Cerebral venous thrombosis with intracerebral hemorrhage in a patient with C1Q nephropathy and acute pancreatitis: a rare clinical constellation

Aswin Vinitha *

Staff Nurse, Kauvery Hospital, Hosur, Tamil Nadu

*Correspondence

Abstract

Cerebral venous sinus thrombosis (CVST) is an uncommon yet serious and treatable cause of neurological impairment. Clinical manifestations vary widely and often include headache, focal neurological deficits, seizures, papilledema, and altered consciousness. Rarely, CVST may present with rapidly progressive cognitive dysfunction. Early recognition, neuroimaging, and timely multidisciplinary management facilitated gradual neurological recovery.

Key words: Cerebral venous sinus thrombosis (CVST); Glasgow Coma Scale (GCS);

Introduction

Cerebral venous thrombosis is a neurovascular emergency characterized by thrombosis of the dural venous sinuses or cortical veins. Clinical presentation is highly variable and may occur within 12–72 hours following head injury or due to underlying prothrombotic conditions. Typical symptoms include headache, seizures, motor deficits, disorientation, and decreased consciousness. Prompt stabilization, neuroimaging, monitoring, and multidisciplinary interventions are essential. Patients with preserved Glasgow Coma Scale (GCS) and no significant midline shift may be managed conservatively with Antiepileptic, Antihypertensive, Anticoagulation, Anti-edema measures, and Supportive therapy. This report underscores the importance of comprehensive evaluation in a patient who is presented with neurological deficits following trauma.

Case presentation

The patient developed numbness and weakness of the left upper limb for the past 2 days.
He had a headache for 1 week along with intermittent giddiness.
He experienced a fall the previous night following a giddiness episode and sustained a minor head injury.
After the fall, he developed slurred speech, left-sided weakness, and deviation of the mouth to the right.
No history of fever, vomiting, seizures, visual disturbances, or loss of consciousness before arrival.

Past medical history: Systemic Hypertension – on regular medication.

Past surgical history: No previous surgeries.

Vital Signs

On Admission

BP	160/100 mmHg
PR	110/min
RR	22/min
Temperature	97°F
SpO₂	97% on room air
RBS	165 mg/dl

Systemic Examination

CVS	S1 S2 heard, normal
Respiratory system	Clear
Neurological	Left-sided weakness, slurred speech

Imaging

Chest X-ray	No abnormalities
ECG	No abnormalities
ECHO	EF 60%; LVH; Grade I diastolic dysfunction; trivial MR/TR
USG Abdomen	Bulky heterogeneous pancreas; early inflammatory changes; medical renal disease Grade I; bladder wall thickening

Neuroimaging

MRI Brain

Periventricular and subcortical ischemic changes
Small vessel ischemic disease
Right acute subcortical bleed
Right parietal edema
Paracortical vein thrombosis

MR Angiography

Normal arterial circulation

MR Venogram

Patent major venous sinuses
Paracortical venous thrombosis

CT Brain

Right temporal and parietal subarachnoid hemorrhage
Multiple intra-axial hemorrhages
Resolving right parietal ICH
Edema without significant midline shift

Investigations

Investigations	Results
Hb	19.2 g/dl
Platelet count	248000/Cumm
Total Count	13990/Cumm
PH	6.96
PCO2	37mmHg
PO2	32mmHg
HCO3	8.3mmol/L
Lactate	0.8mmol/L
Urea	70.6mg/dl
Creatinine	2.6mg/dl
Sodium	139mmol/L
Potassium	5.2mmol/L
PTT	12.3
INR	1.09
Total Bilirubin	1.3mg/dl
Bilirubin Direct	0.5mg/dl
Bilirubin Indirect	0.7mg/dl
SGOT	41u/l
SGPT	24u/l
Albumin	31
Calcium	8.7mg/dl

Diagnosis

Cortical Venous Thrombosis
C1q Nephropathy- Biopsy Proven
Acute Pancreatitis
Systemic Hypertension
Hyponatremia – SIADH

Medical Management

Initial CT brain imaging revealed a right high parietal intracerebral hemorrhage, maintained midline ventricular alignment, right sylvian subarachnoid hemorrhage, and open basal cisterns. Based on clinical and radiological features, a diagnosis of right high parietal intracerebral hemorrhage with venous infarction and hemorrhagic transformation was made.

