Korean Journal of Cerebrovascular Surgery 2008;10(3):454-458.
Published online September 1, 2008.
Remote Cerebellar Hemorrhage After Surgery for an Unruptured Aneurysm.
Baek, In Hyun , Park, Keun Young , Lee, Jae Whan , Huh, Seung Kon
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea. sk522@yumc.yonsei.ac.kr
Abstract
We report here on 2 cases of remote cerebellar hemorrhage (RCH) that developed after surgery for supratentorial unruptured aneurysm. In both cases, cerebral angiography was performed to diagnose the aneurysms and then screening was conducted for determining if there were any previous bleeding tendencies and comorbidities. After surgery, computed tomography (CT) was immediately performed to check for postoperative hemorrhage or infarction, and the images showed cerebellar hemorrhage that was relatively far away from the surgical site. We present the similarities of the 2 patients' preoperative angiography and CT and their perioperative blood pressure, and we discuss these findings to illuminate the pathophysiology of RCH.
Key Words: Aneurysm surgery, Cerebellar hemorrhage, Venous infarction

Introduction 


  
Remote cerebellar hemorrhage (RCH) after supratentorial craniotomy is an infrequent and poorly understood complication. Although RCH have been described several times in some literatures,2)3)8)10)11)12) its etiology and mechanism have been unclear. We will present 2 cases of RCH after aneurysm surgery and discuss the common findings in both cases. And we reviewed the previous literatures. 

Case reports 

Case 1 
   The patient was a 57-years-old man who was admitted for unruptured aneurysm surgery of an incidental aneurysm of the anterior communicating artery (Acom). He had no significant medical history, except for photoallergic dermatitis and laboratory study could not show any coagulopathy. Preoperative digital subtraction angiography (DSA) showed the unruptured Acom aneurysm without any other remarkable findings and both transverse sinuses were well shown in the venous phase of right vertebral angiogram (Fig. 1A, B). Aneurysm clipping was performed by usual pterional approach. During operation, he was hemodynamically stable. However, in the recovery room, systolic blood pressure (SBP) was up to 170mmHg. Postoperative CT brain images showed the remote cerebellar hemorrhage (Fig. 2A). However, he did not have any neurological deterioration except headache. He did not have any other surgical procedure and was discharged without neurologic deficit. One month after surgery, follow up CT showed the resolution of hemorrhage (Fig. 2B). 

Case 2 
   The patient was a 59-years-old woman who was admitted for incidental Acom aneurysm surgery. She had a history of hypertension and diabetes mellitus. Preoperative DSA showed the unruptured Acom aneurysm with poorly visualized left transverse sinus (Fig. 3A, B). Aneurysm clipping was performed by usual pterional approach. During operation, she was hemodynamically stable and SBP never exceeded 140mmHg. However, during the waking-up from anesthesia, SBP elevated up to 165mmHg suddenly. Although postoperative brain CT showed the remote cerebellar hemorrhage (Fig. 4A), the patient had no neurologic deterioration. On postoperative day 2, the patient s mentality became stuporous. Follow-up CT showed increasing cerebellar hematoma with acute obstructive hydrocephalus (Fig. 4B, C). Emergent decompressive suboccipital craniectomy and hematoma removal was performed. At postoperative month 1, she was fully recovered except mild gait disturbance and discharged. 
   The characteristics of the 2 patients are summarized in Table 1

Discussion 

   RCH after supratentorial craniotomy is uncommon and poorly understood complication. Sometimes it can cause fatal neurologic deterioration.1)5) Some cases have been published in the literature. Konig et al showed an incidence of RCH after superatentorial craniotomy to be approximately 0.3%.7) Cloft reported a higher incidence of about 3.5% after aneurysm surgery.3) An incidence of 4.9 % after temporal lobectomy was reported by Toczek et al.10) However, its etiology and pathophysiology is not clear. 
   Many theories have been proposed to explain the pathophysiology of RCH. We reviewed literatures and summarized them as below: 
   First, cerebrospinal fluid (CSF) overdrainage induces downward displacement of the cerebellum, and mechanical disturbance in the venous system, which leads to stretching or tearing of bridging vermian or posterior mesencephalic veins and tirbutaries.5)11)13) As a result, venous blockade and hypertension are evoked and lead to cerebellar hemorrhage. Also, Poppen and colleagues reported that RCH from following supratentorial surgery could result in a blockade of venous drainage due to brain swelling and increased supratentorial pressure.9) Second, another group of authors proposes that acute loss of CSF and craniotomy induce negative supratentorial and intracranial pressure, which can result in a reciprocal increase in the transmural pressure in veins and venules, traumatize the cerebellar capillaries, and cause intracerebellar hemorrhage.6)7) Third, Farag E. and colleagues suggest that head rotation and neck flexion can induce positional jugular vein compression which leads to venous hypertension and hemorrhage.4) Although most authors agree that the main pathophysiology of RCH is the venous infarction, most literatures did not explain about venous drainage pattern of preoperative DSA. Tucker and colleagues reported that the angiographic finding did not show any other vascular abnormalities.11) 
   In our second case, the ipsilateral transverse sinus was poorly visualized on preoperative DSA. However, angiographic abnormalities were not shown in the first case. Although concomitant findings were not shown in DSA, It was possible for poorly drained transverse sinus in preopretive DSA to be a contributor of RCH and more severe cerebellar edema. Actually, in the second case, the patient had more extensive hemorrhage, aggressive course and neurologic deterioration. Less functioning transverse sinus amplified stretching and tearing of bridging vein which lead to extensive RCH. Forth, Friedmann and colleagues found that elevated intraoperative systolic blood pressure was independent risk factor associated with RCH.5) In our cases, intraoperative blood pressure were stable. However, postoperative SBP elevated suddenly and could not be well controlled. 
   It is thought for the pathophysiology of RCH to be complex including CSF overdrainage, venous flow disturbance, intracranial hypotension, arterial hypertension and head position.(Fig. 5) We can have one question; How can we prevent RCH? First, preoperative DSA should be reviewed by experienced neurosurgeon to identify venous drainage pattern. Second, extreme head rotation and flexion should be avoided for release jugular vein. Finally, after supratentorial craniotomy, expert of neurosurgical anesthesia should emergence the patient carefully to control blood pressure. 

Conclusion 

   In spite of rarity, RCH can cause fatal outcome. And it can be related with several factors. Neurosurgeons should be aware of its possibility and if preoperative DSA show less drained venous system, more careful attention can prevent this complication. 


REFERENCES


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  5. Friedman JA, Piepgras DG, Duke DA, McClelland RL, Bechtle PS, Maher CO, et al. Remote cerebellar hemorrhage after supratentorial surgery. Neurosurgery 49:1327-40, 2001 

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  9. Poppen JL, Kendrick JF Jr, Hicks SF. Brain stem hemorrhages secondary to supratentorial space-taking lesions. J Neuropathol Exp Neurol 11:267-79, 1952 

  10. Toczek MT, Morrell MJ, Silverberg GA, Lowe GM. Cerebellar hemorrhage complicating temporal lobectomy: report of four cases. J Neurosurg 85:718-22, 1996 

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  13. Yoshida S, Yonekawa Y, Yamashita K, Ihara I, Morooka Y. Cerebellar hemorrhage after supratentorial craniotomy: report of three cases. Neurol Med Chir 30:738-43, 1990



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