Drowning, electrical and altitude injury

• Drowning is death from respiratory impairment after submersion or immersion in liquid; about 300,000 people drown each year, and 92% of deaths are in low- and middle-income countries. ^[7]
• Electrical injury ranges from harmless mains shocks to high-voltage and lightning injuries that can stop the heart and burn deep tissues; alternating current in homes is more dangerous than direct current because it causes tetany.
• Altitude illness begins above 2500 m in unacclimatised travellers and runs from acute mountain sickness through high-altitude cerebral oedema (rapidly fatal) to high-altitude pulmonary oedema (up to half die if untreated). ^[2]
• Decompression sickness arises from nitrogen bubbles released during ascent from depth; most type I cases are painful but self-limiting, while type II can paralyse or kill.
• Prevention dominates management in all four conditions: water safety and supervision, electrical safety and lightning awareness, graded ascent with acetazolamide when needed, and dive tables with slow ascent.

By the end of this page you should be able to:

1. Describe the drowning chain from water entry to death, and outline out-of-hospital and in-hospital care, including prognosis.
2. Explain why electrical injury is assessed by voltage, current type and pathway, and how that drives cardiac, muscle, kidney and airway management.
3. Recognise the three altitude illnesses, apply the Lake Louise criteria and the HAPE diagnostic criteria, and state the prevention and treatment regimens recommended by the Wilderness Medical Society (WMS).
4. Identify type I and type II decompression sickness and arterial gas embolism, and outline oxygen and hyperbaric therapy.
5. Give patient education and prevention advice for low-resource and high-risk groups.

These four problems are grouped because each is an environmental or immersion emergency where the first tasks are the same: make the scene safe, stop further injury, support breathing and circulation, and get the patient to definitive care. They share a common theme of hypoxia (drowning and diving), electrical energy (contact and lightning), or hypobaric hypoxia (altitude). Each section below gives enough for a student to recognise the condition, understand why it happens, and manage it safely. Numerical claims are cited to the sources, and guideline editions are named where they are used.

Drowning disproportionately affects children and young people. Children under 5 years account for nearly a quarter of all drowning deaths, and children and young adults aged 0 to 29 years account for over half (57%) of all drowning deaths; the highest rates per population are among children aged 0 to 4 years. ^[7] About 300,000 people drown each year worldwide, and 92% of deaths occur in low- and middle-income countries, where drowning death rates are more than three times higher than in high-income countries. ^[7] Over half of the world's drowning occurs in the WHO Western Pacific Region and WHO South-East Asia Region. ^[7] Since 2000 the global drowning death rate has fallen by 38%, from 6.1 to 3.8 per 100,000 population. ^[7] The male drowning death rate is more than twice as high as the female rate, related to greater water exposure and riskier behaviour. ^{[7] [4]}

Unintentional drowning causes more than 500,000 deaths each year by some estimates. ^[6] In one retrospective emergency department cohort, 60% of admitted patients (15 of 25) did not survive drowning or diving incidents, and hypoxic brain injury was the leading cause of death. ^[6]

• Age: very young children have underdeveloped risk assessment and limited water safety skills; the risk rises when children interact with water outside active adult supervision. ^[7]
• Poverty and inequality: ponds, rivers, lakes and open wells used for bathing, washing and water collection expose people daily in low-resource settings. ^[7]
• Occupational exposure: commercial and subsistence fishing, with tens of thousands of fisher deaths each year. ^[7]
• Climate: drowning accounts for 75% of deaths in flood disasters. ^[7]
• Unsafe water transport and migration across water in overcrowded vessels without safety equipment. ^[7]

Drowning begins with breath-holding. When oxygen falls, laryngospasm and then water entry impair gas exchange, producing hypoxaemia, hypercapnia and acidosis. Coughing and swallowing occur, then loss of consciousness as hypoxia deepens. Cardiac rhythm disturbances and cardiac arrest follow ischaemia; secondary hypoxic injury to the brain and other organs dominates outcome. The duration of submersion and the time to effective ventilation are the strongest determinants of outcome.

Presentations range from a coughing, alert survivor to an unresponsive victim with no pulse. Tachypnoea, cough, crackles, hypoxaemia and altered consciousness are common. Temperature is often low because of cold water, and hypothermia may be neuroprotective in some cases.

