Corresponding author: Dr.Selcuk Peker
P.K.240 34711 Kadıköy Istanbul, Turkey Tel: 90-216-3264559
Fax: 90-216-3275249 peker@atlas.net.tr
Marmara Medical Journal 2004;17(1);28-31
CASE REPORT
DELAYED INTRACEREBRAL HEMORRHAGE AFTER
VENTRICULOPERITONEAL SHUNTING
Selçuk Peker, Koray Özduman, Serdar Özgen, M.Necmettin Pamir
Marmara University Department of Neurosurgery, Marmara University Neurological Sciences Institute, Istanbul, Turkey
ABSTRACT
Delayed intracerebral hemorrhage after ventriculoperitoneal shunt insertion is a rare complication.
Here in we report the case of an 83-year-old female patient with a left posterior cerebral artery aneurysm and hydrocephalus. A hemorrhage at site of insertion was diagnosed on the postoperative day 4 after ventriculoperitoneal shunt insertion.
The causative factor in our patient was probably the disruption of an intracerebral vessel by the ventricular catheter which was initially tamponaded by the intraparenchymal pressure, but later became manifest as the shunt became functional.
Keywords: Intracerebral hemorrhage, Shunt complication, Ventriculoperitoneal shunt
VENTRİKÜLOPERİTONEAL ŞANT TAKILMASINI TAKİBEN GEÇ
DÖNEMDE GELİŞEN İNTRASEREBRAL HEMATOM
ÖZET
Ventriküloperitoneal şant takılmasını takiben geç dönemde intraserebral hematom gelişmesi oldukça nadir görülür.
Bu yazıda sol posterior serebral arter anevrizması ve hidrosefalisi olan 83 yaşında bir bayan hastada, şant takılmasını takiben 4. günde ortaya çıkan intraserebral hematom komplikasyonu bildirilmektedir.
Bu olguda kanamanın nedeninin şant kateterinin arteriosklerotik damar duvarını zedelemesi ve buna bağlı damar duvarındaki harabiyet olduğu düşünülmüştür.
Anahtar Kelimeler: İntraserebral kanama, Şant komplikasyonu, Ventriküloperitoneal şant
INTRODUCTION
Ventriculoperitoneal shunt placement is a routine procedure in daily neurosurgical activity. It is usually a simple and straightforward procedure. Intracranial hemorrhage is very rare after shunt insertion. The literature data shows that most of the cases had early hemorrhages soon after the surgery, but late or delayed intracerebral hemorrhages are very rare.
We report an unusual case with delayed intracerebral hematoma after a shunting procedure. Literature is reviewed and the causative factors are discussed.
CASE REPORT
An 83-year-old woman presented with one-year-history of dizziness. On admission, she had headache and nausea with a blood pressure of 170/80 mmHg. Neurological examination revealed slight ataxia.
A CT scan of the head with and without contrast demonstrated enlarged lateral and third ventricles and a left-sided hyperdense, slightly calcified 1.5x2 cm mass at the tentorial notch (Fig. 1). MR angiogram showed that this was a left posterior cerebral artery saccular aneurysm (Fig. 2).
Marmara Medical Journal 2004;17(1);28-31 Selçuk Peker, et al.
Delayed intracerebral hemorrhage after ventriculoperitoneal shunting
Endovascular interventional treatment of this vascular pathology was denied by the patient and her family. A new CT examination on the 2nd day
showed increased hydrocephalus. Ventriculoperitoneal shunting was performed on
same day without complication. The ventricular catheter was inserted in to the frontal horn through a right frontal burrhole. The cerebrospinal fluid was clear with a pressure of 220 mmH2O. The
catheter was connected to a medium pressure valve.
A control CT was performed immediately after the surgery and no hemorrhage was seen (Fig. 3). The tip of the ventricular catheter was in appropriate place. Postoperatively the patient was also well initially.
On postoperative day 4, she developed a generalized seizure and decreased conscious level. A CT scan showed intracerebral hemorrhage around the ventricular catheter and mild intraventricular hemorrhage (Fig. 4).
Her blood pressure was stable at 160/80mmHg. After the incident the tests for coagulation defects were repeated and no abnormality was found. Her clinical condition got worse over the following days. She eventually developed aspiration pneumonia and expired on the postoperative 18th day.
Fig 3: CT in the postoperative early period Fig 4: CT in the postoperative fourth day.
Blood is visualized around ventricular catheter
Fig 1: Contrast enhanced CT scan shows t: calcified round
mass at the tentorial edge. Fig 2: MR Angiogram reveals a left PCA aneurysm
Marmara Medical Journal 2004;17(1);28-31 Selçuk Peker, et al.
Delayed intracerebral hemorrhage after ventriculoperitoneal shunting
DISCUSSION
Ventricular shunting operations are among the most frequently performed neurosurgical procedures 1. Obstruction or blockage of the ventricular and abdominal ends of the tubing and infection are the most common complications 2. Small hemorrhages in the ventricles, in the subependymal area and around the ventricular catheters are relatively frequently seen 3. The
reason for these early hemorrhages is almost always trauma of the catheter insertion 1-6.
