Environmental pathology

Environmental pathology is the study of conditions that are caused by exposure to environmental factors such as extreme temperature and altitude changes, electricity, wildlife, and any kind of toxin.

Electrical injuries are often multisystem injuries and require a thorough evaluation. Burns of varying degrees are among the most common findings. Exposure to alternating current can lead to potentially life-threatening arrhythmias. Lightning injuries, a rare subtype of electrical injuries, may manifest with characteristic skin findings, such as Lichtenberg figures.

High-altitude illness, which typically occurs at elevations > 8,000 ft (∼ 2,500 m), encompasses acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema. The main trigger is the low level of oxygen, which can lead to hypoxia, tachypnea, polycythemia, pulmonary edema, and cerebral edema during the first hours to days at high altitude.

Covered in this article

• Electrical injury
• High-altitude illness
  • Acute mountain sickness
  • High-altitude cerebral edema
  • High-altitude pulmonary edema

Covered in other articles

• Burns
• Bite wounds
• Animal bites and stings
  • Dog bite
  • Domestic cat bite
  • Snake bites
  • Spider bites
  • Jellyfish stings
  • Hymenoptera stings
• Poisoning
  • Food poisoning
  • CO poisoning
• Substance-related and addictive disorders
  • Differential diagnosis of substance intoxication
  • Alcohol-related disorders
• Organic solvent toxicity
• Metal toxicity
• Carcinogens
• Pneumoconioses
  • Asbestosis
  • Silicosis
  • Rare pneumoconioses
• Hypersensitivity pneumonitis (e.g., Farmer's lung, Pigeon breeder's lung)
• Occupational rhinitis
• Radiation injury
• Diving-related injuries: decompression sickness
• Infection prevention and control
• Occupational skin diseases
  • Irritant contact dermatitis
  • Occupational acne
  • Latex allergy

Electrical current (industrial or residential) injury ^[1]

• Epidemiology
  • Electrical injuries account for approx. 4% of admissions to specialized burn services. ^[2]
  • Setting
    • Children: most often household injury
    • Adults: most often in occupational settings
  • Workplace-related electrical injuries cause approx. 150 deaths per year in the US. ^[3]
• Etiology
  • High-voltage sources (> 1000 V): e.g., lightning strike, industrial devices, power supply lines
  • Low-voltage sources (120–1000 V): e.g., household appliances, extension cords, or wall outlets
• Pathophysiology: Electrical current enters the body (entry point), passes through tissues and organs, and then exits the body (exit point).
  • The majority of tissue damage is a result of thermal injury, which occurs as the electric current converts to heat when entering the tissue.
  • Nonthermal injury includes direct electric injury to nerve tissue and musculoskeletal injury (secondary to tetanic muscle contraction).
  • The severity of the injury depends on:
    • Current
      • Direct current (DC): e.g., in batteries, cars, computers
      • Alternating current (AC): most household electronic devices (e.g., TV, toaster, washing machine) and wall outlets
      • AC is generally more dangerous than DC, because AC is more likely to trigger ventricular fibrillation.
    • Frequency (in Hz): Low-frequency AC (< 300 Hz) causes muscle contraction, which may prevent the individual from letting go of the source, prolonging exposure.
    • Voltage (V): The higher the voltage of a source, the more severe the injury it may cause.
    • Resistance of tissue
      • Dry skin has a higher resistance than wet skin.
      • The lowest resistance is in water.
• Clinical features: Electrical injury often affects multiple systems.
  • Skin: superficial to deep burn
  • Musculoskeletal
    • Tetanic muscle contraction, which can lead to rhabdomyolysis
    • Orthopedic injuries (e.g., fractures)
    • Muscle necrosis
  • Cardiac
    • Arrhythmia: e.g., asystole; , ventricular fibrillation
    • Myocardial infarction
  • Respiratory: paralysis, respiratory arrest
  • Neurologic
    • CNS: loss of consciousness, seizures
    • PNS: paresthesia, numbness, muscle weakness
  • Vascular: acute compartment syndrome, thrombosis, coagulation necrosis
  • Renal: acute kidney injury (e.g., due to rhabdomyolysis)
  • Ocular: cataracts
• Management: In general, individuals with (suspected) electrical injury should be treated as trauma patients (see “Management of trauma patients”). A thorough evaluation and frequent reassessments are necessary, as some injuries may not be visible at first.
  • Prehospital care
    • Personal safety measures must be prioritized.
    • Remove the patient from the current.
    • ACLS if needed
    • Start IV fluid resuscitation.
    • Transport to a specialized trauma or burn center.
  • Complete physical examination: should include complete skin examination with clothes removed
  • Treatment of burns, which may also require airway management and fluid resuscitation (see “Burns”)
  • ECG (for all patients) and cardiac monitoring
  • Laboratory studies: CBC, complete metabolic panel, CK
• Prevention
  • Following workplace safety rules
  • Education about potential sources of household and workplace exposure
  • Outlet guards
  • Proper incorporation of protective circuit-breaking equipment

