Concurrent Occurrence of Ischemic and Hemorrhagic Stroke in a Patient in a Low Resource Setting Hospital, Western Uganda: A Case Report

Introduction

Stroke is a major global health problem and a leading cause of death and long-term disability worldwide.¹ It is broadly classified into ischemic and hemorrhagic subtypes, which differ in pathophysiology, clinical course, and management. Ischemic stroke, accounting for approximately 80–85% of cases, results from cerebral arterial occlusion leading to focal brain infarction, whereas hemorrhagic stroke occurs due to rupture of intracranial blood vessels, causing intracerebral or subarachnoid bleeding.² The concurrent occurrence of ischemic and hemorrhagic strokes in the same patient is uncommon and represents a complex clinical presentation with significant diagnostic and therapeutic implications.

Patients with concurrent ischemic and hemorrhagic strokes often present with acute neurological deficits that may include unilateral weakness, speech disturbances, altered consciousness, seizures, severe headache, or vomiting.³ The coexistence of both stroke subtypes can result in overlapping or atypical clinical features, making early clinical differentiation challenging. Such presentations are associated with higher morbidity and mortality compared to isolated stroke subtypes.⁴

Accurate and timely diagnosis is critical in cases of concurrent ischemic and hemorrhagic strokes. Non-contrast computed tomography (CT) of the brain remains the initial imaging modality of choice to rapidly identify intracranial hemorrhage.⁵ Magnetic resonance imaging (MRI), particularly diffusion-weighted imaging (DWI) and susceptibility-weighted imaging (SWI), provides greater sensitivity for detecting acute ischemic lesions and small hemorrhages.⁶ Additional investigations, including vascular imaging and laboratory evaluation, are often required to identify underlying etiologies such as hypertension, anticoagulant use, vascular malformations, or cerebral amyloid angiopathy.

The simultaneous presence of cerebral ischemia and hemorrhage significantly increases the risk of complications, including cerebral edema, raised intracranial pressure, hemorrhagic expansion, secondary ischemic injury, and neurological deterioration.⁷ These patients are also at increased risk of poor functional outcomes and prolonged hospitalization.

Management of concurrent ischemic and hemorrhagic strokes is particularly challenging due to conflicting treatment priorities. Standard ischemic stroke therapies, such as antiplatelet agents, anticoagulation, or thrombolysis, may worsen intracranial bleeding, while aggressive management of hemorrhagic stroke—such as blood pressure reduction or reversal of anticoagulation—may compromise cerebral perfusion in ischemic areas.⁸ Treatment therefore requires an individualized, multidisciplinary approach focused on hemodynamic stabilization, prevention of secondary brain injury, careful blood pressure control, and close clinical and radiological monitoring. Reporting such cases contributes to the limited body of evidence guiding management strategies for this rare but serious clinical scenario.

Case Presentation

An 83 year old female was referred from a peripheral facility with 3 day symptoms of sudden onset right sided weakness of both upper and lower limb associated with mouth deviation to the right and aphasia which was expressive in nature. There was history of reduced level of consciousness, no convulsions, no change in personality or abnormal sensations. She was unable to swallow. Attendants denied history of fevers or headaches.

Review of other systems revealed a history of decreased appetite and food intake, decreased interaction with the environment.

She was a known hypertensive on amlodipine 10mg once daily with good adherence, no other known chronic diseases, no known food or drug allergies. Was not on any other medications.

Stopped alcohol intake 40 years back, had never smoked cigarettes though she used biomass fuel for cooking. She was a widow that stayed with her daughter, had good social support.

She was sicklooking, not in obvious respiratory distress, unconscious.

BP: 197/115mmhg, pulse 78 b/min, SPO2: 86% on Room air.

Mildly dehydrated, not anemic or jaundiced.

CNS exam: arousable, GCS: 8/15. E2, V1, M5, pupils were equally reactive to light, soft neck, negative kernigs, right arm power 2/5, hypertonic, hyperreflexic, right lower limb power 0/5, hypertonic, hyperreflexive. Sensation and vision could not be assessed because of the low GCS.

NIHHS score was greater than 25.

Cvs: warm peripherals, irregularly irregular pulse, normal JVP, normal s1 and s2, no murmurs or added sounds, no carotid bruit ausculated.

Respiratory: rate, 23breaths/min, equal bilateral air entry, normal breath sounds, basal crepitations.

Per abdomen: normal fullness, soft, non-tender, no palpable organomegalies, normal bowel sounds.

Investigations

Table 1 shows a full blood count.

