Introduction

Traumatic posterior fossa hematoma is very less as compared with spontaneous hematomas associated with hypertension. They are associated with significant mortality and morbidity. They constitute a small subset of total head injury patients.1 As we know, posterior fossa have small volume, and any increase in volume due to any cause may cause increase intracranial pressure, herniation, and deterioration. Traumatic posterior fossa hematomas account for < 1% in all head injury patients.2 3 Liu4 reported the incidence of traumatic posterior fossa hematoma to be 3.7% of total intracranial hematomas. These hematomas may be totally asymptomatic, with a sudden increase in size can lead to rapid deterioration of neurological status.5

Traumatic cerebellar hematoma may be isolated or may be associated with subdural hemorrhage (SDH), extradural hemorrhage (EDH), and subarachnoid hemorrhage (SAH) in posterior fossa. They may present acutely or in delayed manner. The hematoma location, volume, initial Glasgow Coma Scale (GCS) score, status of fourth ventricle, and basal cisterns are important in final outcome. Management of these hematomas nowadays have changed from all surgery to conservative management.1

Authors evaluated outcome of patients on GCS score at admission, location, volume, status of cisterns, fourth ventricle, SAH, and supratentorial lesions. The surgical indications were posterior fossa hematoma with mass effect, midline shift, size greater than 3 cm, effaced basal cisterns, fourth ventricle compression, and associated supratentorial lesions with significant mass effect with midline shift.

Similarly, patients were managed conservatively with respect to hematoma location, size less than 3 cm, normal basal cisterns, and fourth ventricle. In some of these hematomas, early surgical intervention is deemed necessary.5 6 7 9 9 The early results of surgery are good, so surgical intervention if required should not be delayed. The course and prognosis of midline hematoma is worse, so evacuation should be done early.

Methods

From August 2011 to August 2017, approximately 5,100 patients with head injury were admitted in our institute. This study was focused on 21 patients (0.41%) with traumatic posterior fossa hematomas. The clinical findings, mode of injury, initial GCS, various radiological parameters, and final outcome were evaluated in 21 patients using Glasgow Outcome Scale (GOS). GOS was graded into good recovery (GR), moderate disability, severe disability (SD), vegetative state (VS), and death (D).

Initial computed tomography (CT) head was obtained at admission of patient and repeat CT head was done at 6 hours if the patient deteriorated more than 2 points of initial GCS score at admission. On CT scan, hematoma location, size, status of basal cisterns (normal or compressed), status of fourth ventricle (normal or compressed), associated SAH, and supratentorial lesions were evaluated. Hematoma volume was assessed by using formula A*B*C/2, where A is maximum transverse diameter of hemorrhage on CT, B is anterioposterior diameter, and C is number of CT slices showing hematoma.10

Hematomas were classified as type 1 vermian hematoma (Fig. 1) and type 2 hemispheric hematoma involving superficial two-thirds of the hemisphere (Figs. 2 and 3). Injury is classified as coup, countercoup, and acceleration-deceleration type. Time to reach hospital is important as it affects overall morbidity and mortality of patient.

Results

Clinical and Radiological Findings

Out of 21 patients, 18 were male and the rest females. Most of the patients were in the age range of 30 to 60 years. The mode of injury was road traffic accident (15 patients) and fall (6 patients). Duration between sustaining injury and reporting to hospital was 4 hours in 11 patients and 5 to 8 hours in 10 patients. GCS score on admission ranged from 3 to 15 as shown in Table 1. The location of hematoma was type 1 (8 patients) and type 2 (13 patients). Nine patients had isolated posterior fossa hematoma and 12 patients presented with associated intracranial lesions.

