Drowning (Submersion Injury) Nursing Care Plans

A drowning patient hits your unit hypoxic, often hypothermic, and sometimes in arrest. Your job is airway, oxygenation, cerebral perfusion, rewarming, and watching for the pulmonary edema that can show up hours after the water is out of the lungs. This guide covers how to assess, prioritize, and intervene.

What is drowning?

Drowning is the third leading cause of unintentional injury death worldwide, accounting for more than 360,000 deaths annually. Submersion leads to rapid hypoxemia. Aspirated water pulls plasma into the lungs, producing hypoxemia, acidosis, and hypovolemia, and it strips pulmonary surfactant, damaging the capillary membrane. Severe hypoxia can also come from pure asphyxia, submersion without any aspiration.

Skip the old terms. "Near-drowning," "secondary drowning," "wet drowning," and "dry drowning" have been retired because they muddy documentation. Use drowning, fatal drowning, non-fatal drowning, and rescue.

Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid, and the outcome is fatal or non-fatal. Fatal drowning ends in death. Non-fatal drowning is stopped before death and the patient survives.

The WHO grades non-fatal drowning by respiratory impairment right after the process stops:

• Mild: breathing, involuntary distressed coughing, fully alert.
• Moderate: difficulty breathing and/or disoriented but conscious.
• Severe: not breathing and/or unconscious. Further graded by decline from prior functional capacity, no morbidity, some morbidity, or severe morbidity.

Rescue means you pulled someone out who was submerged but never developed respiratory symptoms or impairment.

Three risk factors drive most drownings: inability to swim or overestimating swimming ability, risk-taking behavior, and inadequate adult supervision. A drowning patient may be unresponsive. Watch for cold or pale skin, abdominal distension, vomiting, cough with pink frothy sputum, shortness of breath, lethargy, and chest pain.

Freshwater drowning is far more common than saltwater. Fresh water washes out surfactant and produces atelectasis. Saltwater pulls fluid into the alveoli by osmosis and produces pulmonary edema.

Nursing Care Plans & Management

Management centers on stabilizing the airway, delivering oxygen, maintaining cerebral perfusion, continuous monitoring, rewarming, starting CPR when needed, and heading off complications.

Nursing Problem Priorities

1. Maintain airway patency and adequate oxygenation.
2. Support gas exchange.
3. Watch for pulmonary edema, aspiration pneumonia, and neurological deficits.
4. Support the patient and family.
5. Teach water safety, drowning prevention, and CPR.

Nursing Assessment

Assess for the following:

• Coughing or gasping for air
• Difficulty breathing or shortness of breath
• Cyanosis of skin or lips
• Altered mental status or confusion
• Fatigue or exhaustion
• Chest pain or discomfort
• Vomiting or foaming at the mouth
• Frothy, pink-tinged sputum
• Cool, clammy skin
• Loss of consciousness
• Severe respiratory distress or respiratory failure
• Hypothermia
• Seizures
• Cardiopulmonary arrest
• Coma or unarousable state

Factors related to the cause:

• Aspiration (freshwater or saltwater)
• Bronchospasm
• Pulmonary capillary membrane damage
• Pulmonary edema
• Surfactant loss
• Cerebral edema
• Gas exchange insufficiency
• Increased intracranial pressure (ICP)
• Prolonged hypoxemia
• Fluid shift from intravascular to interstitial space
• Contaminated water aspiration
• Gastric contents aspiration
• Increased secretions
• Conductive heat loss
• Prolonged submersion in cold water

Nursing Goals

• The patient maintains optimal gas exchange: ABGs in usual range, oxygen saturation 90% or higher, alert and responsive or no further decline in level of consciousness, relaxed breathing, baseline heart rate.
• The patient maintains cerebral perfusion: alert and responsive, no neurological deficits, normoreactive pupils, normal or baseline motor function.
• The patient shows stable vital signs and no signs of increased ICP.
• The patient maintains adequate fluid volume: urine output greater than 30 mL/hour, normotensive blood pressure, heart rate less than 100 beats per minute, balanced intake and output, good skin turgor, moist mucous membranes, palpable peripheral pulses, stable weight, normal electrolytes.
• The patient stays free of infection: normal vital signs, no purulent drainage from wounds, incisions, or tubes.
• The patient achieves adequate cardiac output: strong peripheral pulses, normal vital signs, urine output greater than 30 mL/hour, warm dry skin, no further decline in level of consciousness, and fewer dysrhythmias.
• The patient maintains effective thermoregulation with stable temperature and pulse and stays free of cardiovascular and neurological injury.
• The patient and caregiver verbalize the condition, its complications, perform necessary procedures, and start needed lifestyle changes.

