What is the most likely diagnosis, appropriate investigations, treatment, and two critical complications to monitor in a 25-year-old primiparous woman 7 days after an uncomplicated caesarean section who presents with severe progressive headache, occasional visual blurring, nausea, lethargy, blood pressure of 130/80 mm Hg, and bilateral papilledema?

Most Likely Diagnosis

The most likely diagnosis is cerebral venous thrombosis (CVT), specifically postpartum cerebral venous sinus thrombosis. This 25-year-old woman presenting 7 days post-cesarean section with progressive headache, visual disturbances, nausea, lethargy, and bilateral papilledema has the classic presentation of CVT in the puerperium 1.

Diagnostic Reasoning

The puerperium carries a 12 per 100,000 deliveries risk of CVT, with cesarean section being an additional risk factor 1. The clinical presentation fits perfectly:

• Increased intracranial pressure symptoms: Progressive headache (present in 90% of CVT cases), bilateral papilledema, visual blurring, and nausea 1
• Timing: 7 days postpartum falls within the high-risk puerperium period, when most pregnancy-related CVT occurs 1
• Risk factors: Cesarean delivery increases CVT risk through hypercoagulability worsened by delivery trauma and volume depletion 1

The blood pressure of 130/80 mmHg makes late postpartum eclampsia less likely, though it cannot be completely excluded. Post-dural puncture headache would not cause papilledema.

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Investigations

Immediate imaging (within 24 hours) is mandatory:

1. MRI brain with MR venography (MRV) - This is the gold standard and must be performed urgently 2, 3

   • If MRI unavailable within 24 hours, perform CT brain followed by CT venography 2
   • MRV/CTV is mandatory to exclude cerebral sinus thrombosis 2
   • Look for: absence of flow void in venous sinuses, direct visualization of thrombus

2. Lumbar puncture with opening pressure measurement - Perform ONLY after imaging excludes mass lesion 2

   • Measure opening pressure in lateral decubitus position
   • Opening pressure >25 cm H₂O confirms elevated intracranial pressure 2
   • CSF analysis to exclude infection/inflammation

3. Laboratory investigations:

   • Complete blood count with platelets
   • Coagulation profile (PT, aPTT)
   • Thrombophilia screening: Factor V Leiden, prothrombin G20210A mutation, protein C, protein S, antithrombin III 1
   • Homocysteine levels 1
   • Renal and hepatic function
   • Urine protein-to-creatinine ratio (to exclude eclampsia)

4. Ophthalmology assessment:

   • Formal visual field testing
   • Visual acuity documentation
   • Fundoscopy to grade papilledema severity

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Treatment

Immediate anticoagulation is the cornerstone of CVT management, even in the presence of hemorrhagic infarction:

Acute Phase Management

1. Start low-molecular-weight heparin (LMWH) immediately upon diagnosis confirmation 3

   • Enoxaparin 1 mg/kg subcutaneously twice daily, or
   • Dalteparin 100 units/kg subcutaneously twice daily
   • Do NOT delay anticoagulation while awaiting thrombophilia results

2. Seizure prophylaxis and management:

   • If seizures occur: Levetiracetam 500-1000 mg IV, then 500 mg twice daily orally
   • Consider prophylactic antiepileptics given 40% seizure risk in CVT 1

3. Manage elevated intracranial pressure:

   • Elevate head of bed 30 degrees
   • Acetazolamide 500-1000 mg twice daily (if opening pressure confirmed elevated)
   • Avoid aggressive diuresis that could worsen hypercoagulability

4. Supportive care:

   • Adequate analgesia for headache
   • Maintain euvolemia (avoid dehydration)
   • Monitor neurological status closely

Transition to Long-term Anticoagulation

• After 5-10 days of LMWH, transition to oral anticoagulation 3:
  • Rivaroxaban 15 mg twice daily for 3 weeks, then 20 mg once daily, OR
  • Warfarin (target INR 2-3)
  • Continue for minimum 3-6 months

Surgical Intervention

• Decompressive surgery only if:
  • Progressive neurological deterioration despite anticoagulation
  • Large hemorrhagic venous infarction with mass effect
  • Impending herniation

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Two Critical Complications to Monitor

1. Seizures (Focal or Generalized)

Seizures occur in 40% of CVT patients and can develop at any time during the acute phase 1.

Monitoring strategy:

• Continuous neurological observations every 2-4 hours initially
• Watch for: focal motor activity, altered consciousness, generalized tonic-clonic activity
• Have IV levetiracetam immediately available at bedside
• Consider prophylactic antiepileptic therapy given high risk

Why critical: Seizures indicate cortical venous infarction/hemorrhage and can cause secondary brain injury, aspiration, and status epilepticus.

2. Venous Hemorrhagic Infarction with Neurological Deterioration

Hemorrhagic transformation occurs frequently in CVT and can cause rapid deterioration 1.

Monitoring strategy:

• Serial neurological examinations every 2-4 hours
• Watch for: worsening headache, declining consciousness (GCS), new focal deficits (hemiparesis, aphasia), pupillary changes
• Repeat neuroimaging (CT or MRI) urgently if any deterioration
• Monitor for signs of herniation: bradycardia, hypertension, irregular respirations

Why critical: Hemorrhagic infarction with mass effect can lead to herniation and death. Bilateral thalamic involvement from deep venous system thrombosis causes rapid coma 1. Despite hemorrhage, anticoagulation should be continued as benefits outweigh risks.

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Critical Pitfalls to Avoid

• Do NOT withhold anticoagulation due to presence of hemorrhagic infarction - this is a common mistake; anticoagulation is still indicated
• Do NOT attribute symptoms to post-dural puncture headache - PDPH does not cause papilledema 4
• Do NOT delay imaging to perform lumbar puncture first - always image before LP to exclude mass lesion 2
• Do NOT dismiss normal blood pressure - CVT can occur with normal BP, unlike eclampsia which typically shows hypertension