Survival data from a single-centre retrospective study of drowning and diving admissions: patients needing cardiopulmonary resuscitation (CPR) were far less likely to survive; all non-survivors had a Glasgow Coma Scale score of 3; and non-survivors had lower pH (6.7 versus 7.4) and higher lactate (14.8 versus 4.3 mmol/L), myoglobin, CK-MB quotient and blood glucose. ^[6] In that cohort, all four patients who received CPR for up to 10 minutes had two survivors, while none of the eleven patients receiving CPR for more than 10 minutes survived; no patient survived when no-flow time exceeded 5 minutes. ^[6] Treating clinicians should not use any single laboratory value as a decision rule, because the sample was small and retrospective.

Other causes of sudden water-related death include cardiac arrhythmia, myocardial infarction, stroke, seizure, trauma (including diving into shallow water), and hypothermia. In divers, consider arterial gas embolism and decompression sickness (below).

Core support: oxygen saturation, arterial blood gas (pH, lactate), glucose, electrolytes, renal function, CK and cardiac biomarkers as clinically indicated, chest imaging, and ECG. Hypothermia requires core temperature measurement. Most data come from retrospective single-centre work with small numbers, so interpret results cautiously.

There is no single severity score for drowning. In practice, the key questions are: how long was the person submerged, when did effective ventilation and CPR start, what is the core temperature, and what is the neurological state after resuscitation.

Immediate (out of hospital):

1. Ensure scene safety. Remove the person from the water.
2. Clear the airway of visible debris, but do not spend time trying to drain water from the lungs; water in the airways is scant and drainage attempts only delay ventilation. ^[6]
3. Give rescue breaths early. If breathing is absent or abnormal, start CPR with rescue breaths rather than compression-only CPR.
4. Do not routinely immobilise the cervical spine unless there is a history of diving, a fall, trauma or neurological findings; in-water spine immobilisation delays rescue and is not required for uncomplicated drowning.
5. Use an automated external defibrillator for shockable rhythms.
6. Warm and dry the victim; prevent further heat loss. Do not delay CPR for warming.

In hospital:

• Airway and breathing: give high-flow oxygen, assess for pulmonary oedema and aspiration, and intubate early if the airway is unprotected or oxygenation is failing.
• Circulation: follow advanced life support. Fluids and vasopressors as clinically indicated.
• Temperature: treat hypothermia; core rewarming for profound hypothermia.
• Investigations: arterial blood gas, lactate, glucose, electrolytes, renal function and CK.
• Neurological care: consider targeted temperature management after cardiac arrest per local protocol.
• Diving-related cases: give 100% oxygen and consider hyperbaric oxygen therapy for severe cases. ^[6]

Prognosis after drowning depends mainly on submersion time, water temperature, speed of resuscitation and pre-existing disease. Non-survivors most often die of hypoxic brain injury. ^[6]

WHO advises covering wells, using doorway barriers and playpens, fencing swimming pools and otherwise controlling access to water hazards; community-based supervised childcare for pre-school children; teaching school-age children basic swimming, water safety and safe rescue skills; setting and enforcing safe boating, shipping and ferry regulations; and building resilience to flooding with disaster preparedness and early warning systems. ^[7] A WHO investment case estimated that scaling up day-care and basic swim skills for children could prevent hundreds of thousands of drowning deaths and injuries by 2050. ^[7] UN and World Health Assembly resolutions on drowning prevention provide the global roadmap, and 25 July is World Drowning Prevention Day. ^[7]

• Children: highest rates; active supervision and barriers are critical.
• Occupational fishers and water transport workers: high exposure.
• Low-income communities near water without lifeguards or barriers.

Prioritise supervision, barriers around water, and teaching safe rescue and early ventilation rather than aggressive in-water techniques. A single responder who gives rescue breaths early may change outcome more than advanced equipment.

Electrical injury is tissue and organ damage caused by electrical current passing through (or over) the body. Burns are one part; cardiac, renal, muscular, neurological and sensory complications may dominate.

