TRANSPORT MEDICINE 0031-3955/93 $0.00 + .

20

DROWNING AND
NEAR-DROWNING
Daniel L. Levin, MD, Frances C. Morriss, MD,
Luis O. Toro, MD, Lela W. Brink, MD,
and Gary R. Turner, MD

Several different terms used in this discussion of near-drowning and

drowning need to be defined initially to avoid later confusion. 30. 49
Drowning: Death from asphyxia while submerged or within 24 hours of submersion.
Near-drowning: An episode of sufficient severity to warrant medical attention for the
victim that may eventually lead to morbidity and mortality.
Drowning without aspiration of water: Death from respiratory obstruction and asphyxia
while submerged in water or within 24 hours of submersion.
Drowning with aspiration of water: Death within 24 hours from changes secondary to
aspiration of water while submerged.
Near-drowning without aspiration: Survival of a victim, at least temporarily, after
suffering asphyxia from submersion in water.
Near-drowning with aspiration: Survival of a victim, at least temporarily, after submer-
sion in and aspiration of water.
Secondary drowning: Death from complication~ after submersion (e.g., adult respiratory
distress syndrome [ARDS], pneumonia, neurogenic pulmonary edema) more than 24
hours after the drowning that is directly attributable to submersion.
Immersion syndrome: Sudden death, probably vagally mediated, due to cardiac arrest
after contact with cold water (coincident use of drugs such as alcohol or sedatives may
contribute to pathogenesis of this syndrome).
Submersion injury: Any submersion resulting in hospital admission or death (e.g.,
near-drowning, drowning, spinal cord injury).
Save: Water rescue or removal of victim from water by someone who perceived
individual to be a potential victim of submersion injury.

INCIDENCE AND EPIDEMIOLOGY

The incidence and epidemiology of near-drowning and drowning in chil-

dren less than 19 years of age is not specifically a pediatric intensive care unit/

From The University of Texas Southwestern Medical Center (DLL, FCM, LOT, LWB);
and Children's Medical Center of Dallas (DLL, FCM, LOT, LWB, CRT), Dallas, Texas

PEDIATRIC CLINICS OF NORTH AMERICA

VOLUME 40 • NUMBER 2 • APRIL 1993 321

322 LEVIN et al

transport subject, but because these events are largely preventable they are
worthy of discussion. Approximately 6000 non-boat drownings, 1200 boat-
related drownings, 500 motor vehicle-related (submerged) drownings, and
1000 drownings of undetermined intent or suicide occur annually in the United
States. 1, 2, 11, 18, 20, 25, 36, 42, 43, 51, 53 Drowning in children is a worldwide problem
occurring in every area of the globe. 3, 16, 18, 24, 25, 28, 36 It has been a problem since
medieval times, and it is distressing that it continues as such. 17 When one
realizes that near-drownings are three to five times as frequent as drownings
and, it is estimated, there are 10 times as many saves as drownings, it is easy
to understand why near-drowning and drowning are problems of epidemic
proportions. The United States Consumer Product Safety Commission
(USCPSC) estimates that in 1985, 3000 children less than 5 years old were
treated in hospital emergency departments because of submersion accidents in
residential pools. Approximately 235 children less than 5 years of age drowned
in swimming pools in 1983. The number of pool drownings is roughly the
same as the number of poisoning deaths (245) recorded for the same age
group in 1969 before the enactment of the poison prevention packaging act.'2
Approximately 85% of the deaths are in male subjects, with a maximum in-
cidence in the 10- to 19-year-old age group (Fig. 1). In the adolescent age group,
drowning represents the third most common cause of death overall and is
second only to motor vehicle injuries as a cause of accidental death. The bi-
modal nature of the curve in Figure 1 represents the peak risks for 1- to
2-year-olds and again for older male teenagers, but the complete absence of a
second peak in female subjects suggests a sex-related etiology among male
victims.
In the pediatric intensive care unit at Children's Medical Center, Dallas,
Texas, from July I, 1975, through December 31, 1991, 248 victims less than 19
years of age were seen (Table 1). Of them, 200 (81%) were 5 years of age or

1000

800
0
0
0
0
0
0 600
0
...
Q)
a.
Ul
~

iii
Q)
c

o------~----~----~----~~
o 20 40 60 80
Age of Victim
Figure 1. Drowning rate in the United States, 1977-1979, for males (top line) and females
(bottom line). (From Spyker DA: Submersion injury. Pediatr elin North Am 32:113-125,
1985.).
 DROWNING AND NEAR-DROWNING 323

