Environmental pathology

Last updated: November 14, 2023

Summarytoggle arrow icon

Environmental pathologies are conditions caused by exposure to environmental factors such as extreme temperature, rapid changes in ambient pressure, electricity, wildlife, and environmental and occupational toxins and irritants.

Electrical injuries typically manifest with burns, cardiac dysrhythmias, and/or traumatic injuries. Lightning injuries can manifest with fixed dilated pupils, cardiorespiratory arrest, and characteristic skin findings such as Lichtenberg figures. Individuals with an electrical injury require a thorough assessment for burns, cardiac complications (e.g., with a screening ECG), and traumatic injuries. Management may include ATLS, ACLS, cardiac monitoring, and treatment of complications such as fractures.

High-altitude illnesses result from inadequate acclimatization to the low partial pressure of inspired oxygen found at elevations > 2500 m (∼ 8000 feet). Manifestations include acute mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema. Management involves descent, supplemental oxygen, and possible pharmacotherapy. Preventative measures include staged ascent and prophylactic medications.

Diving-related illnesses are caused by rapid changes in ambient pressure. Decompression illness is caused by the presence of gas bubbles in the blood or tissue and manifests as musculoskeletal pain, altered mental status, and/or circulatory collapse. Treatment involves 100% oxygen and hyperbaric oxygen therapy (HBOT). Barotrauma is caused by a large pressure difference between the ambient environment and air-filled structures such as the middle ear, sinuses, and/or lungs. Treatment is usually conservative but rare, life-threatening complications (e.g., pneumothorax) may occur.

Agricultural health hazards include green tobacco sickness and anhydrous ammonia poisoning.

Other environmental pathologies are covered in separate articles; see “Overview of environmental pathologies” for links.

Overviewtoggle arrow icon

Poisoning/toxin exposure

Electrical, thermal, and radiation injury

Injuries related to changes in ambient pressure

Animal-related conditions

Work-related conditions

Electrical and lightning injuriestoggle arrow icon

Electrical injury [1][2][3]


  • Electrical injuries account for approx. 4% of admissions to specialized burn services. [4]
  • Setting
    • Children: most often a household injury
    • Adults: most often found in occupational settings
  • Workplace-related electrical injuries cause approx. 150 deaths per year in the US. [5]

Etiology [1][3]

Pathophysiology [1][3]

Electrical current enters the body (entry point), passes through tissues and organs, and exits the body (exit point).

  • Thermal injury: conversion of electrical energy to heat within tissue
  • Nonthermal injuries: direct electrical injury (e.g., to nerves) or mechanical trauma (e.g., due to falls or tetanic muscle contraction)
  • Injury severity depends on:
    • Current
      • Direct current (DC): e.g., found in batteries, cars, computers
      • Alternating current (AC): found in most household electronic devices (e.g., TV, toaster, washing machine) and wall outlets
      • AC is more likely to cause ventricular fibrillation; DC is more likely to cause asystole. [7]
    • Frequency (Hz): Low-frequency AC (< 300 Hz) can cause muscle contractions, which may prolong exposure.
    • Voltage (V): High voltage is associated with a higher risk of traumatic injury, deeper skin burns, and higher mortality than low voltage.
    • Skin resistance
      • Dry skin has the highest resistance.
      • Skin submerged in water has the lowest resistance.

AC is more dangerous than DC because it is more likely to cause ventricular fibrillation and muscle contraction, leading to prolonged contact with the electrical source. [3][8]

Clinical features [1][9]

Electrical injury often affects multiple systems, and the extent of visible skin damage does not always correlate with the degree of deep tissue injury.

Severe deep tissue and/or organ damage may be present despite little or no apparent skin injury. [1][3]

Management of electrical injuries [1][2][3]

Prehospital care

  • Prioritize provider safety measures.
  • Remove the patient from the source of the current.
  • Initiate ACLS and ATLS as needed.
  • Start IV fluid resuscitation.
  • Transport to a specialized trauma or burn center.

Initial management

Anticipate the need for advanced airway management in patients with high-voltage head and/or neck burns, as the injury may be deeper than is apparent on initial examination. [1]

High-voltage injury and/or significant symptoms [1][3][7]

Do not rely on troponin and/or CK-MB levels to screen for cardiac injury, as their diagnostic utility in patients with electrical injury is unknown. [2][7]

Frequent reassessment is necessary, as some electrical injuries may have delayed manifestations (e.g., acute compartment syndrome).

Low-voltage injury and minimal symptoms [1][3]

  • No additional diagnostics are indicated if symptoms are minimal and localized.
  • After providing local wound care, consider discharge with return precautions.