• Low-voltage electrical injury (LVEI): exposure below 1000 volts; most household appliances operate below 240 V. ^[3]
• High-voltage electrical injury (HVEI): more than 1000 volts, usually occupational (power lines, electrified railways). ^[3]
• Lightning: counts as HVEI and may involve 30,000 to 110,000 volts per strike. ^{[3] [4]}

Electrical injuries affect more than 30,000 people each year in the United States and account for about 4% of burn centre admissions in adults and children. ^[3] About 3% are fatal, with HVEIs responsible for roughly 40% of fatalities and lightning for about 5%. ^[3] Males are disproportionately affected, mostly through occupational exposure. ^[3]

Lightning is rare but dangerous. Global lightning mortality is estimated at 0.2 to 1.7 deaths per million per year, and in most developed countries below 0.3 per million per year, though rural and agriculture-dominated areas may see about six per million per year. ^[4] Worldwide, over 100 lightning strikes occur each second, and lightning accidents make up only 2 to 4% of high-voltage accidents. ^[4] The male-to-female ratio is about 5 to 1 for lightning strikes. ^[4] In an Austrian Alps analysis, 64 lightning victims included 54 men; 93.8% survived, with all deaths on scene; most occurred June to August between noon and 22:00, and 46.9% on a Saturday or Sunday. ^[4]

• Contact with mains electricity (LVEI) or high-voltage conductors (HVEI), including railway and power-line contact.
• Lightning: outdoor and mountain activity in summer afternoons, sheltering under trees, carrying metal objects, being on ridges.
• Children: increasingly rare because of better safety standards; mostly low-voltage household contact.

The severity depends on voltage, current (amperes), type of current, duration of contact, pathway through the body and tissue resistance. Nerves, muscles and blood vessels conduct well and are damaged most; bone, tendon, skin and fat resist more. Alternating current in homes is more dangerous than direct current because the oscillation produces tetanic contractions that prolong contact; lightning uses direct current. ^[3]

Pathways matter: a vertical pathway exposes brain, heart, lungs, respiratory muscles and uterus, whereas horizontal or lower-body pathways cause more local injury. ^[3] Joule heating, electroporation and protein denaturation damage cell membranes and muscle, releasing creatine kinase and myoglobin and causing rhabdomyolysis, compartment syndrome and acute kidney injury even when skin burns look small.

Lightning is a special case: up to 100,000 amperes, 0.3 to 2.2 million volts, conduction of only 0.02 to 100 milliseconds, and temperatures of 25,000 to 30,000 degrees C. ^[4] Most of the current travels along the outside of the body (flashover/surface effect), which explains why many survive; burns are usually first- and second-degree. ^[4]

Systemic features by organ group, as summarised in current reviews:

Cardiovascular: arrhythmias are common in the first few hours. Sinus tachycardia and premature ventricular contractions are the most common; ventricular fibrillation, ventricular tachycardia and asystole occur. Patients with LVEI more often develop ventricular arrhythmias, while HVEI patients are at higher risk of pulseless electrical activity and asystole; lightning confers the greatest risk of fatal arrhythmia. An initial ECG is essential. ^[3]

Musculoskeletal: electrical injury can cause fractures and dislocations from tetany; posterior shoulder dislocation is the most commonly described joint injury. Deep muscle injury exceeds skin findings, so have a low threshold for imaging. ^[3]

Rhabdomyolysis: serum creatine kinase above five times the upper limit of normal, typically above 1000 IU/L, with myoglobinuria, hyperkalaemia and acute kidney injury; treatment should not be delayed awaiting results. ^[3]

Compartment syndrome: rising pressure in a fascial compartment, diagnosed clinically (pain out of proportion, pain with passive stretch) or by measurement (intracompartmental pressure above 30 mmHg, or a delta pressure of diastolic blood pressure minus compartment pressure under 30 mmHg). ^[3] Circumferential burns are a particularly strong risk factor.

Renal: acute kidney injury from rhabdomyolysis. KDIGO criteria apply: low urine output (below 0.5 mL/kg/h for at least 6 hours), creatinine rise of 0.3 mg/dL within 48 hours, or 1.5 to 2 times baseline. Electrical burns need a higher urine output target than thermal burns (around 1 mL/kg/h) during fluid resuscitation. ^[3]

Respiratory: arrest from diaphragm and intercostal paralysis, seen more in lightning and HVEI, plus inhalation injury, pulmonary haemorrhage and acute respiratory distress syndrome; suspect carbon monoxide or cyanide toxicity where there has been fire or smoke.

