Many of the following emergencies are first aid measures the diver should undertake himself.
Insure your divers are familiar with these disorders and self-aid measures they can take prior to
your arrival at the scene.
Transport rapidly to nearest hyperbaric chamber at or below the pressure altitude of the point of
departure. If possible administer 100% oxygen by demand-valve mask during transport.
Note: Transportation by air at an altitude up to 200 feet above the point of departure may be
entertained without major risk of worsening the symptoms, but should NOT be considered when
ground transportation is readily available and would not take much longer.
When in doubt consult your DMO/HMO/DMT.
Diving Operations: Non-Trauma
1. In the case of a diving accident the victim and swim buddy will be brought on board the medic's
boat. If the victim and swim buddy come up on the beach, medic will transit to beach.
2. Medic will administer 100% oxygen and perform a physical/neurological assessment to determine
if treatment is required.
3. Diving supervisor will recall the divers. Once all divers are on the surface and off dive status, a
muster will be taken and the diving supervisor releases medic to transport vehicle.
4. If medic determines that the diver requires recompression, the diving officer will contact the
chamber to initiate primary chamber recall, and activate EMS (if available).
5. Medic administers medical treatment as necessary to stabilize victim for transportation. If patient
needs to be brought to the beach, medic's boat can be beached.
6. Victim will be loaded into EMS vehicle if available. If EMS is not available in appropriate time
span, the diving officer's vehicle will be used for transport to the recompression facility. Patient's
swim buddy will accompany to the chamber.
7. Diving officer will accompany emergency vehicle to chamber. Note: The DMO will notify person
Who stayed in area to contact chain of command and inform them of the situation.
8. Back at the dive site, all divers will be recovered by the boats left on the scene or can be directed
to turtle-back (off dive status) to the beach. Gear will be loaded and divers transported from area.
9. Diving supervisor will contact the Diving Officer when all divers have been recovered and again
when they have returned to the area.
Diving Operations: Trauma
1. The victim and the swim buddy will be brought on board the medic's boat. If the victim and swim
buddy come up on the beach, medic will transit to the beach.
2. Medic will administer 100% oxygen and perform physical exam to determine if treatment is
3. If medic determines that the victim has a life/limb/sight threatening injury, the diving officer will
call 911 via cellular phone to contact EMS. Diving officer will inform operator of situation.
4. Diving supervisor recall divers.
5. Medic administers treatment to stabilize the victim for transport. If patient need to be brought to
beach, medic's boat can be beached.
6. Victim will loaded into the EMS vehicle. If EMS is not readily available, the diving officer's vehicle
will be used for emergency transport. When all divers are on the surface, off dive status, and a
muster has been accomplished, the diving officer, medic, victim, and the swim buddy will transit
to the appropriate facility or designated area by EMS.
Note: In cases requiring trauma care and recompression, transport patient to hospital with a
chamber. This can be via ambulance or Life-Flight™ (or equivalent), depending upon patients
condition. If Life-Flight™ is required, the diving officer will designate a qualified person to prepare the LZ.
7. Back at the site, all divers will be recovered by boat left on the scene, or will turtle-back off dive
status to the beach.
8. Diving supervisor will contact the diving officer when all divers have been recovered and again
when they have returned to the area.
Note: The diving officer will notify the chain of command to inform them of the situation.
Open Circuit Diving Emergencies Pulmonary Overinflation Injuries (POI): Characterized by a sudden onset occurring immediately, during or after ascent (unconsciousness or other neurological symptoms within 10 min). Injuries include subcutaneous emphysema, mediastinal emphysema, pneumothorax and arterial gas embolism (AGE). May have respiratory arrest.
Signs & Symptoms: Crepitation and swelling of the neck, voice change, dyspnea, difficulty swallowing. Syncope, shock, shortness of breath, dizziness, blurred vision, vertigo, paralysis or weakness of extremities, loss of sensation and chest pain.
Note: Some patients with AGE may exhibit a ‘lucent interval’, where the symptoms will improve for a short time after initial onset. Do not delay evacuation in such cases.
1. ABCs / High flow O2 / IV NS/LR KVO
2. Begin resuscitation if required.
3. 100% O2 (or highest concentration available) via tight fitting aviator’s mask and demand valve.
4. If pneumothorax identified, treat accordingly.
5. Arrange for immediate evacuation and recompression.
Decompression Sickness (DCS): DCS is usually seen after surfacing, with the majority of cases occurring within 3 hrs after completion of dive. Signs & Symptoms can occur immediately or after a sustained period, however onset of symptoms after 24 hours is highly unusual.
DCS is Divided Into Type I and Type II:
Type I DCS usually affects the muscular-skeletal system (pain only), cutaneous system
(rashes, hives, itching) or the lymphatic system (blotching, pain, discomfort).
Type II DCS usually manifest itself in the joints or CNS.
Note: 15-30% of Type I DCS will progress to Type II if symptoms occur immediately after
surfacing or if left untreated.
Mechanical Effects of DCS are Divided Into Two Categories: Intravascular and Extravascular.
Intravascular effects of bubbles include blockage, pain and obstruction of blood supply.
Extravascular effects cause pain, tissue distortion and disruption.
