Rapid Enlargement of Ventricles
within Seven Hours
after Head Injury
Hiroshi Takagi, M.D., Yoshio Tamaki, M.D.,
Seiji Morii, M.D., and Takashi Ohwada, M.D.

We report a case of acute enlargement of the ventricles
within 7 hours after head injury that was documented by
repeated computerized tomography. It is suggested that
the pathophysiological mechanism for this rapid enlargement of ventricles may be due to the raised intracranial
pressure (ICP) that results from obstruction of cerebrospinal fluid pathways by subarachnoid hemorrhage, in addition to the elevation of ICP aggravated by frequent focal
convulsive seizures.
Takagi H, Tamaki Y, Morii S, Ohwada T: Rapid
enlargement of ventricleswithin seven hours after
head injury. Surg Neurol 16:103-105, 1981

to verbal command. He scored 8 points on the Glasgow
Coma Scale. There was no paresis of any extremity. Pupils
were equal and reacted to light. Laboratory examination
showed a leukocyte count of 36,600/mma; serum glutamic-oxaloacetic transaminase (SGOT) was 78; serum
glutamic-pyruvic transaminase (SGPT) was 28, and lactate
dehydrogenase (LDH) was 1,508 units. Peritoneal lavage,
performed because of the suspicion of liver contusion, was
negative. Plain roentgenograms demonstrated no fracture
of the skull. CT scan, which was performed 31/2 hours after
the accident, showed slightly enlarged ventricles, but there
was no suggestion of an intracranial hematoma or cerebral
It has been reported that posttraumatic communicating contusion (Fig. 1A).
hydrocephalus develops within days and weeks after a
During the observation period in the intensive care unit,
closed head injury [4, 7]. We have had occasion to demon- the patient's state of consciousness gradually deteriorated.
strate rapid ventricular enlargement within 7 hours after The right pupil began to dilate and the left deep tendon
head injury by means of a computerized tomographic (CT) reflexes were exaggerated, with a positive plantar response.
scan. This enlargement was treated by ventricular drainage Right-sided focal convulsive seizures with complete loss of
with continuous monitoring of intracranial pressure (ICP) consciousness occurred six times. At this time, 7 hours after
without any shunting procedure. A CT scan performed the accident, the CT scan was repeated and demonstrated
nine months after the accident showed the ventricles were a marked enlargement of the ventricles compared with the
of normal size and shape.
previous CT scan (Fig. IB). Right lateral ventricular drainage was done and a subdural balloon was installed for
Case Report
monitoring of intracranial pressure. Macroscopically, the
This 4-year-old right-handed boy was struck by an au- cerebrospinal fluid was slightly bloody.
tomobile on April 16, 1980. After losing consciousness for
Immediately after the ventricular drainage, the ana few minutes he began to cry, became agitated, and vom- isocoria disappeared. The patient's state of consciousness
ited. He was brought to the Division of Critical Care Medi- improved rapidly, and he began to respond to verbal com.
cine of Kitasato University and was evaluated 3 hours after mands a few hours later. The level of intracranial pressure at
the accident.
which ventricular fluid was drained was set at 10 mm Hg for
On his arrival, his vital signs were within normal limits. the first two days; it was then increased, continuing at 20
He had a contusion on his scalp in the right occipital region mm Hg for the next four days. After six days, ventricular
and tenderness over the right upper quadrant of the abdo- drainage was stopped. Monitoring of intracranial pressure
men. He responded to noxious stimuli but did not respond was continued for another 24 hours, when it was stopped
(Fig. 2). Isotope cistemography done 30 days after the injury revealed ventricular reflux at 3 hours; however, the
isotope could not be detected at 48 hours. CT scan perFromthe Departmentof Neurosurgeryand Divisionof Critical Care Medi- formed 35 days after the accident showed slightly enlarged
cine, KitasatoUniversity, Schoolof Medicine, Kanagawa, Japan.
lateral and third ventricles, but other findings were normal
Address reprint requests to Dr. Hiroshi Takagi, Department of
Neurosurgery,KitasatoUniversitySchool of Medicine, 1-15-1, Kitasato, (Fig. 3A). The patient was discharged home 36 days after
Sgamihara-shi, Kanagawa-Ken,Japan 228.
the head injury without any neurological deficits. He was
Key words: acute head injury; posttraumatic hydrocephalus;intracranial put on 40 mg of diphenylhydantoin twice a day and had
pressure; ventriculardilatation
had no convulsive seizures in the nine months since then.
0090-3019/81/080103-03501.25 © 1981 by Little, Brown and Company (Inc.)

