Stresses in SCUBA and Breath-Hold Diving

  • Michael B. Strauss, MD; Phi-Nga Jeannie Le, MD; and Stuart S. Miller, MD
  • Volume 06 - Issue 1

Part V: Near-drowning and Drowning

In the four previous issues of Wound Care and Hyperbaric Medicine, we introduced the subject of stimulus/stress—response/resolution and used this as the basis for discussing the physical, physiological, psychological, and no-panic syndrome stresses of diving.1-4 In this article we will discuss the ultimate and most dreaded stress of all water related activities: suffocation in the water. It is associated with oxygen deprivation to the brain with loss of conscious as well as various degrees of insult to the lungs. Unfortunately, the body’s reactions/responses to these devastating stresses are very limited in the absence of restoration of ventilation. The responses that somewhat mitigate these stresses are observed in the diving reflex and hypothermia, both of which will be discussed. Although 33 different definitions have been ascribed to drowning incidents, we will refer to them as near-drowning and drowning.5 The near-drownings are further subdivided into events with no residual neurological problems and events with neurological residuals (Figure 1). While this article considers the subjects of near-drownings and drownings in general, as much of the information as possible will relate to SCUBA and breath-hold diving activities.

Figure 1: Drowning and the Spectrum of Near-Drownings


Legend: Drownings and near-drownings must always be considered in the context of the event, i.e, loss of consciousness while submerged, and the outcomes. The outcomes range from no residuals to coma. It is suspected that transient LOCs almost always go unreported.

Key: LOC = Loss of consciousness


Extensive literature exists on near-drownings and drownings and is excellently summarized in articles by Golden et al. (1997) and Szpilman et al. (2012).6,7 Another authoritative source of information on near-drownings and drownings comes from the 2002 and 2011 World Congresses on Drowning (WCOD), with the resulting information adopted by the World Health Organization (WHO). The WCOD uses the Utstein template and defines drowning as “…experiencing respiratory impairment from submersion/immersion in liquid.”8 It supplements drowning information with outcomes that include death, morbidity, or no morbidity. Other terms such as wet, dry, near, passive, delayed/secondary, and the time interval between the event and pronouncing the victim dead are used to describe drownings, but the WCOD consensus is that these terms should no longer be used.

Whereas drowning deaths throughout the world generate large numbers, it is fortunate that only a small proportion occur in SCUBA divers. Statistics on SCUBA diving related drowning deaths from the Divers Alert Network (DAN) show that approximately 100 deaths (with about a 10 percent variance from year to year) occur in SCUBA divers in the USA, and approximately half are designated as drownings without any established etiologies for the loss of consciousness while submerged.9 The data from drowning deaths  in  snorkelers  and breath-hold divers is less well documented since these incidents tend to be lumped into all deaths where a mortal submersion occurs, and the recording of such deaths, especially for surface swimmers and snorkelers, is even less rigorous. The collection of data on breath-hold diving related drownings is being initiated by DAN, but numbers are not known to us at this time. Furthermore, there is no incentive to report near- drownings, especially those with no residual lung or brain injury. In the USA, near-drownings are estimated to be 500-600 times more common than deaths from drowning.10 Regardless, any loss of consciousness in a water-related activity is a serious concern and especially tragic when the activity is voluntary and done for recreational, fitness, and/or sports-related purposes.

The actual number of drowning deaths throughout the world is unknown, with estimates as high as over 500,000 in 2001 and 372,000 in 2012, according to the WHO. In the USA 40 percent of drownings occur in children younger than four years old.6 Drowning is a leading cause of death worldwide in children five to fourteen years of age. In the USA it is the second leading cause of non-disease, injury-related deaths (secondary to motor vehicle accidents) in children one to four years of age.7 In terms of exposure adjusted person-time estimates, Szpilman et al. note that the chances of drowning is 200 times higher than such estimates from motor vehicle accidents.7

This article describes the precursors/risk factors associated with near-drowning and drowning, the pathophysiological events that occur with submersion injury, factors that influence favorable outcomes, and patient management from first response interventions to definitive management for victims that lose consciousness in the aquatic environment. Special consideration is given to relating these subjects to SCUBA and breath-hold divers. The question of whether or not to use the term “drowned” has some pertinence and is discussed next.

Never Say Drowned

Although death occurring while immersed in water is tantamount to drowning, and is the terminology we advocate, the admonition of “never say drowned” should always be remembered (Figure 2) and is well founded for two reasons. First, never say “drowned” because recoveries, some seemingly miraculous, have occurred after unconscious victims of immersion have been rescued and revived. Some recoveries have occurred after immersions of up to 60 minutes.7,11 Age, absence of panic, the oxygen conserving/diving reflex, and cold water are factors associated with recoveries from prolonged (up to 30 minute) immersions and, in part, reflect the body’s limited responses to the anoxic stress of submersion. A corollary to this admonition of “never say drowned” is the hypothermic victim with a profound bradycardia or asystole immersed for less than 30 minutes. Only after rewarming with no evidence of recovery should the victim be labeled as dead and nonresuscitatable. How these factors associated with the diving reflex affect recovery for the unconscious victim of water immersion will be discussed later in this article.

Figure 2: Why "Never Say Drowned"

figure-2Legend: When a victim is found unconscious in the water, they should not automatically be labeled as dead. About 90% of the victims recover. Furthermore, the caregiver should ascertain the cause of the loss of consciousness so etiology-specific appropriate care is provided.

A purported (but not verified) record for recovery after prolonged immersion is that of a newborn being cast into a toilet bowl when the mother  did not want to keep the baby. As the information goes, after two hours she reconsidered her decision and retrieved the immersed neonate. Miraculous spontaneous breathing and recovery occurred.
Comment: The new born status, the cold water, and the oxygen-conserving reflex are factors that would have contributed to a miraculous recovery of this sort. The oxygen-conserving reflex is strongly exhibited in the fetus and the newborn with its most characteristic sign being that of bradycardia, an objective sign of the fetal distress syndrome.12

The second reason for “never say drowned” is that in many victims of water immersion a preceding event leads to the loss of consciousness in the water. If the problem that led to the loss of consciousness is not recognized and appropriate interventions are not initiated, recovery will be hampered. For example, loss of consciousness from a cardiac event while immersed requires markedly different treatment than that from water aspiration associated with a blackout (see reference 4) or from unconsciousness due to an arterial gas embolism. This caveat of ascertaining the reason for the loss of consciousness while immersed is especially true for the near-drowning victim, where appropriate immediate early management is so crucial to achieve good outcomes. Often when a drowning occurs it makes the headlines of the local newspaper; however, follow-up information as to the cause of the loss of consciousness is almost never reported.