Neurological: acute loss of consciousness, seizures, stroke, peripheral neuropathy; delayed sequelae can appear days to years later. Routine seizure prophylaxis is not recommended unless high-risk. Sensory complications include tympanic membrane rupture (classically in lightning), vertigo, corneal erosions and cataracts.

Cutaneous: small, well-demarcated entry and exit wounds; characteristic patterns include "crocodile skin", metallization and periorbital "crow's feet". Lichtenberg figures are transient, fern-like erythematous markings seen in lightning and resolve within 24 hours. Visible burns underestimate deeper damage, so consult burn services early.

Lightning-specific syndromes include keraunoparalysis (transient paralysis of limbs, often with mottled cyanosis), most obvious in the legs, and spasm of small cutaneous vessels. Most deaths are from cardiac arrest due to ventricular fibrillation and asystole, and from respiratory centre paralysis with apnoea. ^[4] The continuous current can paralyse the respiratory centre, cause prolonged apnoea, and lead to secondary hypoxia, so prolonged CPR may be needed. ^[4]

ECG on arrival for all electrical injuries; ECG monitoring for at least 24 hours if there was loss of consciousness, an abnormal ECG, a history of cardiac disease, HVEI or lightning. ^[3] Serum creatine kinase on arrival and trended serially over 24 to 48 hours, even if initially normal. Basic laboratory panel (full blood count, renal function, electrolytes, glucose). Imaging as indicated: plain radiographs for focal pain, restricted movement, or suspected fracture or dislocation; CT or MRI when focal neurological deficits or head injury are suspected; intracompartment pressure when examination is unreliable. Cardiac biomarkers (troponin, CK-MB) are not helpful for risk stratification after electrical injury and are reserved for patients with chest pain, haemodynamic instability or ECG changes suggesting acute coronary syndrome. ^[3]

There are no widely accepted specific guidelines for electrical injury; management follows ATLS and burn protocols. The Wilderness Medical Society provides a standard protocol for lightning: ATLS principles, routine ECG, head CT if there is loss of consciousness or a direct head strike, ophthalmological evaluation, bilateral ear examination and superficial burn care. ^[3]

1. Scene safety first; assume the source is still live.
2. Advanced cardiac life support for cardiac arrest; first responders should perform vigorous resuscitation in lightning victims, who may be more responsive. ^[3] If several people are struck, contrary to usual triage, priority goes to the person with no vital signs. ^[4]
3. Airway and breathing, including intubation for respiratory arrest or unprotected airway. Ventilate and oxygenate; 100% oxygen where indicated.
4. Cardiac monitoring as above; treat arrhythmias per advanced life support.
5. Assess for rhabdomyolysis and start intravenous fluids promptly with Lactated Ringer's. The Parkland formula (4 mL per percent total body surface area per kg body weight in 24 h, half in the first 8 h) or the modified Brooke formula may guide volumes, but resuscitation is best titrated to urine output (target 1 mL/kg/h for electrical injuries). ^[3]
6. Consider mannitol for myoglobinuria and treat hyperkalaemia if needed.
7. Manage compartment syndrome early, with fasciotomy when indicated; consult surgery for circumferential or high-voltage injuries.
8. Burn care by depth; early burn unit or surgical consultation for deep injury.
9. Manage neurological, sensory and pain symptoms with a multimodal analgesic approach.
10. Support kidney function and monitor for acute kidney injury.

Complications include arrhythmia, respiratory arrest, acute kidney injury, compartment syndrome and limb loss, infection, cataracts and delayed neurological syndromes. Mortality is highest in HVEI and lightning but low overall where early resuscitation is provided.

Prevention means safe electrical practice: isolation, lockout procedures, protective equipment for electrical workers, and public education on mains and rail hazards. Lightning safety: follow "when thunder roars, go indoors"; avoid peaks, ridgelines and open terrain in the afternoon; do not shelter under trees or in small shelters; discard metal objects; adopt the lightning position (crouching, feet together, only one point of ground contact) if caught in the open; keep group members separated. ^[4]

Children (mostly low-voltage household shocks but may have pocket-burn at the oral commissure), occupational workers, and older adults with comorbid cardiac disease.

Focus on scene safety and ATLS: ECG and creatine kinase where available, creatine kinase–driven ABCs, generous fluids titrated to urine, early surgical consultation, and evacuation to a burn centre.

