A case of cerebellar hemangioblastoma causing obstructive hydrocephalus

Jenma Rakkini1*,Subathra Devi. M2,Mahalakshmi3

1Nursing Supervisor, Kauvery Hospital, Cantonment, Trichy, Tamil Nadu

2Nurse Educator, Kauvery Hospital, Cantonment, Trichy, Tamil Nadu

3Nursing Superintendent, Kauvery Hospital, Cantonment, Trichy, Tamil Nadu

*Correspondence

Abstract

Cerebellar hemangioblastomas are rare, highly vascular tumors that can present with nonspecific neurological symptoms. We report a case of a 68‑year‑old male who presented with progressive memory impairment for three months, mild gait disturbance, and slowing of motor activity for six months, along with occasional urinary urgency and incontinence. Neuroimaging revealed a cerebellar hemangioblastoma arising from the rostrum of the cerebellar vermis, causing obstructive hydrocephalus. The patient underwent surgical excision but developed severe postoperative complications, including neurogenic stress cardiomyopathy and refractory cardiogenic shock, ultimately leading to death. This case highlights the importance of early diagnosis, multidisciplinary management, and vigilant postoperative nursing care in patients with posterior fossa tumours.

Key words: Cerebellar hemangioblastomas; Obstructive hydrocephalus

Introduction

Cognitive decline in elderly patients is a common clinical problem and may be associated with several neurological disorders. When memory impairment is accompanied by gait disturbance and urinary symptoms, an underlying intracranial pathology should be suspected. Differential diagnoses include Normal Pressure Hydrocephalus, Parkinson’s disease, and posterior fossa tumors. Cerebellar hemangioblastomas, although uncommon, can cause obstructive hydrocephalus due to their location and mass effect. Early recognition and prompt intervention are crucial to prevent morbidity and mortality.

Case Presentation

A 68‑year‑old male presented with progressive memory impairment for three months and mild difficulty in walking with slowing of motor activity for six months. There was no history of headache, vomiting, or visual disturbances. The patient reported occasional urinary urgency and incontinence.

Social History

  • No history of smoking or alcohol consumption
  • No known drug allergies

Past Medical History

  • Type 2 Diabetes Mellitus
  • Systemic Hypertension
  • Benign Prostatic Hyperplasia

(All on regular treatment)

Past Surgical history: Nil

Physical Examinations

Conscious and oriented at admission

Blood Pressure120/70 mmHg
Heart Rate70 beats/min
Respiratory Rate20 breaths/min
Oxygen Saturation97% on room air
Temperature98.7°F
Glasgow Coma ScaleE4 V5 M6

Motor Examination

Spinal or cranial deformityNil
TremorsNoted in all 4 limbs
Romberg signPositive

Relevant Investigation

DateParameterResult
24/02/2026Blood Group and Rh Type - AutomatedA Positive
Urea Serum25 mg/dL
Creatinine0.6 mg/dL
Platelet Count201000 cells/µl
Total RBC Count4.31 ML/10^9
Mean Corpuscular Volume (MCV)89.3
Hepatitis B Surface Antigen (HBsAg)Negative (0.08)
Hepatitis C Antibody (Anti HCV)Non - Reactive (0.01)
25/02/2026Aspartate Aminotransferase 19 U/L
HbA1c9.40%
28/02/2026Bicarbonate24 mEq/L
Creatinine1.1 mg/dL
Urea Serum68 mg/dL
Potassium4.0 mmol/L
Sodium139 mmol/L
Chloride107 mmol/L
Alkaline Phosphatase84 U/L
Indirect Bilirubin0.9 mg/dL
Alanine Aminotransferase (ALT/SGPT)44 U/L
Globulin3.1 g/dl
Direct Bilirubin0.3 mg/dL
Albumin, Serum3.6 g/dl
Total Protein6.7 g/dl
Gamma - Glutamyl Transferase24 U/L
Aspartate Aminotransferase138 U/L
Total Bilirubin1.3 mg/dL
Calcium Serum9.2 mg/dL
Phosphorous3.0 mg/dL
Magnesium2.4 mg/dL
01/03/2026BE(B)-2.2 mm Hg
Glucose In Glucometer POCT205 mg/dL
Chloride Blood109 mEq/L
02 Saturation97.20%
K +4.5 mmol/L
Glucose201 mg/dL
HCO3(c)23.7 mmol/L
PCO244 mm Hg
pH Blood7.34
Haematocrit40%
Glucose In Glucometer POCT211 mg/dL
Phosphorous3.5 mg/dL
Magnesium2.9 mg/dL
Calcium Free Ionized4.55 mg/dL
02/03/2026Haematocrit41%
Sodium144 mmol/L
Urea Serum114 mg/dL
Creatinine1.1 mg/dL
Potassium5.3 mmol/L
Potassium4.8 mmol/L
03/03/2026Blood Ketone (POCT)6.3
NT Pro BNP (N - Terminal B Type )14300 pg/mL
Potassium4.7 mmol/L
Chloride113 mmol/L
Bicarbonate27 mEq/L
Cortisol Random66.3 µg/dL
Sodium152 mmol/L
Procalcitonin12.3 ng/mL

Imaging

MRI Brain revealed a lesion suggestive of a hemangioblastoma arising from the rostrum of the cerebellar vermis, protruding into the cerebral aqueduct, with surrounding vasogenic edema causing mass effect and secondary moderate obstructive hydrocephalus.

