Environmental pathology

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.

Poisoning/toxin exposure

• CO toxicity
• Organic solvent toxicity
• Metal toxicity
• Carcinogen exposure

Electrical, thermal, and radiation injury

• Electrical injury
• Lightning injury
• Heat stroke
• Burns
• Hypothermia
• Frostbite and nonfreezing cold injuries
• Radiation injury

Injuries related to changes in ambient pressure

• High-altitude illnesses
  • Acute mountain sickness
  • High-altitude cerebral edema
  • High-altitude pulmonary edema
• Diving-related illnesses
  • Decompression illness
  • Nitrogen narcosis
  • Barotrauma on descent or ascent

Animal-related conditions

• Animal bites and stings
  • Dog bite
  • Domestic cat bite
  • Snake bites
  • Spider bites
  • Jellyfish stings
  • Hymenoptera stings
• Zoonotic diseases

Work-related conditions

• Work-related respiratory conditions, e.g.:
  • Hypersensitivity pneumonitis
  • Asbestosis
  • Silicosis
  • Other pneumoconioses
• Work-related infectious diseases
• Occupational rhinitis
• Occupational skin diseases
• Agricultural health hazards

Electrical injury ^[1][2][3]

Epidemiology

• 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]

• High-voltage sources (≥ 1000 V): e.g., lightning strike, industrial devices, power supply lines, conducted electrical weapon (CEW) ^[6]
• Low-voltage sources (< 1000 V): e.g., household appliances, extension cords, wall outlets

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.

• Skin: superficial to deep burn
• Musculoskeletal
  • Tetanic muscle contraction can lead to rhabdomyolysis or fracture.
  • Muscle necrosis
  • Acute compartment syndrome
  • Fractures (e.g., cervical spine fractures)
• Cardiovascular
  • Arrhythmia: e.g., asystole; , ventricular fibrillation
  • Myocardial infarction
  • Hypovolemia, e.g., due to burns, traumatic hemorrhage, and/or third spacing in injured tissue ^[3]
  • Thrombosis, coagulation, necrosis
• Respiratory: paralysis, respiratory arrest ^[7]
• Renal: acute kidney injury (e.g., pigment-induced AKI due to rhabdomyolysis)
• Neurological
  • CNS: loss of consciousness, seizures, head injury, spinal cord injury
  • PNS: paresthesia, numbness, muscle weakness
• Ocular: cataracts, retinal 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

• ABCDE assessment: following the ATLS algorithm
  • Airway management including C-spine immobilization
  • Mechanical ventilation as needed
  • Immediate hemodynamic support
• Immediate diagnostics: ECG ^[7]
• Focused history and physical examination
  • History: voltage and type of current, associated trauma (e.g., fall, blast), underlying medical conditions (e.g., heart disease)
  • Examination: evaluation for burns, head trauma, eye injury, cardiopulmonary abnormalities, musculoskeletal trauma, and neurological injury

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]

• Additional diagnostics
  • Laboratory studies: CBC, CMP, urinalysis, CPK, myoglobin
  • Imaging based on clinical suspicion: e.g., echocardiography , additional trauma diagnostics ^[7]
• Treatment
  • IV fluid resuscitation with a goal urine output of 1–1.5 mL/kg/hour ^[1][3]
  • Pain management as needed
  • Burn management: Consult a burn surgeon; consider transfer to a burn center.
  • Management of specific injuries and additional consults (e.g., orthopedics, cardiology) as appropriate
• Disposition and monitoring
  • Initiate continuous cardiac monitoring.
  • Admit to a monitored setting.

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]

Prevention

• 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
  • Blast injury: due to rapid heating and expansion of surrounding air
  • Cardiopulmonary arrest: due to transient stunning of the cardiac conduction system and/or the brain stem
  • Thermal burns: superficial or, less commonly, deep

Clinical features ^[3][8][10]

• Clothing: often singed, torn, and/or tattered, with melted metal items (e.g., zippers) ^[11]
• Skin: Signs may be minimal or absent despite substantial other injuries.
  • Burns: typically superficial
  • Lichtenberg figure: branching (fern‑like), erythematous patterns on the skin (pathognomonic for lightning injury)
  • Metalization: deposition of metal particles into the skin at sites where metallic objects (e.g., jewelry) are in contact with the body
• Respiratory: central apnea ^[3][10]
• Cardiac
  • Arrhythmia (common): e.g., ventricular fibrillation, asystole
  • QTc prolongation, depressed cardiac contractility, pericardial effusion, acute myocardial injury
• Neurological
  • Immediate onset
    • Pupillary dilation, anisocoria ^[3][8]
    • Loss of consciousness, seizures, amnesia
    • Keraunoparalysis: transient flaccid paralysis and sensory loss with signs of vascular spasm (e.g., pulselessness) ^[10]
    • Peripheral nerve injury, intracranial hemorrhage, traumatic brain injury
  • Delayed onset: myelopathy, complex regional pain syndrome ^[12]
• Vascular: vascular spasm ^[1]
• ENT: tympanic membrane rupture
• Ocular: cataract, retinal detachment

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]