Table 1. NEAR-DROWNING PATIENTS IN CHILDREN'S MEDICAL CENTER

PEDIATRIC INTENSIVE CARE UNIT
Known Cases
Near- of Severe Brain
Year Drownings Expired Damage
1975 (July to December) 3 1
1976 8 4
1977 4 3
1978 11 4
1979 4 2
1980 11 4 1
1981 12 4 1
1982 14 4 1
1983 21 8 3
1984 20 6 3
1985 23 7 3
1986 26 7 6
1987 23 8 4
1988 25 9 2
1989 15 4 1
1990 10 8 1
1991 17 3 2

Total 248 86 (35%) 28(11%)

younger (Fig. 2). Overall, 35% died and 11 % suffered severe neurologic residua,
many of whom eventually died. This experience is similar to that reported in
most major centers in the United States, Canada, England, Australia, and New
Zealand.
The USCPSC undertook a prospective analysis of near-drowning and
drowning events in eight counties (five in southern and northern California,
one in Arizona, two in Florida) between May 1 and September 3D, 1986.42 There
were 142 near-drownings and drownings in children less than 5 years of age
during this 5-month study, making it easy to accept that drowning is the
number one leading cause of accidental death in children less than 5 years of
age in California, Arizona, Florida, and Texas and the third overall cause in
the United States. The incidents in young children mostly occur in private
swimming pools (Table 2), regardless of geographic location. 19 Although
drownings can occur in any (even a small) body of water,>3, 47, 49 the leading
identified cause for this astounding rate of accidents is the lack of an ade-
quate barrier for small children between their own homes or yards and the
pool. 12, 13, 16, 38, 40, 41, 49, 52 These children are not intruders; they are drowned in
their own pools or in the pools of friends or relatives in whose homes they
are invited guests. The accidents occur more frequently in warm weather but
can occur any month of the year (Fig. 3). There is a predominance of male
over female victims even in younger victims, and female victims are almost
missing from the later peak period because the later peak is related to water
sports, boating, the daredevil syndrome, voluntary hyperventilation, and,
most especially, alcohol. For victims brought to the hospital, there is a high
morbidity-mortality ratio compared with other forms of accidental injury re-
quiring medical attention.
324 LEVIN et al

MS

Number of Patients
o. . . • 10 • • • • 20 • • • • 30 . • • • 40 • • • • 50 • • •
0-6 MOS_

7-12 Mos
13-18 Mos

19-24 Mos
2 Yrs
3 Yrs
4 Yrs
5 Yrs
6 Yrs

----
7 Yrs
8 Yrs
9 Yrs
10 Yrs
11

12

13
Yrs
Yrs
Yrs ---
14

15
Yrs
Yrs

-
Figure 2. Age of near·drowning victims, Children's Medical Center, Dallas, Texas (1975-
1991).

PATHOPHYSIOLOGY

The Drowning Episode

Several pathogenic mechanisms of death can occur while a drowning victim
is submerged." 26. 31. 38 Brain death, the common final pathway, may be caused

Table 2. LOCATION OF NEAR-DROWNING ACCIDENTS, JULY 1,1975, TO

DECEMBER 31,1991, CHILDREN'S MEDICAL CENTER PEDIATRIC INTENSIVE CARE
UNIT
Number of
Location Patients
Pool 164 (66.1%)
Lake 21 (S.4%)
Bathtub 22 (S.S%)
Bucket 6 (2.4%)
Hot tub 10 (4.0%)
Toilet 2 (O.S%)
Miscellaneous/unknown 23 (9.3%)
Total 24S
 DROWNING AND NEAR-DROWNING 325

Number of Patients
o • • • • 10 • • • • 20 • • • • 30 • • • • 40 • • • • 50 • • • • 60
Jan _

Feb •
Mar
Apr
May
Jun
Jul
Auq
Sep
Oct
Nov
Dec

Figure 3. Month of near-drowning accidents, Children's Medical Center, Dallas, Texas

(1975-1991).

by cerebral hypoxia, carbon dioxide narcosis, laryngospasm, pulmonary re-

flexes, or vagally mediated cardiac arrest (Fig. 4). Whereas drowning is
technically death due to submersion in water and aspiration of water, the latter
three causes of death are due to submersion alone without aspiration of water.
The volume of water aspirated or swallowed may be large or small, and
the depth of water may be shallow. Laryngospasm may occur, and hypoxia

Dr"!"...,.......,o.

