Spontaneous Subarachnoid Hemorrhage as a Rare Manifestation of Dengue: A Case Report

INTRODUCTION

According to the World Health Organization (WHO), an estimated 50–100 million people contract dengue annually, with approximately 500,000 cases progressing to dengue hemorrhagic fever (DHF), resulting in around 22,000 deaths—mostly among children.^[1] Model-based estimates suggest that India accounts for nearly one-third of the global dengue burden, with approximately 33 million symptomatic cases annually.^[2] Among the officially reported cases, India has seen a significant increase, with numbers rising from 157,315 in 2019 to 289,235 in 2023, according to data from the National Center for Diseases Control.^[3] In Asian countries, the mortality rate for severe dengue ranges between 0.5% and 3.5%.^[2,4]

Dengue fever (DF) is a viral, mosquito-borne illness commonly seen in tropical and subtropical regions. It is caused by the dengue virus and transmitted to humans through the bites of infected Aedes aegypti and Aedes albopictus mosquitoes.^[2] The disease presents with a wide clinical spectrum, ranging from asymptomatic infection to severe complications such as multiorgan failure. Typical clinical features include fever, leukopenia, and thrombocytopenia. In most cases, the illness is self-limiting. Diagnosis can be confirmed by detecting IgM antibodies after seven days, indicative of an acute infection, while the presence of IgG antibodies suggests a previous exposure. Early detection is possible using Enzyme-linked immunosorbent assay ELISA-based identification of the Non-structural protein 1(NS1) antigen during the acute phase (days 1–7).^[1] In some cases, the infection may compromise vascular integrity, leading to plasma leakage—a hallmark of DHF—which can result in hemorrhagic manifestations.^[2,1] Severe cases may progress to intravascular volume depletion, culminating in dengue shock syndrome (DSS) or multiorgan dysfunction, collectively referred to as expanded dengue syndrome.^[1] Neurological complications (NCs) in dengue are uncommon. Recent studies report neurological involvement in 1–20% of dengue infections, with rare occurrences of SAH and other intracranial hemorrhages.^[4-6] Case reports as recent as 2024–2025 have detailed SAH, including cases linked to hemophagocytic lymphohistiocytosis and aneurysmal rupture.^[7]

This case presents a rare manifestation of expanded dengue syndrome, featuring subarachnoid hemorrhage (SAH) and hydrocephalus in a previously healthy 65-year-old male with severe thrombocytopenia. This unusual presentation underscores the complexity of severe dengue and the diagnostic and therapeutic challenges it poses for clinicians.

CASE REPORT

A 65-year-old male presented to the emergency department with complaints of headache and vomiting for two days. He had experienced a single episode of loss of consciousness lasting approximately 20 minutes, followed by an altered sensorium, which necessitated endotracheal intubation at an outside hospital. Additionally, the patient reported a history of 2–3 episodes of fever one week prior, which had resolved with over-the-counter medication.

On neurological evaluation, his Glasgow Coma Scale (GCS) score was E1VtM4, and pupils were bilaterally equal and reactive to light. On general physical examination, the patient was intubated, afebrile, and hemodynamically stable (pulse: 94/min, blood pressure: 130/82 mmHg, respiratory rate: 16/min, SpO₂: 99%). Arterial blood gas analysis (ABGA) was within normal limits. Both abdominal and respiratory examinations were unremarkable.

Initial laboratory investigations revealed a total leukocyte count of 11,000/cmm, a significantly reduced platelet count of 15,000/cmm, hemoglobin level of 13.3 g/dL, and a hematocrit of 40.7%. Renal function tests and serum electrolyte levels were within normal limits.

An emergency non-contrast computed tomography (NCCT) scan of the head revealed subarachnoid hemorrhage (SAH) along the sulcal spaces of the bilateral frontoparieto-temporal lobes, interhemispheric fissure, basal cisterns, and bilateral Sylvian fissures. Additionally, intraventricular hemorrhage (IVH) was observed in both lateral ventricles, along with marked ventricular dilatation and periventricular ooze, suggestive of hydrocephalus. The findings were consistent with Fisher Grade 4 SAH [Figure 1].

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Figure 1:

(a–c) Axial non-contrast Computed Tomography (CT) scans of the brain at different levels showing hyperdensities within the cerebral sulci of the bilateral fronto-parieto-temporal regions, interhemispheric fissure, basal cisterns, and Sylvian fissures suggestive of subarachnoid hemorrhage (SAH). Intraventricular extension of blood is noted in both lateral ventricles, with ventricular dilatation and periventricular ooze, indicative of acute hydrocephalus. Overall findings correspond to Fisher Grade 4 SAH.