Lightning injury ^[1][4]

• Definition: a type of electrical injury that is caused by a lightning strike
• Epidemiology ^[5]
  • Approx. 250 lightning injuries per year in the US
  • Responsible for 20–30 deaths per year in the US (death rate of ∼ 10%)
• Pathophysiology: A lightning strike is a type of electrical discharge that has voltages above 10 million volts, which generates a shock wave and extreme heat inside the body in less than a second (low exposure time).
• Clinical features
  • Skin
    • Burns: typically superficial
    • Scorched hair on the scalp
    • Lichtenberg figure: branching (fern‑like), erythematous patterns on the skin (pathognomonic for lightning injury)
    • Metalization: deposition of metal particles into the skin at places where metallic objects (e.g., jewelry) touch the body
  • Cardiac: arrhythmia, e.g., ventricular fibrillation (most common fatal arrhythmia), asystole
  • Vascular: vascular spasms
  • Neurologic
    • Varying degrees of CNS and PNS dysfunction are possible.
    • Onset may be delayed.
  • ENT: tympanic membrane rupture
  • Ocular: cataract, retinal detachment
  • Permanent damage (e.g., complex regional pain syndrome) is common.
• Diagnostics
  • Diagnosis is based on history (e.g., patient with altered mental status found outside in an open space) and clinical findings.
  • Findings on clothing suggestive of lightning injury
    • Grouped holes in clothes
    • Laceration of leather and shoe soles
    • Traces of melting on the body from metal (belt buckles, wristwatches)
• Prevention: appropriate behavior during thunderstorms
  • Avoid swimming outdoors.
  • Find a safe, enclosed shelter.
  • Stay away from concrete floors, walls, and electronic equipment.

Acute mountain sickness (AMS) ^[6]

• Onset
  • Typically 6–12 hours after arrival at high altitude
  • Earlier or later onset possible (ranging from 1–24 hours after arrival)
• Precipitating factors
  • Fast ascent
  • Higher risk in extreme altitude >18,000 ft (∼ 5,500 m)
  • Previous symptoms of altitude sickness
• Pathophysiology: The partial pressure of oxygen of inspired air (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. The physiologic changes typically become significant at elevations > 8,000 ft (∼ 2,500 m). See “Acclimatization.”
  • Early changes
    • Hypobaric hypoxia triggers ventilation → tachypnea and respiratory alkalosis → increases glycolysis → increased 2,3-BPG synthesis → right shift of oxygen dissociation curve → enhanced tissue oxygenation
    • Sickling of red blood cells
  • Late changes
    • Polycythemia
    • Sickling of red blood cells
    • Arterial pH returns to normal through bicarbonate excretion (renal compensation)
    • Pulmonary hypertension
    • Cor pulmonale and right ventricular hypertrophy

• Clinical features
  • Headache (most common)
  • Fatigue
  • Dizziness
  • Anorexia, nausea, vomiting
  • Peripheral edema
  • Nose bleeding
  • Sleep disturbances
• Diagnostics: usually diagnosed clinically based on the development of symptoms only after ascending to high altitude
• Treatment: Symptoms may resolve spontaneously after 12–48 hours of acclimatization.
  • Drugs (symptomatic)
    • NSAIDs for headaches
    • Acetazolamide: increases renal excretion of bicarbonate
    • Dexamethasone
  • Supplement oxygen
  • Descent from altitude
• Prevention
  • Acclimating to 6,000 ft before ascending higher
  • For climbers: supplemental oxygen
  • Avoid alcohol consumption.
  • Drugs: acetazolamide, dexamethasone

High-altitude cerebral edema (HACE)

