Published online Nov 28, 2026. doi: 10.5528/wjtm.124522
Revised: August 12, 2026
Accepted: October 10, 2026
Published online: November 28, 2026
Processing time: 140 Days and 5.4 Hours
Sickle cell disease homozygous SS (SCD-SS) is the most prevalent hemoglo
We report an 8-year-old girl with SCD-SS and a history of ischemic stroke re
The absence of secondary stroke prevention in a child with SCD-SS proved fatal. Transcranial Doppler screening and exchange transfusion therapy are potentially life-saving interventions. Expanding access to these therapies across sub-Saharan Africa is an urgent priority.
Core Tip: This case highlights the fatal consequences of absent secondary stroke prevention in a child with sickle cell disease homozygous SS (SCD-SS). An 8-year-old girl who survived an initial ischemic stroke subsequently developed a fatal hemorrhagic stroke in the setting of Plasmodium falciparum malaria, without having received secondary preventive care. In sub-Saharan Africa, limited access to transcranial Doppler screening and exchange transfusion programs continues to place children with SCD-SS at high risk of recurrent cerebrovascular events. This report underscores the urgent need to strengthen early screening and secondary stroke prevention strategies in resource-limited settings.
- Citation: Ahouangansi SER, Ouohi A, Koffi L, Kossonou AM, Kouamé KI, Toure WC, Bédié YV, Kakou KM, N’dah ES, Koné K, Adingra SCE, Aboudramane K, Ayé YD. Fatal hemorrhagic transformation after ischemic stroke in a child with sickle cell disease SS: A case report. World J Transl Med 2026; 12(4): 124522
- URL: https://www.wjgnet.com/2220-6132/full/v12/i4/124522.htm
- DOI: https://dx.doi.org/10.5528/wjtm.124522
Sickle cell disease (SCD) is the most prevalent hemoglobinopathy in sub-Saharan Africa, accounting for nearly 80% of global cases, with more than 515000 affected births annually according to the Global Burden of Disease Study 2021[1]. The brain is one of the principal target organs of this disease. Ischemic stroke affects approximately 11% of children with SCD before the age of 20 years and results from chronic vascular inflammation, progressive endothelial injury, and silently evolving arterial stenosis[2]. Hemorrhagic stroke is rarer but is frequently associated with irreversible consequences when it occurs[2].
Beyond the classical atherothrombotic, cardioembolic and small-vessel mechanisms, hematological disorders constitute a frequently unrecognized cause of both ischemic and hemorrhagic stroke. They account for approximately 1.3% of all acute strokes and represent the leading etiology among ischemic strokes of unusual cause; moreover, an acute cere
Pediatric stroke in SCD is particularly devastating as it is largely preventable. Transcranial Doppler (TCD) screening allows identification of high-risk children before the occurrence of a first cerebrovascular event by detecting accelerated flow velocities suggestive of progressive arterial stenosis[4]. Regular exchange transfusion therapy, targeting a hemoglobin S (HbS) fraction below 30%, has demonstrated robust efficacy in reducing stroke recurrence[5]. These are not experimental interventions; they are evidence-based tools recommended by international guidelines and have been proven to save lives when appropriately implemented.
We report the case of a child with SCD who did not receive any structured secondary preventive strategy and who, in the setting of a Plasmodium falciparum malarial episode, developed hemorrhagic transformation of a prior ischemic stroke.
An 8-year-old girl with homozygous SCD (SCD-SS; SSFA2 genotype), diagnosed in early childhood. She had received multiple blood transfusions and had previously sustained an ischemic stroke in October 2025, resulting in left hemiplegia. Her family history was unavailable. She was admitted to the intensive care unit (ICU) because of impaired consciousness and seizures.
Five days before admission, the patient developed intense frontal headache, fever, and recurrent generalized tonic-clonic seizures. Her family initially brought her to the Centre Hospitalier Régional d’Aboisso, where a thick blood smear identified Plasmodium falciparum malaria with a parasitemia of 800 trophozoites/µL. Intramuscular artemether was initiated, although the dose was not recorded. Owing to persistent seizures, progressive coma, and limited technical resources at the regional hospital, she was transferred to the pediatric emergency department and subsequently admitted to the ICU of Centre Hospitalier & Universitaire d’Angré, Abidjan, Côte d’Ivoire.
No special notes.
No special notes.