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The patient underwent emergency neurosurgical intervention, during which a right-sided external ventricular drain (EVD) was placed [Figure 2]. Controlled cerebrospinal fluid (CSF) drainage was maintained over the following six days until clearance of blood from the CSF was achieved. Subsequently, a definitive procedure was performed, and a left-sided ventriculoperitoneal (VP) shunt was inserted.

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Figure 2:

(a–c) Axial non-contrast Computed Tomography (CT) scans of the brain at different levels showing an external ventricular drain (EVD) catheter in situ within the right lateral ventricle, with partial clearing of intraventricular hemorrhage and reduction in ventricular size compared to initial imaging. Residual hyperdensities within the sulci and ventricles are seen, consistent with resolving subarachnoid and intraventricular hemorrhage.

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A comprehensive diagnostic workup was conducted in collaboration with the departments of medicine and neurology to identify the etiology of subarachnoid hemorrhage (SAH) and thrombocytopenia. Postoperatively, digital subtraction angiography revealed no evidence of arteriovenous malformation (AVM) or intracranial aneurysm. There was no history of recent head trauma.

Given the severe thrombocytopenia at presentation, a full coagulation profile was evaluated. Peripheral blood smear and rapid antigen tests for malaria were negative. However, the dengue-specific IgM antibody test returned positive. Liver function tests revealed moderate elevations in SGOT (233 IU/dL) and SGPT (122 IU/dL), while abdominal ultrasonography showed hepatosplenomegaly. Coagulation parameters—including clotting time (CT), prothrombin time (PT), D-dimer levels, and activated partial thromboplastin time (aPTT)—were within normal limits. Bleeding time (BT) was prolonged 6 minutes and 40 seconds. Blood cultures were sterile.

The clinical picture was consistent with dengue fever (DF) presenting with a hemorrhagic complication in the form of SAH, without evidence of shock but with significant thrombocytopenia.

Management included multiple single-donor platelet transfusions, fluid resuscitation guided by central venous pressure, empirical antibiotics, decongestive therapy, proton pump inhibitors, and anticonvulsant medications. Following placement of the left-sided ventriculoperitoneal (VP) shunt, the patient demonstrated marked neurological and clinical improvement. He regained consciousness and began following commands. He was discharged in a stable condition on postoperative day 9. A follow-up non-contrast CT (NCCT) head scan was performed on day 14 during his outpatient department (OPD) visit Figure 3.

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Figure 3:

(a, b) Axial non-contrast Computed Tomography (CT) scans of the brain showing a left-sided ventriculoperitoneal (VP) shunt catheter in situ with well-decompressed ventricles and resolution of intraventricular and subarachnoid blood. The absence of periventricular ooze indicates effective cerebrospinal fluid (CSF) diversion and restoration of normal ventricular size following shunt placement.

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DISCUSSION

Currently, approximately 2.5 billion individuals— representing nearly 40% of the global population—reside in regions at risk of dengue virus transmission. The disease is endemic in at least 100 countries across Asia, the Americas, Africa, the Pacific, and the Caribbean. Dengue hemorrhagic fever (DHF) was first documented during the 1950s in outbreaks in the Philippines and Thailand.^[8] Commonly referred to as “breakbone fever” due to the severe musculoskeletal pain it causes, dengue is a mosquito-borne viral illness transmitted primarily through the bite of infected female Aedes aegypti mosquitoes.

The dengue virus exists in four distinct serotypes—DEN-1, DEN-2, DEN-3, and DEN-4. Infection with one serotype confers lifelong immunity against that specific strain; however, subsequent infections with different serotypes significantly increase the risk of severe complications, including DHF and dengue shock syndrome (DSS), both of which may be life-threatening. According to the 2011 revised World Health Organization (WHO) classification, dengue is categorized into dengue fever (DF), DHF (with or without shock), and expanded dengue syndrome.^[1]

Although DF is not inherently fatal, delayed diagnosis, reinfection with a different serotype, or the presence of underlying comorbidities may predispose patients to severe manifestations. The typical incubation period ranges from 4 to 10 days, followed by an acute symptomatic phase lasting 2 to 7 days. Clinical presentation includes a sudden onset of high-grade fever (often reaching 40°C/104°F), frequently exhibiting a biphasic pattern. Other symptoms comprise retro-orbital pain, headache, nausea, vomiting, myalgia, arthralgia, rash, and lymphadenopathy. In severe cases, dengue may progress to a critical phase marked by plasma leakage, hemorrhagic complications, and hypotension.^[1]

According to WHO guidelines, a diagnosis of DHF requires the presence of the following criteria: (1) acute febrile illness lasting 2–7 days; (2) hemorrhagic manifestations such as a positive tourniquet test; (3) thrombocytopenia with platelet count <100,000/mm³; and (4) evidence of plasma leakage, including hemoconcentration, pleural effusion, ascites, or hypoalbuminemia.^[1] Severe dengue with profound thrombocytopenia can result in organ dysfunction and significant bleeding, most frequently from the gastrointestinal tract. Other critical signs include hematemesis, severe abdominal pain, respiratory distress, fatigue, and altered mental status.