Cerebral CO 2
Hypoxia

Brain
Death
Figure 4. Pathophysiology leading to brain death in drowning victims.
326 LEVIN et al

may follow without the active aspiration of water in as many as 10% of victims.
This is probably caused by a small amount of water entering the larynx or
trachea and eliciting a reflex causing spasm.
When a sober victim is first submerged, a period of initial voluntary apnea
occurs (Fig. 5). There may not be a struggle, but swimming movements occur.
Younger victims may simply sink to the bottom. In the younger age group
(less than 5 years), the diving reflex (Fig. 6) may be stimulated and make a
significant difference in survival. 7, 8,21, 30,45,48 Within seconds of the victim's face
touching cold water and before consciousness is lost, a reflex mediated by the
trigeminal nerve sends sensory afferent impulses to the central nervous system

Submersion

~ 1~ LarynqOB,..,

V01U"["" ..... 00, ..rcoBi.

Break Point

1
Voluntary Breathing -,----
(If conscious)
~ Aspiration
~
./
./
./
./
Secondary Apnea ./
./

l /
./
'/

Involuntary Gasping

1
Respiratory Arrest ----------~~~ Hypoxia --------'~~ Dysrythmia

Cardiac Arrest
t

Brain Death
1
Figure 5. Sequence of respiratory reflexes occurring in drowning.
 /colTter
DROWNING AND NEAR-DROWNING 327

Startle *
Response

Still Conscious Face

Tr,.LnAl
Nerve

1
CNS
(medUll~

Bradycardia
I ~ Shunting of
Blood from
Skin and viscera

tSABP / \

Cerebral Coronary
Circulation

Improved
Survival
Figure 6. The diving reflex .• = May be absent in infants taught to "swim" or be waterproofed
at early age.

(eNS) medullary respiratory center, which causes bradycardia and shunting of

blood from cutaneous and splanchnic vascular beds to the cerebral and coronary
circulations (i.e., the diving reflex). Systemic arterial blood pressure increases
as well. These reflex changes are independent of peripheral chemoreceptors
and baroreceptors and are augmented by progressively colder water tempera-
tures and the startle response. Infants who are taught to swim at a young age
("waterproofing") and who are not afraid of the water may lack a startle
response and may be at greater risk for near-drowning. The victim can hold
his or her breath voluntarily until the break point is reached, as determined by
the oxygen and carbon dioxide levels (peripheral and central chemoreceptors,
respectively). The break point is when an individual takes an involuntary
breath, which occurs at Paco2 levels of 51 mm Hg and Pao2 of 73 mm Hg after
87 seconds at rest in normal human volunteers.
After voluntary hyperventilation the break point can be prolonged to 140
seconds (paco2 , 46 mm Hg, and PaoZ, 58 mm Hg) at rest and 85 seconds
(paco 2, 49 mm Hg, and PaoZ, 43 mm Hg) with exercise. The break point may
not occur while the victim is conscious if he or she has voluntarily hyperven-
tilated to low Paco2 values before submersion and hyperventilation is followed
by exercise (underwater swimming). Hypoxia may cause loss of consciousness
before activation of carbon dioxide receptors causes voluntary breathing move-
ments.31
328 LEVIN et al

Within seconds of the first submerged breaths, secondary apnea occurs

and, if followed by involuntary gasping under the water lasting for several
minutes, respiratory arrest follows. Dysrhythmias occur due to hypoxia, and
eventually cardiac arrest and brain death occur. Once aspiration of fluid takes
place, metabolic acidosis and systemic arterial hypertension persist even if the
victim is saved or pulled from the water.
How long hypoxia can be tolerated by an individual victim is a frequently
asked question. It depends on many factors, including the age of the victim,
previous health, water temperature, and promptness and effectiveness of the
rescue effort.5, 6, 20, 32, 33, 35 Young victims usually survive if submersion is less
than 3 minutes and up to 10 minutes in water 10° to 15°C. Survival after longer
submersions (15 to 20 minutes) is occasionally reported, and even longer times
of up to 40 minutes rarely are compatible with eventual recovery from near-
drowning in cold water (0° to 15°C). Although the effect of surface cooling in
young children (large body surface area-mass ratio) and core cooling due to
aspiration and swallowing of cold water may play some role in patient survival
after prolonged submersion by decreasing cerebral metabolic rate, an active
diving reflex with bradycardia and shunting of the circulation to the cerebral
and coronary circulations may be the most significant factors in survival rather
than a decrease in cerebral metabolic rate. The importance of moderate hypo-
thermia (33°C) of the brain in preventing brain injury is becoming increasingly
understood, however. 10 In older victims, cold water may inhibit effective
swimming movements in even accomplished swimmers and induce vagally
mediated cardiac dysrhythmias and coma in individuals with a body tempera-
ture less than 34°C.