On admission to the ICU, the patient was febrile and tachycardic. Neurological examination revealed a Glasgow Coma Scale score of 11/15 and a left-sided pyramidal syndrome consistent with sequelae of her prior ischemic stroke. No signs of active bleeding, hepatosplenomegaly, or lymphadenopathy were noted. The pediatric National Institutes of Health Stroke Scale (PedNIHSS) is not routinely used in our unit and was therefore not scored prospectively on admission. Retrospective appraisal of the documented findings, namely impaired consciousness with a Glasgow Coma Scale score of 11/15, complete left hemiplegia involving both the upper and the lower limb, and inability to cooperate with language, sensory and cerebellar testing, indicated severe neurological impairment. No reliable numerical score was able to be assigned a posteriori, however, because several of the PedNIHSS items cannot be evaluated formally in a child with altered consciousness and recurrent seizures. The absence of a prospectively recorded PedNIHSS score is acknowledged among the limitations of this report.
Laboratory investigations performed on admission revealed a hemoglobin level of 7.6 g/dL (normal range: 11.5-15.5 g/dL for children aged 6-12 years), consistent with severe anemia. Procalcitonin level was 0.29 ng/mL (normal range: < 0.5 ng/mL), which was within normal limits and argued against bacterial superinfection. Cerebrospinal fluid analysis was clear and sterile, without pleocytosis or elevated protein levels, effectively ruling out bacterial meningitis. Peripheral blood smear confirmed active Plasmodium falciparum infection with a parasitemia of 800 trophozoites/µL. The HbS fraction was not measured at admission.
Initial cerebral computed tomography (CT) demonstrated a subacute ischemic infarction involving the territories of the right anterior cerebral artery (ACA) and right middle cerebral artery (MCA) (Figure 1). On day 4 of hospitalization, following acute neurological deterioration, emergency CT revealed diffuse subarachnoid hemorrhage, diffuse cerebral edema, and an 8-mm right subfalcine herniation, consistent with hemorrhagic transformation of the ischemic lesion (Figure 2). Cerebral magnetic resonance (MR) angiography was not available at the time of admission and, therefore, could not be performed.
Transthoracic echocardiography was likewise not performed during the hospital stay; no clinical argument for a cardiac embolic source was identified at the bedside, and the neurological instability of the child took priority in a unit where the examination is not available around the clock. A cardiac source of embolism, in particular infective endo
Electroencephalography: Electroencephalography (EEG) was not performed. EEG remains unavailable on an emergency or continuous basis in our institution, and the hemodynamic and neurological instability of the child precluded any transfer to conduct this examination. Consequently, non-convulsive seizures and non-convulsive status epilepticus could not be excluded once clinical control of the convulsive episodes had been obtained with midazolam, levetiracetam and phenobarbital. A persistent electrical seizure burden may therefore have contributed, undetected, to the secondary neurological deterioration observed on day 4.
Genetic testing: Hemoglobin electrophoresis performed at the time of the initial diagnosis confirmed homozygous SCD (SSFA2 genotype). No additional genetic testing was performed during the current hospitalization.
The patient was managed jointly by the pediatric intensive care, pediatric neurology, and hematology teams. Given the unavailability of exchange transfusion facilities and cerebral MR angiography at the institution, neurosurgical con
The final diagnoses were as follows: (1) Acute Plasmodium falciparum malaria with cerebral involvement; (2) Subacute ischemic infarction of the right ACA and MCA territories in the setting of SCD-SS-associated vasculopathy; (3) Hem
Initial management included anticonvulsant therapy with midazolam and levetiracetam, intravenous artesunate for the treatment of malaria, packed red blood cell transfusions, and dexamethasone for cerebral edema associated with the ischemic lesions. In the ICU, the patient received continuous multiparameter monitoring, phenobarbital for seizure control, continuation of intravenous artesunate, and isogroup-isorhesus packed red blood cell transfusions.
On day 2, a brief and fragile improvement was observed, with the Glasgow Coma Scale score increasing to 11/15. However, on day 4, the score dropped to 5/15 and was associated with anisocoria and meningeal signs. Emergency CT confirmed diffuse subarachnoid hemorrhage with subfalcine herniation (Figure 2). Despite maximal intensive care support, the patient died on day 5. No autopsy was performed owing to cultural and familial reasons.
This case is of triple interest from epidemiological, pathophysiological, and therapeutic perspectives.
Stroke represents one of the most severe neurological complications of SCD in children. Without preventive strategies, approximately 11% of children with SCD-SS experience a clinically apparent stroke before the age of 20 years[2]. Among children with TCD velocities exceeding 200 cm/second, the risk of stroke reaches approximately 40% within 3 years of screening in the absence of transfusion therapy[4,6].