Management

• High-risk lightning strike ^[10]
  • Management is similar to patients with high-voltage electrical injuries.
  • Obtain ECG and echocardiography for all patients.
  • Admit for continuous cardiac monitoring for ≥ 24 hours.
  • See “Management of electrical injuries” for further information.
• Low-risk lightning strike ^[3]
  • Typically, no specific diagnostics or treatment are required.
  • Consider discharge after arranging outpatient follow-up to assess for delayed effects. ^[8]

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]

Prevention

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]

• Provide ACLS and ATLS as needed.
• Obtain an ECG.
• Begin continuous cardiac monitoring in high-risk patients.
• Initiate IV fluid therapy to maintain target diuresis of 1–1.5 mL/kg/hour.
• Perform a focused physical examination to assess for:
  • Burns
  • Trauma
  • Compartment syndrome
  • Neurological injury
• Obtain diagnostic testing based on history and examination findings.
• Begin treatment based on injury severity.

Overview ^[3][17]

• High-altitude illnesses can occur at altitudes above 2000–2500 m (∼ 6500–8000 feet) as a result of unsuccessful acclimatization.
• Manifestations range from acute mountain sickness to high-altitude pulmonary edema and high-altitude cerebral edema.
• Initial management includes supplemental oxygen and cessation of ascent or rapid descent.

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.”

• Early changes: Hypobaric hypoxia triggers ventilation → tachypnea and respiratory alkalosis → increased glycolysis → increased 2,3-BPG synthesis → right shift of oxygen dissociation curve → enhanced tissue oxygenation
• Late changes
  • Polycythemia
  • Arterial pH returns to normal through bicarbonate excretion (renal compensation).
  • Pulmonary hypertension
  • Cor pulmonale and right ventricular hypertrophy

Clinical features of AMS ^[20]

• Onset: typically 4–12 hours (range 1–24 hours) after arrival ^[21][22]
• Headache (most common)
• Fatigue
• Dizziness
• Anorexia, nausea, vomiting
• Peripheral edema
• Sleep disturbance

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]

• Carbon monoxide poisoning
• Dehydration, exhaustion, hypothermia
• Hypoglycemia and/or hyponatremia
• CNS pathology

Treatment ^[3][17]

• Stop ascent until symptoms resolve and descend if symptoms do not improve or worsen.
• Mild AMS : symptomatic treatment with analgesics (e.g., ibuprofen) and antiemetics (e.g., ondansetron)
• Moderate to severe AMS
  • Oxygen therapy (target SpO₂ > 90%)
  • Pharmacological therapy: acetazolamide (preferred) OR dexamethasone (off-label) ^[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.

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

• Onset: typically 12–72 hours after arrival ^[3]
• Symptoms of AMS (e.g., headache)
• Altered mental status; (e.g., gradual loss of consciousness, stupor, coma)
• Ataxia
• Visual impairment
• Bladder dysfunction
• Bowel dysfunction

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

Diagnostics ^[22]

• Imaging: CT head, MRI head
• Laboratory studies: CBC, CMP, carboxyhemoglobin level, toxicology screen
• Lumbar puncture (for suspected CNS infection or hemorrhage)

Differential diagnoses ^[3][22]

• Differential diagnoses of acute mountain sickness (e.g., hypothermia)
• Acute stroke

Treatment ^[3][17][22]

• Descend immediately.
• High-flow oxygen titrated to target SpO₂ of > 90%
• Critical rescue medication: dexamethasone (off-label) ^[17]
• Hyperbaric oxygen therapy (HBOT) if available

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]

Pathophysiology

• Similar to acute mountain sickness: 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

• Onset: typically 2–4 days after arrival
• Cough (initially dry, but may become productive with pink, frothy sputum)
• Shortness of breath
• Weakness
• Chest tightness
• Crackles or wheezing
• Cyanosis
• Tachypnea and tachycardia

Diagnostics ^[3][19][22]

• Lung ultrasound: pulmonary edema, B lines; see also “POCUS in acute heart failure”
• Chest x-ray: patchy infiltrates
• ECG: tachycardia and evidence of right heart strain
• Echocardiography: elevated pulmonary pressure, normal LV function

Differential diagnoses ^[3][22]

• Exacerbation of asthma or COPD
• Pneumonia
• Acute heart failure
• Pulmonary embolism

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]

• Descend immediately.
• Oxygen therapy with target SpO₂ of > 90%; CPAP if in the hospital setting
• Portable HBOT if available
• Pharmacotherapy if immediate descent and oxygen therapy are not feasible.
  • Nifedipine (off-label) ^[17]
  • OR phosphodiesterase inhibitors : sildenafil or tadalafil ^[17]

Prevention of altitude illness ^[17][22]

• Staged ascent and oxygen during sleep
• Prophylactic medication
  • AMS/HACE: acetazolamide or dexamethasone (if risk factors for altitude illness are present)
  • HAPE: nifedipine (preferred) or phosphodiesterase inhibitors (if the individual has a history of HAPE)