Nursing Interventions and Actions

1. Improving Gas Exchange

Prolonged hypoxia sets the patient up for alveolar fluid aspiration, vagally mediated pulmonary vasoconstriction, hypertension, and fluid-induced bronchospasm. Fresh water is hypotonic relative to plasma and disrupts surfactant, producing alveolar instability, atelectasis, decreased compliance, and marked ventilation/perfusion (V/Q) mismatch.

1. Assess level of consciousness. Within 3 minutes of submersion, drowning patients are unconscious and at risk for cerebral edema. Experienced swimmers can faint from hypoxia after hyperventilating off their carbon dioxide, and deep-water divers can black out on ascent.

2. Assess respiratory rate, depth, and rhythm. Changes here are early warning signs. Impaired gas exchange shows up as rapid shallow breathing or hypoventilation, and hypoxia raises the work of breathing. Aspiration of as little as 1 to 3 mL/kg of fluid significantly impairs gas exchange.

3. Auscultate breath sounds. Crackles come from fluid in the airways and pulmonary edema. Wheezing means bronchospasm. Water in the airway triggers coughing and laryngospasm, and when the laryngospasm breaks, the patient may aspirate a larger volume.

4. Watch for nasal flaring, stridor, retractions, and accessory muscle use. These signal the patient working to increase chest excursion. Early hypoxia is limited to the period of apnea or hypopnea and may resolve with initial rescue.

5. Watch for worsening pulmonary edema. Pink frothy sputum is the classic sign and points toward mechanical ventilation. Postobstructive edema after laryngospasm, neurogenic pulmonary edema, and ARDS from altered surfactant all complicate the course.

6. Monitor oxygen saturation and ABGs. Keep saturation at 90% or greater. Falling PaO2 and pulse oximetry with rising PaCO2 signal respiratory failure. ABGs are the most reliable parameter in asymptomatic or mildly symptomatic patients and should include co-oximetry to detect methemoglobinemia and carboxyhemoglobinemia.

7. Monitor chest X-ray. Get a film on every submersion victim to gauge aspiration and lung injury. Radiographic findings lag the clinical picture by 24 hours. The film may also show aspiration, pulmonary edema, segmental atelectasis, or foreign bodies.

8. Maintain the airway and assist ventilation while protecting the cervical spine. A patent airway is always first. Assume cervical spine injury in any drowning, especially after a dive. The first priority is restoring oxygen to the cells and preventing further hypoxic damage.

9. Provide oxygen. If the patient is breathing spontaneously, give supplemental oxygen by mask. Move early to intubation with PEEP, or CPAP/BiPAP in an awake, cooperative, less hypoxic patient, if hypoxia or dyspnea persists despite 100% oxygen.

10. Insert a nasogastric tube as indicated. Use it to remove swallowed water and debris. Go orogastric if there is head or facial trauma.

11. Anticipate intubation and mechanical ventilation. Pulmonary injury produces an ARDS picture: pulmonary edema, atelectasis, hyaline membrane formation, and capillary injury. Early intubation and ventilation prevent full decompensation and maintain oxygenation.

12. Assist with endotracheal intubation. Intubation may be needed when the patient cannot hold a PO2 above 60 to 70 mm Hg on 100% oxygen by face mask. In an alert, cooperative patient, trial BiPAP/CPAP first if available.

13. Use PEEP for ventilated patients. Intubated submersion patients often need PEEP to maintain oxygenation in noncompliant lungs.

14. Monitor patients on ECMO closely. ECMO helps selected patients: respiratory failure unresponsive to conventional or high-frequency ventilation, a reasonable chance of neurologic recovery, and persistent hypothermia from cold-water drowning.