Table 1: Risk-taking that Leads to Near-drowning and Drowning in Divers

Problem Comments/Examples
General Risk Factors (see reference 1)
1. Exceeding one's capabilities Diving too deeply (nitrogen narcosis), swimming to/returning from dive sites (exhaustion)
2. Lack of awareness of diving conditions Open water dives (disorientation), cave diving, hull penetrations (panic), diving in currents, rip tides, traversing surf zones (exhaustion and panic)
3. Alcohol and illicit drug use Impairs judgment (panic, disregard for risks, increased susceptibility to nitrogen narcosis) (see reference 2)
Special Risks Associated with SCUBA Diving (see reference 2)
1. Equipment related Lack of familiarity (buoyancy control), inoperable or in need of servicing (equipment failures), loss of monitors—flooding, dead battery (disorientation, uncontrolled ascents, decompression obligations)
2. Entanglements Especially with kelp and hull penetrations (panic, exhaustion of air supply)
3. Exposure and exhaustion Hypothermia, surface swimming against currents (exhaustion)
4. Sensor failures, wrong gas mixtures Insufficient oxygen partial pressures (hypoxia) with closed circuit rebreathers
Special Risks Associated with Breath-hold Diving (see reference 4)
1. Profound hyperventilation Blackout from hypoxia before CO2, elevation signals the diver to breathe
2. Deep dives with hypoxia on ascent Diffusion at blackout (see reference 4)
1. Diving with medical problems Impaired heart function, uncontrolled diabetes, seizure disorder, stroke residuals
2. Diving in dangerous environments  Overhead boats (propeller/head injuries), polluted waters (toxic chemicals), sharks
3. Envenomation from marine animals Usually from carelessness (stonefish) or handling (blue-ringed octopus, sea snakes)


Causes and Risks Factors for Near- drowning and Drowning

There are multiple reasons why near-drowning and drowning occur. Probably the least frequent is that of forceful immersion as a consequence of homicide, attempted homicide, or torture. Conversely, the most frequent cause for near-drowning and drowning is that of risk-taking, especially with respect to diving (Table 1). Several subcategories of risk-taking exist: first there is risk-taking associated with exceeding one’s diving capabilities. Second there is risk-taking due to unawareness of the diving conditions or challenges. Third there is risk- taking with equipment-related situations. Fourth there is risk-taking associated with alcohol and/ or illicit drug use in association with water-related activities. Alcohol has been reported in about 50 percent of drowning deaths, although the majority of these are in non-diving related water associated activities.15 Other risk factors are those of SCUBA diving without adequate supervision/pre-dive briefings and disregarding the buddy system.


A 1994 event that made news headlines was that of a woman who drove her car into a pond with two of her children inside in order to kill them.13 This is the epitome of a forced immersion.
Another news headliner is that of waterboarding as an interrogation technique. Of all forceful interrogation techniques, including drugs, sensory deprivation, absence of sleep, bodily harm, etc., water- boarding presumably is the most effective and the quickest from which to obtain responses.14
The technique of waterboarding is relatively simple. The victim is securely bound, placed on  a slight downward incline, and the face covered with a cloth. Water is then used to block the nostrils until the victim is on the verge of suffocation. The urge to breathe apparently makes this the most effective interrogation technique without inflicting bodily harm, although deaths, presumably from aspiration of vomitus and/or cardiac causes, have been mentioned.
Comment: The bottom line is that oxygen deprivation before loss of consciousness (in the absence of no-panic syndromes) can be such a profound stimulus to breathe it can generate confessions even in the most hardened suspects.

In addition, several factors are associated particularly with breath-hold diving. Profound hyperventilation before submersion is a significant risk factor for loss of consciousness during underwater swimming and breath-holding diving activities.4 Another risk factor in this category is the breath-hold dive with resulting diffusional blackout.4 Finally, there are serious risks for those who attempt to set world unlimited and free dive breath-hold depth records (now greater than 500 feet).

In SCUBA diving excess risks are associated with inadequate training, lack of familiarity with equipment, and/or poor fitness.1,16As mentioned earlier, drowning deaths in SCUBA divers are rare with reported deaths in the USA consistently remaining around 100 (±10%) per year.9 Especially significant risks to SCUBA divers include diving too deeply with air, resulting in nitrogen narcosis; panic, which is frequently caused by entanglement; and depletion of air supply. Drowning deaths from decompression sickness and arterial gas embolism are exceedingly rare because the victims are usually on the surface when symptoms manifest themselves and a buddy diver is usually in attendance. Other SCUBA diving causes/risk factors associated with loss of consciousness in the water include hypothermia and exhaustion. With closed circuit rebreather diving, drowning deaths most often occur due to hypoxia from insufficient oxygen partial pressures caused by human error or equipment malfunctions.3,17There are also medical conditions that can cause loss of consciousness in water such as myocardial infarction, heart arrhythmias, stroke, seizure and hypoglycemia.4 Trauma from boating accidents and shark bites (with acute blood loss) can be another cause of loss of consciousness in the water. Finally, there is the potential (possibly non-existent) for loss of consciousness in divers from venomous marine animal bites and stings, such as from the sea snake and the blue-ringed octopus.

Related Near-drowning and Drowning Terminology

A number of other terms associated with drowning are eschewed by the WCOD in favor of the simple outcome terminology of morbidity,  no  morbidity, or mortality after water immersion, as previously mentioned. The problem with this simplified terminology is that additional descriptions are required in order to define and/or explain the morbidity. Nonetheless, it is important to be aware of other terminology associated with near-drowning and drowning. Sudden (instantaneous) drowning was described by Keatinge in 1977.18 He postulated that the immediate loss of consciousness and drowning deaths in aviators whose planes were shot down over the cold North Sea waters was due to uncontrollable gasps in the near freezing water. If the head were submerged, water would be aspirated and consciousness almost immediately lost due to brain hypoxia. Wet and dry drowning refers to whether or not enough water is aspirated to cause electrolyte imbalances in the body. Further discussion of this will occur later in this article. Secondary drowning refers to the delayed onset of pulmonary edema after a near-drowning episode19 and is most frequently reported in near- drownings of children. It is believed to be due to a hypoxic insult to the alveolar capillaries, which gradually lose their integrity so that diffusion of serum into the alveoli occurs and causes the victim to become progressively hypoxic with dyspnea, tachypnea, confusion, agitation, and eventually lose consciousness. Treatment requires all measures necessary to manage pulmonary edema including breathing enriched oxygen mixtures, diuretics, intubation, and positive end-expiratory pressure ventilation.