Aspirated Fluid

Victims may aspirate fresh water or salt water and foreign matter either
from the water itself or as stomach contents. Although the salinity of sea water
varies, it usually has 34.48 g/kg (3.5%) of dissolved salts, of which 29.54 g/kg
(2.9%) is sodium chloride. 31 The Dead Sea in Israel is, for example, much
different in both the quantity and nature of its salts. Fresh water also contains
some salts and organic material. The contents of spas, bathtubs, cleaning pails,
toilets, lakes, rivers, ponds, and stagnant water must be analyzed to know
what the victim has aspirated.
After the victim inhales sea water, the hypertonic fluid pulls water from
the circulation into the lungs, resulting in fluid-filled but perfused alveoli
(pulmonary edema). Pulmonary surfactant is washed out. The victim develops
hypovolemia and greater amounts of sea water inhalation (> 11 mLlkg) and
blood volume can decrease to as little as 65% of the normal.
Aspiration of fresh water can cause an increase in blood volume because
the hypotonic fluid is absorbed into the circulation when large amounts of fluid
are aspirated. Surfactant is altered in a combination with regional hypoxia and
intrapulmonary shunt, leading to systemic hypoxemia that causes reflex pul-
monary arterial vasoconstriction, myocardial depression, and an alteration of
pulmonary capillary permeability. These events all lead to return of fluid to the
lung and sudden pulmonary edema (Fig. 7).
Drowning victims seen alive in hospitals rarely have aspirated enough
fluid to cause life-threatening changes in blood volume, although pulmonary
edema is common. For the same reason, hospitalized victims of either sea
water or fresh water accidents rarely have electrolyte disturbances (Table 3).
 DROWNING AND NEAR-DROWNING 329

Fresh water
Aspiration

Surf.ctant
Altered
~ ~"'ionalHypoXi'
Intrapulmonary
Shunt

Absorption into
Circulation

Atelectasis

t
1
Circulating
Blood Volume

Systemic
/ H y p o X••lo
Systemic
Hypoxemia

Pulmonary Arterial
Vasoconstriction

+Capillary
Pulmonary
PeJ:meability

Myocardial ~
Depression ~

Pulmonary Edema
Figure 7. Pathophysiology of pulmonary edema formation in near-drowning victims.

Table 3. USUAL LABORATORY VALUES AFTER NEAR-DROWNING

Sea Water Fresh Water
Range Mean Range Mean
Sodium 132-160 147 mEq/L 126-146 137 mEq/L
Potassium 3.2-5.4 4 mEq/L 2.6-6.3 4 mEq/L
Chlorine 96-127 106 mEq/L 88-116 98 mEq/L
Hemoglobin 14.8 g/dL 14.2 g/dL
Hematocrit 43% 44%

Modified from Modell JH: Drowning. In Staub NC, Taylor AE (eds): Edema. New York, Raven
Press, 1984, pp 679-693; with permission.
330 LEVIN et al

Victims of sea water near-drowning would be expected to have hemoconcen-

tration and victims of fresh water near-drowning to have hemodilution, but
they do not. Fresh water near-drowning victims should have hemolysis with
hyperkalemia and plasma-free hemoglobin, although hyperkalemia is rare. An
increased level of endogenous catecholamines even causes kaliuresis, and serum
potassium levels are usually decreased. Plasma-free hemoglobin levels are
usually less than 500 mg/dL and are not believed to cause renal dysfunction
from plugging of tubules.