Day 1

On assessment, the patient’s Glasgow Coma Scale (GCS) score was E3V4M6. Pupils were bilaterally equal (2 mm) and reactive to light. Motor examination showed left-sided weakness (4/5). The patient was managed conservatively with antiepileptic, antihypertensive, anti-edema therapy, analgesics, and supportive measures. He was maintained under strict neuro-monitoring in the ICU.

A subsequent repeat CT brain demonstrated persistent right parietal intracerebral hemorrhage with surrounding edema, mild compression of the right lateral ventricle, and a slight increase in mass effect. Due to worsening cerebral edema and rising intracranial pressure, a decision was made to intubate and sedate the patient. He was then managed with controlled mechanical ventilation and neuromuscular paralysis.

Multidisciplinary consultations were obtained.

Neurology advised continuation of ongoing conservative neuro-management.
Gastroenterology evaluation with ultrasound abdomen indicated early pancreatitis.
Nephrology was consulted due to a known history of proteinuria; nephroprotective measures were recommended.

In view of progressive cerebral venous thrombosis, therapeutic anticoagulation infusion was initiated to prevent further thrombotic extension. The patient continued to receive close neurological observation, anticoagulation therapy, and supportive care in the ICU.

Day 2

The patient was reassessed for altered sensorium. His GCS was E4VTM6, with pupils equal and reactive. Neurologically, he continued to show left-sided relative paucity. Serial CT brain scans demonstrated no new hemorrhages, and gradual reduction in mass effect. The patient remained on anticoagulation infusion, anti-edema therapy, and ventilator support.

Day 3

The patient showed improvement in respiratory parameters and was successfully extubated. Anticoagulation was shifted from infusion to oral anticoagulant therapy.

Day 4

Neurological status improved further (GCS E4V5M6) and pupils remained reactive.

Day 5

A follow-up CT brain revealed a resolving right temporoparietal intracerebral hemorrhage with decreased edema and no midline shift. He was transferred to the ward; however, during ambulation, he experienced a syncopal episode and was returned to the ICU for observation. After stabilization, he was shifted back to the ward.

Day6

EEG showed right temporal dysfunction, prompting adjustment of antiepileptic medications. The patient continued to receive multidisciplinary input and neurorehabilitation.

After a week, the patient demonstrated steady neurological and functional improvement. Repeat CT brain imaging showed resolving right parietal hemorrhage without midline shift. Mobility, cognition, and sensorimotor function improved with rehabilitation support.

Nursing Management

Seizure Precautions

The bed was kept in a low position, and side rails were padded.
Emergency seizure medications were kept readily available at all times.
Any seizure activity was closely monitored, and the duration and characteristics were documented promptly.

Anticoagulation Monitoring

Anticoagulants were administered strictly as prescribed.
The patient was monitored for any signs of bleeding, including bruising, hematuria, or drop in hemoglobin.
Laboratory parameters such as PT, aPTT, platelet count, and renal function were monitored regularly to ensure safe therapeutic levels.

Pain Management

Pain was assessed routinely using an appropriate pain scale.
Analgesics were administered as ordered to maintain comfort.
A calm and quiet environment was provided to minimize discomfort and anxiety.

Fluid & Electrolyte Balance

Intake and output were monitored vigilantly.
The patient was assessed for signs of dehydration or fluid overload.
Intravenous fluids were administered according to medical instructions.

Prevention of Complications

Pressure injury prevention measures were implemented consistently.
The patient was repositioned frequently, and pressure-relieving devices were used.
Deep vein thrombosis prophylaxis was maintained through passive and active limb exercises.
Strict aseptic techniques were followed for all invasive lines to prevent infection.

Nutritional Support

Swallowing ability was assessed before initiating oral intake.
A modified diet was provided based on the patient’s tolerance and risk of aspiration.
The patient was monitored for signs of aspiration and malnutrition.

Psychosocial Support

Emotional reassurance was provided to both the patient and family.
Clear explanations regarding the illness, treatment plan, and prognosis were given.
Family involvement in care was encouraged to enhance patient support and comfort.