Both DF and DHF are associated with varying degrees of thrombocytopenia. While platelet counts may drop below 10 × 10⁹/L, severe bleeding remains rare, with most patients presenting only with minor manifestations such as epistaxis, petechiae, or gingival bleeding. However, the precise incidence and predictors of these complications remain inadequately defined.^[2,9]

In the absence of neurological complications (NC), management of dengue is largely supportive, emphasizing fluid resuscitation and judicious platelet transfusion in patients with critical thrombocytopenia.^[1] Currently, there is no specific antiviral therapy or widely accessible vaccine. Preventive strategies remain the cornerstone of disease control. A global dengue vaccine candidate is currently undergoing phase III clinical trials in multiple countries to evaluate its efficacy and safety.

Neurological manifestations in dengue are rare, occurring in fewer than 1% of cases.^[10] These complications may arise due to direct viral neurotropism, hemorrhagic sequelae, or secondary to multiorgan dysfunction. Reported neurological complications include encephalopathy, encephalitis, aseptic meningitis, intracranial hemorrhages, Guillain–Barré syndrome, myelitis, mononeuropathies, and polyneuropathies.^[5,11]

In the present case, the patient exhibited clinical signs of intracranial involvement. Neuroimaging confirmed the presence of subarachnoid hemorrhage (SAH) with associated hydrocephalus—a rare complication in the context of DHF. Although initial suspicion focused on a vascular anomaly such as an arteriovenous malformation (AVM) or aneurysm, digital subtraction angiography excluded these possibilities. Notably, the patient had no prior medical or familial history suggestive of cerebrovascular pathology.

The diagnosis of dengue fever was confirmed through a positive IgM serology, accompanied by marked thrombocytopenia. The patient required urgent neurosurgical intervention, initially via placement of an external ventricular drain (EVD) followed by a definitive left-sided ventriculoperitoneal (VP) shunt. Supportive management included multiple single-donor platelet transfusions, volume resuscitation, antibiotics, anticonvulsants, and proton pump inhibitors. The patient exhibited substantial neurological recovery, was discharged in stable condition on postoperative day 9, and showed no residual deficits during follow-up.

This case underscores a rare but potentially fatal manifestation of DF, in which SAH and hydrocephalus necessitated prompt neurosurgical intervention. Early recognition and a multidisciplinary approach were instrumental in achieving a favorable outcome.

Previous literature has documented similar presentations. Patey O et al. reported focal SAH in a patient with transient thrombocytopenia due to DF.^[12,13] MDPR Fernando et al. described a case involving subarachnoid, retinal, and vitreous hemorrhages in DHF.^[3,14] Jensenius et al. reported a fatal SAH in a Norwegian traveler with dengue fever, despite the absence of vascular anomalies on autopsy.^[7,15]

Lee I-K et al. described SAH in the context of DSS. Other reports have noted subdural hematomas, intracerebral hemorrhages, and dengue-associated encephalopathy.^{[9-13, 16,17]} Kumar R et al. presented a case of acute subdural hematoma in a child during the convalescent phase of DHF, which was successfully managed surgically.^[18] Cam . also reported intracranial hemorrhage in a case of dengue-associated encephalopathy.^[8]

These reports, including the present case, highlight the spectrum of neurological involvement in DF and DHF and reinforce the necessity for early diagnostic imaging and timely intervention to mitigate morbidity and mortality in such rare presentations.

CONCLUSION

Although neurological complications (NCs) in dengue fever (DF) are rare, clinicians must remain alert to the possibility of serious manifestations such as subarachnoid hemorrhage (SAH). Neurological symptoms in patients with DF should not be misattributed to febrile delirium or toxic encephalopathy, as such misinterpretations may lead to delayed diagnosis and critical delays in intervention. Early neuroimaging and timely management—including neurosurgical procedures such as intraventricular drainage when indicated—can substantially improve patient outcomes.

In dengue-endemic regions, healthcare providers should maintain a high index of suspicion for rare but life-threatening complications such as SAH, especially in the presence of thrombocytopenia and altered sensorium. Furthermore, differential diagnoses must be thoroughly considered and ruled out through appropriate investigations, including other etiologies of thrombocytopenia such as severe malaria, leptospirosis, gram-negative septicemia, disseminated intravascular coagulation (DIC), or co-infections.