What is the differential diagnosis and management for a patient presenting with acute onset diplopia, chicken pox (varicella) lesions, and hypertension?

Differential Diagnosis and Management of Acute Diplopia with Varicella and Hypertension

Primary Differential Diagnosis

This patient requires immediate evaluation for hypertensive emergency with neurological involvement, specifically hypertensive encephalopathy or intracranial hypertension, as diplopia combined with elevated blood pressure represents acute hypertension-mediated organ damage until proven otherwise. 1

Critical Diagnostic Considerations

Hypertensive Emergency with Neurological Manifestations:

• Diplopia is a recognized neurological symptom of hypertensive encephalopathy and intracranial hypertension, occurring alongside other subtle neurological features that can progress to seizures, lethargy, cortical blindness, and coma if untreated 1, 2
• The presence of any neurological symptom—not the absolute BP value—defines this as a hypertensive emergency requiring immediate intervention 3, 4
• Hypertensive encephalopathy occurs in 10-15% of patients with malignant hypertension, and advanced retinopathy may be absent in up to one-third of cases 1

Varicella Zoster Virus (VZV) Neurological Complications:

• Diplopia from cranial nerve palsy occurs in less than 30% of herpes zoster ophthalmicus (HZO) cases, with sixth nerve palsy being the most common cranial nerve involvement 5, 6
• VZV can cause vasculopathy leading to stroke, cranial nerve palsies, and optic neuropathy even without visible skin lesions 5
• The temporal relationship (chickenpox 10 days ago with recurrent lesions) raises concern for VZV reactivation or disseminated disease 5

Idiopathic Intracranial Hypertension (IIH):

• Can present with diplopia (typically from sixth nerve palsy), papilledema, headache, and visual disturbances 2, 7, 8
• However, the acute onset (1 day) and concurrent severe hypertension make this less likely as the primary diagnosis 2

Secondary Causes to Consider:

• Intracranial hemorrhage or ischemic stroke (focal neurological lesions are rare in pure hypertensive encephalopathy but must be excluded) 1
• Posterior reversible encephalopathy syndrome (PRES), which is a form of hypertensive encephalopathy 4, 2
• Thrombotic microangiopathy associated with malignant hypertension 1

Immediate Diagnostic Workup

Mandatory Laboratory Studies:

• Hemoglobin, platelet count (assess for thrombotic microangiopathy) 1, 4
• Creatinine, sodium, potassium, LDH, haptoglobin (evaluate for hemolysis and renal damage) 1, 4
• Quantitative urinalysis for protein, urine sediment for erythrocytes, leucocytes, cylinders, and casts 1, 4

Essential Diagnostic Examinations:

• ECG immediately to detect ischemia, arrhythmias, or left ventricular hypertrophy 1, 4
• Fundoscopy to identify papilledema, flame-shaped hemorrhages, cotton wool spots, or Grade III/IV hypertensive retinopathy 1, 2
• MRI brain with contrast (preferred over CT) to evaluate for hypertensive encephalopathy, PRES, intracranial hemorrhage, ischemic stroke, or VZV vasculopathy 3, 5
• Troponin if cardiac ischemia suspected 1

VZV-Specific Testing (if neurological complications suspected):

• PCR and serology on paired serum and cerebrospinal fluid samples if MRI shows abnormalities or clinical suspicion for VZV neurological involvement 5
• Lumbar puncture should be performed after neuroimaging excludes mass effect or increased intracranial pressure 5

Additional Studies Based on Presentation:

• Chest X-ray or point-of-care ultrasound if pulmonary edema suspected 1
• CT-angiography of thorax/abdomen if aortic dissection considered 1, 3

Immediate Management Algorithm

Step 1: Triage and Monitoring

• Admit to ICU immediately for continuous arterial blood pressure monitoring 4
• Measure BP in both arms and lower limb to detect pressure differences from aortic dissection 1
• Perform repeated BP measurements, as BP may fall considerably without medication in some patients 1

Step 2: Blood Pressure Management

If Hypertensive Emergency Confirmed (acute organ damage present):

• Target: Reduce mean arterial pressure (MAP) by 20-25% within the first hour 3, 4
• Then reduce to 160/110-100 mmHg over the next 2-6 hours 3
• Initiate intravenous antihypertensive therapy immediately 3
• Preferred agents: Labetalol or nicardipine for hypertensive encephalopathy 4
• Avoid rapid BP lowering beyond recommended targets to prevent cardiovascular complications and cerebral hypoperfusion 1

If Hypertensive Urgency (no acute organ damage):

• Treat with oral BP-lowering medication or adaptation of current regimen 1
• Avoid short-acting nifedipine due to rapid, uncontrolled BP falls 1
• Consider captopril, labetalol, or nifedipine retard 1
• Observe for at least 2 hours to evaluate efficacy and safety 1

Step 3: VZV-Specific Treatment

If VZV Neurological Complications Confirmed or Highly Suspected:

• Initiate intravenous acyclovir immediately for patients with neurological signs/symptoms or abnormal imaging 5
• Antiviral treatment should be started within 48-72 hours of HZ onset to decrease pain and reduce complications 5
• Patients with isolated cranial nerve palsy can be managed with oral antivirals 5
• Prognosis for visual recovery is excellent for isolated ocular motor cranial nerve palsy 5

Step 4: Transition to Oral Therapy

• Begin oral antihypertensives after 6-12 hours of parenteral therapy once BP stabilized 4
• Gradually transition over 24-48 hours using combination therapy with RAS blockers, calcium channel blockers, and diuretics 4

Critical Pitfalls to Avoid

Do not dismiss diplopia as "benign" in the setting of elevated BP, as this represents a neurological symptom significantly increasing likelihood of intracranial pathology 3

Do not rely solely on neurological examination, as absence of focal deficits does not exclude hypertensive encephalopathy, PRES, or early stroke 3, 4

Do not delay neuroimaging while attempting BP reduction, as identifying underlying pathology guides appropriate BP targets and treatment intensity 3

Do not assume focal neurological lesions are due to hypertensive encephalopathy alone—they should raise suspicion for intracranial hemorrhage or ischemic stroke 1, 2

Do not overlook VZV as a cause of diplopia, especially with recent chickenpox history, as cranial nerve palsies can occur even without visible HZO 5

Post-Stabilization Considerations

Screen for secondary hypertension, as 20-40% of malignant hypertension cases have identifiable secondary causes including renal parenchymal disease, renal artery stenosis, pheochromocytoma, and primary aldosteronism 4

Monitor for resolution of diplopia: Microvascular disease-related cranial nerve palsies (from hypertension/diabetes) resolve spontaneously in 87% by 5 months and 95% by 12 months 6

Recognize prognostic implications: Without treatment, hypertensive emergencies have 1-year mortality >79% with median survival of only 10.4 months, but with appropriate management, survival has improved significantly 4