Outcome

The patient demonstrated marked neurological recovery over the course of treatment. Serial neuroimaging showed gradual resolution of the intracerebral hemorrhage, with corresponding improvement in cerebral edema. His Glasgow Coma Scale improved to E4V5M6, and motor strength on the left side progressively increased with physiotherapy and neurorehabilitation.

Renal function and pancreatic biomarkers stabilized with supportive management and specialist input. EEG abnormalities were addressed through optimization of antiepileptic therapy, resulting in improved neurological stability.

Condition at Discharge

At the time of discharge, the patient was conscious, alert, and fully oriented, with stable vital parameters and no signs of neurological deterioration. He tolerated an oral diet without difficulty and maintained normal bowel and bladder function. Motor function had improved sufficiently for him to ambulate with assistance.

The patient was discharged on oral anticoagulants and antiepileptic medications, with clear instructions regarding adherence, monitoring for adverse effects, and recognition of warning symptoms. He was advised to attend regular follow-up appointments with the Neurology, Nephrology, and Gastroenterology departments for continued evaluation of cerebral venous thrombosis, renal status, and pancreatic recovery. In addition, he was referred for ongoing neurorehabilitation to support progressive functional improvement and optimize long-term recovery outcomes.

Discussion – Medical Aspects

Cerebral venous thrombosis remains a challenging diagnosis due to its broad spectrum of clinical presentations. In this case, the patient had multiple predisposing factors—including recent trauma, underlying C1q nephropathy, and acute pancreatitis—all of which likely contributed to a transient hypercoagulable state, precipitating cortical venous thrombosis.

Neuroimaging played a pivotal role in diagnosis and monitoring. MR venography remains the gold standard for confirming venous occlusion, while CT imaging was crucial for detecting hemorrhagic transformation and monitoring cerebral edema.

Despite the presence of intracerebral hemorrhage, timely therapeutic anticoagulation was essential for preventing propagation of the thrombus and promoting venous recanalization—a standard, evidence-based approach in CVT management. The patient’s clinical course required dynamic management of complications, including raised intracranial pressure, seizures, acute kidney injury, and early pancreatitis.

A coordinated multidisciplinary approach involving neurology, critical care, nephrology, and gastroenterology ensured comprehensive management of multisystem involvement. Early initiation of rehabilitation significantly contributed to functional improvement.

Discussion – Nursing Aspects

Nursing care played an integral role throughout the patient’s hospitalization. Continuous neurological monitoring enabled early detection of changes in consciousness and motor function. Strict seizure precautions prevented secondary complications, while meticulous anticoagulation monitoring ensured therapeutic safety.

Preventive measures including pressure injury prevention, DVT prophylaxis, and maintenance of aseptic techniques were essential in reducing hospital-acquired complications. Fluid and electrolyte balance monitoring supported stabilization of renal and metabolic parameters.

Nutritional assessment and aspiration precautions ensure safe oral intake during recovery. Emotional support to both the patient and family facilitated coping and enhanced treatment adherence.

Nursing vigilance and timely interventions were instrumental in maintaining patient stability and promoting progressive recovery.

Conclusion

This case highlights the importance of early recognition and comprehensive management of cerebral venous thrombosis with intracerebral hemorrhage. Despite presenting with multiple complications including acute pancreatitis, acute kidney injury, and underlying C1q nephropathy the patient improved significantly due to timely neuroimaging, early anticoagulation, aggressive management of cerebral edema, and a strong multidisciplinary approach.

Effective nursing care further contributed to the prevention of complications, stabilization of neurological status, and holistic recovery. The case underscores that coordinated medical and nursing interventions are essential for favorable outcomes in complex neurovascular emergencies.

Cerebral venous thrombosis with intracerebral hemorrhage in a patient with C1Q nephropathy and acute pancreatitis: a rare clinical constellation

Cerebral venous thrombosis with intracerebral hemorrhage in a patient with C1Q nephropathy and acute pancreatitis: a rare clinical constellation

Aswin Vinitha *

Nursing Management

Seizure Precautions

Anticoagulation Monitoring

Pain Management

Fluid & Electrolyte Balance

Prevention of Complications

Nutritional Support

Psychosocial Support

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