Signs & Symptoms: Skin: Localized or spreading prickly, itching, tingling or burning sensation; Rash and/or blotching. Pain: Pain in joints of arms and/or legs; Pain may grow in intensity, particularly with activity; Chest pain or SOB (The Chokes). CNS: Cranial Nerve deficits (vision, eye movements, smell, taste, hearing, speech); ear (The Staggers); hemiparesis, personality changes, amnesia, unconsciousness. Spinal Cord: Paraplegia, paresthesia, muscle weakness, bladder paralysis, urinary and fecal incontinence and radiating pain.
Caution: Chokes in the presence of DCS is a rare but grave sign. Most commonly seen in aviators from rapid decompression or from emergency ascents during saturation dives.
1. ABCs / High flow O2 / IV NS/LR KVO
2. Begin resuscitation if required.
3. 100% O2 (or highest concentration available) via tight fitting aviator’s mask and demand valve.
Signs & Symptoms: Pain not relieved by valsalva. Hemorrhage and/or edema in ear canal. In severe cases the tympanic membrane (TM) may rupture.
1. Stop descent and attempt to equalize.
2. If above fails: Ascend to shallower depth and attempt to equalize.
3. If above fails: Abort dive, clear obstruction and clear ear canal. Keep ear canal dry. No diving
until ear is healed. No ear drops if TM ruptured. Consider antibiotics if damage to TM is
moderate to severe.
Middle Ear Squeeze
Signs & Symptoms: Ear feels full or blocked, tinnitus, pain (relieved immediately if TM ruptures), hemorrhage in middle ear or possible vertigo.
1. If in water, stop descent/ascent and return to comfortable depth. Continue as for ear squeeze.
2. Continue slowly until equalized or abort dive.
3. Decongestants. No ear drops if TM ruptured. Consider antibiotics if damage to TM is moderate to severe.
Signs & Symptoms: Pain over affected sinus on descent (pain will subside with equalization), blood or mucus from the nose on ascent.
1. Symptomatic pain relief.
2. Decongestants. Antibiotics if infected.
Signs & Symptoms: Gum Abscess: Dull pain on ascent. Root Abscess: Dull pain on descent.
1. Analgesics PRN.
2. Dental repair.
Reverse Squeeze: May be external ear, sinus or dental.
Signs and Symptoms: Sharp pain on ascent (pain is relieved by descending a few feet [bouncing]); bloody discharge in mask.
1. Bounce 5-10 feet as needed to relieve pressure.
2. Decongestants. No ear drops if TM ruptured. Consider antibiotics if damage to TM is moderate to severe.
Closed Circuit Diving Emergencies 02 Toxicity: Pulmonary and CNS
Pulmonary: Results from long exposures to elevated O2 partial pressures characterized by lung irritation with coughing and painful breathing. Symptoms become increasingly worse as long as elevated levels of O2 are breathed.
CNS: Signs and symptoms may be convulsive or non-convulsive.
1. Diver unable to carry on effective breathing.
2. Period of unconsciousness or CNS impairment following convulsion may be similar to AGE.
3. No attempt should be made to insert any object between the clenched teeth of the diver
4. There may be no warning of an impending convulsion to provide the diver the opportunity to
surface. Buddy lines are essential!
Non-Convulsive: May occur suddenly and dramatically. May have a gradual onset. Think VENTID:
Visual: Tunnel vision (a decrease in peripheral vision) or blurred vision.
Ear symptoms: Tinnitus.
Nausea and/or vomiting
Twitching: Generally involves the facial muscles, but can involve arms/legs.
Irritability: Change in diver's mental status.
1. Assume position behind victim and release victims weight belt unless wearing a dry suit.
2. Leave mouthpiece in the victims mouth. If not in mouth do not attempt to replace it. If time
permits switch mouthpiece to surface position.
3. Grasp diver around chest above Underwater Breathing Apparatus (UBA) or between the UBA and
divers body. If difficulty in gaining control is experienced, use whatever means necessary.
4. Making a controlled ascent, maintain pressure on victim’s chest to assist exhalation.
5. If additional buoyancy is required, activate the victim’s life jacket. The rescuer should not
release their weight belt or inflate their life jacket.
6. Once on the surface, inflate victim's lifejacket, remove the victim's mouthpiece and switch the
mouthpiece valve to surface to prevent the rig from flooding and weighing the diver down.
7. Signal for emergency pick-up.
8. Once the convulsion has subsided open the airway by tilting the head back slightly.
9. Ensure breathing. Do rescue breathing if needed.
Hypercarbia (C02 Buildup): Generally results from inadequate ventilation or failure of absorbent canister to remove C02 from exhaled gas. May also result from flooding of the canister.
1. Perform dip test on UBA before dive.
2. Do not exceed canister duration limits for the water temperature.
3. Ensure one-way valves in the supply and exhaust hoses are present and work.
4. Swim at a relaxed and comfortable pace.
5. Avoid skip breathing-Skip breathing does not save gas in a closed circuit unit.
Signs & Symptoms:
1. Increased respiratory rate and depth of breathing.
2. Labored breathing
Note: The presence of a high partial pressure of O2 may reduce the early symptoms of CO2 buildup. Elevated levels of CO2 may result in an episode of CNS toxicity on a normally safe dive profile.