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.:
  • Decompression sickness type I and II
  • Arterial gas embolism
• Risk factors for DCI include:
  • Environment-related factors
    • Prolonged and deep diving
    • Air travel shortly after diving
  • Patient-related factors
    • Obesity, older age
    • Low fitness level, strenuous exertion during the dive
    • Hypothermia or hyperthermia
• 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]
  • Musculoskeletal: myalgia and arthralgia (most common)
  • Neurological
    • Numbness and paresthesias
    • Headaches, altered mental status, visual disturbances, stooping posture
    • Spinal cord involvement: weakness, paralysis, sensory dysfunction, loss of sphincter control
  • Inner ear: vertigo, ataxia, hearing loss
  • Cardiopulmonary: chest pain, dyspnea, cough
  • Cutaneous: pruritus and cutis marmorata
• Diagnostics ^[24]
  • Primarily a clinical diagnosis based on diving history and timing of symptom onset
  • Chest x-ray: to rule out pneumothorax
• Differential diagnosis ^[24][26]
  • Barotrauma
  • Contaminated air
  • Oxygen toxicity
  • Immersion pulmonary edema
  • Coincidental CNS disorder, e.g., stroke
• Management: Maintain the patient supine during treatment. ^[26][27]
  • ABCDE assessment and administration of 100% oxygen
  • Dive medicine consultation and hyperbaric oxygen therapy (recompression) as soon as possible ^[27]
  • Cautious IV fluids with fluid balance monitoring ^[24][27]
• Complications
  • Arterial gas embolism in patients with atrial septal defect, e.g., patent foramen ovale
  • Prolonged neurological deficit ^[26]
• 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]

• Etiology
  • Can occur after brief and shallow (< 3 m) dive as a result of pulmonary barotrauma on ascent
  • Can also develop in those with DCS and atrial septal defect, e.g., patent foramen ovale
• Onset: usually within 10 minutes of surfacing ^[3]
• Clinical features: focal neurologic deficits, altered mental status, arrhythmias, and/or circulatory collapse
• Management
  • ABCDE assessment and administration of 100% oxygen
  • Dive medicine consultation and HBOT as soon as possible
  • Cautious IV fluids with fluid balance monitoring
  • See “Arterial air embolism” in “Nonthrombotic embolism” for further details.
• Prevention: Avoid breath holding during ascent.

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]

• Definition: injury to the structures of the ear caused by a rapid change in ambient pressure without adequate equalization of the pressure between the middle or inner ear and the external environment
• Epidemiology: Ear barotrauma is the most common flying and diving-related injury. ^[31]
• 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 ^[29]
• Clinical features
  • Acute onset of symptoms (e.g., during rapid descent while diving, during airplane descent)
  • Middle ear barotrauma (MEBT)
    • Stabbing ear pain or pressure
    • Conductive hearing loss
    • Tympanic membrane rupture, blood in the ear canal
    • Transient vertigo and nausea if the tympanic membrane ruptures
  • Inner ear barotrauma (IEBT)
    • Persistent vertigo and/or ataxia
    • Sensorineural hearing loss
    • Tinnitus
    • Nausea and vomiting
• Diagnostics ^[29][32]
  • Clinical diagnosis based on diving history and timing of symptom onset
  • Possible supportive findings
    • Otoscopy: hemotympanum, ruptured tympanic membrane
    • Hearing studies (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
• Differential diagnosis: inner ear DCS ^[30]
• Management ^[29][33]
  • Stop descent if possible.
  • Symptomatic treatment: analgesics, oral and topical decongestants
  • ENT consult for:
    • Antibiotics if the tympanic membrane is ruptured
    • All suspected cases of IEBT
    • Consideration of systemic steroids if otoscopy is abnormal
    • Surgery in selected cases
  • Additional measures for IEBT
    • Bed rest and head elevation
    • Avoid activities that increase inner ear pressure (e.g., Valsalva maneuver, coughing, straining on the toilet).
• Prevention ^[33][34]
  • Avoid diving if eustachian tubes are plugged.
  • Consider oral and/or nasal decongestants (e.g., pseudoephedrine) prior to flying or diving.
  • Tube opening maneuvers (preferred) or nonforceful Valsalva maneuvers while diving or flying
  • Consider myringotomy tubes in at-risk patients
• Prognosis ^[3]
  • MEBT typically resolves with conservative therapy.
  • IEBT may result in persistent hearing loss, vertigo, and tinnitus.

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]

• Epidemiology: second most common diving injury
• Clinical features
  • Sinus pain on descent
  • Epistaxis on ascent
• Management
  • Conservative treatment of symptoms
  • Monitor for delayed sinusitis.

Pulmonary barotrauma ^[3]

• Definition: alveolar rupture caused by expansion of air in the lungs during rapid ascent
• Risk factors ^[3]
  • Breath holding during ascent
  • Asthma
  • COPD
  • Mucus plugging
• Clinical features
  • Chest pain
  • Subcutaneous crepitus
  • Hemoptysis
• Complications: pneumothorax, AGE, alveolar hemorrhage, subcutaneous emphysema
• Management ^[25]
  • Provide 100% oxygen.
  • Treat complications (e.g., thoracostomy for pneumothorax).

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

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
  • 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 ^[36]

• 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!