The originality of this case lies in the sequential occurrence of an ischemic stroke followed by a hemorrhagic meningeal complication in a child with SCD-SS who already had neurological sequelae. Although ischemic stroke represents the most common cerebrovascular manifestation in pediatric SCD, hemorrhagic strokes remain considerably less common and occur primarily in young adults. In the Cooperative Study of Sickle Cell Disease cohort[2], the incidence of hem
In SCD, stroke does not occur in isolation but results from the convergence of at least six distinct pathophysiological mechanisms capable of acting simultaneously and potentiating one another. Acute hypoxia, linked to a drop in oxygen saturation or a sudden decrease in hemoglobin, constitutes a major triggering factor[7]. This is compounded by progressive cerebral vasculopathy, characterized by arterial stenoses and moyamoya-type vascular remodeling, which silently erodes cerebrovascular reserve over time[8]. Severe anemia associated with a high HbS fraction induces a compensatory increase in cerebral blood flow that further compromises already vulnerable vascular territories. Acute febrile infections may also exacerbate this condition by sharply increasing cerebral metabolic demand precisely when the brain has the least reserves to cope[9]. In older adolescents with SCD, classical cardiovascular risk factors such as hypertension and dyslipidemia may further increase vascular burden[10]. Finally, rapid increases in hemoglobin level following transfusion can itself become harmful by inducing hyperviscosity capable of triggering new vascular events[11,12]. In our patient, most of these mechanisms were simultaneously active. Her HbS was uncontrolled, recurrent seizures were present, and she had active malaria. Each of these factors independently increased the risk of cerebrovascular deterioration; together, they likely contributed to the fatal outcome.
The hemorrhagic transformation that occurred on day 4 remained clinically difficult to anticipate at the bedside. Within an extensive ischemic territory, disruption of the blood-brain barrier leads to loosening of tight junctions and progressive loss of vascular structural integrity. During spontaneous reperfusion, fragile microvessels that have lost the protective function of the blood-brain barrier become vulnerable to rupture[13]. Massive cerebral edema further worsens the condition by increasing intracranial pressure to levels exceeding vascular resistance. This process is compounded by the chronic vascular lesions of SCD, including endothelial inflammation, vascular wall rigidity, and microaneurysm formation, all of which contribute to cumulative flaws in an already compromised cerebrovascular network[14]. Per
Early seizures deserve specific attention in this case, as they were present from the very onset of the illness, recurred despite treatment, and preceded the hemorrhagic event by several days. Seizures occurring during the acute phase of a cerebrovascular event are not a simple epiphenomenon; they arise within the temporal window in which potentially salvageable penumbral tissue still exists, and they abruptly raise cerebral metabolic demand, cerebral blood flow and intracranial pressure in a brain that has already exhausted its vascular reserve.
This prognostic weight has been documented in subarachnoid hemorrhage. In a prospective hospital-based series of 184 patients with non-traumatic subarachnoid hemorrhage[15], very early in-hospital death (i.e. within the first 72 hours) occurred in 9.8% of the patients, and those who died early were significantly more likely to have presented with seizures, progressive neurological deficit, altered consciousness, limb weakness and sensory involvement. After multivariate analysis, progressive neurological deficit and limb weakness remained independent predictors of very early death. Our patient combined almost all of these clinical markers, having early and recurrent generalized seizures, a progressive deterioration of consciousness from 11/15 to 5/15, and hemiplegia, with death occurring within 24 hours of the radiological documentation of the subarachnoid hemorrhage. This clinical trajectory is fully consistent with the severe early prognosis reported for subarachnoid hemorrhage presenting with such features, and supports regarding early seizures in a child with SCD not merely as a complication to be treated but as a warning sign that justifies immediate intensification of neurological monitoring and repeat cerebral imaging.
The absence of exchange transfusion therapy was not a peripheral detail in this case but rather a central aspect of the patient’s unfavorable outcome. Maintaining HbS below 30% reduces blood viscosity, limits vaso-occlusion, and stabilizes the cerebrovascular environment[5,6]. Without adequate secondary prevention, cerebrovascular injury may progress unchecked.