1. Increase ventilation (if skip breathing is a cause) and decrease exertion level.
2. Abort dive, return to surface and breathe air.
3.During Ascent: While maintaining a vertical position the diver should activate the bypass valve
to add fresh gas to his UBA. If related to canister flood out the vertical position will reduce
chance of caustic cocktail.
4. If unconscious follow procedure for underwater convulsion.
Caution: If CO2 toxicity is suspected the dive should be aborted even if symptoms dissipate at the surface. The decrease in symptoms may be a result of the reduction of partial pressure of CO2 as the diver ascends and will reappear upon return to depth.
Hypoxia: Caused by the partial pressure O2 being too low to meet metabolic needs. In closed circuit diving, cause is the result of too much inert gas (nitrogen) in the breathing loop due to an inadequate purge.
Signs & Symptoms:
1. Frequently no warnings signs prior to loss of consciousness.
2. 0ther symptoms include confusion, uncoordination, dizziness and convulsions.
NOTE: If symptoms of unconsciousness or convulsions occur at the beginning of a closed circuit dive, hypoxia, not O2 toxicity is the most likely cause.
1. If unconscious or incoherent at depth the dive buddy should add O2 to the stricken diver’s UBA.
2. Bring diver to the surface. Remove mouthpiece and allow diver to breathe fresh air. If
unconscious, check breathing and circulation, maintain an open airway and administer 100% 02.
Chemical Injury: Theintroduction into of a caustic alkaline solution into the upper airway is the result of water leaking into the canister and coming in contact with C02 absorbent. Generally occurs when diver is in a horizontal or head down position.
Signs & Symptoms:
1. Rapid breathing or headache related to buildup of C02.
2. Choking, gagging, foul taste and burning of the mouth and throat, will begin immediately.
1. Immediately assume an upright position.
2. Depress the manual bypass valve continuously and make a controlled ascent to the surface,
exhaling through the nose to prevent over-pressurization.
3. Should signs of system flooding occur during underwater purging, abort the dive.
4. Rinse mouth out several times with fresh water. Several mouthfuls should then be swallowed. If
only seawater is available, rinse mouth, do not swallow.
Note: Do not use acid solutions or induce vomiting. Uncontrolled ascent is common. Monitor for AGE.
Rapid Field Neurological Examination: This examination is designed to detect suspected problems in the CNS and serves as a monitor for changes in neurological functions resulting from DCS or POI’s. The exam should be conducted on any diver who experiences pain, discomfort, alteration in sensation or body function, or any other symptom within 24 hours of completion of a dive. The exam should be repeated every 30-45 minutes and if a diver's condition deteriorates.
Neurological Examination Checklist Patient's Name: ______________________ Date/Time: __________
Description of Symptoms: ________________________________
Type of dive last performed? _____ Depth? _______How long? _________
Number of dives in last 24 hours? ______
Was symptom noted before, during, or after dive? ______
If during, was it while descending, on the bottom, or ascending? _______________
Has symptom increased or decreased? __________
Have any other symptoms developed? ___________
Has pt had a similar symptom before? ______ When? ____________________
Has pt ever had DCS or air embolism before? ________ When? _________________
Mental Status Examination:
1. Is patient orientated to time, place, person, and recent events?
2. Evaluate speech for clarity and appropriateness.
COORDINATION (+ or --)
STRENGTH (1-5 scale)
REFLEXES (1-4 Scale)
Sensory Exam: Normal light touch/pressure sensation to: Fingers, hands, forearm, upper arm, legs, toes and trunk. (see dermatome chart, page 43).
Table 9-5, Navy Diving Manual:
Required Surface Interval Before Ascent to Altitude After Diving
Increase in Altitude
Repetitive Group Designator
Wait 48 Hours Before Flying
When using Table 9-5, use the highest repetitive group designator obtained in the previous 24-hour period
Table 9-5 may only be used when the maximum altitude achieved is 10,000 feet or less. For ascents above
10,000 ft, consult NAVSEA 00C for guidance.
The cabin pressure maintained in commercial aircraft is maintained at a constant value regardless of the
actual altitude of the flight. Though cabin pressure varies somewhat with aircraft type, the nominal value is
8,000 ft. For commercial flights, use a final altitude of 8,000 ft to compute the required surface interval before
No surface interval is required before taking a commercial flight if the dive site is at 8,ooo ft or higher. In this
case, flying results in an increase in atmospheric pressure rather than a decrease.
No repetitive group is given for air dives with surface decompression on oxygen or air. For these surface
decompression dives, enter the standard air table with a sea level equivalent depth and bottom time of the dive
to obtain the appropriate repetitive group designator to be used.
For ascent to altitude following a non-saturation helium-oxygen dive, wait 12 hours if the dive was a
no-decompression dive. Wait 24 hours if the dive was a decompression dive.
Note 1: For Non-Special Tactics personnel, flying after diving rules are as follows:
Do not fly for 24 hours after a no-decompression dive.
Do not fly for 48 hours following a decompression dive.