Altitude illness is a collective term for syndromes occurring in unacclimatised people who travel above 2500 m (high altitude 2500 to 3500 m; very high 3500 to 5500 m; extremely high over 5500 m). ^[2] The spectrum runs from acute mountain sickness (AMS), through high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE), to mild peripheral oedema which may not denote illness. Recommendations below draw on the 2024 Wilderness Medical Society Clinical Practice Guidelines for the prevention, diagnosis and treatment of acute altitude illness, as summarised in a 2025 appraisal of WMS guidelines ^[1] and a 2026 BMJ practice pointer ^[2], which bases its advice on the 2024 WMS and 2024 UIAA Medical Commission guidelines.

AMS may occur in up to 25% of people who ascend rapidly above 2500 m. ^[2] HACE may occur in up to 1% of travellers at 4000 to 5000 m, and HAPE in up to 6% at 4500 m. ^[2] A wider review reports AMS in up to 25%, HACE leading to death in as little as 24 hours if untreated, and HAPE mortality up to 50% if untreated. ^[1]

• Rapid ascent (more than 500 m sleeping-altitude gain between nights), especially above 3000 m. ^[2]
• High starting sleeping altitude (over 2800 m on day 1, for example flying into a high-altitude city).
• Previous history of moderate or severe AMS, HACE or HAPE.
• Intense exertion regardless of fitness; fitness and youth are not protective. ^[2]
• Altitude illness can occur in healthy people from around 2000 m. ^[1]

Hypobaric hypoxia (falling barometric and partial pressure of oxygen) triggers hypoxic cerebral vasodilatation and intracellular oedema in AMS and HACE, and exaggerated hypoxic pulmonary vasoconstriction with raised pulmonary artery pressure and non-cardiogenic pulmonary oedema in HAPE. ^[2] Sleeping altitude (not the day's maximum) drives risk, because recovery overnight is what matters; hence the guidance uses sleeping altitude gain and extra acclimatisation days.

AMS: headache plus at least one of nausea or vomiting, fatigue, lassitude or dizziness, according to the 2018 Lake Louise criteria as reported in the WMS summary. ^[1] Symptoms appear during or after the first night at altitude, usually 4 to 12 hours and up to 72 hours after arrival. ^[1]

HACE: deterioration of severe AMS with truncal ataxia (inability to perform a tandem gait), altered mental status, slurred speech and severe lassitude; clinical picture resembles alcohol intoxication. Without treatment, coma and death can develop within 12 to 24 hours. ^{[1] [2]}

HAPE: dyspnoea on mild exertion out of proportion to previous days or to companions, clear drop in exercise capacity, non-productive cough, fatigue and weakness, progressing to dyspnoea at rest and pink frothy sputum. Diagnosis requires two of four symptoms (chest tightness or pain, dyspnoea at rest, cough, decreased exercise tolerance) and two of four signs (crackles or wheezes, cyanosis, tachypnoea, tachycardia). ^[1]

For persistent symptoms on return to low altitude, consider other diagnoses: alcohol hangover, carbon monoxide poisoning, dehydration, exhaustion, hyponatraemia and migraine for apparent AMS; intracranial lesions, seizure disorder, stroke, hypoglycaemia, drug intoxication, hypothermia, hyponatraemia for HACE; and anxiety attack, bronchospasm, myocardial infarction, heart failure, pneumonia, pulmonary embolism, pneumothorax and mucus plugging for HAPE. ^[2]

Use the Lake Louise AMS score (headache plus gastrointestinal symptoms, fatigue or weakness, or dizziness) and the HAPE symptom/sign criteria above. ^[1] Severity also follows WMS risk stratification: low, moderate or high risk based on prior altitude illness history, day-1 sleeping altitude and rate of ascent (see the table). ^[2]

Altitude illness is clinical. Pulse oximeters are not recommended for diagnosing or confirming altitude illness, because readings do not correlate reliably with symptoms. ^[2] Assess cardiopulmonary comorbidities before travel; contraindications to high-altitude travel include advanced restrictive or obstructive lung disease, decompensated heart failure, recent myocardial infarction or stroke (within 6 months), unstable angina, poorly controlled seizure disorder, pulmonary hypertension, sickle cell disease, high-risk pregnancy, and untreated high-risk cerebrovascular abnormality. ^[2]

Prevention (travel advice):