Table 1 Complete Blood Count with Differentials

Table 2 shows a renal function test and electrolyte.

Table 2 Renal Function Tests and Electrolytes

Table 3 shows d dimers.

Table 3 D-Dimer Test

Table 4 shows lipid profile.

Table 4 Lipid Profile

Imaging

Figure 1 shows Non contrasted brain CT scan.

Figure 1 Non contrasted brain CT scan. Note: Showed ischemic lesion in the left frontal parietal area and heamorrhagic lesion in the cerebellum.

Findings were of acute heamorrhagic stroke involving the cerebellum and ischemic stroke involving the left sided frontal parietal lobe.

Figure 2 shows an Electrocardiogram that showed features of an irregularly irregular rhythm.

Figure 2 Electrocardiogram. Note: showed fast atrial fibrillation.

Impression: elderly patient of hypertension with ischemic and hemorrhagic stroke secondary to poorly controlled hypertension and atrial fibrillation complicated with probable increased ICP and aspiration pneumonia.

The patient was managed supportively since thrombolysis was both unavailable and unsafe due to concurrent hemorrhage, antiplatelet therapy was not given either.

Airway was secured by nasogastric tube insertion and positioning, proper feeding technique was taught and implemented. Amlodipine 10mg was administered and blood pressure monitored. Atovastatin 40mg once daily, oxygen therapy and antibiotics to cover aspiration pneumonia. Hypertonic saline and bed elevation were administered for increased ICP.

Physiotherapy with 2 hourly turning was initiated. Attendants were educated about the diagnosis and prognosis. Blood pressure was mildly controlled, patient was weaned off oxygen in the following days, there was mild improvement in focal neurological deficits and level of consciousness to GCS of 12/15. E4, M5, V3.

Admission lasted 4 days, they were discharged against medical advice due to financial constraints, follow up of patient condition while home was also not possible for same reasons.

Discussion

Epidemiology and Clinical Significance

Available epidemiological data indicate that the vast majority of stroke cases present as a single pathological subtype. Reports of simultaneous ischemic and hemorrhagic strokes occurring in different brain territories are rare and largely limited to isolated case reports and small case series.^4,5 In Africa, hospital-based studies provide limited but more direct estimates. A prospective study conducted in Sikasso, Mali, reported ischemic stroke in 74.8% of patients, hemorrhagic stroke in 21.5%, and mixed stroke in 3.7%.⁹

This rarity may reflect both the infrequency of the underlying mechanisms and underdiagnosis, particularly in resource-limited settings where advanced neuroimaging modalities may not be routinely available. In this case, the patient was managed without appropriate imaging and referred 3 days after symptom onset which possibly worsened the patients outcome.

Clinical Presentation

Patients with concurrent ischemic and hemorrhagic strokes often present with acute neurological deficits, including unilateral weakness, speech disturbances, altered level of consciousness, seizures, severe headache, or vomiting.⁶ The coexistence of both stroke subtypes may lead to overlapping or atypical clinical features, making early clinical differentiation difficult. Such presentations are associated with higher morbidity and mortality compared with isolated ischemic or hemorrhagic strokes.⁷ The presented patient’s presentation was a complex interplay between possible causes of the strokes for example hypertension, atrial fibrillation and thrombocytopenia and the symptoms of focal neurological deficits plus reduced level of consciousness.

Elevated urea and creatinine were thought to be acute kidney injury while the elevated d dimers probably pointed to wide spread thrombotic events with platelet depletion and subsequent heamorrhagic stroke. Confirmation of mechanisms and outcomes where not locally available.

Proposed Pathophysiological Mechanisms

Several mechanisms have been proposed to explain the concurrent occurrence of ischemic and hemorrhagic stroke.

Intracranial arterial dissection is one important mechanism, as it may cause luminal narrowing or occlusion leading to ischemia while simultaneously weakening the vessel wall and predisposing to hemorrhage. Intracranial dissections are increasingly recognized as causes of mixed stroke presentations, particularly in younger patients and those without traditional vascular risk factors.⁸

Severe hypertensive small-vessel disease is another proposed mechanism. Chronic hypertension leads to lipohyalinosis and fibrinoid necrosis of penetrating arteries, predisposing some vessels to occlusion and infarction while others rupture, resulting in hemorrhage in different brain regions.¹⁰ This mechanism is especially relevant in older patients and those with long-standing uncontrolled hypertension.

