Simultaneous occurrence of cerebral bleed and infarct

Amitesh Aggarwal; Luv Bansal; Meenakshi Jain

doi:10.4103/upjimi.upjimi_1_21

CASE REPORT

Year : 2021 | Volume : 15 | Issue : 1 | Page : 56-58

Simultaneous occurrence of cerebral bleed and infarct

Amitesh Aggarwal¹, Luv Bansal², Meenakshi Jain³
¹ Department of Medicine, University College of Medical Sciences and GTB Hospital, New Delhi, India
² Department of Neurology, GB Pant Hospital, New Delhi, India
³ Department of Internal Medicine and Critical Care, Max Multispeciality Hospital Noida and Patparganj, India

Date of Submission	28-Oct-2021
Date of Decision	04-Jan-2022
Date of Acceptance	01-Feb-2022
Date of Web Publication	13-Apr-2022

Correspondence Address:
Dr. Luv Bansal
Department of Neurology, GB Pant Hospital, New Delhi
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/upjimi.upjimi_1_21

Abstract

BACKGROUND: Simultaneous occurrence of ischemic and hemorrhagic stroke is extremely rare although the pathology of both types of strokes is similar. However, this poses challenges in management of such cases.
CASE DETAIL: An 80-year-old Indian housewife presented to the hospital in altered sensorium with no significant comorbidity in the past. On neurological imaging, she was found to have both intracerebral infarct and bleed. She was managed conservatively.
CONCLUSION: There are challenges in management of these types of patients as treatment is different in both scenarios. This case raised the question regarding the routine management of such cases. In the absence of published guidelines, individual tailoring of treatment is needed.

Keywords: Bleed, cerebral, hemorrhage, infarct, stroke

How to cite this article:
Aggarwal A, Bansal L, Jain M. Simultaneous occurrence of cerebral bleed and infarct. J Intern Med India 2021;15:56-8

How to cite this URL:
Aggarwal A, Bansal L, Jain M. Simultaneous occurrence of cerebral bleed and infarct. J Intern Med India [serial online] 2021 [cited 2023 Mar 24];15:56-8. Available from: http://www.upjimi.com/text.asp?2021/15/1/56/343023

Introduction

Multiple ischemic infarcts and multiple hemorrhagic infarcts involving different arterial territories are rare clinical events. It is reported in 1.3% of acute bihemispheric infarcts and cardioembolism is the most common etiology.^[1] Multiple hemorrhagic infarcts were reported as unusual by Kohshi et al. who reported two such cases.^[2] Existing literature suggests that occurrence of cerebral bleed and cerebral infarct together in a patient is even rarer although both types of stroke share the common vascular pathology of atherosclerotic changes in small perforating arteries. There are challenges in management of these types of patients as treatment is different in both scenarios.

Case Report

An 80-year-old housewife of Indian origin was brought to the hospital with altered sensorium for the past 4 days. It was sudden in onset. She was not speaking to anyone, bed ridden, and not accepting meals. There was no history of preceding fever, seizures, and head trauma. There was no history of hypertension, diabetes mellitus, or cerebrovascular incident in the past. She was nonsmoker, nonalcoholic, vegetarian by diet and belonged to the lower middle class strata.

On examination, she was conscious but disoriented. Her blood pressure was 100/64 mmHg in with regular pulse. Cardiovascular, abdominal, and respiratory examination was unremarkable. Neurologic examination showed positive Babinski's sign on the right side. Tone was decreased in all four limbs and she was moving all the four limbs spontaneously. Fundus examination was normal.

Laboratory workup including complete blood counts, blood sugar, lipid profile, electrocardiography, kidney, and liver function tests were unremarkable. Serum electrolytes showed hyponatremia with serum sodium levels of 126 meq/dl. The noncontrast computed tomography of head at the time of presentation revealed hyperdensity (68–72 HU) with surrounding edema measuring 2.0 cm × 1.8 cm in left parieto-occipital lobes suggestive of bleed plus another hypodense (10–26 HU) lesion in right parietal and occipital lobes with loss of gray white matter interface suggestive of infarct with no midline shift [Figure 1] and [Figure 2].

