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 Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 28  |  Issue : 3  |  Page : 193-195

Sub acute expansion of hypertensive intracerebral hematoma


Department of Neurosurgery, Narayana Medical College Hospital, Chinthareddypalem, Nellore, Andhra Pradesh, India

Date of Web Publication5-Jan-2015

Correspondence Address:
Amit Agrawal
Department of Neurosurgery, Narayana Medical College Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-4958.148525

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  Abstract 

Intracerebral hemorrhage (ICH) is usually secondary to systemic arterial hypertension, sudden in onset, rapidly progressive, fulminating disease, with profound neurological deficit and high mortality. In majority of the survivors of ICHclots are usually absorbed with minimal scar formation; however, in uncommon circumstances the clot can liquefy and expand causing delayed deterioration that require urgent hematoma evacuation to hasten the recovery. We discuss a case of a 40-year-old male, where the patient had delayed deterioration in his neurological status and a follow-up computed tomography (CT) scan showed sub-acute expansile intracerebral hematoma.

Keywords: Expanding intracerebral hematoma, Intracerebral hematoma, Hematoma, Hypertension


How to cite this article:
Agrawal A. Sub acute expansion of hypertensive intracerebral hematoma. J Med Soc 2014;28:193-5

How to cite this URL:
Agrawal A. Sub acute expansion of hypertensive intracerebral hematoma. J Med Soc [serial online] 2014 [cited 2020 Oct 20];28:193-5. Available from: https://www.jmedsoc.org/text.asp?2014/28/3/193/148525


  Introduction Top


Intracerebral hemorrhage (ICH) is usually secondary to systemic arterial hypertension, sudden in onset, rapidly progressive, fulminating disease, with profound neurological deficit and high mortality. [1],[2],[3] In majority of the survivors, the natural evolution of the clots is by absorption, leaving a residual small scar or cyst. [4] In uncommon circumstances, the hematoma can liquefy [5] or can become encapsulated thus behaving like slowly expanding lesions, with progressive neurological deficits. [1],[2],[3],[6]


  Case Report Top


A 45-year-old man presented in emergency room with a history of sudden onset of weakness of left upper and lower limbs 10 days back. He lapsed into altered sensorium at the same time. He was gradually improving in the sensorium, but again it was followed by decreased sensorium. He developed respiratory difficulty as well. He was diagnosed to have high blood pressure. He had blood pressure of 180/120 mmHg at the time of admission. He had bilateral crepitation. His other general and systemic examination was unremarkable. Neurologically, he was in altered sensorium with Glasgow coma scale (GCS) of E2 V2 M5. Pupils were bilateral equal and reacting to light. He had left upper facial nerve palsy. He had grade 1/5 weakness in left upper and lower limbs with planters' extensor and decreased all deep tendon reflexes. His initial computed tomography (CT) scan showed right basal ganglionic hematoma with mild peri-lesional edema and mass effect [Figure 1]. A repeat CT scan showed significant expansion and increase in size of basal ganglionic hematoma (particularly hypodense component) with increase in peri-lesional edema, mass effect and midline shift [Figure 2]. The patient underwent right frontal trephine craniotomy and evacuation of liquefied intracerebral hematoma. Post-operatively he was kept on elective ventilation and could be weaned off over a period of one week. Follow- up scan showed good evacuation of hematoma, decrease in peri-lesional edema and mass effect [Figure 3]. He recovered in speech, obeying commands but had weakness of left upper and lower limbs of grade 3/5.
Figure 1 : Initial CT scan showing right basal ganglionic hematoma with peri-lesional edema and mass effect

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Figure 2 : CT scan at the time of presentation to the emergency showing significant expansion and increase in size of hematoma with peri-lesional edema

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Figure 3 : Post-operative CT scan showing evacuation of hematoma and resolution of peri-pesional edema and mass effect