• Onset: typically 12–72 hours after arrival at high altitude
• Risk factor: ascending to altitude > 12,000 ft (∼ 3,700 m)
• Pathophysiology
  • 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
  • Gradual loss of consciousness
  • Ataxia
  • Visual impairment
  • Bladder dysfunction
  • Bowel dysfunction
  • Stupor and coma
• Diagnostics
  • MRI head: edema and microhemorrhages in the corpus callosum
  • Consider lumbar puncture to rule out other causes.
• Treatment
  • Immediate descent
  • Oxygen supplement
  • Dexamethasone (used as a critical rescue medication that improves the symptoms)
• Prevention: acetazolamide (accelerates acclimatization), dexamethasone

High-altitude pulmonary edema (HAPE) ^[7]

• Onset: typically 2–4 days after arrival at high altitude
• Risk factor: quick ascent to altitude > 14,500 ft (∼ 4420 m)
• Pathophysiology
  • Similar to AMS: A decrease in the partial pressure of arterial oxygen causes vasoconstriction in different organ systems.
  • Hypoxic pulmonary vasoconstriction → increased pulmonary arterial and capillary pressures → pulmonary hypertension
  • Pulmonary hypertension and inflammatory responses → accumulation of extravascular fluid and proteins in the alveolar spaces → pulmonary edema
• Clinical features
  • Cough (initially dry but may progress to produce pink, frothy sputum)
  • Shortness of breath
  • Weakness
  • Chest tightness
  • Crackles or wheezing
  • Cyanosis
  • Tachypnea and tachycardia
• Diagnostics: based primarily on history and clinical features
  • Chest imaging (x-ray or CT): patchy peripheral and nodular infiltrates
  • Bronchoalveolar lavage (BAL): exudate and mild alveolar hemorrhage
  • Echocardiography: noncardiogenic pulmonary edema with normal ejection fraction
• Treatment
  • Immediate descent
  • Oxygen supplement
  • Nifedipine: reduces pulmonary vascular resistance, PA pressure, and systemic resistance
• Prevention
  • Sildenafil or tadalafil (dilates pulmonary vessels, reducing pulmonary vasoconstriction and hypertension)
  • Nifedipine

Decompression sickness

• Definition: : the formation of air bubbles in the tissue and venous circulation caused by a rapid decline in barometric pressure within the body
• Etiology
  • Rapid decompression
    • Rapid ascent when scuba diving
    • Leaving a caisson or a hyperbaric chamber (e.g., in tunneling projects)
  • Risk factors
    • Insufficient diving experience
    • Air travel soon after diving
    • Preexisting right-to-left shunt (e.g., in patent foramen ovale)
    • Atrial septal defect
• 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)
• Clinical features
  • Musculoskeletal: myalgia and arthralgia (most common)
  • Neurological
    • Headaches, altered mental status, visual disturbances, vertigo, ataxia, and a stooping posture
    • Spinal cord involvement: weakness, paralysis, sensory dysfunction, and loss of sphincter control
  • Cutaneous: pruritus and cutis marmorata
  • Cardiopulmonary: chest pain and dyspnea
• Management
  • 100% hyperbaric oxygen
  • Hydration
  • Patient positioning (left lateral decubitus position, lowering the head of the bed)
• Complications
  • Arterial air embolism
  • Circulatory collapse and death
• Prevention
  • Avoid situations involving a rapid decline in barometric pressure.
  • Follow diving safety guidelines (e.g., pay attention to diving limits, make safety stops during the ascent).

References:^[10][11]

Nitrogen narcosis ^[12]

• Definition: a syndrome caused by increased nitrogen levels from breathing compressed air while diving at depth
• Onset: diving at depths ≥ 100 ft
• Risk factors: use of alcohol, sedatives, analgesics before diving
• Pathophysiology: ↑ ambient pressure under water → ↑ partial pressure of nitrogen → ↑ solubility in neuronal membranes → ↓ excitability → intoxication and narcosis
• Clinical features: severity of symptoms increases with diving depth; symptoms disappear rapidly after ascending to shallower depths
  • Altered mental status (e.g., euphoria, confusion, hostility), unconsciousness, coma
  • Loss of fine motor skills
• Diagnostics: clinical diagnosis
• Treatment: immediate ascent
• Prevention: switching from nitrogen-based mixtures to helium-based mixtures or staying above 100 ft

Ear barotrauma (barotitis media, aerotitis media)