In pregnant patients, consider admission for monitoring (including fetal heart tracing) regardless of symptoms or voltage of injury. [1][7]


  • Following workplace safety rules
  • Education about potential household and workplace electrical exposures
  • Utilization of outlet guards and incorporation of circuit breakers

Lightning injury [1][10]

Epidemiology [10]

  • ∼ 400 lightning injuries per year in the US
  • ∼ 40 lightning-related deaths per year in the US

Pathophysiology [3][8]

  • Lightning strikes can be direct or indirect (e.g., transfer of current from struck object or the ground to the individual)
  • Very brief (< 1 second) exposure to an intense (> 106 V) electrical discharge → flashover effect (most of the current travels along the outside of the body) → lower risk of deep tissue injury compared with other electrical injuries [3]
  • Mechanisms of injury

Clinical features [3][8][10]

Blunt trauma and cardiopulmonary arrest are more common than severe burns in lightning strike victims. [3]

Suspect a lightning strike in any patient found outdoors with altered mental status or cardiopulmonary arrest during a thunderstorm even if evidence of external injury is absent. [3]


Do not terminate resuscitation based on the presence of fixed, dilated pupils and respiratory arrest, as these features do not always signify permanent brain injury in lightning strike victims. [3][13]


Advise individuals to adhere to the following recommendations during a lightning storm:

  • Avoid swimming outdoors.
  • Find a safe, enclosed shelter.
  • Stay away from concrete floors, walls, and electronic equipment.

Conducted electrical weapon (CEW) injury [1][14][15]

  • Definition: injury from a weapon that delivers a high voltage but low amperage electrical charge, causing temporary neuromuscular incapacitation (NMI); also known as a Taser® or stun gun
  • Clinical features
    • Often minor or absent [14][15]
    • May be associated with traumatic injuries secondary to NMI-induced fall
  • Management [1][3][14]
    • Assess for and manage any concomitant conditions, e.g., agitation, alcohol or drug intoxication, psychiatric conditions.
    • Assess for and treat any associated injuries, e.g., wounds caused by barbed projectiles or TBI caused by falls.
    • In symptomatic individuals and/or after exposure of > 15 seconds, obtain an ECG and consider observation for 6–8 hours. [3][15][16]

Acute management checklist for electrical injuriestoggle arrow icon

High-altitude illnessestoggle arrow icon

Overview [3][17]

Risk factors for altitude illness [17][18]

  • Patient-related: age < 50 years, history of migraines, previous altitude illness
  • Rapid ascent pattern: e.g.,
    • Ascent to > 3500 m (∼ 11,500 feet) from < 1200 m in one day
    • Increase in sleeping altitude of > 500 m/day (∼ 1650 feet) above 3000 m (∼ 9850 feet)

Acute mountain sickness (AMS) [3][17][19]

AMS is characterized by the onset of headache and other nonspecific symptoms after rapid ascent to above 2000–2500 m (∼ 6500–8000 feet). [20]

Pathophysiology [21]

PiO2 and oxygenation decrease at high altitudes. Acclimatization (a normal compensatory process that occurs in response to the low level of oxygen at high altitude) occurs in different organ systems during the first hours to days. Physiological changes typically become significant at elevations > 2500 m (∼ 8000 feet); see “Acclimatization.”

Acclimatization to high altitude
Parameter Early changes Late changes
PAO2 and PaO2
PACO2 and PaCO2
Arterial pH
  • Normal (due to renal compensation)
  • Normal
Arterial O2 content
  • Returned to normal

Clinical features of AMS [20]

Diagnostics [19][22]

AMS is usually a clinical diagnosis based on the development of symptoms after ascending to high altitude.

Differential diagnoses of acute mountain sickness [3][17]

Treatment [3][17]

Ascent may be resumed after symptoms of AMS have resolved; consider prophylactic use of acetazolamide. [17]

High-altitude cerebral edema (HACE) [17][19][22]

High-altitude cerebral edema is an uncommon but potentially life-threatening manifestation of AMS characterized by encephalopathy.


  • Not fully understood, but generally considered to be an extreme progression of AMS with the same underlying pathophysiology
  • Most likely, increased cerebral vascular permeability and cerebral blood flow lead to high intravascular pressure and cerebral edema.

Clinical features

The key diagnostic findings in HACE are altered mental status and ataxia. [17]

Diagnostics [22]

Differential diagnoses [3][22]

Treatment [3][17][22]

HACE is a medical emergency and requires immediate descent and treatment.

High-altitude pulmonary edema (HAPE) [3][17][23]

High-altitude pulmonary edema is a noncardiogenic pulmonary edema occurring shortly after rapid ascent, typically to > 4500 m (∼ 14,500 feet), and is the most common cause of death in individuals ascending rapidly to high altitude. [23]


Clinical features

Diagnostics [3][19][22]

Differential diagnoses [3][22]

If a patient with a recent history of ascent to high altitude presents with a normal leukocyte count and rapidly improves with oxygen therapy, HAPE is more likely than pneumonia.