Dive Scenario: A healthy, fit, well-trained SCUBA diver loses consciousness on the bottom in about 30 feet of water with no apparent cause. Fortunately, the dive buddy recognizes the situation and brings the unconscious diver to the surface. Immediate cardiopulmonary resuscitation is initiated and breathing and heart activity resume. The victim, while still unconscious, is brought to a nearby hyperbaric chamber where he is recompressed on a Navy Treatment Table 6-A (maximum depth of 165 feet) because of suspected arterial gas embolism. Near the end of the six-plus hour treatment the semiconscious diver becomes agitated. Immediately on completion of the treatment table the patient is transferred to an emergency department where he requires intubation for hypoxemia. Subsequent x-rays demonstrate extensive pulmonary edema.
Comment: Many questions arise with this scenario, including why loss of consciousness occurred almost immediately on reaching the shallow bottom depth. An arrhythmia is probably the best explanation for this since no equipment or gas mixture problems were found during the investigation. Second, did the victim experience an arterial gas embolism since consciousness was lost on the bottom and not upon surfacing? Did the treatment table with high pressure oxygen breathing contribute to the pulmonary edema? Regardless, the onset of pulmonary edema (as manifested by agitation and confusion secondary to hypoxemia and “white out” of the lungs later obtained on a chest x-ray) was presumably due to the alveolar insult with delayed manifestation from water aspiration. These findings occurred nearly six hours after retrieval from the water and are postulated to be an example of “delayed” drowning.
Pulmonary edema, apparently in the absence of near-drowning, has been reported in SCUBA divers without loss of consciousness while diving.20 The cases described occurred in cold water, but mention of water aspiration was not noted. The pathophysiology and management appear to be the same as described for secondary drowning.
Comment: It is known that small amounts of water aspiration into the lungs precipitates changes in lung function (described later in this article). Whether occult aspiration of water during the dive or moisture in the breathing gear was a contributing factor is not known.

Another variant of “delayed” drowning was associated in a breath-holding thoracic squeeze episode.21 Three hours following an apparent full recovery after loss of consciousness and retrieval during ascent of a breath-hold dive (i.e., diffusional blackout—see reference 4), the victim became progressively hypoxic and failed to respond to treatment measures. Autopsy demonstrated serum and blood in the alveoli. The three-hour latency period represented the time it took for serum and blood to accumulate in the alveoli and reflected the characteristics of a delayed drowning.

Figure 3: Swann's Dog Studies from the 1940s


Legend: During the first author's time in medical school, this was the prevailing information on what happened (in humans) in near-drownings and drownings from which test questions were derived.


Evolution of the Understanding of the Pathophysiology and Management of Near-drowning

The understanding of what happens in near- drowning has evolved from total misinformation to a sound physiological basis today. Based on dog studies by Swann in the late 1940s, distinction was made between what occurs in fresh- and saltwater drownings (Figure 3).22 Therapy was consequently directed at maintaining electrolyte balance because of hemodilution with freshwater drownings and hypernatremia with saltwater drownings.

Swann’s study involved immersing anesthetized canines in fresh water and salt water. Dogs, apparently as a natural response to immersion, aspirate large quantity of waters (in contrast to humans); enough to cause severe disturbances in electrolytes and red blood cells (RBCs). In fresh water hemodilution, hyponatremia, and RBC hemolysis were observed in the canine model. In salt water the opposite occurred with hemoconcentration, hyponatremia, and crenation of the RBCs.
Comment: Observations in human near-drowning and drowning events indicate in almost all occurrences that insufficient water is aspirated to alter electrolytes or RBCs. More than 1.5 quarts of water need to be aspirated before significant changes in intravascular fluids and electrolytes occur. However, in almost all near-drowning and drowning events in humans, water is aspirated and differentiates the drowning as a “wet” type, as will be discussed shortly.

Modell in the late 1970s found that fluid and electrolyte imbalances were not the reason morbidity was associated with near-drownings.23 Rather, it was due to hypoxia. With the newly acquired avail- ability of arterial blood gas measurements, Mod- ell showed that blood oxygen tensions fell precipitously with asphyxia in water, approaching nearly zero within 10 minutes (Figure 4).

Figure 4: Modell's Blood Gas Studies in Drownings


Legend: Modell demonstrated that hypoxia was the pathophysiological event that initially occurred in drownings.

Table 2: Modell's Method for Pulmonary Management of Drownings

Category I II III



Insp Force

Vital Cap










Chest PT



>25 cm H2O

>500 cc






<25 cm H2O

<500 cc



Swan Ganz

Key: CAP = capacity, cc = cubic centimeters, cmH2O = centimeters of water, CPAP = continuous positive airway pressure, Insp = inspiratory, IPPB = intermediate positive pressure breathing, PaO2 = partial pressure of arterial oxygen (mmHg), PEEP = positive end-expiratory pressure, PT = physical therapy, WNL = within normal limits


He advocated using advanced pulmonary life support measures to achieve adequate blood oxygenation to protect the brain, and his approach utilized three categories of severity using blood gasses and respiratory parameters (Table 2). For the more severe presentations continuous positive airway pressure (CPAP) was used, and in the most severe situations positive end-expiratory pressure (PEEP) was initiated. Modell observed that if the near-drowning victim arrived in the emergency department alert, 100 percent recovery was observed. If the sensorium was blunted, 90 percent recovery occurred. However, if the victim was comatose at the time of arrival full recovery with his techniques only occurred in 50 percent of the near-drowning victims.

Subsequently, Conn amended Modell’s recommendation to stress cerebral resuscitation in comatose patients after near-drowning.24 He advocated “HYPER” therapy, which was an  acronym for interventions to modify hydration, ventilation, body temperature, excitability, and rigidity (Table 3). With use of his “HYPER” therapy in 18 patients who arrived comatose, he observed that 61 percent had full recovery and only 5.5 percent had residual brain damage. He contrasted this in 21 patients using Modell’s approach where 28 percent had full recovery and 38 percent had residual brain damage.