2. Maintaining Cerebral Tissue Perfusion & Cardiac Output

Hypoxic-ischemic brain injury is the major determinant of survival and long-term outcome after drowning. Primary CNS injury starts with tissue hypoxia and ischemia. Prolonged hypoxia drives both primary and secondary injury, especially in older patients who cannot reach core hypothermia quickly.

1. Assess level of consciousness using the Glasgow Coma Scale (GCS). The GCS tracks verbal, motor, and pupillary responses. Early cerebral hypoxia shows as restlessness and anxiety, then agitation, confusion, lethargy, and coma. A patient who is alert or mildly obtunded on arrival has an excellent chance at full recovery. A comatose patient, one receiving CPR on arrival, or one with fixed dilated pupils and no spontaneous respirations has a poor prognosis.

2. Watch for seizure activity. Cerebral irritation or trauma raises seizure risk. Seizures may follow acute cerebral hypoxia or may have triggered the loss of consciousness in the first place. Seizures raise cerebral metabolism and oxygen demand.

3. Control environmental stimulation. Stimuli can spike ICP. No evidence shows ICP monitoring changes drowning outcomes, though it may have a role in severe ARDS to gauge the effect of permissive hypercarbia and PEEP.

4. Assess cranial nerve responses, especially the vagus nerve. An absent gag reflex means the airway needs protection. Aspirated fluid produces pulmonary edema, atelectasis, airway spasm, and pneumonitis, all of which worsen hypoxia. Cold water stimulating the vagus nerve can cause primary cardiac arrest.

5. Monitor blood pressure. Vasodilation during rewarming can drop pressure unless you watch closely. Anticipate intra-arterial monitoring for ongoing shock. Profound hypotension can occur during and after resuscitation, especially when rewarming brings vasodilation.

6. Monitor temperature. Severe submersion hypothermia decreases myocardial contractility and vasomotor tone. Remember that many patients are hypothermic from prolonged submersion, not true cold-water submersion.

7. Monitor skin temperature, color, and peripheral pulses. Peripheral vasoconstriction produces cool, pale, diaphoretic skin and weak pulses. The diving reflex, triggered by cold water on the face, causes breath-holding, bradycardia, and intense peripheral vasoconstriction and can drive autonomic instability.

8. Palpate peripheral pulses for at least 1 minute before starting compressions. Sinus bradycardia and atrial fibrillation do not need immediate treatment, and pulses can be very weak in a hypothermic or bradycardic patient.

9. Assess for dysrhythmias. Low perfusion, acidosis, hypoxia, hypothermia, or electrolyte imbalance can produce dysrhythmias that drop stroke volume and cardiac output. Primary arrhythmias such as long-QT syndromes and catecholaminergic polymorphic ventricular tachycardia can be fatal during swimming.

10. Monitor urine output. Oliguria signals inadequate renal perfusion from low cardiac output. A hypothermic patient can be significantly hypovolemic from cold diuresis, where early vasoconstriction shifts blood centrally, volume receptors sense overload, antidiuretic hormone drops, and urine output climbs.

11. Monitor ethanol levels and toxicology screen. Alcohol or drugs may have contributed and can mask true loss of consciousness. Alcohol contributes to roughly 20% of all drowning deaths, rising to 30% of recreational aquatic deaths and 41% of river drownings, and to nearly half in some age groups.

12. Monitor glucose. Both hypoglycemia and hyperglycemia raise mortality and are especially harmful to the injured brain. Target normoglycemia.

13. Assess hemodynamic monitoring if in place. CVP reflects right-sided filling pressures; pulmonary artery diastolic pressure (PADP) and pulmonary capillary wedge pressure reflect left-sided volume. Arterial and central venous catheters help track cardiac output.

14. Perform ECG monitoring. ST-segment changes after non-fatal submersion may come from takotsubo cardiomyopathy, coronary artery spasm, hypothermia, hypoxia, or, less often, ischemia from coronary artery disease.

15. Lift the patient from the water in a prone position; promote comfort once stable. Lifting upright can drop pressure as the body moves from water to air. Once stable, a position of comfort lowers oxygen consumption and myocardial workload.