Diagnosis 

  • Cerebellar hemangioblastoma causing obstructive hydrocephalus
  • Type 2 diabetes mellitus
  • Systemic hypertension

Surgical Management

The patient was placed in the prone position under sterile conditions, and a midline suboccipital incision was made extending from 3 cm above the superior nuchal line to the level of the C2 arch. Following adequate exposure, a bilateral craniotomy was performed up to the margin of the transverse sinus and torcula. The dura was opened in a V-shaped manner, and under microscopic guidance, the pia and vermian cortex were incised and explored along the paramedian cerebellar region. As the lesion could not be identified initially, intraoperative ultrasound was used, and a gelatin sponge with a titanium clip was placed as a marker. The wound was temporarily closed, and the patient was shifted for an intraoperative CT scan, which showed the lesion slightly right of the midline and more superficial. The patient was then returned to the operating room, repositioned, and re-explored using microscopic guidance based on CT findings. A reddish vascular mass was identified at the anterior vermian surface and right paramedian cerebellum, and it was completely excised, suggestive of a hemangioblastoma. The dura was closed using a dural substitute, bone flaps were fixed with screws and plates, and the wound was closed in layers. No blood transfusion was required, and the patient was electively ventilated and shifted to the Neuro ICU for further monitoring.

Management

POD 0: The patient was in the Neuro ICU on mechanical ventilation with stable airway findings. Blood pressure was 170/90 mmHg. Initially, GCS was low due to relaxants, but later improved to E4 VT M6. We monitored ABG regularly, ABG showed severe metabolic and lactic acidosis.

POD 1: The patient remained sick with stable GCS but borderline BP. doctors monitored POCUS showed persistent LV dysfunction with pleural effusion. MRI showed post-surgical changes with edema and hydrocephalus. Trial extubation failed. Later, the patient developed acidosis and cardiogenic pulmonary edema. Treatment with diuretics, acidosis correction given as per doctor advice, and digoxin was started after cardiology review.

POD 2: The patient continued to have stress cardiomyopathy and pulmonary edema. GCS was slightly reduced, but the patient was arousable. Weaning was not tolerated. Immediately escalated to doctor, Clopilet was started, and cardiology co-management was ongoing.

POD 3: GCS was stable initially but later decreased. Severe LV dysfunction persisted, though acidosis and pulmonary edema improved. Medical management was continued, and tracheostomy was planned. Cardiology medications were adjusted as per doctor advice.

POD 5: The patient developed tachycardia, tachypnea, fever, and high blood sugar with worsening condition.

Outcome

The patient deteriorated with persistent shock, worsening sensorium, and sluggish pupils. Arterial BP was 84/68 mmHg. At 8.45 pm the patient went into cardiac arrest, CPR was initiated as per ACLS protocol, and the patient was declared dead at 9.15pm on 03.03.2026

Cause of Death

  • Immediate Cause: Refractory cardiogenic shock due to stress cardiomyopathy
  • Antecedent Cause: Status post suboccipital craniotomy and tumor excision
  • Underlying Cause: Cerebellar hemangioblastoma.

Nursing Management

  • Continuous neurological monitoring (GCS, pupil reaction, signs of raised ICP)
  • Airway management with mechanical ventilation and oxygenation support
  • Regular suctioning and prevention of ventilator-associated complications
  • Hemodynamic monitoring (BP, heart rate, perfusion)
  • Every 2nd hourly position changed as per protocol
  • Administration and titration of vasopressors as prescribed
  • Cardiac monitoring and early identification of stress cardiomyopathy
  • Strict fluid balance monitoring (intake–output charting)
  • Blood glucose monitoring and insulin infusion as needed
  • Infection prevention and aseptic surgical site care
  • Skin care and prevention of pressure ulcers
  • Nutritional support as per patient condition
  • Monitoring for complications (AKI, pneumomediastinum, shock)
  • Preparation for procedures (extubation trial, tracheostomy)
  • Documentation and timely reporting of changes
  • Providing emotional support and communication with family

Discussion

Neurogenic stress cardiomyopathy is a known complication following prolonged brainstem or posterior fossa surgeries. Diagnostic criteria include transient left ventricular apical or mid‑ventricular akinesia/dyskinesia, absence of significant coronary artery disease, new ECG changes, and exclusion of myocarditis, pheochromocytoma, or intracranial hemorrhage. In this case, stress cardiomyopathy significantly contributed to postoperative deterioration and mortality.

Conclusion

This case illustrates the complexity and severity of postoperative complications following cerebellar tumor surgery. Despite timely surgical intervention, intensive care management, and meticulous nursing care, the patient developed fatal neurogenic stress cardiomyopathy. The case underscores the importance of early diagnosis, vigilant postoperative monitoring, multidisciplinary collaboration, and high‑quality nursing care, while acknowledging that outcomes may still be unfavourable in critically ill patients.

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