Underlying cerebrovascular disorders such as moyamoya disease, cerebral amyloid angiopathy, and vasculitis have also been associated with mixed ischemic and hemorrhagic events. Moyamoya disease is characterized by progressive stenosis of major intracranial arteries with fragile collateral vessel formation, conferring a dual risk of cerebral ischemia and hemorrhage.¹¹

Systemic and hematologic factors, including coagulopathies, thrombophilia, and anticoagulant use, may further contribute to a mixed stroke pattern. In such cases, thrombotic and hemorrhagic events may coexist, particularly in the presence of endothelial dysfunction or vascular fragility.¹²

Distinction from Hemorrhagic Transformation

It is essential to distinguish true concurrent ischemic and hemorrhagic strokes from hemorrhagic transformation of an ischemic infarct. Hemorrhagic transformation represents secondary bleeding within an infarcted region and typically occurs within the same vascular territory. In contrast, concurrent ischemic and hemorrhagic strokes involve distinct lesions in separate brain regions, reflecting independent pathological processes rather than progression of a single ischemic event.³

Diagnosis

Accurate and timely diagnosis is critical in cases of concurrent ischemic and hemorrhagic strokes. Non-contrast computed tomography (CT) of the brain remains the initial imaging modality of choice for rapid identification of intracranial hemorrhage.¹³ Magnetic resonance imaging (MRI), particularly diffusion-weighted imaging (DWI) and susceptibility-weighted imaging (SWI), offers greater sensitivity for detecting acute ischemic lesions and small hemorrhages in different vascular territories.¹⁴

Additional investigations, including vascular imaging and laboratory evaluation, may assist in identifying underlying etiologies such as arterial dissection, hypertension, anticoagulant use, vasculopathies, or cerebral amyloid angiopathy. In our setting, only a non-contrast CT scan was performed due to availability and financial constraints.

Complications

The simultaneous presence of cerebral ischemia and hemorrhage significantly increases the risk of complications, including cerebral edema, raised intracranial pressure, hematoma expansion, secondary ischemic injury, and neurological deterioration.¹⁵ These patients are at increased risk of poor functional outcomes and prolonged hospitalization. These would explain the lowered level of consciousness in our patient though confirmatory measurement of intracranial pressure was not available and so it’s management was not optimum.

Management

Management of concurrent ischemic and hemorrhagic strokes is particularly challenging due to competing treatment priorities. Standard therapies for ischemic stroke—such as antiplatelet agents, anticoagulation, and thrombolysis—may exacerbate intracranial bleeding. Conversely, aggressive blood pressure reduction or reversal of anticoagulation aimed at limiting hemorrhagic expansion may compromise cerebral perfusion in ischemic regions.⁴

Consequently, management must be individualized, emphasizing stabilization, cautious blood pressure control, prevention of secondary brain injury, and treatment of underlying etiologies rather than strict adherence to conventional stroke protocols.

In this case, although the patient was in atrial fibrillation, anticoagulation was considered contraindicated due to the presence of intracranial hemorrhage and was therefore not administered; antiplatelet therapy was also withheld. Mild blood pressure lowering was instituted, statins were administered, and supportive care including oxygen therapy and antibiotics was provided. Management of increased intracranial pressure which would be a hall mark in this presentation was done with only hypertonic saline with only mild improvement, any further management both medical and possible surgical decompression were not available.

Prognostic Implications

The prognosis of patients with simultaneous ischemic and hemorrhagic strokes remains poorly defined due to limited data. Available evidence suggests poorer outcomes compared with isolated stroke subtypes, attributable to greater neurological burden and restricted therapeutic options.⁵ Early recognition and multidisciplinary management are therefore essential to optimize outcomes.

Limitations

1. Late patient presentation after onset of neurological deficits, patient was admitted after 3 days.
2. Poor imaging quality and further imaging to diagnose causation and direct treatment was not available.
3. Inability to measure and successfully manage increased intracranial pressure in this patient due to limited therapeutic resources.
4. Financial constraints limited patient’s stay in hospital, the family requested a discharge against medical advice.
5. Follow up of patient after discharge was not made possible by the family.

Conclusion

Although rare, the simultaneous occurrence of ischemic and hemorrhagic strokes in different brain regions is a recognized clinical entity with important diagnostic and therapeutic implications. Multiple mechanisms, including intracranial arterial dissection, hypertensive small-vessel disease, and underlying vasculopathies, may contribute to this presentation however in a low resource setting, investigating and managing them is severely limited making an already challenging medical dilemma almost impossible to manage with any long term success. Awareness of this phenomenon is crucial to guide advances in investigation and individualized management strategies. Further studies are required to establish optimal treatment approaches and long-term outcomes for this uncommon but complex condition.