Intracranial lesions were supratentorial contusion (11), SDH (2), EDH (2), SAH (9), IVH (1), diffuse axonal injury (DAI) (1), hydrocephalus (HCP) (2), and SDH in posterior fossa in 1 patient (Fig. 3C). Basal cisterns were compressed in 9 and normal in 12 patients. Fourth ventricle had intraventricular hemorrhage (IVH) in 3, was compressed in 3, and normal in 15 patients. Associated injuries were found in 8, and skull fracture was seen in 15 patients. Out of 8 patients, only 1 had splenic injury which was managed conservatively and 1 patient had hemothorax which was managed by intercostal tube drainage.

Close

Fig. 1 (A) Computerized tomography scan revealing vermian hematoma (type 1). (B) Postoperative scan after suboccipital craniectomy and hematoma evacuation (type 1).

Export to PPT

Fig. 1 (A) Computerized tomography scan revealing vermian hematoma (type 1). (B) Postoperative scan after suboccipital craniectomy and hematoma evacuation (type 1).

Close

Fig. 2 (A) Computerized tomography scan revealing preoperative image type 2 hematoma. (B) Postoperative scan showing complete removal of hematoma.

Export to PPT

Fig. 2 (A) Computerized tomography scan revealing preoperative image type 2 hematoma. (B) Postoperative scan showing complete removal of hematoma.

Close

Fig. 3 (A) Computerized tomography scan revealing bilateral type 2 hematoma. (B) Computerized tomography revealing type 2 hematoma. (C) Computerized tomography revealing type 2 hematoma with subdural hemorrhage.

Export to PPT

Fig. 3 (A) Computerized tomography scan revealing bilateral type 2 hematoma. (B) Computerized tomography revealing type 2 hematoma. (C) Computerized tomography revealing type 2 hematoma with subdural hemorrhage.

