Summary
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.
Animal bites and stings are a common cause of visits to the emergency department. Symptoms vary in severity, depending on the organism. Local findings typically include pain, swelling, and paresthesia. Systemic signs of envenomation may be limited to nonspecific symptoms (e.g., nausea and vomiting) or lead to neurotoxicity, autonomic dysfunction, and shock.
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.
Overview
Covered in this article
- Electrical injury
- Animal bites and stings
- High-altitude illness
Covered in other articles
- Burns
- Bite wounds
- Poisoning
- Substance-related and addictive disorders
- Organic solvent toxicity
- Metal toxicity
- Carcinogens
- 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
Electrical injury
Electrical current (industrial or residential) injury [1]
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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]
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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
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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
- Current
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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
- 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
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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
- Prehospital care
-
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
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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).
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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
- ENT: tympanic membrane rupture
- Ocular: cataract, retinal detachment
- Permanent damage (e.g., complex regional pain syndrome) is common.
-
Skin
-
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.
Animal bites and stings
For the general management of animal bites, see ”Bite wounds” and “Rabies risk assessment.”
Snake bites [6][7]
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Epidemiology [8]
- ∼ 5,000 venomous snake bites per year in the US
- Crotaline snakes (pit vipers, e.g., rattlesnakes, copperheads, cottonmouths) are responsible for the majority of snake bites in the US.
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Clinical features
- “Dry bites” (bites without envenomation): minor local symptoms
- Envenomation leads to varying degrees of local and systemic symptoms that depend on the amount and toxicity of the venom (see table below).
Common snake bites | ||||
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Rattlesnakes | Coral snakes | Black mamba snake | ||
Distinguishing features |
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Geographic location |
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Venom |
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Clinical features of envenomation | Local |
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Systemic |
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- Diagnostics: usually based on history (description of possible identifying features of the snake) and clinical features
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Management
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Antivenom administration
- For pit viper bites: crotalidae polyvalent immune fab
- Adverse effects: hypersensitivity, serum sickness
- Pressure immobilization and/or tourniquets are not recommended as part of routine management in the US. [9]
- Patients must be closely watched for signs of cardiovascular instability and respiratory compromise.
-
Antivenom administration
Spider bites
- Diagnosis of spider bites is usually based on history and clinical presentation.
- General treatment includes cleaning of the wound, cooling, and analgesia.
- They rarely require specific medical treatment.
Common spider bites | |||
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Brown recluse spider | Widow spider | ||
Distinguishing features |
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Geographic location |
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Venom |
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Clinical features | Local |
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Systemic |
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Specific treatment |
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Scorpion sting
- Most scorpion stings in the US are painful but do not cause severe symptoms.
Bark scorpion sting
- Geographic location: southwestern US
- Pathophysiology: venom contains a neurotoxin that inhibits the inactivation of the sodium channels → prolonged depolarization → neuronal membrane hyperexcitability
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Clinical features
- Mild: local pain, swelling, and paresthesia at the sting site
- Severe: cranial nerve dysfunction, autonomic dysfunction, neuromuscular toxicity (e.g., fasciculations, muscle jerks), rarely acute pancreatitis
- Diagnostics: based on history and clinical features
- Treatment: antivenom administration for severe cases
Jellyfish sting
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Geographic location
- Worldwide in coastal waters
- Box jellyfish: Hawaii, Northern Australia, tropical Atlantic
- Pathophysiology: Jellyfish have tentacles with specialized capsules (nematocysts) that attach to the skin and release venom. The toxicity of the venom depends on the species.
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Clinical features
- Local envenomation
- Initial pain
- Sting develops into a linear urticarial lesion.
- Severe stings can be complicated by skin necrosis.
- Systemic envenomation: anaphylaxis, cardiac arrest
- Local envenomation
- Diagnostics: based on history and clinical features
-
Treatment: Routine management depends on the jellyfish species and the geographic location. [10]
- Apply topical vinegar: recommended only for some jellyfish species (e.g., box jellyfish)
- Remove attached tentacles and rinse the sting site with seawater.
- Immerse in hot water for pain relief.
- Administer antivenom in the case of severe stings (e.g., stings affecting large areas, systemic symptoms).
Hymenoptera sting
- Examples: bees, wasps, yellow jackets, hornets, fire ants
- Geographic location: worldwide
- Pathophysiology: Insects from the Hymenoptera order release venom into tissue when stinging, triggering a local skin reaction and potentially life-threatening systemic reactions.
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Clinical features
- Local skin reaction at the site of the sting
- Initial pain
- Swelling and redness appear within minutes of the sting event.
- Usually resolves within hours
- Large local reactions (LLR): gradually extending area of swelling and redness (typically > 10 cm) that lasts for days [11]
- Systemic allergic reactions, anaphylaxis are possible
- Local skin reaction at the site of the sting
- Diagnostics: primarily a clinical diagnosis
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Treatment
- Removal of the stinger if it is still lodged in the skin
- Cold compresses
- Analgesia (NSAIDs)
- Observation of patients with multiple stings or a history of systemic reactions or other allergies
- Severe cases
- Oral prednisone for LLR to reduce significant swelling
- Systemic reactions (anaphylaxis): See ”Management of anaphylaxis.”
High-altitude illness
High-altitude illness refers to a group of syndromes that can occur at high altitudes (typically over 8,000 ft or 2,500 m).
Acute mountain sickness (AMS) [12]
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Onset
- Typically 6–12 hours after arrival at high altitude
- Earlier or later onset possible (ranging from 1–24 hours after arrival)
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Precipitating factors
- Fast ascent
- Higher risk in extreme altitude >18,000 ft (∼ 5,500 m)
- Previous symptoms of altitude sickness
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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
- Early changes
Acclimatization to high altitude | ||
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Parameter | Early changes | Late changes |
PAO2 and PaO2 |
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PACO2 and PaCO2 |
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Arterial pH |
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Hb |
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Arterial O2 content |
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- Clinical features
- Diagnostics: usually diagnosed clinically based on the development of symptoms only after ascending to high altitude
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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
- Drugs (symptomatic)
-
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
-
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) [13]
- 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
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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
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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
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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