A late or delayed hemorrhage at the site of the ventricular catheter is very rare. There are only some case reports in the literature 1-6.
As an early complication, Udvarhelyi et al. 7 first
reported two cases with intracerebral hemorrhage after ventriculoperitoneal shunt insertion. Sayers 8
reported six cases of intracerebral hemorrhage among 1390 shunted cases.
Matsumura et al 6 reported the first case with CT
pictures of delayed intracerebral hemorrhage after shunting.
In our institution all patients with ventricular shunt insertions, undergo a control CT scan few hours after the of surgery. We had some patients with small hemorrhages around the catheter or in the ventricles, but none of them presented any clinical significance. We had only one patient with delayed intracerebral hemorrhage.
There are some possible mechanisms for intracerebral hemorrhages after shunt insertion; a bleeding disorder, antiaggregant or anticoagulant therapy, surgery induced disseminated intravascular coagulation, disruption of an intracerebral vessel by the catheter, hemorrhage into an intracerebral tumor, hemorrhage from a vascular malformation or spontaneous vascular rupture secondary to progressive degenerative vascular changes 1-6.
In the preoperative period all the laboratory tests were performed to discover any coagulation defects. The medications such as warfarin Na or acetylsalicylic acid were discontinued one week before the surgery. Because of these reasons it is very unlikely for these factors to be a causative factor.
Disseminated intravascular coagulation (DIC) has been described after head trauma, operation for brain tumor and after ventriculoperitoneal shunt insertion 1. The proposed mechanism for
DIC-induced hemorrhage in these instances is release
of brain thromboplastin as well as other substances found in the choroid plexus and meninges that act like plasminogen activators 1.
Hemorrhage into a cerebral tumor or hemorrhage due to a vascular malformation can also be seen in shunted patients. However, none of these seemed to be the causative factor in our patient.
The disruption of an intracerebral vessel by the catheter or spontaneous vascular rupture secondary to progressive degenerative vascular changes appears to be the most likely mechanisms.
Snow 1 reported a case of idiopathic
hydrocephalus with delayed hemorrhage. The hemorrhage was found at the catheter insertion site on the postoperative 5th day. The author
concluded that the normal pulsations of the cerebrospinal fluid transmitted to the ventricular catheter may have helped the catheter to erode a blood vessel with subsequent intracerebral hemorrhage. This mechanism may have been the reason in our patient too. Savitz 2 reported five
patients with delayed hemorrhages and he suspected of the same mechanism.
Mascalchi 5 reported a patient who had a
hemorrhage 14 days after the shunt insertion. As a causative factor, changes in the intracranial and interstitial pressures heading to parenchymal or intravascular pressure changes in a hypertensive patient were suggested. Yet if this mechanism was operational, hemorrhage could have occurred in any part in the brain. Indeed in most of the patients delayed intracerebral hemorrhages were seen around the ventricular catheter.
Bavbek and Göksel 3 reported a patient which has
been shunted after posterior fossa tumor surgery. Their patient had multiple hematomas on the postoperative 18th day. These authors suspected
from the decompressive surgeries and prolonged increased intracranial pressure in their patient. Woollam and Millen 9 showed that in nontraumatic conditions, the hypoxia of the endothelial cells may lead to perivascular hemorrhage. At the insertion site, the traumatic edema of the cerebral tissue may cause this hypoxia.
We conclude that the mechanism of bleeding in our patient might be the disruption and irritation of the arteriosclerotic small diameter arteries of the brain near the catheter. The disruption was probably initially tamponaded by the high intraparenchymal pressure.
Marmara Medical Journal 2004;17(1);28-31 Selçuk Peker, et al.
Delayed intracerebral hemorrhage after ventriculoperitoneal shunting
Delayed intracerebral hemorrhage after ventricular shunting is rare. The mechanism is not clear, but the surgeon must be aware of this complication.
REFERENCES
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2. Savitz MH, Bobroff LM. Low incidence of delayed intracerebral hemorrhage secondary to ventriculoperitoneal shunt insertion. J Neurosurg 1999; 91:32-34
3. Bavbek M, Göksel M. Multiple delayed intracerebral hematoma after ventriculoperitoneal shunting. Turk Norosirurji Dergisi (in Turkish) 1997; 7:82-84
4. Kubokura T, Nishimura T, Koyama S. Delayed intracerebral hemorrhage following VP shunt operation. No Shinkei Geka 1988; 16(5 suppl):523-527
5. Mascalchi M. Delayed intracerebral hemorrhage after CSF shunt for communicating “normal-pressure” hydrocephalus. Case report. Ital J Neurol Sci 1991; 12:109-112
6. Matsumura A, Shinohara A, Munekata K, Maki Y. Delayed intracerebral hemorrhage after ventriculoperitoneal shunt. Surg Neurol 1985; 24:503-506
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9. Woollam DH, Millen JW. Vascular tissue in the central nervous system. In: Mickler J, editor. Pathology of the central nervous system, Vol. 1. New York: McGraw-Hill 1968: 486-498