16. Rewarm as appropriate. Use warm humidified oxygen, blankets, head wrap or over-the-bed heaters, and IV fluids warmed to 98.6° to 104° F. Core temperature may be very low, so rewarm slowly to avoid a rapid release of metabolites. In a hypothermic patient in cardiac arrest, continue resuscitation until core temperature reaches 32 to 35°C (89.6°F).

17. Start a vasopressor for refractory hypotension. Start an infusion such as norepinephrine. Vasopressors raise systemic vascular resistance, mean arterial pressure, and organ perfusion.

18. Give inotropic agents as ordered. Digoxin, amrinone, dobutamine, or dopamine improve contractility and cardiac output. Short-term dobutamine is reasonable for admitted patients with severe systolic dysfunction, low blood pressure, and significantly reduced cardiac output to preserve systemic flow and protect organs.

19. Give plasma volume expanders as ordered. Give IV crystalloids to counter immersion diuresis and correct other contributors. Rapid volume expansion uses isotonic crystalloid (20 mL/kg) or colloid.

20. Assist with extracorporeal CPR (ECPR). When conventional CPR is failing and ECMO is available, ECPR may be a salvage option case by case. It uses percutaneous veno-arterial ECMO as a bridge to maintain organ perfusion.

21. Provide supplemental oxygen. Give oxygen by nasal cannula or face mask to maintain normal SpO2. Noninvasive positive-pressure ventilation can improve oxygenation and bridge to intubation or be weaned off in 1 to 2 days.

22. Institute seizure precautions. Pad the side rails, keep the bed low, and provide head protection if needed. Remove nearby hazards. The patient may be unaware of their actions during a seizure.

23. Elevate the head of the bed and keep the head and body midline. This promotes venous drainage and reduces ICP. A lateral position with the neck slightly flexed lets saliva drain and keeps the tongue forward.

24. Reduce unnecessary stimuli. Cut noise, close curtains, and avoid unnecessary activity to lower seizure risk. Seizures after hypoxic brain injury are common but hard to spot in sedated or paralyzed ICU patients.

25. Limit suctioning. Hypoxia and the Valsalva from suctioning can raise ICP and seizure risk. Check for metabolic triggers in any patient with breakthrough seizures.

26. Give anticonvulsants as ordered. Drug therapy is the primary approach to seizures. Treat clinical seizures, and consider treatment for non-convulsive seizures or status epilepticus, though the outcome benefit is unclear. Prophylactic anticonvulsants are unproven.

27. For signs of increased ICP:

27.1. Maintain oxygenation. Adequate oxygenation prevents further hypoxic damage. Care may include endotracheal intubation with 100% oxygen at 5 to 10 cm PEEP, which also protects against aspiration of gastric contents.

27.2. Monitor EEG as indicated. Continuous EEG in critically ill patients showed seizures in 13% of cases, with 92% exclusively non-convulsive. EEG guides treatment and prognosis.

27.3. Monitor serum electrolytes. Changes depend on the type and amount of fluid aspirated. Avoid a hypoosmolar state in hypoxic encephalopathy, which can worsen cerebral edema and secondary brain injury.

3. Promoting Optimal Fluid Balance

Hypovolemia can follow fluid loss from increased capillary permeability. Aspiration of at least 11 mL/kg is needed to alter blood volume, and more than 22 mL/kg before significant electrolyte changes appear. In children, swallowing large volumes of fresh water, rather than aspiration, is the likely cause of clinically significant hyponatremia.

1. Assess intake and output. Even with adequate intake, fluid shifting into the extravascular space can cause dehydration and low output. Accurate I&O guides replacement.

2. Monitor urine-specific gravity. This shows the degree of concentration or dilution. Acute renal impairment is common in drowning and, while usually mild, can require dialysis.

3. Assess for crackles and shortness of breath. These signal fluid in the lungs. With saltwater aspiration, crackles and congestion may not mean fluid overload, since salt water pulls fluid from the circulation into the alveoli. Fresh water moves the opposite way, rapidly across the alveolar-capillary membrane into the microcirculation, and disrupts surfactant.

