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| CASE REPORT |
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| Year : 2014 | Volume
: 28
| Issue : 3 | Page : 193-195 |
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Sub acute expansion of hypertensive intracerebral hematoma
Amit Agrawal
Department of Neurosurgery, Narayana Medical College Hospital, Chinthareddypalem, Nellore, Andhra Pradesh, India
| Date of Web Publication | 5-Jan-2015 |
Correspondence Address:
Amit Agrawal
Department of Neurosurgery, Narayana Medical College Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0972-4958.148525
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 |
| Introduction | |  |
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 | | |
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 | | |
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 | | |
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 | | |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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