Table 3:  The Five Components of Conn's "HYPER" Therapy


Note:  With Conn's "HYPER" therapy, 61% of his 18 patients who arrived comatose demonstrated full recovery and only 5.5% had residual brain damage. He contrasted this with experiences where 28% of patients had full recovery and 38% had residual brain damage.


Current management for near-drownings is based on improved understanding of the pathophysiology of water immersion and optimization of management. In 85-90 percent of human drownings, water is aspirated and consequently the event could be considered a “wet” near-drowning, drowning event. This is confirmed at autopsy by the findings of diatoms from the aspirated water in the alveoli. The other small percentages of drownings are “dry” types where water does not enter the alveoli secondary to laryngospasm.

Drowning victims are too busy struggling (unless blackout has occurred) and too “air hungry” to yell for help. Once water enters the alveoli, four pathophysiological events occur (Figure 5). These include 1) decreased lung compliance, 2) ventilation-perfusion mismatching, 3) intrapulmonary shunting,  and 4) surfactant washout. The common final denominators are hypoxemia and acidosis that lead to secondary problems of encephalopathy, acute respiratory distress syndrome, cardiac problems (ischemia, infarction, and/or arrhythmias), and renal shutdown.

All therapy is directed at maintaining adequate arterial blood saturations (above 90 percent) and acid-base balance including CPAP, PEEP, vasopressors, fluids, diuretics, acid buffers, intubation with barbiturates for sedation, etc. If aspiration of contaminated water is suspected, antibiotics are given. Finally, the use of steroids for reducing cerebral edema is controversial and apparently neither Modell nor Conn used them in their resuscitation protocols. An excellent algorithm for the evaluation and management of drowning victims has been generated by Szpilman et al.7 They grade the victim from “Dead” to “Rescue” with six intermediate grades (1 to 6) based on the duration of immersion and the physical examination findings at the time of presentation to the emergency department. Management is specified for each grade with accompanying survival rates. Hyperbaric oxygen would seem a logical adjunct for mitigating the brain pathophysiology of hypoxia and cerebral edema (see text box below). Unfortunately, we are not aware of any reports of using HBO for such.

Hypothermia and hyperbaric oxygen (HBO) are two other therapeutic interventions that may have roles in improving outcomes for brain insult consequences of near-drowning, as well as other brain injuries. While Conn mentions hypothermia to slow brain metabolism it tends not to be used in near-drownings, though there is increasing awareness of its use for acute traumatic brain injuries.
The use of HBO is even more controversial. Since the acute brain insult in near-drowning is a combination of hypoxia and edema, possibly coupled with a reperfusion injury element, the acute use of HBO has justification (Figure 6).25-26 Laboratory studies show significant improvements in outcomes when HBO is used in their models and the treatment has been coupled with hypothermia for a possible additive benefit.27-29

The Diving Reflex

Near-drownings, and the seemingly miraculous recoveries that have been observed after rescues, require a discussion of the diving reflex. The diving reflex is a series of innate responses that are associated with immersion in water (Figure 7). The reflex is highly developed in diving mammals and other aquatic animals, allowing them to remain submerged from six minutes (porpoises) to two hours (blue whales).30 This series of physiological responses conserve oxygen and direct blood flow exclusively to the two most vital organs needed to safely continue the breath-hold dive; namely, the heart and the brain. The diving reflex  has three  components: 1) bradycardia, 2) vasoconstriction with shunting of blood to all body systems (except the heart and brain), and 3) anaerobic metabolism. Absence of panic, minimizing moments of the extremities, immersion in cold water, and young age (especially the fetus) facilitate the effectiveness of the diving reflex.

Figure 5: Sequence of Events in Diving-related Near-drownings and Drownings


Legend: Modell demonstrated that hypoxia was the pathophysiological event that initially occurred in drownings.


Figure 6:  The Role of the Acute Use of Hyperbaric Oxygen for Near Drownings


Legend: The mechanisms of hyperbaric oxygen (HBO) have applications for the pathophysiology of near drowning, especially with respect to the brain injury.

The diving reflex is initiated by water coming in contact with the nasal branch of the trigeminal nerve, and the effect can be very profound. For example, heart rates in the seal slow by 90 per- cent to 10 beats per minute during the diving re- flex.30,31 Selective vasoconstriction is intense with almost total cessation of blood flow to all areas of the body except the heart and brain. This allows the oxygen content of the blood to meet the oxygen needs of the brain and thereby maintain consciousness during the dive. Anaerobic metabolism allows muscles for propulsion and feeding purposes to function in the absence of the usual oxygen requirements for aerobic metabolism. The “cost” of this is an oxygen deficit in the tissues that is met after surfacing by breathing air, which resolves bradycardia and vasoconstriction.
As previously mentioned, elements of the diving reflex exist in humans. Heart rates have been observed to decrease 40 percent in experienced breath-hold divers with immersion.30 Other components of the diving reflex, such as vasoconstriction and anaerobic metabolism, also occur in humans. Vasoconstriction offers some protection from hypothermia by decreasing perfusion to the extremities. This helps maintain core temperature while reducing heat loss from extremities through the radiator effect of the relatively large surface area to mass of the limbs. Conditioning directly leads to improved tolerance of elevated levels of carbon dioxide and decreased levels of oxygen as well as the consequences of anaerobic metabolism.

First-response Interventions for Near-drowning victims 

The first step in any near-drowning event is retrieval of the victim from the water. If on the surface, the Red Cross water safety adage of “throw, tow, row and only then go” is sound advice. Certainly, the rescuer should not be put in jeopardy. What is worse than a drowning is a double drowning with the rescuer as the second victim. The next steps in the first response interventions are 1) getting the victim to a stable platform like a boat if in open water or the shore if nearby and 2) activating the Emergency Response System (best initiated by dialing 911 if in the USA). After this, basic life support (BLS) measures, which continue to evolve, should be initiated (Table 4). While performing BLS, the hypothermic victim should not be rewarmed. The reason for this is the hypothermic victim may be in asystole, and during the rewarming the initial cardiac response is likely to be ventricular fibrillation, which is rapidly fatal if not immediately corrected. Once advanced support with an automated external defibrillator is available and intravenous (IV) access established, rewarming while continuing resuscitation should be done.

