Pathophysiology
The sequence begins with panic, struggle, and breath holding. This results in rapid
development of hypoxemia and hypercapnea. At some point voluntary efforts at breath
holding are overcome and aspiration of significant quantities of water may occur. Large
quantities of water may be swallowed and vomited leading to aspiration of gastric
contaminants.
Respiratory and metabolic acidosis occurs from hypoxia and anaerobic cellular activity.
Freshwater and saltwater will dilute/ washout surfactant leading to atelectasis,
ventilation/perfusion (VQ) mismatch and destruction of the alveolar capillary membrane.
This can occur with as little as 2.2ml/kg of aspirant. Non-cardiac pulmonary edema results
from the direct pulmonary injury, surfactant loss, inflammatory mediators, and cerebral
hypoxia.
Cardiovascular complications occur as a result of hypoxia, acidosis and hypothermia,
not from the fluid or electrolyte shifts as previously proposed. For these shifts to
occur, 10 to 22 ml/kg of water would need to be aspirated or the incident would have to
occur in a very high solute environment such as the Dead Sea.
Supraventricular tachycardia (SVT) is common and may simply
occur from hypoxia or a massive catecholamine release. The EKG may demonstrate Osborne
Waves, a small notch on the descending R-wave that is associated with hypothermia.
In
very cold water, the diving reflex may account for cardiovascular collapse. Arrest seldom
occurs from ventricular fibrillation except in cases of significant hypothermia (core body
temperature <28 degrees centigrade). Central Nervous System (CNS) damage is caused by
hypoxia and ischemic changes. This may be lessened in patients given CPR and in those who
are hypothermic (due to its protective effect on the cerebral metabolism).
Severe neurologic damage may occur in up to 15 to 20 percent of near drowning patients.
However, 10 to 20 percent of patients that present in coma with fixed and dilated pupils
who are aggressively resuscitated recover completely.
Other less common sequela are renal failure (anoxia, hemolysis, or
rhabdomyolysis) and
disseminated intravascular coagulation (DIC) (pulmonary endothelial damage, hypoxia, and
acidosis).
Pertinent History
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Circumstances surrounding incident including drug or alcohol usage.
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Duration of time submerged.
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Water temperature.
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Water contamination (i.e. sewage).
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Condition of the patient on discovery, initial extrication and during transport.
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General medical history.
Medical Management
On scene:
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Initiate rescue breathing immediately.
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Extricate from the water using full spine precautions if mechanism of injury dictates.
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Re-evaluate airway, breathing, and circulation (ABCs) and apply ACLS / ATLS
measures as needed. Begin supplemental oxygen if available.
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Immediately transport to the medical department initiating measures to prevent further
hypothermia.
In the medical department:
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Evaluate and treat ABCs.
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Start an IV; administer 100% oxygen via nonrebreather mask, cardiac monitors and pulse
oximetry.
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Perform rapid neurologic exam (GCS is useful).
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Expose and initiate rewarming if hypothermic.
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Use a low range thermometer (refrigerator thermometer will work).
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Raise the ambient room temp above 90 degrees.
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Infuse warmed IV solution as needed.
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Place warmed IV bags in axillas, groin, behind neck, and around scalp.
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Cover with warmed blankets.
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Perform a secondary exam. Pad spine board if unable to clear the spine clinically or
radiographically.
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Insert a Foley to monitor urine output, state of hydration, and renal function.
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Place a NG tube (assure airway protection). Empty the gastric contents to prevent
aspiration and improve ventilation.
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Institute standard supportive therapy.
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Observe closely.
When initiating the IV, draw lab samples. Depending on the ships lab
capabilities, run a CBC, electrolytes,
glucose, BUN,
creatinine and coagulation
profile.
Obtain an ECG and chest radiograph. Continuously monitor pulse oximetry and the cardiac
rhythm. Do not use steroids or antibiotics empirically. However, if the water was
contaminated (i.e. sewage), appropriate antibiotic coverage (and immunization if
applicable), should be initiated. If the mechanism of injury is significant (e.g., fall
from the deck of a ship or pier), institute full spinal immobilization during extrication
from the water. Initial clues for CNS injury include priapism, Cushing reflex, and
paradoxical respiration. Rescue breathing should begin in the water with supplemental
oxygen ASAP. Lung drainage procedures generally do not improve tissue oxygenation
significantly.
If endotracheal intubation is necessary because of hypoxemia, 5-10 cm of positive end
expiratory pressure (PEEP) may be helpful. Observe very closely for circulatory
compromise. The patient that presents in full arrest is not dead until he is warm and
dead. Continue resuscitative measures until the core temperature reaches 33ºC (92º F).
Disposition
If the patient is asymptomatic from the onset of the rescue through evaluation, observe
in medical for 6 hours. If the patient remains completely asymptomatic during observation
and has no lab, cardiac or radiological abnormalities, then discharge. If symptoms were
noted at any point, observe the patient until the symptoms completely resolve at which
time the patient can be discharged with close follow-up.
When should
the patient be evacuated to higher level of care?
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Continued tachypnea, dyspnea, or cyanosis.
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Radiologic evidence of aspiration or pulmonary edema.
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Dysrhythmias or ECG evidence of cardiac ischemia.
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History of apnea, cardiac arrest, altered level of consciousness.
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Associated trauma.
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Significant co-morbid disease.
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Your department is overwhelmed with other patients.
Remember that near drowning sequel may occur rapidly; hence, continual monitoring
while in medical is required.
Pearls
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Get the help of a colleague or a consultant (radio, VTC, e-mail, plain old telephone
service (POTS), global satellite communications (INMARSAT), etc). Share your findings and
concerns. Keep good records.
-
Consider other common military injury complications (blast injury, inhalation injury
(carbon monoxide fumes, gas), and burns.
References
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Clinical Practice of Emergency Medicine 2nd ed. Ann L. Harwood-Nuss,
Lippincott-Raven 1996.
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Emergency Medicine: A Comprehensive Study Guide 4th ed., Judith E.
Tinitnalli, McGraw-Hill Inc., 1996
Prepared by LCDR Steven L Banks, MC, USN, Emergency Medicine Department, Naval
Medical Center San Diego, San Diego, CA (1999).
Approved for public release; Distribution is unlimited.