Pulmonary Pathophysiology

The pulmonary pathologic events include increased peripheral airway

resistance; variable degrees of laryngospasm; reflex pulmonary vasoconstriction,
leading to pulmonary hypertension; decreased lung compliance; fall in venti-
lation-perfusion ratios; fluid shifts across the alveolar membrane; surfactant
loss (salt water) or alteration in its properties (fresh water); foam and froth
production; and anatomic changes in alveolar epithelial cells. 15, 31, 38
When fluid is aspirated, a reflex via vagal efferents causes obstruction of
the peripheral airways. The reflex is predominantly mediated through osmo-
lality rather than volume of fluid; therefore its occurrence is more prominent
with fresh water inhalation. Small volumes of fresh water (1 mLlkg) can cause
pulmonary vasoconstriction and result in pulmonary hypertension. Larger
volumes of fluid (2.5 mLlkg) lead to vascular perfusion of nonventilated alveoli,
and combined with loss or inactivation of surfactant, alveolar collapse and
pulmonary hypertension result in decreased lung compliance. Within minutes
of aspiration of small amounts of fresh water, an intrapulmonary shunt due to
perfusion of nonventilated areas can increase from the normal 5% to 18% to as
much as 75%. Although young victims may appear normal clinically within
minutes or hours of the event, it may take days for the intrapulmonary shunt
to return to pre-event levels.
As mentioned previously, fresh water moves across the endothelial and
capillary membranes into the circulation, and plasma moves in the opposite
direction, drawn by the hyperosmolality of sea water in alveoli. Surfactant is
washed out by sea water and altered by fresh water. The airways may become
obstructed by laryngospasm, bronchoconstriction, foam, mucus, inhaled foreign
material, and stomach contents.

Neurologic Pathophysiology

Metabolic acidosis and hypoxemia rapidly alter the blood-brain barrier,

and even if the patient is saved at this point, cerebral edema occurs. Edema
causes hemispheric swelling and shifts of brain across compartments (hernia-
tion). The edema probably does not cause brain cell injury but is an indication
of the extent of the original and any subsequent hypoxic episodes. If the
hypoxia is severe enough, brain death occurs. 21,22,34,35,50
Neurologic residua include prolonged unconsciousness with subsequent
recovery (rare, but more likely when event occurred in cold water), blindness,
electroencephalographic changes, dilation of ventricles due to brain atrophy,
and persistent coma, leading to death (more usual in patients with prolonged
coma). We have treated two patients who developed cortical blindness after
near-drowning but eventually recovered their vision.
 DROWNING AND NEAR-DROWNING 331

Cardiovascular Pathophysiology

The cardiovascular system in children is remarkably stable.z9 Most victims

have healthy hearts that can be resuscitated after prolonged periods of ischemia.
Electrocardiographic (ECG) changes, primarily bradycardia or asystole, can
occur. Some victims may have ventricular fibrillation and need cardioversion
during resuscitation. Systemic arterial blood pressure may be normal, high, or
low, depending on oxygenation, acid-base balance, cardiac function, peripheral
vascular resistance, the level of circulating endogenous and exogenous cate-
cholamines, and elevated intracranial pressure (ICP).

Renal Pathophysiology

Renal function is usually normal, but albuminuria, hemoglobinuria, oli-

guria, and anuria can occur. The dysfunction is probably due to ischemia rather
than tubular damage from free hemoglobin.

PREDICTABILITY OF OUTCOME

When the victim is first seen, predicting the outcome is extremely difficult.20,
22,24,32,34, 35 No one finding (pulselessness, apnea, fixed and dilated pupils,
duration of event, water temperature) reliably predicts outcome; therefore all
victims who are submerged for an unknown length of time, except those with
putrification, should receive cardiopulmonary resuscitation (CPR), This position
has been questioned recently.33 When admitted to the emergency department,
although certainty of outcome is still difficult to predict, those victims who are
pulseless, apneic, or flaccid and comatose have a high likelihood of dying or
surviving with extreme neurologic residua. Patients admitted to the pediatric
intensive care unit with apnea and signs of increased ICP have a high likelihood
of death or survival with severe neurologic residua. Patients who are awake or
have blunted awareness or responsiveness but who are not comatose have an
excellent chance of survival with full recovery.