• Follow a low-risk gradual ascent: sleep below 2800 m on day 1, ascend no more than 500 m/day above 3000 m, and build in an extra acclimatisation day for every 1000 m of gain. ^[2]
• Remain well hydrated; avoid alcohol. Physical fitness and youth are not protective. ^[2]
• Pre-acclimatisation and staged ascent help; hypoxic tents are not recommended for AMS prevention. ^[1]
• Acetazolamide 125 mg orally every 12 hours starting the night before ascent above 2800 m for moderate-risk travellers; consider doubling to 250 mg every 12 hours for high risk. It is started the night before and continued for 2 to 4 days after reaching and staying at maximum altitude, or until descent. ^[2]
• Dexamethasone 2 mg orally every 6 hours or 4 mg every 12 hours when acetazolamide is contraindicated, for example after anaphylaxis to a sulphonamide or Stevens-Johnson syndrome. ^[2]
• For HAPE-prone individuals, nifedipine extended release 30 mg orally every 12 hours starting 24 hours before ascent, or a phosphodiesterase-5 inhibitor (tadalafil 10 mg every 12 hours, or sildenafil 50 mg every 8 hours), or dexamethasone 8 mg every 12 hours. ^[2]
• Ibuprofen 600 mg three times daily may help prevent high-altitude headache. ^[2]
• Ginseng and Ginkgo biloba are not recommended; acetaminophen and budesonide inhalation are discouraged for AMS prevention. ^[1]

Treatment:

• Stop further ascent for mild or moderate AMS. Descend immediately (at least 300 to 500 m or to the last tolerated altitude) for severe AMS, HACE or HAPE. ^{[1] [2]}
• Supplemental oxygen targeting SpO2 over 90%; portable hyperbaric chamber when descent is not possible or is delayed. ^[1]
• Acetazolamide 250 mg orally every 12 hours and dexamethasone 4 mg every 6 hours (AMS) or 8 mg once then 4 mg every 6 hours (HACE) until symptoms subside. ^[2]
• For HACE or concurrent HAPE/HACE, add dexamethasone 2 mg every 6 hours or 4 mg every 12 hours to the regimen, with caution in neurologically impaired HAPE patients. ^[1]
• HAPE: nifedipine is only an alternative when oxygen, descent or a hyperbaric chamber is not available; phosphodiesterase inhibitors may be used; avoid diuretics (risk of volume depletion); acetazolamide is not recommended for HAPE treatment. ^[1]
• CPAP may be considered as an adjunct when oxygen or vasodilators are unavailable. ^[1]

AMS has an excellent prognosis with cessation of ascent. HACE can kill within 12 to 24 hours. HAPE carries up to 50% mortality if untreated.

Graded ascent and acclimatisation are free and effective. Pharmacological prevention is most important for high-risk itineraries (rapid ascent, field research, pilgrimage). In low-resource settings, education about symptom recognition, stopping ascent and descending, and access to oxygen and portable chambers are the key interventions.

Children, pregnant travellers (high-risk pregnancy is a contraindication), and people with cardiopulmonary comorbidities need specialist advice.

Decompression sickness is caused by bubbles of inert gas (mainly nitrogen) released into tissues and circulation during ascent from a dive, when falling ambient pressure outstrips the ability of tissues to equilibrate. Arterial gas embolism arises when alveolar gas enters the systemic circulation through a ruptured pulmonary vein, often after breath-holding ascent or pulmonary barotrauma.

Diving accidents are relatively uncommon; one German registry reported about 62 diving accidents in a single year, and forensic case series are small. ^[6] Drowning is the commonest forensic cause of death in fatal diving incidents, so drowning and diving injuries are often analysed together. ^[6]

During descent, nitrogen dissolves in blood and tissues in proportion to the partial pressure (Henry's law). During ascent, falling pressure causes supersaturation, and gas forms bubbles in joints, tendons, spinal cord, brain and lungs. Tissues with high fat content, such as brain and spinal cord, are especially susceptible because nitrogen dissolves readily in fat. Bubble-related mechanical damage and inflammatory vascular injury follow. Symptoms usually occur 15 minutes to 36 hours after the dive, and in most cases within 6 hours. ^[5]

