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Spontaneous intracerebral hemorrhage (ICH) is a common condition that often leads to death or disability. Accurate prediction of the outcome and decisions regarding the treatment of ICH patients are important issues. We report a case of thalamic hemorrhage with an intraventricular hemorrhage that was suddenly migrated into the third and fourth ventricles in its entirety 8 hours after symptom onset. To our knowledge, this case is the first report of spontaneous migration of thalamic ICH into ventricles, and we suggest a possible mechanism for this case with a brief review of the literature.
The worldwide incidence of spontaneous intracerebral hemorrhage (ICH) ranges from 10 to 20 cases per 100,000 population, and increases with age14,16). Several studies have identified individual clinical and radiological variables that are correlated with mortality in ICH. These include the hematoma size or volume, Glasgow coma scale (GCS) score, presence of hydrocephalus, intraventricular extension, degree of midline shift, level of consciousness, age, fever, hyperglycemia, and pulse pressure1,2,4-7,11,13,16,18,19).
It is difficult to compare the effectiveness of medical and surgical treatment in patients with ICH and it is frequently necessary to perform both forms of treatment, as they are often complementary3).
We experienced a case of right thalamic ICH with intraventricular hemorrhage (IVH). The hematoma volume was about 12 mL. Initially, the patient was treated conservatively. However, 8 hours after symptom onset, the patient abruptly became semi-comatose, and computed tomography (CT) revealed that the entire thalamic ICH had been suddenly migrated into the third and fourth ventricles. Emergency external ventricular drainage (EVD) and bifrontal decompressive craniectomy were performed. However, he died five days later. We introduce this case with a brief review of the literature.
A 31-year-old man was hospitalized because he becane stuporous abruptly. He had no history of trauma, hypertension, tumor, infectious disease, or previous surgery. On physical examination, his systolic blood pressure was 130-140 mmHg. On neurological examination, he was stuporous, and his pupil size was 3/2 mm, with no light reflex. His GCS score was 9. Brain CT on admission showed a right thalamic ICH (3.5 × 2.3 × 3.0 cm), with intraventricular extension and a midline brain shift of about 0.8 cm. The estimated total volume of the ICH was about 12 mL (Fig. 1). Eight hours after symptom onset, he suddenly became semi-comatose, and his pupils were 5/5 mm, with no light reflex. Follow-up brain CT showed no evidence of rebleeding, but the entire right thalamic ICH had migrated into the ventricular system suddenly, with marked hematoma accumulation in the third and fourth ventricles. The suprasellar and prepontine cisterns were obliterated and severe brain swelling with pseudo-subarachnoid hemorrhages (SAH) was noted (Fig. 2). We performed emergency EVD on right Kocker's point for correction of non-communicating hydrocephalus. Follow-up brain CT after EVD showed decreased ventricle size, but remained intraventricular hemorrhage in both lateral ventricles, and ill defined low density lesions were seen on brain stem, medial frontal, temporal and occipital lobe. This lesion was suggested acute cerebral infarction due to increased intracranial pressure (ICP) (Fig. 3). Emergency bifrontal decompressive craniectomy was carried out in order to decrease ICP. However, his level of consciousness was deteriorated. He became comatose, and both pupils were fully dilated, with no light reflex. Magnetic resonance imaging (MRI) revealed acute infarction in posterior cerebral artery territory, including the pons and mid-brain (Fig. 4). He died five days after symptom onset.
ICH accounts for 10-15% of all strokes and is associated with a high mortality rate3,7,10). Indeed, the 30-day mortality for ICH is 34-53%4,7,14). Strong associations with poor outcome are known for mass effect and size, intraventricular extension, and decreased level of consciousness1,2,4-7,9,10,14,16,18-20).
Early neurological deterioration (END) is common after an ICH; it occurs in 20-40% of patients and is associated with a poor prognosis12). The identification of predictors of END may help in designing therapeutic strategies for ICH. High body temperature, neutrophil count, and plasma fibrinogen on admission are independent predictors of END. Hyperthermia may be a result of the acute-phase reaction and inflammatory response. The fibrinogen levels may reflect the activation of inflammatory mechanisms responsible for tissue damage around the hematoma12).
The mass effect, which results from the volume of the hematoma, the edematous tissue surrounding the hematoma, and obstructive hydrocephalus with subsequent herniation, remains the chief secondary cause of death in the first few days after ICH. Progressive elevation of intracranial pressure is seen in patients with massive ICH3,15,16). Extension of the ICH into the ventricles occurs in association with large, deep hematomas6,16). The presence of blood in the ventricle may be related to the development of obstructive hydrocephalus or a direct mass effect if the ventricular blood is located on a periventricular structure, which is associated with global hypoperfusion of the overlying cortex6,9,15,16). In our case, intraventricular extension of the hematoma was seen, but there was no obstructive hydrocephalus initially. In one quarter of patients with ICH, secondary deterioration of consciousness occurs within the first 24 hours, and worsening cerebral edema is implicated in the neurological deterioration that typically occurs within 24-48 hours after the onset of hemorrhage8,9,16).
A comparison of the effectiveness of medical and surgical treatment in patients with ICH is difficult and both forms of treatment frequently complement each other1,3). A recent study suggested that aggressive, timely reversal of transtentorial herniation, through the use of hyperventilation and osmotic agents improved the long-term outcome16). The surgical removal of any hemorrhage is beneficial because it reduces the hematoma volume, lowers ICP, improves perfusion in the affected hemisphere, prevents secondary enlargement of the hematoma, and reduces neurotoxic edema3,8,9,14). The surgical results may be better if patients are selected for surgery earlier, before they deteriorate3,7,20). This is associated with decreased 30-day mortality, although the overall morbidity and mortality did not differ significantly in patients who underwent surgery compared with those who did not4,14).
ICP may not respond to conservative management strategies, necessitating a decompressive craniectomy. Positive effects of bifrontal craniectomy on both ICP and the clinical outcome of head-injury patients have recently been reported20). The effects of craniectomy include regression of blood congestion, reduced edema formation, and increased edema absorption. The ideal time when a craniectomy should be performed and the exact effects of a decompressive craniectomy on ICP and cerebral tissue oxygenation remain unclear17). The indications for a craniectomy are a decrease in local brain tissue oxygen pressure (ptiO2 below 10 mmHg, coupled with ICP exceeding 20 mmHg, or a pro-gradient increase in ICP of at least 25 mmHg, resistant to conservative treatment3,17).
In our case, follow up CT scans revealed that the entire hematoma was migrated into the ventricular system abruptly, and pseudo-SAH was newly developed in basal cisterns at 8 hours after onset. The mechanism for the development of a pseudo-SAH has not been elucidated fully. Severe brain edema compresses the dural sinuses, compromising the venous drainage from the brain and resulting in engorgement of the superficial veins, which stand out against the edematous low-attenuated brain parenchyma, mimicking an SAH and narrowing or disappearance of hypo-attenuated CSF space as an additional factor generating a pseudo-SAH20). A possible cause for this sudden migration of the hematoma into the ventricles may be that the hemispheric ICP was increased suddenly and pushed it into the ventricle. The causes of increased hemispheric ICP are unknown, but we postulate that a gradual increase in cerebral edema around the hematoma and compromising the venous drainage from the brain may be causes.
We report an extremely rare case involving the sudden migration of a thalamic ICH into the 3rd and 4th ventricles. A sudden migration of an ICH with pseudo-SAH may indicate increased ICP. Immediate ICP control, with medical and surgical treatment, is necessary in such patients.