In sub-Saharan Africa, malaria and SCD frequently coexist, and their interaction can lead to severe consequences[16-18]. In children with the SSFA2 genotype, malaria may accelerate hemolysis, worsen anemia, increase blood viscosity, amplify vaso-occlusive processes, and critically promote capillary rupture in already ischemic cerebral tissue. In the present case, the malaria episode appears to have been the trigger that set the cascade leading to hemorrhagic trans
The interaction between Plasmodium falciparum malaria and cerebrovascular complications has been increasingly recognized in recent literature. Alabi et al[19], in a systematic review, reported that Plasmodium falciparum is associated with hemorrhagic stroke occurrence through mechanisms involving microvascular obstruction, endothelial activation, and hypercoagulability. However, to the best of our knowledge, hemorrhagic transformation of a prior ischemic stroke triggered by a malarial episode in a child with SCD-SS has not been reported in the literature. This rarity constitutes one of the major clinical contributions of the present case[16-18].
Corticosteroid administration in this context warrants critical consideration. Strouse et al[20] demonstrated, in a study involving children with SCD, that recent corticosteroid use was significantly associated with primary hemorrhagic stroke, independently of other risk factors. The proposed mechanism involves a rebound sickling effect following steroid discontinuation, accompanied by transient increases in blood viscosity, hemodynamic instability, and additional microvascular fragility.
In the present case, corticosteroid therapy was initiated to control cerebral edema associated with the extensive ischemic lesion, which constituted its primary clinical indication. However, it is impossible to retrospectively exclude the possibility that corticosteroid administration may have contributed to precipitating or worsening the hemorrhagic transformation observed on day 4. This association does not imply that corticosteroid therapy was contraindicated in this emergency setting but underlines the necessity of a rigorous benefit-risk assessment before corticosteroid administration in children with SCD presenting with active cerebrovascular injury. When corticosteroid use is deemed indispensable, close neurological surveillance, intracranial pressure monitoring, and strict control of blood viscosity are essential.
A hemorrhagic cardioembolic stroke, in particular one secondary to infective endocarditis, is an essential differential diagnosis that must be formally addressed in this presentation. Children with SCD-SS are exposed to repeated bacteremia, functional asplenia, chronic anemia with a hyperkinetic circulatory state, and repeated venous access, all of which increase the risk of infective endocarditis. Endocarditis may produce a septic embolic infarction that undergoes secondary hemorrhagic transformation, or may cause the rupture of an infectious intracranial aneurysm presenting as diffuse subarachnoid hemorrhage, a radiological picture superimposable on the one observed in our patient.
Recognition of this mechanism matters because the short-term prognosis of cardioembolic stroke is poorer than that of the other ischemic stroke subtypes. In a prospective registry of 1500 consecutive stroke patients[21], cardioembolic infarction accounted for 15.4% of cases and was characterized by sudden onset of the neurological deficit (79.7%) and altered consciousness (31.2%), significantly more often than atherothrombotic (46% and 24%) or lacunar (38% and 1.9%) infarction; early embolic recurrence occurred in 6.5% of patients, in 60% of them within the first 7 days, and in-hospital mortality reached 27.3%, against 21.7% for atherothrombotic and 0.8% for lacunar infarction. Sudden onset, early recurrence and rapid impairment of consciousness thus define a clinical profile that overlaps considerably with the course observed in our patient.
In the present case, several elements made the argument against infective endocarditis, including absence of peripheral embolic or immunological stigmata, a procalcitonin level within the normal range (0.29 ng/mL), clear and sterile cerebrospinal fluid, and identification of an alternative and sufficient explanation combining SCD-SS cerebral vasculopathy, severe anemia and acute Plasmodium falciparum malaria. Nevertheless, no blood culture result was available and no echocardiographic study was performed, so that a cardiac embolic source could not be formally ruled out. In retrospect, transthoracic echocardiography, ideally combined with blood culture assessment, should have been part of the initial etiological work-up, and we consider that any child with SCD presenting with stroke, fever and altered con
Cerebral CT remains the first-line imaging tool in resource-limited settings, as it is rapid, widely accessible, and essential for distinguishing ischemic from hemorrhagic lesions. However, CT alone cannot identify the hemodynamic abnor
Cerebral MR angiography, when available, provides a valuable morphological complementary assessment by mapping arterial stenoses, occlusions, and moyamoya-type vascular anomalies that TCD alone cannot fully characterize[5]. In the present case, the patient did not benefit from any of these surveillance modalities after her first stroke. Her vasculopathy likely progressed silently until the occurrence of the fatal cerebrovascular complication.