• Type I (less severe): musculoskeletal pain ("the bends", about 90% of cases), lymphatic swelling and pain, and skin bends (itching, rash, marbling). Upper limbs are affected about three times more often than lower limbs. ^[5]
• Type II (more severe): neurological (headache, confusion, cognitive dysfunction, visual disturbance, weakness, hemiparesis, paraparesis, incontinence), spinal cord symptoms, pulmonary ("chokes": inspiratory burning, substernal pain, dyspnoea, cough), inner-ear ("staggers": vertigo, tinnitus, hearing loss), and shock. ^[5]
• Arterial gas embolism: cerebral or coronary symptoms, typically within 10 to 20 minutes of surfacing, often multi-system. ^[5]
• Subclinical DCI: fatigue, "heavy head", mild aching joints, usually self-limiting and more common after deep dives. ^[5]

Decompression sickness type II can mimic spinal cord trauma, stroke and myocardial infarction. The timing of onset relative to a dive is the key clue; a dive within the previous 36 hours should raise the diagnosis.

Clinical diagnosis. Imaging is used to exclude other causes (stroke, cord compression). Measurement of oxygenation and exclusion of pulmonary barotrauma guide care.

1. Stop diving, rest (avoid exertion), keep the patient still, warm and hydrated.
2. Give 100% oxygen immediately; this is the primary therapeutic intervention, with hyperbaric oxygen therapy in severe cases, per the 2023 S2k guideline for diving accidents. ^[6]
3. Urgent transfer to a hyperbaric centre for recompression; minimise further depth changes during transport where possible, and avoid flying or altitude exposure.
4. Add fluids and monitor for neurological change and shock.
5. Treat pain and institute appropriate trauma care.
6. Any diver with neurological or cardiopulmonary symptoms needs emergency evaluation.

The main objective of emergency treatment in both drowning and diving accidents is rapid management of hypoxia to prevent irreversible neurological injury and loss of function. ^[6]

Outcome depends on speed of oxygen therapy and recompression. Neurological DCS carries risk of permanent deficit. About 30% of spinal cases have low-back or pelvic girdle pain before or alongside neurological symptoms. ^[5]

Follow dive tables or computer algorithms, limit depth and time, and ascend slowly with safety stops; allow adequate surface interval; avoid flying or altitude soon after diving; ensure fit-to-dive assessment and training. Decompression tables and oxygen-enriched regimens have evolved to reduce this risk.

Commercial divers, military divers and recreational divers with patent foramen ovale are at higher risk of paradoxical (shunt-mediated) decompression sickness.

Immediate high-flow oxygen and flat or supine positioning (or left lateral if vomiting), with urgent referral to the nearest recompression chamber, remain the practical essentials where a chamber is not locally available.

Electrical burn care overlaps with Burns; cardiopulmonary resuscitation with Cardiac arrest and life support; hypothermia management overlaps with Hypothermia and hyperthermia. Referral pathways should follow local burning, trauma and emergency networks.

• Drowning kills about 300,000 people a year, 92% in low- and middle-income countries; take children to water safety and supervision early. ^[7]
• In drowning, the priority is rapid rescue and ventilation; long scene delays and CPR durations over 10 minutes are associated with very poor survival. ^[6]
• Low-voltage (below 1000 V), high-voltage (above 1000 V) and lightning (tens of thousands of volts) injuries differ greatly in lethality; skin burns underestimate deep damage in all three.
• Alternating current causes tetany and prolonged contact, making it more dangerous than direct current at similar voltage.
• High-voltage and lightning injuries need ECG and creatine kinase, fluid resuscitation and early surgery; cardiac biomarkers do not stratify risk alone. ^[3]
• Lightning deaths most often follow cardiac arrest from ventricular fibrillation and asystole; prolonged CPR may be required and triage is reversed, treating the pulseless first. ^[4]
• Altitude illness begins above 2500 m; graded ascent (300 to 500 m per day), acclimatisation days and acetazolamide 125 mg twice daily are the cornerstones of prevention. ^[2]
• Lake Louise criteria define AMS; HAPE needs two of four symptoms and two of four signs; untreated HAPE carries up to 50% mortality and HACE can kill within 24 hours. ^{[1] [2]}
• Decompression sickness follows ascent and occurs mostly within 6 hours; type I is usually painful but self-limiting, type II can be fatal.
• Emergency management of diving accidents starts with 100% oxygen and proceeds to hyperbaric recompression in severe cases. ^[6]