High Altitude Retinal Hemorrhage (HARH)

1. Introduction

High-Altitude Retinal Hemorrhage (HARH) is a retinal vascular complication occurring at high altitude, typically above 3,500–4,000 meters, due to hypobaric hypoxia–induced microvascular injury.

It is considered part of the spectrum of high-altitude illness, along with:

  • Acute Mountain Sickness (AMS)
  • High-Altitude Cerebral Edema
  • High-Altitude Pulmonary Edema


2. Epidemiology

Factor

Details

Altitude

>3,500–4,000 m (common >5,000 m)

Incidence

20–40% above 5,000 m (often asymptomatic)

Symptomatic cases

Minority

Risk factors

Rapid ascent, severe hypoxemia, strenuous exertion

Seen in:

  • Mountaineers
  • Military personnel
  • High-altitude trekkers
  • Pilots in unpressurized aircraft


3. Pathophysiology 

Stepwise Mechanism

1️⃣ Hypobaric Hypoxia

↓ Atmospheric pressure
↓ PaO₂
↓ Retinal oxygen delivery

2️⃣ Retinal Vasodilation

  • Hypoxia → local nitric oxide–mediated vasodilation
  • Increased retinal blood flow

3️⃣ Increased Capillary Pressure

  • Hyperemia
  • Increased hydrostatic pressure
  • Fragile capillary rupture

4️⃣ Blood–Retinal Barrier Disruption

  • Increased permeability
  • Microvascular leakage
  • Hemorrhage formation


Mechanism

Explanation

Venous congestion

Hypoxia → increased hematocrit → increased viscosity

Valsalva effect

Strenuous climbing → intrathoracic pressure ↑

Cerebral venous hypertension

Seen with HACE

Autoregulation failure

Severe hypoxia impairs retinal vascular autoregulation

Important: HARH reflects systemic hypoxic stress — not a primary eye disease.


4. Clinical Presentation

A. Asymptomatic (Most Common)

  • Incidentally detected on fundus exam
  • Peripheral hemorrhages

B. Symptomatic

Symptom

Cause

Blurred vision

Macular involvement

Scotoma

Central retinal hemorrhage

Visual field defect

Parafoveal bleed

Floaters

Vitreous involvement

Usually:

  • Painless
  • Unilateral or bilateral


5. Fundoscopic Findings

Typical Features

  • Flame-shaped hemorrhages
  • Dot-blot hemorrhages
  • Often near optic disc
  • Usually peripheral
  • Macular involvement → vision loss

No papilledema unless associated with HACE.


6. Differential Diagnosis 

Condition

Distinguishing Feature

Diabetic retinopathy

Chronic microaneurysms, exudates

Hypertensive retinopathy

AV nicking, cotton wool spots

Central retinal vein occlusion

“Blood and thunder” appearance

Terson syndrome

Associated with SAH

Leukemia-related hemorrhage

Systemic cytopenias

Especially differentiate from:

  • Terson syndrome


7. Diagnosis

Primarily clinical:

✔ High altitude exposure
✔ Fundoscopy

Additional tools:

  • Optical coherence tomography (OCT)
  • Fundus photography

No routine imaging needed unless:

  • Severe visual loss
  • Suspicion of CNS pathology


8. Management 

 1. Descent (Definitive Treatment)

  • Immediate descent if:
    • Visual symptoms
    • Associated HACE
    • Severe AMS

 2. Oxygen Therapy

  • Supplemental oxygen
  • Improves retinal oxygenation
  • Also treats concurrent HACE/HAPE

 3. Rest and Avoid Exertion

  • Prevent Valsalva-induced worsening

 4. No Routine Steroids

Unless:

  • HACE present → Dexamethasone

 5. No Anticoagulation


9. Prognosis

  • Usually spontaneous resolution in 2–8 weeks
  • Vision typically recovers fully
  • Rarely:
    • Persistent scotoma
    • Macular scarring


10. Prevention 

Strategy

Rationale

Gradual ascent

Allows acclimatization

Avoid >500 m/day above 3,000 m

Standard recommendation

Acetazolamide prophylaxis

Reduces AMS risk

Avoid excessive exertion

Prevents venous pressure spikes

Prophylaxis follows same principles as prevention of:

  • Acute Mountain Sickness
  • High-Altitude Cerebral Edema