International guidelines clearly recommend that, after a first ischemic stroke in a child with SCD, regular exchange transfusions must be initiated to maintain the HbS below 30%, and should be continued long term[5,22]. Simple packed red blood cell transfusions, such as those received by our patient, are not considered a substitute. Although they increase total hemoglobin levels, they do not adequately reduce the HbS fraction and may paradoxically increase the risk of hyperviscosity[5,22]. In Côte d’Ivoire and many other countries in sub-Saharan Africa, access to TCD screening and structured exchange transfusion programs remains severely limited owing to equipment shortages, inadequately trained personnel, fragmented care pathways, and insufficiently resourced healthcare systems[23,24]. These limitations continue to pose major barriers to secondary stroke prevention in children with SCD.
Retracing the current patient’s clinical course, five major and avoidable failures can be identified. First, her HbS fraction was never monitored after the first stroke, and the key essential intervention was never performed. Second, no structured secondary prevention program was established, including the absence of an exchange transfusion protocol, regular TCD surveillance, or specialized neurovascular follow-up. Third, the malarial episode, a known and serious aggravating factor in SCD, occurred in a patient with no physiological protection against its effects. Fourth, the progression of the underlying cerebral vasculopathy remained undetected because the diagnostic tools required to monitor it were unavailable or had never been deployed. Fifth, admission to the ICU occurred at an advanced stage in the clinical trajectory, thereby limiting the opportunity to offer effective neuroprotective intervention. Individually, each of these shortcomings posed a considerable threat to the patient; together, they contributed to the fatal outcome.
This case report has several limitations inherent to its resource-limited context. First, the absence of cerebral MR angiography prevented precise characterization of the underlying vasculopathy, particularly the extent of arterial stenoses and the possible presence of a moyamoya-type network, whose documentation would have provided important pathophysiological and prognostic data. Second, the HbS fraction could not be measured at admission, preventing objective assessment of the degree of sickling at the time of neurological decompensation and precluding quantitative evaluation of the association between circulating sickle cell burden and the severity of the hemorrhagic event. Finally, no autopsy was performed owing to cultural and familial reasons, limiting understanding of the anatomopathological mechanisms leading to death and preventing the formal exclusion of other associated vascular lesions.
Three further limitations must be explicitly acknowledged. First, no echocardiographic study was performed during the hospital stay, which prevented formal exclusion of a cardiac source of embolism, in particular infective endocarditis, and constitutes a significant gap in the etiological work-up of a child presenting with stroke and fever. Second, EEG was not available, so that non-convulsive seizures and non-convulsive status epilepticus could not be ruled out once the convulsive episodes had been clinically controlled. Third, the PedNIHSS score was not recorded prospectively on admission, which limits the objective and reproducible quantification of the initial neurological severity and any com
This case highlights the extreme vulnerability of children with SCD in sub-Saharan Africa when secondary stroke prevention is absent. Clinically, this case advocates for early multidisciplinary management integrating pediatrics, neurology, hematology, and critical care specialists. Secondary stroke prevention in SCD should rely on rigorous clinical and neuroradiological surveillance, systematic use of chronic transfusion therapy or exchange transfusion, and the introduction of hydroxyurea according to current indications.
At the health system level, this case calls for urgent development of adapted care protocols in resource-limited settings, incorporating cerebrovascular risk stratification using TCD velocimetry, establishment of rapid referral pathways, and better access to cerebral imaging. Implementation of these measures is important to reduce preventable morbidity and mortality associated with neurovascular complications of SCD across sub-Saharan Africa.
Several research avenues emerge from this case profile. Prospective multicenter cohorts are needed in sub-Saharan Africa to establish the true incidence of hemorrhagic transformation after ischemic stroke in children with SCD-SS and to identify its predictors, including the HbS fraction, the transfusion regimen and concomitant malaria. The interaction between Plasmodium falciparum infection and SCD cerebral vasculopathy warrants dedicated pathophysiological studies combining biomarkers of endothelial activation, hemolysis and blood-brain barrier disruption. The benefit-risk balance of corticosteroid therapy for cerebral edema in children with SCD and acute cerebrovascular injury should be assessed specifically, since current evidence rests mainly on retrospective data. Finally, implementation research is required to define simplified, affordable and locally sustainable models of secondary prevention, including task-shifted TCD screening performed by trained non-specialists, manual partial exchange transfusion protocols adapted to limited blood-bank capacity and wider use of hydroxyurea, and to measure their real impact on stroke recurrence and mortality among African children with SCD.
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