29%
Variability in incidence is attributed to
complex Pathology of PTH and
discrepancy in diagnostic criteria.
Incidence in our study is 2.08% though
the hospital admission biases exist.

22. Patients who underwent
decompressive craniectomy had high
chance of developing hydrocephalus.
Various hypotheses have been
proposed

23. CELLULAR LEVEL
Schaller et al . In particular, reduction
cerebral metabolic rate of glucose
(CMRglc) documented the high
susceptibility of oxygen metabolism to
perfusion disturbance
The increase of glucose metabolism
not only correlates with the restitution
of CBF but is a good predictive value
for clinical outcome after cranioplasty.

24. Yoshida et al. observed decreased
activity of phosphocreatine (PCr)
before and a significant improvement
after cranioplasty
Phosphocreatinine plays a pivotal role
in cellular metabolism, and the
increase in its activity after
cranioplasty reflects profound changes
in mitochondria and neuronal
metabolism.

25. DC itself being risk factor for
development of hydrocephalus as the
trauma events lead to surgical debris
which may lead to mechanical
blockade.

26. Since Arachnoid granulations act as
pressure valves, and inflammation of
this lead to the circulation and
absorption disturbance of
cerebrospinal fluid

27. And when the skull is removed too
close to the midline, the external force
compressing the veins mainly during
the diastolic phase is reduced, causing
an increase in venous outflow and
extracellular fluid absorption and a
decrease in brain parenchyma volume,
which causes ventriculomegaly and
hydrocephalus.

28. In post decompressive craniectomy
there is loss of insulating factors
which alter temperature gradients and
reduction of the core temperature of
the brain leading to alteration of
cerebral blood flow ,which may
contribute to the reduction in
neurological function

29. In our study of the 32 patients 22
patients underwent decompressive
craniectomy and 16 patients
developed hydrocephalus before
cranioplasty.
Early cranioplasty will lead to
restoration of normal intracranial
pressure dynamics and resolution of
hydrocephalus

30. Our study has analysed that
advantages of placement of lumbar
drain before the cranioplasty in
patients where ventriculomegaly with
flap bulge is there but CT does not
show PVO .

31. CONCLUSION
 Clinical development of post traumatic
hydrocephalus is known to be multi factorial. This
study sought to determine risk factors and
prognostic correlation.
 Our retrospective analysis suggests that
Decompressive craniectomy and delay in bone
flap replacement increase the risk of development
of PTH, but due to small population size, statistical
significance was unable to be established.