Note 2: Special Tactics flying after diving regulations reflect the current recommendations for flying after diving in the US Navy Diving Manual. As per AFSOC Policy the flying after diving rules for Pararescue and Combat Controllers assigned to Special Tactics Teams is given in Table 9-5, Navy Diving Manual. Exception: Flying is allowed immediately after a 100% oxygen (LAR-V) dive, if no other breathing mixture was used. Caution:These rules apply for OPERATIONAL MILITARY DIVES ONLY. Longer surface intervals before flying are safer, and should be used in training and recreational dives.
Additional Notes (Diving): USAF/SAM, Hyperbaric Medicine Division, San Antonio, TX
level of exertion at altitude and individual susceptibility.
Signs & Symptoms: Headache, fatigue, loss of appetite, dizziness and irritability (symptoms frequently mimic a bad hangover). Dry cough is common. Dyspnea at rest is not common and frequently precedes or indicates High Altitude Pulmonary Edema (HAPE).
Caution: Ataxia is not common with AMS alone: A person who has AMS and ataxia probably has High Altitude Cerebral Edema (HACE) and requires urgent evacuation to a lower altitude.
Mild AMS: Headache, anorexia, nausea and malaise.
Moderate AMS: Severe headache, vomiting, decreased urine output.
Severe AMS: Dyspnea at rest, ataxia, decreased level of consciousness and +/- pulmonary rales.
Mild AMS: Descend minimum of 1000 ft., rest and acclimatize. Diamox, 250mg b.i.d. or 500mg QD (sustained release form). Mild analgesia (Tylenol) for headache or phenergan if significant nausea.
Moderate AMS: Descend immediately a minimum of 1000 ft. Oxygen 2-4 LPM by mask. Acetazolamide as above. Consider Decadron, 4 mg, PO, IM or IV q. 6 hrs (does not speed acclimatization, but will reduce symptoms). Hyperbaric therapy (Gamow bag or equivalent) if descent is delayed or impossible.
Severe AMS: Same as for moderate, but IMMEDIATE descent is mandatory. If descent is delayed, hyperbaric therapy while awaiting descent or evacuation.
Note 1:DO NOT use sleeping medication or other sedating drugs to treat sleep disturbances at altitude. Use of these medications is thought to increase the incidence of HACE. Sleep disturbances usually resolve with proper acclimation. Acetazolamide may be helpful
Note 2: Diamox (acetazolamide), a carbonic-anhydrase inhibitor/diuretic, can speed acclimatization to altitude and decrease symptoms of AMS. The dose is 125-500 mg q. 24 hours, preferably starting 1-2 days prior to ascent, and continuing for at least one day after ascent. This is a sulfa-based medication, and should not be given to patients allergic to sulfa.
Note 3: Decadron (Dexamethasone) 4 mg PO, IM or IV q. 6 hours may prevent AMS if deployment to altitude is required without time for acclimatization. Note this does NOT speed acclimatization, but reduces the symptoms of AMS. Best used in quick in/out operations where altitude exposure is transient.
High Altitude Cerebral Edema (HACE): A severe form of AMS characterized by alterations of consciousness, ataxia, confusion, drowsiness, stupor, coma and death. Progression from AMS to
HACE usually occurs over 12-72 hrs. HACE and High Altitude Pulmonary Edema (HAPE) can and frequently do appear at the same time in the same patient.
Caution: A person who has symptoms of AMS and develops an altered metal status or ataxia is most likely in the early stages of HACE and requires immediate treatment.
Signs & Symptoms: Similar to severe AMS. Ataxia, confusion, impaired mentation and severe lassitude. Patients with AMS who are not improving within 24 hours should be suspected of having early HACE.
Caution: A person with AMS who develops ataxia most likely has early HACE, and needs emergency descent.
Treatment: Emergency descent by a minimum of 1000 ft but preferably more (the lower the better). Hyperbaric bag while awaiting descent or evacuation. Oxygen 2-4 LPM by mask. If an IV is started, run at KVO. Decadron, 4 mg PO, IV or IM every 6 hrs.
Warning: Do not delay descent while awaiting evacuation. If possible, have evacuation aircraft meet you at a lower elevation.
High Altitude Pulmonary Edema (HAPE) Mild, Moderate, Severe: HAPE is more common in young and healthy individuals, usually occurring 2-4 days after getting arriving at altitude, and most commonly on the second night at altitude. Rarely occurs below 8,000 ft. An individual that does not seem to be acclimatizing to altitude, or has AMS symptoms increasing after being on the mountain for 36 hrs or more, must be suspected of having HAPE.
Signs and Symptoms:
Mild HAPE: Dyspnea on exertion, easily fatigability, especially with uphill travel, +/- rales in lung bases.
Moderate HAPE: Dyspnea, weak, fatigue with travel on level ground, raspy cough, possible nail bed cyanosis, headache, decreased appetite, +- rales (usually bilateral).
Severe HAPE: Dyspnea at rest, productive cough (frothy, occasionally blood tinged sputum), extreme weakness, orthopnea, cyanosis, rales.
Treatment: Oxygen, high flow if possible. Immediate emergency descent. Hyperbaric bag if not able to descend immediately.
Note: Use of Lasix and/or Morphine in HAPE is controversial, DO NOT use without direct physician order.