MONITORING AND LABORATORY TESTS

Monitoring of the victim at the accident site includes checking for the
presence of pulse, respirations, purposeful movement, and color.5, 26 In the
ambulance or emergency department, heart rate, ECG, respiratory rate, sys-
temic arterial blood pressure, temperature, Glasgow Coma Scale score, serum
electrolyte values, serum glucose and hematocrit values, and urinalysis must
be checked. A chest roentgenogram must be taken, and for those with CNS or
respiratory signs, arterial blood gas and pH values must be determined. The
possibility of concomitant injuries, especially to the head and neck, must be
considered.
In the pediatric intensive care unit mild to moderately involved patients
must be observed for signs of respiratory distress from aspiration of water or
stomach contents and for signs of neurologic complications such as head
trauma, seizures, or increased ICP. Severely involved victims almost certainly
need intubation and assisted ventilation. In addition, they need placement of
a central venous pressure catheter, arterial catheter, bladder catheter, nasogas-
332 LEVIN et al

tric tube, and rarely, a pulmonary artery catheter for treatment of severe
persistent pulmonary edema or decreased cardiac output.
The need for ICP monitoring is quite controversial. Some authors 8 , 114
believe that although ICP can be monitored and even treated, monitoring and
treatment do not alter outcome, and all victims with elevated ICP have a poor
outcome with either death or severe neurologic residua. Others8 have noted
that some victims with no measured increase in ICP also have a poor outcome
and therefore, ICP monitoring need not be done in any victims. Others 34 , 46
believe that elevated ICP in combination with calculated cerebral perfusion
pressure is highly predictive of a poor outcome and that it should be monitored
for that reason. Still other authors 30 argue that although those patients with an
elevated ICP have a uniformly poor outcome because the treatment of increased
ICP necessitates interventions that may be harmful, especially for the brain,
these interventions should not be used in the absence of a documented increase
in ICP. Thus, according to this position, all patients who are severely involved
must have ICP monitored. Because none of these statements is based on a
prospective, randomized clinical trial, however, we believe that the subject is
unresolved and still awaits such a study.

TREATMENT

In the Field

Cardiopulmonary resuscitation must be given as quickly as possible. 5, 33

The one most devastating aspect of the drowning episode is hypoxemia, and
mouth-to-mouth or mouth-to-nose ventilation must be given promptly, even
in the water if necessary. All parents, child care personnel, and pool owners
or supervisors should be certified in CPR. Supplemental oxygen must be given
to all victims as soon as possible until it is proved that they no longer need it.
Rescuers need to be cognizant of possible head and neck injuries and of the
necessity for preventing aspiration of stomach contents. Once trained personnel
arrive, bag and mask ventilation with proper positioning of the jaw and tongue,
use of supplemental oxygen, and, on occasion, tracheal intubation may be
needed. Inserting an intravenous catheter may be necessary for administration
of fluids and medications (e.g., sodium bicarbonate, epinephrine) at the site,
although epinephrine may be given intratracheally if the patient is intubated.
Intraosseous infusion of fluids and medications is another route to consider.
Rarely, cardioversion for defibrillation is needed in the field.

In the Emergency Department

All patients must be given oxygen until it is proved that they no longer
need it by chest roentgenogram, arterial blood gas and pH determinations, or
noninvasive pulse oximetry. All patients must have their stomach contents
removed, particularly if they are not completely awake or lack intact protective
airway reflexes. Because victims can swallow large amounts of fluid, they may
vomit and aspirate the stomach contents even when they are neurologically
intact; prolonged hospitalization for ventilatory care or even death can result
from such an episode. All victims need to have their head and neck assessed
for concomitant trauma. Severely affected patients may continue to need
 DROWNING AND NEAR-DROWNING 333

advanced cardiac life support, intubation and ventilatory assistance, and cardiac
support with inotropic and vasoactive agents.

Transport

Several issues are of major concern when it is necessary to transport a

victim from a referral center to a tertiary care center. Heart and respiratory rate
monitoring need to continue en route, and a large bore intravenous catheter
needs to be in place. Health care personnel should provide sufficient inspiratory
oxygen to assure a peripheral oxygen saturation of greater than 90%. If the
patient is intubated, one should make certain of the proper position of the tip
of the endotracheal tube and of the absence of pneumothorax. The endotracheal
tube also should be secured. An ideal situation is the documentation of an air
leak around the endotracheal tube when 20 cm H 20 positive pressure is applied
to the tube. Patients with near-drowning, especially those with aspiration of
stomach contents, are at risk for pneumothorax, and this needs to be considered
if the patient should suddenly deteriorate during transport.
In intubated or neurologically depressed patients a nasogastric tube must
be placed and the stomach contents evacuated. If wheezing is present, adequate
suctioning of the endotracheal tube should be done and bronchodilators can
be used.
Isotonic fluids at a rate sufficient to maintain a normal systemic arterial
blood pressure for age should be given, but fluid restriction for cerebral edema
must be kept in mind. Early use of inotropic agents such as dopamine or
dobutamine may maintain adequate cardiac output without administering
excessive fluids and aggravating cerebral injury.
Other measures for cerebral protection subsequent to hypoxia that can be
administered during transport include adequate oxygenation and oxygen carry-
ing capacity; sufficient alveolar ventilation; use of an osmotic diuretic and
sedation and neuromuscular blockade in a patient believed to have a cerebral
hypoxic-ischemic insult who is struggling and may increase intracranial pressure
by effort; valsalva maneuvers; and increased systemic arterial blood pressure.