4. Note changes in heart rate and blood pressure. Profound hypotension can occur during and after resuscitation, especially with rewarming and vasodilation. Hypoxemia can also damage the myocardium directly and lower cardiac output.

5. Monitor labs: hematocrit, serum electrolytes, renal function. Hematocrit shows hemodilution or concentration. Dehydration raises serum sodium; hemodilution lowers it. Hypokalemia may follow increased urine output. If creatinine is elevated, with marked metabolic acidosis, abnormal urinalysis, or significant lymphocytosis, repeat serial creatinine.

6. Monitor central venous pressure. Severe hypovolemia drops CVP and signals the need for volume expanders.

7. Insert and maintain an indwelling urinary catheter. This allows close monitoring of renal function and prevents retention, which can cause renal dysfunction and infection.

8. Make fluids accessible to the conscious, stable patient. Offer tolerable fluids that replace electrolytes, such as a sports drink or broth.

9. Assist with central venous and arterial line insertion as ordered. These support fluid administration and hemodynamic monitoring. Use central access cautiously in hypothermic patients to avoid stimulating the atrium and triggering dysrhythmias.

10. Give fluid volume expanders as ordered. Volume expanders increase or retain circulating volume and correct imbalances. Rapid expansion uses isotonic crystalloid (20 mL/kg) or colloid.

11. Give inotropic agents as prescribed. See Pharmacologic Management.

4. Administering Medications and Pharmacologic Support

1. Dobutamine. Use dobutamine as temporary IV inotropic support until the acute factors resolve or definitive treatment is in place. Give short-term inotropic support in cardiogenic shock to preserve systemic flow and protect against end-organ damage.

2. Sodium bicarbonate. Correct metabolic acidosis with sodium bicarbonate. Most acidosis resolves with improved oxygenation and corrected volume depletion. Bicarbonate raises plasma bicarbonate, buffers excess hydrogen ions, and raises pH.

3. Broad-spectrum antibiotics. Choose based on suspected or cultured pathogens, local resistance, and patient factors. Common choices for respiratory infection here include ceftriaxone, cefepime, or ampicillin-sulbactam.

4. Antifungals. Scedosporium apiospermum is hard to treat, with susceptibility varying by species. S. aurantiacum has the highest resistance profile and may respond only to voriconazole. Combinations of voriconazole, itraconazole, and posaconazole with caspofungin may work. Other options include fluconazole, voriconazole, or amphotericin B.

5. Initiating Measures for Infection Control & Management

Chemical pneumonitis is more common than pneumonia, especially after submersion in a chlorinated pool or a bucket of cleaning product. After initial recovery, patients can develop nonpulmonary infections, including brain abscess, osteomyelitis, and soft-tissue infections with unusual fungal, amebic, and bacterial pathogens. Keep a high index of suspicion.

1. Assess temperature. Fever signals the response to infection. Uncommon infections can present late and atypically, so watch for pneumonia and CNS infection.

2. Assess for respiratory difficulty. Early assessment drives early intervention. Sinus, lung, and CNS infections from unusual soil and waterborne organisms are usually insidious, often more than 30 days after the injury.

3. Auscultate breath sounds. Rhonchi and wheezes suggest retained secretions needing expectoration or suctioning. A patient with a brief, witnessed submersion and immediate resuscitation may be asymptomatic, but symptomatic patients show wheezing, coughing, tachypnea, dyspnea, or hypoxia.

4. Monitor sputum amount, color, and odor. Yellow or yellow-green sputum points to respiratory infection and reflects either resolving pneumonia or a developing secondary infection.

5. Monitor white blood cell count and cultures. A rising WBC signals infection. Culture blood from every patient who aspirated water to identify the pathogen and guide therapy. Organisms common after submersion include Pseudallescheria boydii, Scedosporium apiospermum, Naegleria, Balamuthia, Burkholderia, Aeromonas, and Francisella philomiragia.

6. Monitor chest X-ray. Aspiration of contaminated water raises pneumonia risk. The film may also show pulmonary edema, segmental atelectasis, or foreign bodies.