Caution: The definitive treatment for HAPE is descent to lower altitude. Descend as soon as the diagnosis is suspected. Use of Nifedipine in HAPE: Use of the calcium-channel blocker, nifedipine, has been advocated as an adjunct treatment for HAPE. While it appears to be effective, this medication has significant side effects, most notably severe hypotension which may preclude ambulation. Dose of nifedipine is 10 mg sublingually, followed by 30 mg of the slow-release formulation every 12-24 hours, or 10 mg sublingually every 4 hours, titrated to response. Do not use this medication without direct physician order. Nifedipine is an adjunct for treatment of HAPE and does not substitute for oxygen and descent. UV Keratitis (Snow Blindness):Ultraviolet burn of the cornea caused by intense UV and reflected UV light at altitude. Can also be caused by prolonged exposure to UV light in an arctic/snow environment.
Signs & Symptoms: Pain to the eyes (feels as if there is sand in the eyes), usually starting 4-6 hrs after UV exposure. Light sensitivity, tearing, and headache.
Differential Diagnosis: Foreign body in eyes, conjunctivitis, acute close-angle glaucoma, iritis.
Treatment: Usually a self-limiting problem resolving within 12-24 hrs. Remove contact lenses if present. Eyes will be very sensitive to light. Protect from light to tolerance. Oral medications for pain control.
Prevention: Wear sunglasses with good UV blocking lenses, preferably with side shields.
Additional Notes (High Altitude Injuries):
Cold Weather Operations Guidelines and Considerations Individual Related Risk Factors: Characteristics that are generally accepted to be risk factors for cold injury include: Fatigue, alcohol use, dehydration, inadequate nutrition, lack of cold weather training and experience and tobacco use.
Some of the individual risk factors for cold injury are common consequences of operating in the field. Fatigue, inadequate nutrition and dehydration are encountered in every deployment. Assuring adequate rest, complete consumption of meals and forced hydration, controls these factors.
Environmental Risk Factors: Cold exposure can occur on land, in water or in aircraft. Cold land environments are generally classified as either wet-cold or dry-cold.
Wet-cold environments have ambient temperatures above freezing to about 60 F with wetness
ranging from fog to heavy rain and are associated with non-freezing peripheral injuries, such as
trench foot. Usually, many hours to days of exposure are required to cause injury.
Dry-cold environments have ambient temperatures below freezing. Precipitation, if present, is in
the form of dry snow. Dry-cold environments are associated with freezing peripheral injuries,
which can develop in a few minutes to hours.
Frostbite (1st, 2nd, 3rd, 4th Degree): Frostbite is the most common cold induced injury encountered in the field. Clusters of cases occur during cold weather operations, frequently from poor planning or inattention.
Clinical Manifestations: Initially, all frozen tissue has the same appearance: Cold, hard and bloodless. Digits, ears and exposed facial skin are the most commonly injured areas.
1. Limited in extent involving skin that has had a brief contact with very cold air or metal.
2. Skin is initially white, thaws quickly becoming wheal-like, red and painful.
3. Area may become edematous but will not blister.
1. Initial appearance as 1st degree.
2. Freezing involves deeper layers of skin and occurs with prolonged exposure.
3. Limitation of motion appears early.
4. Thawing is rapid with return of mobility and appearance of pain.
5. Blisters form over the affected area.
6. Cold sensitivity may persist.
1. Initially the frozen tissue is stiff and restricts mobility.
2. After thawing, mobility is restored briefly, but the affected skin swells rapidly and bloody blisters
3. Significant skin loss follows thawing through mummification and sloughing.
4. Residual cold sensitivity is common.
1. Frozen tissue has no mobility.
2. Thawing restores passive mobility, but the intrinsic muscle function is lost.
3. Skin perfusion is poor.
4. Blisters and edema do not form.
5. Affected area shows necrotic changes.
6. Significant permanent anatomic and functional loss is the rule.
1. Early detection is essential in cold injury management.
Frostbite injuries are insidious. Injured tissue, which was painful while getting cold, is
anesthetic when frozen and is often covered by a glove or boot.
2. Protect injured area from further exposure and trauma by the best means available.
3. Active warming of frozen tissue should be deferred until there is no risk that the tissue will be
re-exposed to freezing cold.
Refreezing a frostbite injury aggravates the injury so severely that current practice
recommends that frozen parts not be actively re-warmed until protection from refreezing
can be assured.
The frozen part should not be deliberately kept frozen by packing in snow or continued cold
4. Expeditious evacuation and protection of the patient is required.
area in groin or axilla, however active rewarming is the preferred treatment, if possible.
Active rewarming is best accomplished by immersing the frostbitten tissue in warm water
(102-103 F). The tissue must not be exposed to temperatures in excess of 102-103 F.
Rewarming is very painful. Morphine may be required for pain control.
6. Every frostbite casualty must be thoroughly examined for hypothermia, traumatic injuries,
dehydration and hypovolemia.