Rewarming techniques include removal of wet garments to prevent evaporative heat loss, shielding from wind, covering with warm blankets or clothing, application of warm water bottles to axillary and groin areas, instillation of warm IV fluids, and inhalation of warm, humidified air. Usually multiple techniques are used for additive warming effects. Heimlich “hugs” (abdominal thrusts) are not recommended for drowning victims as the maneuver is not effective in expelling water from the lungs and may precipitate vomiting that can lead to lung aspiration.

Figure 7: Components of the Oxygen Conserving/ Diving Reflex


Legend: The diving/O2 conserving reflex is initiated by water coming in contact with the terminal branches of the trigeminal nerve. Andersen's classic experiment with the duck shows how profound it is in prolonging survival with immersion apnea.31 It has been observed in a variety of animals, but best appreciated in the diving mammals. Components of the diving reflex can be observed in humans. The reflex is obliterated by struggling and panic.

We do not advocate in-water resuscitation although a published report indicates otherwise.32 In-water resuscitation—alternating mouth-to-mouth breaths with repeated chest level “bear hugs”—is not only difficult to do in the water, but is ineffective. Consequently, we advocate getting the victim to a stable platform as soon as possible where effective cardiopulmonary resuscitation can be done. Cold water immersion (i.e., in water substantially below body temperature) may slow metabolism as well as augment the diving reflex to improve the chances of survival.
Because of differential cooling of the core, which tends to remain warmer than the extremities whose temperatures approach that of the surrounding water, tourniquet use might be considered during the rewarming process. This is to prevent the rush of cold blood from the extremities from entering the core as a consequence of the obliteration of the diving reflex, which occurs with rewarming. Remember with vasoconstriction as a component of the diving reflex, warm core blood flow to the extremities is reduced, which lessens heat loss through the extremities due to their large surface area to mass ratio as compared to the core.
With core temperature monitoring and use of extremity tourniquets, as the victim of near- drowning plus hypothermia warms, the extremity tourniquets are reduced in a serial fashion. This is believed to prevent the temperature afterdrop observed with the rewarming of the hypothermic victim.


Table 4: Highlights in the History of Cardiopulmonary Resuscitation

1. In the beginning...He (God) breathed the breath of life into Adam's nostrils and the man became a living creature. (Genesis 2:7)

2. There are anecdotal commentaries throughout the ages for recovery of drowning victims

  • Mothers breathing life into their drowned children's nostrils
  • Restoring life to drowned victims by teeter-tottering them
  • Drowned victims coming back to life when transported on a wagon over a bumpy road

3. 1740 Paris Academy of Science: Mouth-to-mouth resuscitation recommended for drowning victims

4. 1767 Amsterdam Society for Recovery of Drowned Victims

  • Advocated resuscitation by means of mouth-to-mouth breathing or use of bellows
  • Utilized "fumigation" to stimulate the victim with orally or rectally insufflated tobacco smoke

5. 1903 George Crille, a surgeon, introduced the technique of external cardiac compression

6. 1950-1973 Various techniques for artificial resuscitation

  • Back pressure technique (victim prone, resuscitator straddles the victims's thighs and rhythmically applies pressure to the lower rib cage
  • Holger-Nielsen back pressure plus arm lift with resuscitator straddling the victim's head

7. 1954 James Elam reported that expired air was adequate to maintain adequate oxygenation

8. 1964-1963 cardiopulmonary resuscitation was developed under the auspices of the American Heart Association headed by Leonard Scheris

9. 1973 to present National Conferences on CPR and ECC approximately every four years with refinement of techniques and simplification of applications. Items such as rhythms, exchanges of rescuers, ABCs (airway, breathing, cardiac compressions), activation of the ERS ( Emergency Response System), advanced life support and pediatric advanced life support qualifications, and use of the AED ( Automated Electrical Defibrillator). Heimlich maneuver for expelling foreign objects reported in 1974

10. 2010 American Heart Association Guidelines with CAB (chest compressions, airway, and breathing) management, nearly uniform rates, simplified exchanges of rescuers, improved AEDs, and higher quality training manikins.

The unconscious SCUBA diver imposes additional challenges.If the diver is unconscious on the surface, measures as just described are appropriate. Inflating the buoyancy compensator (BC) and ditching gear in the water will lessen the exertion required by the rescuer to bring the victim to shore or the diving platform. More controversial is the management of the SCUBA diver who is found unconscious on the bottom. Three different “schools of thought” exist for handling this challenge:

First Option: Replace the regulator in the victim’s mouth, gain control of the head with the head carry (as has been taught in Red Cross lifesaving and water safety courses), cradle the head on the rescuer’s chest while extending the victim’s neck, then perform a slow swimming ascent aided, possibly, by improving buoyancy through judicious inflation of the rescuer’s BC. Once on the surface, the measures described for the near-drowning victim found on the surface are employed.

Second Option: Swim the victim to the surface with or without ditching the SCUBA tanks and regulator by grasping the victim’s BC straps with or without improving buoyancy with the rescuer’s BC. A variation of this is placing the rescuer’s second stage octopus regulator into the victim’s mouth before ascending.

Third Option: Swim the victim to the surface with or without ditching the victim’s gear by grasping the victim’s fins and letting the head dangle in the downward position during the ascent. Again, inflation of the rescuer’s BC can be used to improve buoyancy.

We advocate the head control option for several reasons. With head control and neck extension of the unconscious victim, there is less chance of an arterial gas embolism occurring during ascent from retained air in the lungs whose egress is blocked by the flexed neck. Should the unconscious victim still execute agonal respiratory efforts, the regulator in the mouth may prevent aspiration of water. Finally, should spontaneous breathing resume during the ascent process, the regulator will provide an air supply and allow resumption of oxygen delivery to the brain and other tissues.

Unconscious SCUBA divers using closed circuit re- breathers (CCR) present additional challenges.33 Should water enter the breathing circuit, its reaction with the soda lime in the carbon dioxide scrubber will cause the breathing mixture to become caustic, which could cause severe respiratory system injury if breathing is resumed. Because of the special techniques utilized for CCR SCUBA, additional hazards must be considered.2 These include seizure from oxygen toxicity and loss of consciousness from hypoxia. If the patient is seizing, is it recommended that ascent not be initiated until the seizure has ended.33 With blackout from hypoxia breathing efforts may continue, so it is important that an air supply be maintained for the victim during ascent. The supply would preferably be from the open circuit pony bottle that CCR divers are recommended to carry. Finally, because of the ability for long, deep dives with CCR, it is likely that a decompression obligation or manifested decompression sickness will occur once the victim is brought to the surface. This possibility must be considered in the definitive management of the victim, as will be discussed in the next section.