7. Encourage hand hygiene. Hand hygiene reduces the spread of infection and antimicrobial resistance.

8. Institute isolation precautions as appropriate. Use isolation based on the infection type, antibiotic response, the patient's health, and any complications.

9. Encourage rest and nutrition. Both support healing and natural resistance. Encourage self-care as tolerated to build strength and immune recovery, and adequate nutrition lowers infection risk from static secretions.

10. Encourage incentive spirometry once neurologically stable. It improves lung expansion and reduces alveolar collapse. Lung physiotherapy in ARDS improves performance and quality of life.

11. Keep the patient upright. An upright position promotes lung expansion and air exchange and reduces secretion stasis. Reposition frequently for good pulmonary toilet.

12. Maintain body temperature with cooling or warming blankets. Continued hypothermia raises sepsis risk. Patients with core temperatures below 86°F (30°C) after sudden rapid cold-water immersion slow their metabolism and shunt blood to the heart, brain, and lungs, which may protect the brain during submersion.

13. Suction only as needed and send sputum for culture and sensitivity. Suctioning reduces secretion stasis. In ventilated patients, secretions above and below the ET cuff are an ideal medium for pathogens. Suction cautiously, since it can worsen elevated ICP.

14. Perform chest physiotherapy as needed. This promotes postural drainage. Early rehabilitation during the acute phase improves physical performance and acts as a bridge for ARDS patients.

15. Give antifungals as prescribed. See Pharmacologic Management.

16. Prepare for additional diagnostics as indicated. Bronchoscopy may be needed to remove aspirated debris or vomitus plugs, but there is no role for routine bronchoscopy without clear evidence of foreign-material aspiration.

6. Managing Hypothermia and Preventing Cold Injuries

Hypothermia is common in drowning and usually comes from conductive heat loss during submersion, not from cold-water drowning. It lowers cerebral metabolic rate, but the neuroprotective effect happens only when hypothermia occurs at the moment of submersion with very rapid cooling in water below 5°C.

1. Monitor temperature. Hypothermia is a core temperature below 35°C (95°F). Rectal temperature is reasonable in conscious patients. In severe hypothermia, especially with intubation, an esophageal probe in the lower third of the esophagus approximates cardiac temperature.

2. Monitor environmental temperature. Adjust the room and linens toward normal body temperature. Extract the patient from the cold horizontally whenever possible and begin rewarming as soon as you can.

3. Monitor level of consciousness with the GCS. Neurologic findings should match the core temperature. Function declines even above 35°C. A persistently altered patient may have hypoxic-ischemic injury or non-convulsive status epilepticus.

4. Assess vital signs. As compensation fails, vital signs change. Mild hypothermia shows tachypnea, tachycardia, initial hyperventilation, and cold diuresis. Moderate hypothermia brings proportional drops in pulse and cardiac output, hypoventilation, decreased renal flow, and junctional bradycardia. Severe hypothermia causes oliguria, hypotension, bradycardia, and asystole. Vital signs that do not match the degree of hypothermia point to another diagnosis.

5. Assess blood glucose. Both extremes harm the injured brain. Hyperglycemia that persists during rewarming suggests pancreatitis or diabetic ketoacidosis.

6. Monitor labs. Labs identify complications and comorbidities. Get a toxicology screen when mental status does not match core temperature. A low-normal hematocrit is abnormal in severe hypothermia, since hematocrit rises 2% for each 1°C drop. Rewarming can shift electrolytes rapidly, so reassess often.

7. Monitor ECG changes. Hypothermia hides the ECG changes of hyperkalemia and slows conduction through potassium channels, prolonging the RR, PR, QRS, and QT intervals.

8. Monitor oxygenation cautiously. Hypothermia slows finger pulse oximeter response. Ear or forehead probes are less affected by low temperature and peripheral vasoconstriction.

9. Perform CPR as indicated. Start chest compressions in any hypothermic patient in cardiac arrest. If no pulse is found after 1 minute, start CPR and continue it. With a core temperature of 20 to 28°C, or if it is unknown, give CPR continuously for at least 5 minutes, alternating with periods no longer than 10 minutes without CPR.