7. Dry bulky dressing to the rewarmed area. Splint prn. With hand injuries, splint in position of
function (beer-can or duckbill splint). Make sure that the fingers are separated with kerlex or
8. Give Motrin, 400 mg PO every 8-12 hours (for prostaglandin inhibition, not necessarily for pain
control). Topical aloe vera gel (if available) may be applied to the skin for topical prostaglandin
9. If blisters form, leave intact. If the blisters rupture, cover with antibiotic ointment and apply a
Non-freezing Cold Injury: Non-freezing cold injury results from prolonged exposure of the extremities to wet-cold, but above freezing conditions. The feet are the most common areas of injury: Trench Foot and Immersion Foot.Trench foot occurs during ground operations and is due to the combined effects of sustained cold exposure and restricted circulation. Immersion foot is caused by continuous immersion of the extremity in water. In both cases, the key to prevention is to clean and dry the feet, and put on dry socks at least once every 24 hours.
Clinical Manifestations: The injured tissue is pale, anesthetic, pulseless and immobile, but not frozen. Trench foot or immersion foot can be diagnosed when these signs do not change after
re-warming. The skin is frequently macerated and slightly edematous.
Note: Initially, despite rest and warmth, the injured part remains pale, anesthetic and pulseless. After several hours, a marked redness develops associated with severe burning pain and reappearance of sensation proximally, but not distally. Edema and large blisters develop in the injured areas as blood flow returns. Persistence of pulselessness in an extremity after 48 hrs suggests severe deep injury and high probability of substantial tissue loss.
1. First essential of management is detection.
2. Foot inspection and care every eight hours under cold-wet conditions and dry socks!
3. If suspected, priority evacuation is appropriate.
4. Patient must be moved by litter and extremity protected as in frostbite.
5. Dry covering of injured part and protection from cold may permit spontaneous re-warming.
6. If warming does occur, severe pain will develop, provide adequate pain relief.
7.Caution: Do not massage the injured area.
Hypothermia (Mild, Moderate, Severe): Hypothermia is the clinical syndrome that results from reduced core temperature. By definition, hypothermia is considered to be present when the core temperature is below 95 F. Hypothermia is the result of loss of heat to the environment in excess of the rate of heat production by the body. Operationally, hypothermia occurs as the result of either immersion in cold water or prolonged exposure in cold-wet ground environments.
Mild Hypothermia: Temperature between 90-95 F. Patient usually retains the ability to rewarm spontaneously and does not develop cardiac problems. Mental processes slow, errors in judgment are common! Shivering is common. Note: Bradycardia with PVC’s may occur, however this is physiologic and does not require treatment.
Moderate Hypothermia: Temperature above 86 F. Patient exhibits shivering, may be lethargic and dulled mentally, but is some cases may be fully orientated. Muscles may be stiff and uncoordinated, causing the patient to walk with a stumbling, staggering gait.
Severe Hypothermia: Temperature less than 86 F. Patient may be disorientated and confused and may proceed to stupor and coma. Shivering will stop and physical activity becomes uncoordinated. Muscles may be stiff and rigid. Significant cardiac arrhythmias may develop.
Caution: If the patient appears cold and is not shivering, the patient has severe hypothermia until proven otherwise by measurement of body core temperature.
Treatment: Mild to Moderate Hypothermia
1. Remove all wet clothes.
2. Protect against heat loss and wind chill.
3. Maintain horizontal position.
4. Avoid rough movement and excess activity.
5. Monitor core temperature.
6. Add heat preferentially to the patient's head, neck, chest and groin.
8. Provide warm oral fluids, and sugar sources AFTER uncontrollable shivering stops and the
patient exhibits evidence of rewarming.
Treatment: Severe Hypothermia with Vital Signs
1. Same as mild to moderate.
2. Establish an IV of NS at 75cc/hr (warmed).
3. Heated, humidified oxygen, if available.
4. Evacuate ASAP.
5. Some hypothermia protocols (i.e., State of Alaska) suggest a fluid bolus of 10 cc/Kg of NS,
followed by 5 cc/Kg/hour of NS. This is appropriate if there is no evidence of internal bleeding.
Treatment: Severe Hypothermia with No Vital Signs
1. Assess pulse and respiration for 1-2 min.
2. If pulse and respiration are absent, begin CPR.
3. Observe the cardiac rhythm. If VF, defibrillate immediately.
4. Ventilate with warmed humidified oxygen, if available.
5. Establish IV access and administer warmed saline.
6. Measure rectal (core) temperature.
7. If temperature greater than or equal to 86 F: Continue CPR and give resuscitative
medications as indicated (but at longer intervals). Repeat defibrillation as temperature warms.
8.If temperature is less that 86 F: Continue CPR, withhold IV resuscitation medications,
limit shocks to a maximum of three, and evacuate.
9. Rewarming should not be attempted in the field unless the patient is more than 30 minutes from
Immersion Hypothermia: A subset of hypothermia, immersion hypothermia (hypothermia caused by immersion in cold liquid) has several unique aspects that must be taken into account:
Immersion hypothermia rarely causes death by itself. The usual mechanism of death
involves systemic hypothermia to the point where the victim is unable to keep their airway
above water, followed by drowning.
Caution: Any unresponsive immersion hypothermia victim must be assumed to also have
submersion injury. In such cases, airway, ventilation and circulation take priority over
Warning: Immersion hypothermia victims must be hoisted out of the water in a horizontal position, to avoid a potentially-fatal drop in blood pressure. Use a vertical hoist only if a horizontal hoist (i.e. litter hoist) is tactically unsafe or unavailable. Once in the rescue vehicle, the victim should be kept supine. As with any hypothermia victim, it is vital to handle the victim as gently as possible to avoid provoking cardiac arrhythmias.