• Definition: injury to the structures of the ear caused by a quick change in ambient pressure without adequate equalization of the pressure between the middle ear and the external environment
• Epidemiology: ear barotrauma is the most common flying and diving-related injury ^[13]
• Etiology
  • Flying (most common): e.g., when descending and landing
  • Diving: e.g., during rapid descent
  • Exposure to the sound of gunshots and/or explosions
  • Risk factors
    • Rhinogenic infection
    • Allergic rhinitis
    • Head and neck cancer and/or radiation treatment to these regions
    • Lack of diving experience
• Pathophysiology (diving or flying): rapid descent → increased ambient pressure → creation of a vacuum in the middle ear → increase in blood flow to the middle ear → extravasation of serum to the middle ear or rupture of blood vessels → filling of the middle ear with serous fluid and/or blood or rupture of the tympanic membrane → serous otitis media → transmission of pressure to the inner ear
• Clinical features
  • Acute onset of symptoms (e.g., during rapid descent while diving, during airplane descent)
  • Feeling of pressure and/or stabbing ear pain
  • Hearing loss
    • Conductive hearing loss (most common): frequently occurs as a result of serous effusion within the middle ear or rupture of the tympanic membrane
    • Sensorineural hearing loss: secondary to rupture of the oval or round windows, which results in loss of perilymph from the inner ear
  • Tinnitus, nausea, and/or vertigo
  • Bleeding from the ear canal (if the tympanic membrane is ruptured)
• Diagnostics
  • Clinical diagnosis
  • Otoscopy
    • Hemotympanum
    • Ruptured tympanic membrane
  • Hearing tests (tuning fork, audiogram): conductive or sensorineural hearing loss
  • Tympanometry
    • High negative pressure in the middle ear: eustachian tube dysfunction
    • Large canal volume: tympanic membrane perforation
• Management
  • Conservative
    • Middle ear barotrauma
      • Analgesics
      • Antibiotics are indicated if there is rupture of the tympanic membrane and contamination of the middle ear (e.g., with water).
    • Inner ear barotrauma
      • Bed rest with head elevation
      • Avoidance of maneuvers that may increase pressure in the inner ear (e.g., Valsalva maneuver, coughing)
  • Surgery
    • Indications: unsuccessful conservative management, large rupture of the tympanic membrane, perilymphatic fistula
    • Procedure: myringotomy, tympanoplasty, and/or patching of the round window
• Prevention
  • Avoidance of diving and airplane traveling while congested
  • Oral and/or nasal decongestants prior to flying (e.g., pseudoephedrine)
  • Valsalva maneuver
  • Myringotomy with placement of ventilation tubes
• Prognosis
  • Without inner ear involvement: good (full recovery)
  • With inner ear involvement: possible persistent hearing loss, vertigo, tinnitus

Green tobacco sickness ^[14]

• 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
  • Dizziness, headache
  • Nausea, vomiting
  • Blood pressure fluctuations
• Treatment: usually not required
• Complications: vomiting → dehydration → ↑ 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 ^[15]

• Definition: poisoning with substances containing anhydrous ammonia (e.g., fertilizers)
• Risk factors: occupational exposure (e.g., from farming, manufacturing)
• Etiology: exposure to anhydrous ammonia
• Pathophysiology: contact between anhydrous ammonia and moisture in mucous membranes → production of ammonium hydroxide → corrosive injury due to alkaline pH and hygroscopic properties of ammonia
• Clinical features
  • Inhalation
    • Throat irritation, tightness, and swelling
    • Coughing, dyspnea
  • Skin contact: pain, blisters, necrosis, frostbite (due to liquid ammonia exposure)
  • Eye contact: signs of eye irritation (e.g., lacrimation, pain)
  • Ingestion (rare): nausea, vomiting, abdominal pain
• Diagnostics: clinical diagnosis
• Management
  • First responders should use protective equipment to avoid exposure.
  • Respiratory and cardiovascular support
  • In case of ingestion: do not induce emesis to prevent re-exposure of the esophagus and mouth.
• Complications
  • Respiratory
    • Damage to the respiratory tract (e.g., tracheal burns, alveolar edema), which can cause airway destruction and respiratory failure
    • Asthma, lung fibrosis
  • Dermal: severe burns, deep ulcerations, chronic dermatitis
  • Ocular: temporary or permanent blindness, cataracts, glaucoma
  • Gastrointestinal: corrosive injury of the gastrointestinal tract

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