10. Remove wet clothing and start rewarming. In an awake hypothermic patient, remove wet clothing and start passive rewarming with warm blankets or heating pads. Passive rewarming alone may fail with glycogen depletion, sepsis, or hypovolemia, especially in older adults.

11. Assist with core rewarming. Use warm oxygen, continuous bladder lavage at 40°C, and IV isotonic fluids at 40°C during resuscitation. Warm peritoneal lavage has been used in severe hypothermia.

12. Start active external rewarming for moderate to severe hypothermia. Apply warm blankets, heating pads, radiant heat, warm baths, or forced warm air to the skin. Use this for moderate to severe hypothermia and for mild hypothermia in patients with little reserve or no response to passive rewarming.

13. Rewarm the trunk before the extremities. This minimizes core temperature afterdrop with its hypotension and acidemia from arterial vasodilation. Dangerous afterdrop occurs when trunk and extremities are warmed at the same time.

14. Prepare for thoracotomy in refractory cases. Thoracotomy with open cardiac massage and warm mediastinal lavage is used in refractory hypothermia, since the hypothermic heart often does not respond to drugs or countershock. Extracorporeal blood rewarming is used when lavage or thoracotomy fails or in arrest.

15. Insert central venous access carefully. Use central access cautiously to avoid stimulating the hypothermic atrium and triggering dysrhythmias.

16. Give antibiotics as prescribed. Treat hypothermic patients with an obvious infection source. Patients who fail to raise core temperature above 0.7°C/hour despite proper rewarming should get empiric broad-spectrum antibiotics.

7. Providing Patient Education & Health Teaching

A review of 50 drowning cases that ended in litigation found many deaths followed preventable lapses in basic safety. Most drownings are preventable with simple measures. Community education on water safety, injury prevention, and CPR matters.

1. Assess water safety knowledge. Teaching basic swimming, water safety, and safe rescue skills reduces drowning, as shown in programs across Australia, Bangladesh, China, Thailand, the United States, and Vietnam.

2. Identify risk factors. Drowning rates vary by age, sex, race, ethnicity, and neurodevelopmental disorders. The highest rate is in the 0 to 4 year age group, with children aged 12 to 36 months at greatest risk. About 75% of childhood drowning victims are boys, and boys are at higher risk than girls at every age after the first year. Among children aged 0 to 19, rates are highest among Black and American Indian children.

3. Teach constant supervision around water. Supervise children, especially toddlers, around any water, including bathtubs, toilets, and buckets. Keep toilet lids closed or use a child-safe latch. Empty buckets after use. Baby bath seats do not make unsupervised children safe. Water tanks and cisterns need childproof, solid tops.

4. Correct misperceptions about drowning. In one survey, 48% of parents wrongly believed they would hear splashing or crying if their child was in trouble, 56% believed a lifeguard was the primary person responsible for supervising their child, and 32% reported leaving a child unsupervised in a pool for 2 minutes or longer.

5. Reinforce proper pool fencing. Adequate fencing has cut immersion injuries by more than half. The fence should isolate the pool on all four sides, stand at least 4 feet tall, and have openings no wider than 4 inches.

6. Encourage caregivers to learn CPR. Parents who own pools or take children to pools should learn CPR. At least one caregiver should stay focused on the children at all times, off the phone and out of conversation.

7. Promote flotation devices. Children should wear personal flotation devices in pool areas, but these do not replace constant supervision. Water wings, inner tubes, and noodles are not substitutes for Coast Guard-approved personal flotation devices (PFDs).

8. Teach anti-entrapment and anti-entanglement measures. These include special drain covers, safety vacuum release systems, and filter pumps with multiple drains. Residential pool owners should use them.

9. Encourage swimming lessons and water competency training. Swim skills may be the most important prevention in natural water, where fencing and lifeguarding are impractical. Readiness depends on physical, social, behavioral, emotional, and cognitive skills weighed against environmental risk, not on age alone.

10. Teach boating safety. Everyone boating should be able to swim, wear a Coast Guard-approved PFD, and avoid alcohol and recreational drugs. Boaters should anticipate wind, waves, and water temperature and use protective and insulating garments in cold weather. Children younger than 14 should not operate personal watercraft without adult supervision.