Survival after prolonged submersion in cold water (submersion times up to an hour) has
been reported, although it is not common. This usually requires sudden submersion in very
cold water (usually 45 F or below), and appears to occur mainly in children. Airway
submersion times of greater than 60 minutes are almost certain to be fatal, regardless of water temperature.
Immersion Syndrome is a sudden cardiac arrest caused by massive vagal stimulation as a
result of immersion in very cold water. This occurs within seconds of immersion. Rapid
retrieval from the water and immediate CPR may save victims of this syndrome.
The gasp reflex also can occur on sudden immersion in very cold water. This is an
involuntary reflex gasp, followed by several minutes of hyperventilation. During this time, it
will be very difficult for a victim to perform any self-rescue or survival procedures. Victims
who are not wearing flotation are likely to have serious problems keeping their airway above
Heat Injuries Guidelines and Considerations: Heat injury is usually the result of inadequate fluid intake, poor acclimatization, increased workload or a combination of factors. PREVENTION OF HEAT INJURY IS THE RESPONSIBILITY OF ALL OPERATORS. Proper acclimatization, proper hydration, good work/rest schedules and proper nutrition go a long way to prevent heat illness. However, even with ideal circumstances, heat injury can occur. When working in hot environments, it is imperative to use the buddy system, and keep a close eye on your buddy.
The microclimate (shade, humidity, wind, air circulation, body armor, MOPP gear etc) in the
immediate working area may significantly alter heat stress conditions from one area to another.
It is imperative to keep close tabs on your buddy when operating in high heat stress conditions.
Forced hydration (1-2 quarts of water per hour) may be necessary in high heat stress conditions, along with rest breaks and adequate food intake. Full-strength sports drinks (Gatorade®, Power Aide®, etc) and sodas are too concentrated for adequate hydration. If sports drinks are available, they should be diluted 50/50 with water. Sodas should not be used for hydration!
Note 1: The GI tract of a normal adult can absorb approximately 20 cc’s of fluid per minute. Cool (but not cold) liquids are absorbed better than warm fluids. It is best to stay hydrated by taking small amounts of fluid frequently (10-20 cc’s every 1-2 minutes) than attempt to ‘catch up’ by drinking a liter or two of fluid every hour.
Note 2: Heat exhaustion and heat stroke are a continuum of heat disorders, rather than distinct clinical entities. In the setting of heat illness, any patient with CNS dysfunction should be assumed to have heat stroke until proven otherwise. The presence of sweating in a heat illness victim DOES NOT rule out heat stroke.
Signs & Symptoms: Acute cramping pain, usually in legs and arms, nausea, dizziness. No alteration of consciousness. Treatment: Rule out heat stroke. Rest in shade, drink fluids with electrolytes, gradual return to activity with frequent rests until acclimated.
Signs & Symptoms: Headache, nausea, vomiting, dizziness, anorexia, cramps and/or malaise. Body temperature normal or slightly elevated. MENTAL STATUS NORMAL.
Treatment: Oral fluids if patient can tolerate them, IV hydration with normal saline if not. Rest in cool area. Hydration should be continued until urine is completely clear.
Signs & Symptoms: Bizarre behavior, confusion, delirium, ataxia, seizure and/or coma. Altered mental status in the setting of heat illness is heat stroke until proven otherwise. Body core temperature usually above 105 F. ALTERATION OF MENTAL STATUS.
Treatment: Cool patient by any means available (spraying liquid on patient and fanning him;
immersion in water; cool packs to neck, axilla and groin.). Maintain airway and breathing control as needed. IV with NS or Ringers is indicated. If hypotension is present, give 10 cc/Kg bolus of NS/Ringers, and re-evaluate. Continue IV hydration until urine is clear. Monitor fluid intake and output. Warning: Heat stroke is a true emergency and requires emergency evacuation ASAP.
Water Intoxication/Hyponatremia (low sodium in the blood)
Signs & Symptoms: Similar to heat exhaustion, except that the patient usually has a history of forced hydration with large amounts of water (1-2 liters/hour) combined with high heat load conditions and lack of adequate salt intake from food. Patients have usually been urinating clear or near-clear urine. History of adequate water intake with poor food/electrolyte intake is the hallmark of this disorder. Prevented is aimed at consuming adequate food while in the field or by using electrolyte replacement drinks. Full-strength sports drinks (Gatorade®, Power Aide®, etc) contain too much carbohydrate for proper absorption and adequate hydration. If sports drinks are available, they should be diluted 50/50 with water.
Treatment: If the patient is able to drink fluids, administer small amounts of electrolyte replacement drinks (oral rehydration salts or diluted sports drinks.) frequently. The GI tract can absorb only about 20cc’s of fluid per minute (1200cc/hour), so giving 10cc’s of fluid every 30 seconds is the max oral intake. If the patient is unable to drink, start an IV with normal saline, give a 5cc/Kg fluid challenge over 15 minutes, repeat as necessary.