Definitive Management of near-drownings

After the unconscious diver is at a medical center advanced life-support measures are initiated, or if already started, continued with intubation, artificial ventilation, and intravenous fluids. If no spontaneous heartbeat or breathing is present on arrival at the emergency department, the prognosis for recovery is bleak. A decision to pronounce the victim dead may be made by a physician at that time. However, if the period of immersion was relatively short, that is to say 60 minutes or less, and the victim is markedly hypothermic, rewarming while continuing advanced life support should be considered.7 When normothermic, a decision to continue life support measures should then be made. Medications as indicated are administered, e.g., anti-arrhythmic medications for irregular heart- beat, steroids if aspiration is apparent on chest x-ray, antibiotics if lung infection is a concern (the victim was in polluted water), and sedatives/paralyzing agents if the victim is resisting the ventilator. Blood tests and x-rays will help in decision making for management at this stage.

Once advanced life-support measures are established, it is necessary to decide whether hyperbaric oxygen (HBO) recompression is needed. If decompression was omitted or arterial gas embolism is likely, HBO recompression should be started as soon as possible. Another consideration (which is controversial) is whether to use HBO for brain resuscitation for the anoxic brain insult. If HBO is to be used as an adjunct for acute ischemic brain in- jury, the decision must be made jointly by the family, the attending physician, and hyperbaric medicine specialist.

A retrospective study that reviewed hospital ad- missions for drownings reported that 100 percent recovery was observed if the victim arrived in the emergency department with an intact heartbeat. However, if in-hospital cardiopulmonary resuscitation (CPR) was required, 47 percent of the patients died, 33 percent had residual neurological deficits, and 20 percent had full recovery.34
Comment: The target group for the acute use of hyperbaric oxygen treatments is, of course, the 33 percent group that has residual neurological deficits. Two problems arise with deciding which group requiring in-hospital CPR should receive HBO treatments. first, the group that has residual neurological deficits might not be readily identifiable for hours or days after the restoration of heart function as a result of anoxic insult-related or medically induced coma. Second, if the acute use of HBO is to be effective for brain injury, it needs to be started during the “golden period,” which is thought to be in the two to six hour range after the time of the anoxic insult.

As soon as the near-drowning victim has stabilized, decisions for subsequent management are required. If the person is recovering well, rehabilitation is started for residuals of the neurological injury. If the victim remains in a persistent vegetative state, typical interventions in preparation for transfer to a long-term care facility include tracheotomy, percutaneous endoscopic gastrostomy tube placement, management of contractures, and prevention of pressure ulcers. The prognosis for recovery depends almost entirely on the severity of the anoxic brain injury, and the electroencephalogram may be helpful for determining long-term prognosis. Usually critical care management can resolve the lung injury regardless of the severity of the brain injury. The off-label use of HBO for victims  of near-drowning who have serious residuals, but have plateaued with their rehabilitation, remains controversial.

The use of HBO in near-drownings (as well as with cerebral palsy and traumatic brain injuries) with significant residual brain morbidity has been anecdotally reported. HBO is used to try to mitigate the residual brain injury after recovery from the acute effects of the anoxic brain insult and after victims plateau with respect to rehabilitation efforts. Although some of the experiences with HBO are positive, the minimal functional changes we have observed have not materially affected the victim’s quality of life.
The justification for using HBO in these situations is that there are “idling” neurons in a penumbra zone of injury that regain function with HBO treatments coupled with angiogenesis into the sites resulting in sustained oxygenation of the neurons previously impaired by hypoxia.35
Other controversies of using HBO include the number of treatments that are ideal, which range from 14 (angiogenesis effect) to 100 or more; depths of treatments that range from 1.5 atmospheres absolute (16 FSW) to 2.5 ATA (45 FSW); and whether repetitive series of treatments have benefits.

Favorable Prognostic Signs in Victims of Near-drowning

A number of favorable prognostic signs have been associated with near-drownings. First, the shorter the period of immersion, the better the victim’s prognosis. Szpilman et al. reported that the risk of severe neurological impairment after hospital discharge was 10 percent if the period of immersion were zero to five minutes, 56 percent if six to ten minutes, 88 percent if eleven to twenty-five minutes and nearly 100 percent if greater than twenty- five minutes.7 Other favorable prognostic indicators include immersion in water temperatures less than 50°F, a core temperature of less than 95° F, young age, and time to effective BLS less than 10 minutes.6 Victims of near-drownings who arrive in the emergency department with a spontaneous heartbeat have better than a 50 percent chance of survival, whereas those without spontaneous cardiac activity have less than a 12 percent chance of survival.7 Factors that complement the diving reflex, such as absence of panic, young age, hypothermia, and avoidance of extremity movements, also favor survival. If the victim is alert at the time of the arrival to the emergency department, the chance of survival without neurological residuals approaches 100 percent.23 Other factors that favor a good prognosis at the time of arrival at the emergency department include the female gender, absence of aspiration, time to basic life support of less than 10 minutes, blood pH greater than 7.1, blood glucose greater 112 mg percent, Glasgow Coma Score greater than 6, and the presence of the pupillary response.6

Myths and Unresolved Questions about Near-drownings and Drownings

1. Precise definitions that are established by experts should always be used for a victim who has experienced a loss of consciousness in the water.

Comment: We advocate simplicity; “drowning” if the victim is dead and “near-drowning” if alive after recovery and resuscitation efforts. However, the severity of residual neurological injury in near-drowning ranges on a continuum from none to persistent vegetative state (Figure 1).

2. Drowning, is a sufficient diagnosis for anyone who has lost consciousness in the water.

Comment: As mentioned before, “never say drowned.” It sounds like a paradox to acknowledge this adage, but then use the term drowning. The message is that the underlying cause of the loss of consciousness in water needs to be ascertained, be it from decompression illness, breathhold blackout, cardiac arrest, seizure, trauma, etc. The cause dictates the optimal management for the near-drowning treatment.