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  Discussion Top


Based on histopathological, imaging and intra-operative findings; chronic ICH has been categorized into "non-encapsulated" and encapsulated" [4] or "liquefied collections; and encapsulated, expanding lesions". [7] In present case, the hematoma was characterized by liquefied expanding collection causing clinical deterioration of the patient. When intracerebral hematoma persists for a longer duration there is an overabundant proliferation of the vascular granulation tissue [8],[9] and is characterized by a well-formed ring of contrast enhancement on CT scans, representing both "luxury perfusion" of the surrounding brain and peripheral vascular granulation tissues. [10] It has been a matter of debate that increase in size of hematoma is due to recurrent hemorrhage or due to leaking macrocapillaries with large endothelial gap junctions similar to those found in the capsule of chronic subdural hematomas. [11] It has been recognized since long that in comparison to scans of ordinary resolving hematomas (please see [Figure 4]), CT scans of a chronic ICH will demonstrate peri-lesional edema and mass effect (Please compare with [Figure 2]). [12] At angiography, a ring-like blush has been shown in chronic ICH cases not because of neovascularity but rather representing hyperperfusion in the adjacent brain as a result of loss of autoregulation. [13] The management of a non-encapsulated expanding ICH in patients with stable neurological status is to wait and to follow with serial CT scans to confirm a decrease in the size and radiographic attenuation of the lesion. [4] In patients with clinical deterioration and exansile nature of the hematoma, to hasten the recovery surgical evacuation is indicated. [1],[2],[3],[14]
Figure 4 : CT scan of another patient of right basal ganglionic hematoma showing usual natural history i.e. resolving hematoma with decease in size and less peri-lesional edema (please compare with Figure 2)

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  Conclusion Top


In summary, in majority of the survivors of ICH clots are usually absorbed with minimal scar formation; however, in uncommon circumstances the clot can liquefy and expand causing delayed deterioration that require urgent hematoma evacuation to hasten the recovery.

 
  References Top

1.
Fujii M, Takada Y, Ohno K, Hokari M, Arai T. Slowly progressive expanding hematoma in the Basal Ganglia: A report of 3 cases and a literature review. Brain Nerve 2012;64:295-302.  Back to cited text no. 1
    
2.
Jakubovic R, Aviv RI. Intracerebral hemorrhage: Toward physiological imaging of hemorrhage risk in acute and chronic bleeding. Front Neurology 2012;3:86.  Back to cited text no. 2
    
3.
Qin SQ, Yang Y, Heng XY, Liu YG, Fei C, Zhang QL, et al. Clinical analysis of 42 cases of chronic expanding intracerebral hematoma. Zhonghua Yi Xue Za Zhi 2012;92:2059-62.  Back to cited text no. 3
    
4.
Fiumara E, Gambacorta M, D'Angelo V, Ferrara M, Corona C. Chronic encapsulated intracerebral haematoma: Pathogenetic and diagnostic considerations. J Neurol Neurosurg Psychiatry 1989; 52:1296-9.  Back to cited text no. 4
    
5.
Yashon D, Kosnik EJ. Chronic intracerebral hematoma. Neurosurgery 1978;2:103-6.  Back to cited text no. 5
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6.
Aoki N, Mizuguchi K. Chronic encapsulated intracerebellar hematoma in infancy: Case report. Neurosurgery 1984;14:594-7.  Back to cited text no. 6
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7.
Pozzati E, Giuliani G, Gaist G, Piazza G, Vergoni G. Chronic expanding intracerebral hematoma. J Neurosurg 1986;65:611-4.  Back to cited text no. 7
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8.
Laster DW, Moody DM, Ball MR. Resolving intracerebral hematoma: Alteration of the "ring sign" with steroids. AJR Am J Roentgenol 1978;130:935-9.  Back to cited text no. 8
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9.
Lin SZ, Shih CJ, Wang YC, Tsai SH. Intracerebral hematoma simulating a new growth. Surg Neurol 1984;21:459-64.  Back to cited text no. 9
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10.
Hirsh LF, Spector HB, Bogdanoff BM. Chronic encapsulated intracerebral hematoma. Neurosurgery 1981;9:169-72.  Back to cited text no. 10
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11.
Reid JD, Kommareddi S, Lankerani M, Park MC. Chronic expanding hematomas. A clinicopathologic entity. JAMA 1980;244:2441-2.  Back to cited text no. 11
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12.
Zimmerman RD, Leeds NE, Naidich TP. Ring blush associated with intracerebral hematoma. Radiology 1977;122:707-11.  Back to cited text no. 12
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13.
Leeds NE, Goldberg HI. Abnormal vascular patterns in benign intracranial lesions: Pseudotumors of the brain. Am J Roentgenol Radium Ther Nucl Med 1973;118:576-85.  Back to cited text no. 13
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14.
Hsieh CT, Chang CF. Encapsulated chronic intracerebral hematoma mimicking neoplasm. Acta Neurol Taiwan 2009;18:227-8.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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Abstract
Introduction
Case Report
Discussion
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