In the Pediatric Intensive Care Unit

Pulmonary Management
Pulmonary managemenF6 is a primary factor early in the course of treat-
ment. As mentioned previously, oxygen must be supplied at a rate sufficient
to maintain Sao 2 greater than or equal to 90% even to awake patients until it is
proved they no longer need it. For severely involved patients, positive end-
expiratory pressure is helpful in increasing lung volumes, decreasing oxygen
requirements, and improving systemic oxygenation. Assisted mechanical ven-
tilation is necessary in patients with severe pulmonary edema and evidence of
acute respiratory failure or aspiration pneumonia and for patients with a
pronounced CNS injury (e.g., Glasgow Coma Scale score < 8) with seizures or
neurologic depression.
Prophylactic use of broad-spectrum antibiotics for pneumonia is not indi-
cated, although the high likelihood of aspiration of Pseudomonas in hot tub and
spa victims makes use of antipseudomonal agents in these patients seem
rational. Prophylactic use of corticosteroids for treatment of pulmonary com-
plications has no support whatsoever according to properly performed studies.
334 LEVIN et al

Ongoing management of the pulmonary complications depends on the

patient's condition. In a few patients the pulmonary disease secondary to
aspiration is a major problem, but in most children the lungs improve rapidly,
and neurologic complications are the main problem. In those patients with
significant major lung disease but a reasonable choice for neurologic recovery,
extracorporeal membrane oxygenation has been used successfully by us as well
as others to treat the pulmonary insufficiency!

Neurologic Management
Neurologic complications can be devastating, with approximately 35% to
40% of young victims in most large pediatric centers dying with brain death
and 10% surviving with severe neurologic residua. As indicated previously,
monitoring and management of ICP is a major and controversial subject,
specifically because no prospective randomly controlled studies exist about its
efficacy. If one should choose to measure ICP and calculate CPP, progressive
use of measures, including positioning, hyperventilation with mechanical
ventilation, and osmotic and loop diuretics, is indicated to maintain an ICP
less than 20 mm Hg and CPP greater than 50 mm Hg. There is no evidence
that barbiturate coma or steroids for treating a patient with an elevated ICP are
of any benefit for improving outcome.
Short-acting barbiturates interfere with white blood cell function and
increase the risk of infection. Induced hypothermia not only lacks evidence for
benefit in these patients but its use may actually be harmful because it increases
the risk for infection as a result of an alteration in white blood cell function.
Seizures must be treated in a routine fashion. Hypovolemia can be corrected if
the usual colloid-crystalloid considerations are kept in mind. Electrolyte abnor-
malities and renal failure rarely are specific problems.
Determination of brain death in these patients, as in most, may be difficult,
but because they represent a growing and important source for human organ
donation and transplantation, a specific and rigorous protocol for brain death
must be available and followed from early in the course of treatment.

CONCLUSION

Prevention is more desirable than therapy, and this is particularly true in

near-drowning and drowning in young children. 39 Use of effective barriers with
self-closing, self-latching doors and gates, pool safety covers and house door
opening alarms, for residents, invited guests, and intruders may prevent 70%
to 80% of these incidents in children under 5 years of age. Some authorities
question the accuracy of these estimations. 37 The complexities of human
attitudes and behavior" make the debate over the effectiveness among use of
voluntary safety measures, education of the public, and strict safety legislation
including barrier (isolation) fencing a vigorous and acrimonious one. 27, 37, 44, 54

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Address reprint requests to

Daniel 1. Levin, MD
Pediatric Intensive Care Unit
Children's Medical Center of Dallas
1935 Motor Street·
Dallas, TX 75235