Table 1

Summary of cases

S. no.	Age (y)	Sex (M/F) Durationa	Mode of injury, skull fracture	Associated lesions	Site of impact	GCS (3-15)	Volume, cm3, size (cm)	Type of location (½)	Basal cisterns (N/C)	Fourth ventricle (N/C/IVH)	Associated supratentorial lesions	SAH (A/P)	Intervention	GOS
Abbreviations: A, absent; C, compressed; D, death; DAI, diffuse axonal injury; EDH, extradural hemorrhage; F, female; GCS, Glasgow Coma Scale; GOS, Glasgow Outcome Scale; GR, good recovery; HCP, hydrocephalus; ICD, intercostal tube drainage; IVH, intraventricular hemorrhage; M, male; MD, moderate disability; MVA, motor vehicle accident; N, normal; P, present; SAH, subarachnoid hemorrhage; SD, severe disability; SDH, subdural hemorrhage; VS, vegetative state. Note: D-Site of impact could not be identified (acceleration-deacceleration injury), skull fracture (+, present;-absent). aDuration: Timing from injury to reporting to hospital in hours compared with type 1. SAH and supratentorial contusions were relatively higher in type 1 hematomas. There was no significant difference in other factors.
1	40	M, 4 h	MVA,-	None	Occipital	14/15	16.8 (3.5 cm)	2	N	IVH	No lesion	A	Suboccipital craniectomy	GR
2	40	M, 6 h	MVA,+	None	Frontal	5/15	4 (2)	1	C	N	Right frontal contusion	P	Conservative	D
3	30	F, 7 h	MVA,+	None	Fron tal, occipital	6/15	19.2 (4)	2	C	N	Right fron-to-tempo-ro-parietal acute SDH with IVH	P	Subocipital craniectomy	D
4	12	M, 2 h	MVA,-	None	Occip ital	15/15	2 (2)	2	N	N	No lesion	A	Conservative	GR
5	65	M, 4 h	Fall,+	Abdominal injury	Occip ital	12/15	15.4 (3.5)	2	N	N	No lesion	A	Suboccipital craniectomy	MR
6	47	M, 2 h	MVA,+	Fracture left ulna	Occip ital	13/15	40 (5)	2	N	C	No lesion	A	Suboccipital craniectomy	MR
7	35	M, 3 h	Fall,-	None	Occip ital	13/15	15.4 (3.5)	2	N	N	No lesion	A	Suboccipital craniectomy	GR
8	75	F, 6 h	Fall,+	None	Occiput	7/15	19.2 (4)	2	N	C	No lesion	P	Suboccipital craniectomy	D
9	22	M, 8 h	MVA,+	Fracture femur	Fron tal, occipital	5/15	4 (2)	1	C	N	Left frontal EDH, with bilateral temporal contusions, with hydrocephalus	P	Supratentorial craniectomy	D
10	79	M, 7 h	Fall,+	None	Occip ital	7/15	15.4 (3.5)	2	N	IVH	No lesion	P	Suboccipital craniectomy	VS
11	25	M, 1 h	MVA,-	None	Occip ital	15/15	1 (1)	2	N	N	No lesion	A	Conservative	GR
12	55	M, 3 h	MVA,-	Fracture clavicle	Occip ital	14/15	5.2 (3), 5 (2.5)	2 (bilateral)	N	N	Left temporal contusion	A	Conservative	GR
13	55	M, 2 h	MVA,+	Fracture humerus	Occip ital	13/15	15.4 (3.5)	1	C	IVH	No lesion	A	Suboccipital craniectomy	MR
14	56	F, 6 h	MVA,+	Fracture femur	Fron tal, occipital	7/15	15 (3)	1	C	C	Left frontotemporal contusion	P	Suboccipital and supratentorial craniectomy	D
15	25	M, 5 h	MVA,+	Fracture tibia	Temporal	9/15	1 (1)	2	N	N	Right basifrontal contusion, right temporal EDH, and left temporal contusion, right fron-to-tempo-ro-parietal SDH	P	Conservative	SD
16	47	M, 4 h	Fall,+	None	Frontal	3/15	2 (2)	1	C	N	Right frontal contusion with right frontotemporal acute SDH	P	Conservative	D
17	53	M, 6 h	MVA,-	None	Frontal	6/15	5 (2.5)	1	C	N	Bilateral basifrontal contusions, diffuse axonal injury	P	Conservative	D
18	42	M, 6 h	MVA,+	None, chest injury	Frontal	10/15	15.8 (3.5)	2	N	N	Right frontal contusion with mild hydrocephalus	A	Suboccipital craniectomy, ICD	SD
19	54	M, 8 h	Fall,+	None	Temporal	5/15	12 (3)	2	C	N	Left temporoparietal contusion	A	Conservative	D
20	43	M, 4 h	MVA,+	None	Occipital	9/15	4 (2)	1	C	N	Bilateral frontal contusion	P	Conservative	SD
21	32	M, 4 h	MVA,+	None	Occipital	15/15	5.2 (3)	1	N	N	Right frontal contusion	A	Conservative	GR

Discussion

These hematomas approximately constitute one-fourth of all posterior fossa traumatic lesions,3 11 but their frequency is almost between SDH and EDH.9 12 Sato et al13 established 0.7% incidence of cerebellar contusions. Nagata et al reported their frequency to be between 0.6 and 0.82%. The incidence observed in our series was 0.41%, which correlates well with other figures. Various mechanisms are responsible for these hematomas but remain unclear. These could be coup and countercoup injuries. Coup injuries are thought to be the most frequent mechanism.^1,7,14 Countercoup injuries are considered to be rare.15

Another mechanism for traumatic intracerebellar hematoma involves acceleration and deacceleration injuries.16 In our series, 7/21 patients had coup (33.3), 4/21 (19.0) had countercoup injuries, and the rest (47.6) had acceleration-deacceleration injuries. So, this leads us to the conclusion that acceleration and deacceleration is a common cause as reported previously by Takeuchi et al.17

Delayed or evolving hematoma has been reported previ-ously.18 19 In our series, no cases of delayed or evolving hematoma was reported as repeat scan was done within 6 hours of admission as mentioned previously. However, repeat CT examination is necessary, as delayed hematomas can develop.