Treatment [3][17]

Prevention of altitude illness [17][22]

Diving-related illnessestoggle arrow icon

Decompression illness (DCI)

Overview [24][25][26]

  • DCI encompasses conditions caused by gas bubbles in the blood or tissue due to rapidly decreasing ambient pressure, i.e.:
  • Risk factors for DCI include:
    • Environment-related factors
      • Prolonged and deep diving
      • Air travel shortly after diving
    • Patient-related factors
  • Definitive treatment for most patients is HBOT.

Immediately administer 100% oxygen to all patients with suspected DCI. [24]

Decompression sickness (DCS)

  • Definition: : the formation of air bubbles in the tissue and venous circulation caused by a rapid decline in barometric pressure within the body
  • Etiology: insufficient decompression time following time spent at depth
    • Rapid ascent from depth
    • Exiting a hyperbaric chamber or caisson (e.g., in tunneling projects) without decompression time
  • Pathophysiology: decompression sickness due to diving
    • Descent: ambient pressure increases with diving depth → gases (mostly nitrogen) dissolve into the blood and tissue
    • Controlled ascent: ambient pressure gradually decreases → gas tension exceeds the surrounding pressure → gases slowly come out of solution → gases exhaled
    • Rapid ascent: ambient pressure rapidly decreases → gas tension exceeds the surrounding pressure → gases quickly come out of solution in the blood and tissue → insufficient time for the gas to be progressively breathed out through the lungs → formation of gas bubbles → gaseous obstruction of blood flow (especially in the venous circulation because of its lower pressure and higher gas tension)
  • Onset: typically within hours of surfacing [27]
  • Clinical features [24][26][27]
  • Diagnostics [24]
  • Differential diagnosis [24][26]
  • Management: Maintain the patient supine during treatment. [26][27]
  • Complications
  • Prevention [26]
    • Reduce exposure to large pressure variations.
    • Follow diving safety guidelines (e.g., follow dive table recommendations including decompression stops).

Arterial gas embolism (AGE) [3][27]

Consider AGE if there is acute deterioration shortly after surfacing, as AGE can occur even after brief submersion in shallow depths. [24]

Nitrogen narcosis [3][27][28]

  • Definition: a syndrome caused by breathing nitrogen or another inert gas at high partial pressures
  • Onset: diving at depths of ≥ 30 m (≥ 100 feet)
  • Risk factors: use of alcohol, sedatives, and/or analgesics before diving
  • Pathophysiology: ↑ ambient pressure under water → ↑ partial pressure of nitrogen → ↑ solubility in neuronal membranes → ↓ excitability → intoxication and narcosis
  • Clinical features: Symptom severity increases with diving depth; symptoms disappear rapidly after ascending to shallower depths.
    • Altered mental status (e.g., euphoria, confusion, hostility), unconsciousness
    • Loss of fine motor skills
    • Lack of concern for personal safety
  • Diagnostics: clinical diagnosis
  • Treatment: immediate controlled ascent until symptoms subside
  • Prevention: Use a helium-based gas mixture and/or maintain a depth of < 30 m (100 feet).

Barotrauma [27][29][30]

Barotrauma can occur as a result of unsuccessful equalization of the pressure between the ambient environment and air-filled structures in the body (e.g., middle or inner ear, lungs).

Ear barotrauma [3][27][30]

Forceful Valsalva maneuver during descent may cause IEBT. [27]

Vertigo and ataxia after ascent may indicate inner ear DCS, which requires HBOT. [3]

Sinus barotrauma [3][27]

Pulmonary barotrauma [3]

Untreated pneumothorax is an absolute contraindication for HBOT. [24]

Agricultural health hazardstoggle arrow icon

Green tobacco sickness [35]

  • Definition: a form of nicotine poisoning that predominantly affects tobacco harvesters
  • Risk factors
    • Children and adolescents with environmental exposure to tobacco are at increased risk because of higher sensitivity to nicotine.
    • Wet conditions (e.g., due to rain, dew, sweat) promote nicotine absorption
  • Etiology: nicotine exposure
  • Pathophysiology: transdermal absorption of nicotine from tobacco plants
  • Clinical features
  • Treatment: usually not required
  • Complications: vomitingdehydration↑ risk of heat illness
  • Prognosis: usually resolves without treatment within 24 hours
  • Prevention
    • Wearing personal protective equipment (PPE) such as long pants, long-sleeve shirts, water-resistant clothing, and gloves
    • Educating workers on the symptoms of green tobacco poisoning and the necessity of PPE
    • Washing with soap and water immediately after skin contact

Anhydrous ammonia poisoning [36]

In case of ingestion: do not induce emesis to prevent re-exposure of the esophagus and mouth!

Referencestoggle arrow icon

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