3. Usually near-drownings and drownings occur in the absence of risk factors.

Comment: An analysis of the circumstances surrounding the drowning will usually identify underlying risk factors that lead to the loss of consciousness such as a heart attack from coronary artery disease, excessive hyperventilation leading to blackout, viola- tion of decompression practices, etc. (Table 1).

4. All victims of near-drowning, even if asymptomatic, need to be observed for 24 hours before discharge from the medical center where initially evaluated.

Comment: Although delayed onset of pulmonary edema may occur within the first 24-48 hours after the near-drowning event, if the patient is asymptomatic with normal ventilatory functions observation in the hospital setting is not necessary. However, at discharge the patient and/or family should be aware of delayed onset of pulmonary edema associated with near-drowning and instructed to return the patient to the medical facility immediately if shortness of breath, cough, or other respiratory symptoms occur.

5. The primary concern in near-drownings is the management of the respiratory insult.

Comment: Although adequate ventilation is essential for recovering the victim, management of the possible anoxic brain insult must not be over- looked. Whereas respiratory function will inevitably recover, the neurological injury is more likely to be irreversible.

6. If the period of loss of consciousness while immersed is greater than four minutes, resuscitation efforts should not be initiated.

Comment: Although death of brain neurons occurs after four minutes of anoxia, with intact heart function oxygen physically dissolved in the blood is still being delivered to the brain. This is complemented by the diving reflex, which is initiated by immersion. This prolongs survival and promotes full recovery after immersion exceeding four minutes. In addition, hypothermia can slow metabolism and reduce brain oxygen demands.

7. In the USA children's near-drownings are usually in open waters such as lakes and oceans.

Comment: In the USA, the most common cause of near-drownings and drownings in children occurs when they fall, unwitnessed, into a backyard swimming pool, which is an event typically associated with families affluent enough to have swimming pools. “Water safe” in a child does not guarantee that with clothes, shoes, and possibly restrictive garments on, he/she can swim to safety. Pediatricians have said that the only safe thing to fill a backyard pool with is sand! In third world countries, drownings are usually from play activities in (usually polluted) rivers.

8. In most near-drownings and drownings no water enters the lungs due to the laryngospasm reflex.

Comment: Although the laryngospasm reflex is very profound, and one of the last to be lost with impending death, in 85-90 percent of near-drownings and drownings water is aspirated. This qualifies the drowning as a “wet” type. Even small amounts of aspirated water can alter pulmonary functions and require critical care management.

9. Autopsies of drowning victims always have pathognomonic findings.

Comment: Often autopsies of drowning victims demonstrate no specific findings for the cause of death. Aspiration of sea water may show diatoms in the lung tissues. Heart disease can be confirmed by atherosclerosis of coronary arteries, but deaths from arrhythmias are usually undiagnosable. Thoracic squeeze injury can show edema and blood in the alveoli.

10. Near-drownings and drownings associated with SCUBA diving need not be managed any differently than the problems from other causes.

Comment: Special training and techniques are needed to manage SCUBA divers found unconscious on the bottom. Once at a medical center,   a decision needs to be made as to whether hyperbaric oxygen recompression is needed for omitted decompression and/or arterial gas embolism in addition to the usual advanced life support measures.


The management of near-drowning has made note- worthy advancement in both basic life support as well as advanced life support. Unfortunately, the human only has limited reflexes/responses to the hypoxic insult associated with immersion in contrast to almost all of the other stresses associated with diving. The diving reflex and induced hypothermia by the surrounding water environment are the limited responses the body has to deal with the anoxic immersion stress. Although lung function is usually recoverable with advanced life support interventions, neurological injury is often not recoverable. Consequently, attention to rescue and management must always be directed to preventing anoxic brain injury. Usually, underlying causes lead to unconsciousness in the water, hence, “never say drowned” as the cause. Rather, seek the underlying cause and remember that seemingly miraculous recoveries have occurred after recovering a victim from a presumed drowning. This directs treatment interventions from heart attack management to recompression treatments and from observation only for delayed effects of the immersion to physical therapy. Finally, the best measure for near-drownings and drownings is prevention through water safety and diving knowledge. In no water activities is this truer than in SCUBA and breath-hold diving.