103

104 Surgical Neurology Vol 16 No 2 August 1981

A
CT scan performed at that time demonstrated that the ventricles had become normal in size and shape (Fig. 3B).
Discussion
It has been well recognized that the enlargement of ventricles may be a delayed complication of head injury [4, 7].
With the advent of CT scan, Kishore and associates [4]
reported the incidence of hydrocephalus to be 15% and that
it became evident within 14 to 19 days after head injury at
the latest. It seems to be rare that communicating hydrocephalus causes neurological deterioration of the patient
within hours. This may be due to the fact that injury to the

Fig. /. {A) CT scan 3 t/e h~urs ajter head injury. (B) C T scan 7
h{~urs after head injury. N~Jte the marked enlargement of the ventricles.

Fig. 2. Rec~rd of the intracranial pressure ]or the seven days fiJlbwing
trauma. The level ~f intracranial pressure was changed in a stepwise
tizshion. On day 7, ventricular drainage was discontinued.

mrnt~

VENTRICULAR DRAINAGE

90
80
70

60 rain.

[ t

60
50
40
30
20
10
T~

2nd

4th

6th

7th

3575

doy

Takagi et al: Rapid Enlargement of Ventricles after Head Injury

A

B
Fig. 3. (A) C T scan 35 days after head injury. The shape of the
frontal horns of the lateral ventricles is slightly round and enlarged.
(B) C T scan nine months after head injury. The previously enlarged
ventricles have become normal in size and shape.

105

brain parenchyma is more dominant than the subarachnoid
hemorrhage [8].
The patient described here showed rapid enlargement of
the ventricles within 7 hours after head trauma, as compared with the ventricular size at 3V2 hours after the accident.
The basic pathophysiological mechanism responsible for
this rapid enlargement of ventricles may be the obstruction
of cerebrospinal fluid pathways by subarachnoid hemorrhage [2, 4, 6]. This is suggested by the intracranial pressure measurements, the bloody cerebrospinal fluid, and the
isotope cisternography in this patient. However, we postulate that the rapid enlargement of the ventricles may have
been aggravated also by the convulsive seizures, which may
lead to increase in the intracranial pressure [5] by respiratory compromise [3] and elevation of central venous pressure
[11.
Obviously, the treatment of choice of communicating
hydrocephalus is a shunting procedure, but in the acute
stage of head injury, the diffuse brain injury may make this
inadvisable. This patient was treated with continuous control of intracranial pressure by ventricular drainage for six
days. It is suggested that if the increased intracranial pressure can be controlled in patients with acute communicating hydrocephalus following head injury, some may not
need a permanent shunting procedure.
References
1. CypersJ, Matakas F, Potolicchio ST Jr: Effect of central venous pressure on brain tissue pressure and brain volume. J Neurosurg 22:369373, 1975
2. Foltz EL, Ward AA Jr: Communicating hydrocephalus from subarachnoid bleeding. J Neurosurg 13:546-566, 1956
3. Kin& GW, Gosch HH: Arterial pCO2 effect at various levels of intracranial pressure, in Brock M, Dietz H (eds): Intracranial Pressure; Experimental and Clinical Aspects. Berlin, Heidelberg, New York:
Springer, 1972, pp 210-213
4. Kishore PRS, Lipper MH, Miller JD, Girevendulis AK, Pecker DP,
Vines FS: Post-traumatic hydrocephalus in patients with severe head
injury. Neuroradiology 16:261-265, 1978
5. Lundberg N: Continuous recording and control of ventricular fluid
pressure in neurosurgical practice. Acta Psych Neurol Scand
36(suppl):106, 1960
6. McQueen JD, Jelsma LF: lntracranial hypertension: cerebrospinal fluid
pressure rises followingintracistemal infusion of blood components in
dogs. Arch Neurol 16:501-508, 1967
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Posttraumatic progressivenon-obstructivehydrocephalus:report of two
cases. No To Shinkei 23:1217-1221, 1971
8. Zimmerman RA, Bilaniuk LK: Computed tomography in diffuse
traumatic cerebral injury, in Popp JA, Bourke RS, Nelson LR, Kimelberg HK (eds): Neural Trauma. New York: Raven, 1979, pp 253-262