Note: This is for treatment of acute exertional hyponatremia only, NOT for treatment of
long-standing hyponatremia (usually the result of long-term psychogenic water over consumption, use of diuretic medications or endocrine disease). If long-standing hyponatremia is present start an IV of normal saline at baseline rate and contact medical control.
Prevention: Avoid being the tallest object in an open area. Do not take shelter under single tall trees or next to metal/conducting objects. Stay clear of antennas/radios during thunderstorms. Inside an enclosed vehicle is relatively safe. Seek shelter in a grove of trees if possible. If caught in the open, crouch low with feet together. Team should spread out so a single strike will not hit all team members (hand grenade rules).
Victims may be confused, paralyzed (especially lower extremity paralysis), have fluctuating blood pressure, be unconscious but have vital signs or be in cardiopulmonary arrest. Other injuries can include ruptured TM’s; temporary blindness or deafness, altered mental status or have amnesia. Most symptoms will resolve by themselves over hours to days.
Note: Victims of lightning strike ARE NOT electrically charged and may be touched immediately after injury.
Caution: Remember scene safety: Lightning DOESstrike twice in the same place.
Single Casualty: CPR and ALS as required. Dress any burns and evacuate ASAP.
Multiple Casualties:REVERSE TRIAGE (treat the most seriously injured/apparently dead personnel FIRST, rather than last). Patients who are awake, able to move or talk will likely survive. Patients in cardiopulmonary arrest may only need 1-2 minutes of CPR to regain pulse and respirations. Treat any blast injuries or burns and evacuate ASAP.
Additional Notes (Heat Injuries): VENOMOUS INJURIES Reptiles
Guidelines and Considerations:
There are five venomous snake families:
Crotalidae. Uses hemotoxic venom. Includes all pit vipers (rattlesnake, copperhead, cottonmouth, etc.)
Colubridae. Uses hemotoxic venom. Back fanged snakes. Limits ability to envenomate humans.
Elipidae. Uses neurotoxic venom. Includes cobras, mambas, kraits and coral snakes.
Viperdae. Uses hemotoxic venom. True vipers. Includes puff adders, vipers and desert adders.
Hydrophidae. Uses neurotoxic venom. Sea snakes.
The majority of snakebite victims survive.
Not all bites from poisonous snakes involve injection of venom: Up to 50% of cobra bites and 30%
of rattlesnake bites are ‘dry strikes’, meaning no venom is injected.
Operators should be familiar with the types of venomous snakes found in their area of operation,
and the recommended field treatment of bites.
Note 1: All snake venoms (and some large breed lizards) contain components that are neurotoxic and hemotoxic. You will see neurotoxic reactions to primary hemotoxic venoms and hemotoxic reactions to primary neurotoxic venoms.
Note 2: Bites from large breed lizards (Gila Monster, Komodo Dragon, Monitor, etc) carry a high incidence of infection. Debride aggressively and administer antibiotics.
Warning: Snakebite is a true emergency, requiring fast action and emergency evacuation of the victim.
Hemotoxic Envenomations: Most common with pit vipers (rattlesnakes, copperheads, cottonmouth moccasins, Fer-de-Lance and Bushmaster) and old world vipers.
Signs & Symptoms: Swelling and blistering at bite site; muscle fasciculation, weakness and syncope; nausea & vomiting; chills, hypotension, lymphangitis, and respiratory distress may occur; GI and GU bleeding may occur; Bite site tends to ooze blood constantly. Moderate to severe pain at the bite site, starting within a few seconds of the bite; perioral numbness and tingling; metallic taste in the mouth may occur.
Neurotoxic Envenomations: Most common in bites from Elapids (cobras, coral snakes, kraits), sea snakes, and most snakes found in Australia.
Signs & Symptoms: Mild pain or painless bite site; Numbness or tingling of bite site; perioral numbness and metallic taste in mouth may occur. Muscle weakness, uncoordination, fasciculation’s; difficulty in swallowing and speaking may occur; Visual disturbances, ptosis, respiratory distress, hypotension and convulsions may occur. Respiratory paralysis may occur.
Note: Neurotoxic symptoms may take hours to appear and then progress rapidly.
1. Extractor Pump: The extractor pump (NSN 6545-01-281-1237) is known to be effective in pit viper envenomations and is likely to be effective in elapid envenomations, removing up to 30% of the injected venom load. It should be applied to the bite site as soon as possible after the bite (Pump is most effective if applied within 3 minutes). Empty the bell of the pump as it fills with fluid, and re-apply. Continue for 30-60 minutes.
Note 1: No incisions should be made.
Note 2: Mouth or rubber bulb suction is NOT a substitute for an extractor pump.
2. Compression/Immobilization (Used for neurotoxic-predominant bites): Apply an ace wrap and splint to the bitten extremity. Wrap proximal to distal and slightly tight. Wrap so the extractor pump/bite site is accessible. Do not remove wrap until at a medical facility.
3. Proximal Constriction Band (Used for hemotoxic-predominant bites): Use a 1” wide penrose drain or similar wide band. Place above the bite site, just tight enough to indent the skin (should be loose enough to slip one finger between the band and skin). Check proximal pulses frequently. If the band becomes too tight as a result of swelling, place a second band above the first before releasing the first band. Once a constriction band has been placed, do not remove until at a medical facility. Note: This is not a tourniquet!