  1. Strauss MB, Miller SS. Stresses in SCUBA and breath- hold diving. Part I: Introduction and physical stresses. Wound Care & Hyperbaric Medicine. 2014; 5(1):16- 28 Available from: cals-and-subscriptions/wchm.html
  2. Strauss MB, Miller SS. Stresses in SCUBA and breath-hold diving. Part II: Physiological stresses. Wound Care & Hyperbaric Medicine. 2014; 5(2): 16-28. Available from:
  3. Strauss MB, Covington D, Miller SS. Stresses in SCUBA and breath-hold diving. Part III: Psychological stresses. Wound Care & Hyperbaric Medicine. 2014; 5(3): 16-28. Available from: http://www.bestpub. com/periodicals-and-subscriptions/wchm.html
  4. Strauss MB, P-NJ Le, Miller SS. Stresses in SCUBA and breath-hold diving. Part IV: The No Panic Syndromes. Wound Care & Hyperbaric Medicine. 2014; 5(4):10-27. Available from:
  5. Papa L, Hoelle R, Idris A. Systematic review of definitions for drowning incidents. Resuscitation. 2005; 65(3):255-64.
  6. Golden FSC, Tipton MF, Scott RC. Immersion, near- drowning and drowning. Br J Anesthesth. 1997; 79:214-25.
  7. Szpilman D, Joost JLM, Bierens MD, et al. Drowning (Current Concepts Review Article). N Eng J Med. 2012; 366:2102-10.
  8. van Beeck EF, Branche CM, Szpilman D, et al. A new definition of drowning: towards documentation and prevention of a global public health problem. Bull World Health Org. 2005;83(11):853-6.
  9. Orr D. A Review of SCUBA diving fatalities. Paper presented at: Undersea and Hyperbaric Medical Society Meeting, Gulf Coast Chapter. September, 2014.
  10. Orlowski JP. Drowning, near-drowning and ice-water drowning. J Am Med Assoc. 1988;260:390-1.
  11. Nemiroff MJ, Salz GR, Weg JG. Survival after cold-water near-drowning: the protective effect of the diving reflex. Am Rev Respir Dis. 1977;115:145.
  12. Benson RC, Shubeck F, Deutschberger J, et al. Fetal heart rate as a predictor of fetal distress: A re- port from the collaborative project. Obs Gyn. 1968, 32:259-66.
  13. Rekers G. Susan Smith: Victim or murderer. Centennial: Glenbridge Publishing Ltd; 1995. P. 12, 16.
  14. Wikipedia, the Free Encyclopedia. Waterboarding [Internet]. 2015. Available from: waterboarding
  15. Driscoll TR, Harrison JA, Steenkamp M, Review of the role of alcohol associated with recreation aquatic ac- tivity. Inj Prev. 2004, 10:107-13.
  16. Strauss MB, Busch JA, Miller SS. SCUBA in older aged divers. Wound Care and Hyperbaric Medicine. 2013; 4(3):27-37.
  17. Fock AW. Analysis of recreational closed-circuit re- breather deaths 1998-2010. Diving and Hyperbaric Med. 2013; 43(2):78-85.
  18. Keatinge WR. Accidental immersion hypothermia and drowning. Practitioner. 1977,219:183-7.
  19. Pearn JH. Secondary drowning in children. British Medical Journal. 1980; 281:1103-5.
  20. Slade JB Jr, Hattori T, Ray CS, Bove AA, Cianci P. Pulmonary edema associated with scuba diving. Case reports and review. Chest, 2001; 120:1686-94.
  21. Strauss MB, Wright PW. Thoracic squeeze diving casualty. Aerosp Med. 1971; 42:673-5.
  22. Swann HG, Brucer M, Moore C, Vesien BL. Fresh water and sea water drowning: A study of the terminal cardiac and biochemical events. Texas Rep Biol & Med. 1947;6:423-38.
  23. Modell JH. Pathophysiology and Treatment of Drowning. Springfield: Charles C. Thomas; 1971.
  24. Conn AW, Montes JE, Barker GA, Edmonds JE. Cerebral salvage in near-drowning following classification by triage. Can Anesth Soc J. 1980; 27:201-10.
  25. Strauss MB, Hart GB, Miller SS, et al. Mechanisms of hyperbaric oxygen. Part 1 primary: hyperoxygenation and pressurization. Wound Care and Hyperbaric Medicine. 2012;3(3):27-42
  26. Strauss MB, Hart GB, Miller SS, et al. Mechanisms of hyperbaric oxygen. Part 2 secondary: tissue consequences of hyperoxygenation and pressurization. Wound Care and Hyperbaric Medicine. 2013; 3(4):45-63.
  27. Burt JT, Kapp JP, Smith RR. Hyperbaric oxygen and cerebral infarction in gerbils. Surg Neurol. 1987; 24:265-8.
  28. Sunami K, Takeda Y, Hashimoto M, Hirakawa M. Hyperbaric oxygen reduces infarct volume in rats by increasing oxygen supply to the ischemic periphery. Crit Care Med. 2000; 28:2831-6.
  29. Wada K, Nishi D, Kitamura T, et al. Hyperbaric oxygen therapy enhances the protective effect of moderate hypothermia against forebrain ischemia. Undersea Hyperbaric Med. 2006;33-399-405.
  30. Strauss MB. Physiological aspects of mammalian breath-hold diving: A review. Aerospace Med. 1970; 41:1362-1481.
  31. Andersen HT. Physiological adaptation in diving vertebrates. Physiol Rev. 1966; 46:212-43.
  32. March NF, Matthews RC. New Techniques in external cardiac compression: aquatic cardiopulmonary resuscitation. J Am Med Assoc. 1980; 244:1229-32.
  33. Mitchell SJ, Bennett MH, Bird N, et al. Recommendations for rescue of a submerged unresponsive compressed-gas diver. Undersea Hyperbaric Med. 39:1099-1108.
  34. Oakes DD, Sherck JP, Maloney JR, Charters AC. Prognosis and management of victims of near-drowning. J Trauma. 1982; 22:544-49.
  35. Neubauer RA, Gottlieb SF, Kagan RL. Enhancing “idling” neurons. Lancet. 1990;335:542.

About the Author


Dr. Michael B. Strauss has been “brain- washed” about near-drowning and drowning since taking his first Red Cross Junior Life Saving Course in 1948 from his father, a self-learned “professor” of swimming-related activities. From his mother, a high school graduate genius, he was cautioned about  risk taking in water activities such as never to swim hard after eating a big meal (a subject for another paper). In medical school Dr. Strauss remembers being tested on the differences (now anathema) between fresh and salt water drownings. Later, in his associations with Dr. Ronald Samson, who worked with Dr. Jerome Model, he learned of the hypoxemic/loss of consciousness insults of water immersion. Then from Dr. George Hart, his “mentor of all mentors,” he learned about the mechanisms of hyperbaric oxygen and how they can mitigate hypoxic insults. Finally, Dr. Thomas Asciuto, a hyperbaric medicine colleague and critical care specialist, “fine-tuned” him on the contemporary understanding of the pathophysiology and management of near- drownings. Consequently, these mentors and colleagues deserve special recognition for the genesis of this article.



Phi-Nga Jeannie Le, MD  is  fellowship  trained and board certified in  Undersea  and Hyperbaric Medicine. This is her first of many planned collaborations with the prolific Dr. Strauss. For Dr. Le, any collaboration with the experts and teachers at the Long Beach Memorial Medical Center Hyperbaric Medicine Program is a continuation of lifelong education in  the  specialty  of  undersea and hyperbaric medicine that began at the University of Pennsylvania. Though total physical undersea submersion herself is not her passion—nor will her middle and labyrinth of the ear permit such activity—the clinical science and advancement of the field is. Dr. Le enjoys being the one on the surface taking care of the intrepid land mammals who get themselves into trouble playing sea creatures.



Stuart S. Miller, MD is the associate medical director and director of education of the Hyperbaric Medicine Department at Long Beach Memorial Medical Center. He is board certified in Emergency Medicine and fellowship trained/board certified in Undersea & Hyperbaric Medicine. He has co-authored over 40 articles, posters, and book chapters on hyperbaric medicine, wound care, and diving medicine. He has given numerous lectures and is the course director for undersea and diving medicine CME conferences. He has been an avid SCUBA diver for over 25 years.



Contact Us

Best Publishing Company
631 US Highway 1, Suite 307
North Palm Beach, FL 33408

This email address is being protected from spambots. You need JavaScript enabled to view it.



Copyright © 2018 Best Publishing Company, a company of WCHMedia Group, Inc | All rights reserved
Find more information at