High altitude pulmonary edema: Difference between revisions
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*Noncardiogenic [[pulmonary edema]] due to increased microvascular pressure in the pulmonary circulation | *Noncardiogenic [[pulmonary edema]] due to increased microvascular pressure in the pulmonary circulation | ||
**Hypoxic pulmonary vasoconstriction leads to [[pulmonary hypertension]] | **Hypoxic pulmonary vasoconstriction leads to [[pulmonary hypertension]] | ||
*Most lethal of the altitude illnesses | *Most lethal of the altitude illnesses with mortality approaching 50% if descent is not completed in a timely manner <ref>Lobenhoffer HP, Zink RA, et al. High altitude pulmonary edema: analysis of 166 cases. In: Brendel W, Zink RA, editors. High Altitude Physiology and Medicine. New York, NT: Springer-Verlag; 1982. pp. 219–231</ref> | ||
*Occurs in <1/10,000 skiers in Colorado; 2-3% of Mt. McKinley climbers | *Occurs in <1/10,000 skiers in Colorado; 2-3% of Mt. McKinley climbers | ||
*Typical patient is strong and fit; may not have symptoms of [[altered mental status]] before onset of HAPE | *Typical patient is strong and fit; may not have symptoms of [[altered mental status]] before onset of HAPE | ||
Revision as of 08:01, 21 May 2021
Background
- Also known as HAPE
- Noncardiogenic pulmonary edema due to increased microvascular pressure in the pulmonary circulation
- Hypoxic pulmonary vasoconstriction leads to pulmonary hypertension
- Most lethal of the altitude illnesses with mortality approaching 50% if descent is not completed in a timely manner [1]
- Occurs in <1/10,000 skiers in Colorado; 2-3% of Mt. McKinley climbers
- Typical patient is strong and fit; may not have symptoms of altered mental status before onset of HAPE
- Most commonly noticed on the second night at a new altitude
Risk Factors
- Heavy exertion
- Rapid ascent
- Cold
- Excessive salt ingestion
- Use of a sleeping medication
- Preexisting pulmonary hypertension
- Preexisting respiratory infection (children)
- Previous history of HAPE
Clinical Features
Early
- Dry cough, decreased exercise performance, dyspnea on exertion, localized rales
- Resting SaO2 is very low for the expected altitude but patients often appear clinically better than their saturation (aids in diagnosis)
- Easily desaturates with exertion
Late
- Dyspnea at rest, marked weakness, productive cough, cyanosis, generalized rales
- Cough generates pink, frothy sputum
- Tachycardia and tachypnea correlate with severity of illness
- Altered mental status and coma (from severe hypoxemia)
Differential Diagnosis
High Altitude Illnesses
- Acute mountain sickness
- Chronic mountain sickness
- High altitude cerebral edema
- High altitude pulmonary edema
- High altitude peripheral edema
- High altitude retinopathy
- High altitude pharyngitis and bronchitis
- Ultraviolet keratitis
Pulmonary Edema Types
Pulmonary capillary wedge pressure <18 mmHg differentiates noncardiogenic from cardiogenic pulmonary edema[2]
- Cardiogenic pulmonary edema
- Noncardiogenic pulmonary edema
- Negative pressure pulmonary edema
- Upper airway obstruction
- Reexpansion pulmonary edema
- Strangulation
- Neurogenic causes
- Iatrogenic fluid overload
- Multiple blood transfusions
- IV fluid
- Inhalation injury
- Pulmonary contusion
- Aspiration pneumonia and pneumonitis
- Other
- High altitude pulmonary edema
- Hypertensive emergency
- ARDS
- Flash pulmonary edema
- Immersion pulmonary edema
- Hantavirus pulmonary syndrome
- Missed dialysis in kidney failure
- Naloxone reversal
- Negative pressure pulmonary edema
Evaluation
Workup
- ECG - right strain pattern
- CXR - Progresses from interstitial → localized-alveolar → generalized-alveolar infiltrates
- ABG - Hypoxemia with respiratory alkalosis
Evaluation
- Clinical diagnosis
Expected SpO2 and PaO2 levels at altitude[3]
| Altitude | SpO2 | PaO2 (mm Hg) |
|---|---|---|
| 1,500 to 3,500 m (4,900 to 11,500 ft) | about 90% | 55-75 |
| 3,500 to 5,500 m (11,500 to 18,000 ft) | 75-85% | 40-60 |
| 5,500 to 8,850 m (18,000 to 29,000 ft) | 58-75% | 28-40 |
Management
- Immediate descent is treatment of choice - minimize exertion
- If cannot descend use combination of:
- Supplemental O2 - An oxygen concentrator is often used at high altitude ski resorts after the patient is titrated down to nasal cannula. A portable oxygen tank is used for ambulation. Can completely resolve the pulmonary edema within 36-72hr
- Hyperbaric bag - (e.g. Gamow Bag). Should not delay descent, if possible.
- Keep patient warm (cold stress elevates pulmonary artery pressure)
- Use expiratory positive airway pressure mask
- Nifedipine 30mg ER q12hr (or 20mg normal-release q8hr)[4]
- May consider the other medications listed below that are usually used for prevention
Disposition
- Admission
- Warranted for severe illness that does not respond immediately to descent
- Discharge
- Progressive clinical and X-ray improvement and a PaO2 of 60mmHg or SaO2>90%
- May re-ascend in 2-3 days if mild-moderate symptoms resolved that only required descent as the intervention
Prevention
- Nifedipine 20mg q8hr or 30mg ER q12hr while ascending is effective prophylaxis in patients with prior episodes of HAPE
- Tadalafil 10mg BID 24hr prior to ascent OR Sildenafil 50mg q8hr
- Salmeterol 125 mcg inhaled BID
- Acetazolamide 125mg BID for prevention of hypoxia
See Also
References
- ↑ Lobenhoffer HP, Zink RA, et al. High altitude pulmonary edema: analysis of 166 cases. In: Brendel W, Zink RA, editors. High Altitude Physiology and Medicine. New York, NT: Springer-Verlag; 1982. pp. 219–231
- ↑ Clark SB, Soos MP. Noncardiogenic Pulmonary Edema. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 1, 2020.
- ↑ Gallagher, MD, Scott A.; Hackett, MD, Peter (August 28, 2018). "High altitude pulmonary edema". UpToDate. Retrieved May 2, 2019.
- ↑ Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2014 Update. Wilderness & Environmental Medicine. 2014(25): S4–S14)