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