Figure 1: Axial section of noncontrast computed tomography scan of brain shows a well-defined irregularly outlined hyperdense (HU~ +68-+72) lesion (straight arrow) in left parieto-occipital lobes with peri-lesional hypodensity, suggestive of parenchymal bleed with peri-lesional edema. Another wedge-shaped hypodense area (HU~ +10-+26) noted in the right parieto-occipital watershed zone (curved arrow) with loss of gray-white matter interface, s/o infarct with no midline shift

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Figure 2: Axial section of noncontrast computed tomography scan of brain shows a well-defined irregularly outlined hyperdense (HU~ +68-+72) lesion straight arrow) in left parieto-occipital lobes with peri-lesional hypodensity, suggestive of parenchymal bleed with peri-lesional edema

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She was managed conservatively. During the course of stay in hospital, she developed aspiration pneumonitis leading to sepsis with multi organ dysfunction. Later, she left the hospital against medical advice on request of family members.

Discussion

Few cases of simultaneous occurrence of intracerebral bleed and infarct in a patient have been reported.^[2],[3],[4] The co-occurrence of intracranial hemorrhage and infarct is rare but when they co-occur, management related issues arise. It is known that aggressive blood pressure reduction in intracranial hemorrhage may cause infarct in ischemic penumbra and hemorrhagic transformation may occur in ischemic infarcts.^[5] Vasospasm which is common after subarachnoid hemorrhage may present with both ischemia and hemorrhagic stroke (i.e., call-fleming or reversible cerebral vasoconstriction syndrome).^[6] In this case, hemorrhagic and ischemic infarct occurred in different cerebral hemispheres without any evidence of subarachnoid hemorrhage which ruled out the above possibilities. Hypertension is the most common etiology for both types of stroke. It is recommended to reduce mean arterial pressure to <130 mmHg to reduce hematoma growth during acute phase, however, controversies exist due to the lack of randomized controlled data.^[7] Recent data have however suggested that aggressive blood pressure lowering may decrease effective cerebral perfusion pressure below 60 mmHg and cause acute brain ischemia thus worsening outcomes after the intracranial hemorrhage.^[8],[9] In case of intracranial hemorrhage, the aim is to limit hemorrhage growth and hemostasis with procoagulant agents or surgical evacuation may be required.^[10],[11] For ischemic infarct, the use of antiplatelets and statins has shown improved clinical outcome. However, when both ischemic and hemorrhagic stroke co-occur, antiplatelets are not used due to risk of hematoma expansion. Further, anticoagulants are often not used which increase the risk of peripheral venous thrombosis and cause adverse outcomes.^[5] Use of diffusion-weighted magnetic resonance imaging to detect relation between ischemic brain insult and blood pressure reduction may help in guiding management.^{[8],[9],[10],[11],[12]} Although aspirin use has been shown to be nondetrimental in cases of infarcts with hemorrhagic transformation,^[13] there is a lack of appropriate guidelines and/or clinical studies about the use of antiplatelets and anti thrombotics in such cases.

Acute stroke is a catastrophic event and simultaneous occurrence of both bleed and infarct raises critical challenges in the management. Acute aggressive blood pressure lowering should be avoided in case of stroke and individualized targets may be necessary. During the pro-inflammatory “stroke prone” period, the use of antiplatelets and statins therapy to prevent secondary neuronal injury may be more beneficial even at the expense of hemorrhage growth or recurrent hemorrhage. Other risk factors such as atrial fibrillation, coronary artery stenosis, and hypercoagulable states, if present, should be addressed appropriately. Strict glycemic control should be done with blood sugar levels between 140 and 180 mg/dl.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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