The incidence of poor outcome in previously published series were around 20 to 100% (average 60%),2 and in our series, it was 61.9%. The prognosis was better in good GCS patient and in patients who were promptly operated with surgical indication.20 Summary of published series of posterior fossa hematomas are depicted in Table 4.

D’Avella et al have described protocol for traumatic intracerebellar hematomas as follows:

1. Conservative approach is a treatment option for noncomatose patients with intracerebellar clots 3 cm, except when associated with other EDH or SDH of posterior fossa.

2. Surgery should be done for any patient with any clot > 3 cm.

In our study, surgery was done in 11 patients, out of which 7 patients survived and 4 expired. In our series, type 1 hematomas were more frequent in the poor outcome group due to easy compression of brainstem or involvement of deep cerebellar nuclei which lead to bad prognosis.17

Various factors influencing surgical decision were patients with poor GCS, advanced age, poor general condition, clinical signs of early brainstem damage, bilateral cerebral clots, and associated multiple supratentorial intracranial hemorrhages with evidence of coagulopathy. These factors reflect the peculiar heterogenecity of clinical radiological picture of this subset of posterior fossa hematomas.21

HCP is usually not associated with traumatic intracerebellar clots.11 18 Karasawa et al3 mentioned of acute HCP in 20% of intracerebellar hematomas, while in our series it was 9.52%. The timing of reaching hospital is important and affects overall morbidity and mortality of patients. Most of the patients in the favorable outcome group reported to hospital within 4 to 5 hours, whereas those in the poor outcome group had reported more than 4 to 8 hours. There was single case of posterior fossa hematoma with associated SDH in our series (Fig. 1C). This suggests that associated lesions in posterior fossa hematoma such as SDH and EDH are less.

Posterior fossa hematoma is rare in children and incidence of cerebellar hematoma is much rarer.22 Most frequent mode of injury is fall followed by road traffic accident.23 Trauma is a leading cause of childhood head injury, with Center for Disease Control, stating about half a million emergency department visits in the United States is for traumatic brain injury for children aged 0 to 14 years, with 0 to 4 years being the most vulnerable group.24 Although most cases are seen in young adults, Zuccarello et al25 reported traumatic posterior fossa hemorrhage in children also. Wright9 reported 6 cases and Tsai et al11 reported 2 cases of children in their series. Similarly, in our series, we had a single child. Management of such cases is similar to adult posterior fossa hematoma.

Suboccipital craniectomy with hematoma evacuation is the most preferred surgical approach in posterior fossa.26 27 Clinical with radiological features, types of hematomas, prognostic factors, and final outcome are discussed and mentioned in Table 1 Table 2 Table 3. In summary, patients who reported within 4 hours of trauma, with initial GCS score of between 9 and 15, absent SAH, normal basal cisterns, and normal fourth ventricle had better survival rate. However, older age group and females fared worse in our study as shown in Table 1 Table 2 Table 3. In severely ill subjects, surgery should be individualized for each patient with reasonable salvageability.

Conclusion

Traumatic cerebellar hematoma is a life-threatening condition that requires timely management. Nowadays, with wider availability of CT and intensive neuromonitoring, smaller hematomas can be managed conservatively and larger ones with surgical evacuation in clinically deteriorating patients.

The factors correlated with patient outcome were age, sex, mode of injury, GCS at admission, associated intracranial hematomas, associated SAH, hematoma volume, hematoma location, basal cisterns, status of fourth ventricle, and associated multiple injuries on other body parts. It is hereby concluded that timely surgical intervention should be employed whenever indicated without delay. This study had some limitations, like sample size was relatively small to determine the actual prognostic factors. As these lesions are associated with higher morbidity and mortality, it should be evaluated further to explore pathophysiology for better clinical outcome of patients.