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Immersion, near-drowning and drowning


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or death. However, pulmonary complications may follow aspiration of water without cessation of breathing or loss of consciousness. Thus “near-drowning” should be defined as “survival, at least temporarily, after aspiration of fluid into the lungs”. The importance of the distinction between the two definitions is that aspiration of fluid may lead to later pulmonary complications, even in those
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British Journal of Anaesthesia 1997; 79: 214–225
Immersion, near-drowning and drowning
F. S
C. G
, M. J. T
R. C. S
“Drowning” is defined as “suffocation by
submersion, especially in water”
; it continues to be
the third most common cause of accidental death in
the general population and, for children in many
countries, the second most common cause after road
In the USA, 40% of drowning victims
are less than 4 yr old.
In Britain, the Office of
Population Census reports that child deaths from
this cause continue to be the third most common
cause of accidental death after road accidents and
Near-drowning is defined as “survival, at least
temporarily, after suffocation by submersion in
We would challenge this definition as most
dictionaries define “suffocation” as cessation of
breathing leading to unconsciousness or death.
However, pulmonary complications may follow
aspiration of water without cessation of breathing or
loss of consciousness. Thus “near-drowning” should
be defined as “survival, at least temporarily, after
aspiration of fluid into the lungs”. The importance of
the distinction between the two definitions is that
aspiration of fluid may lead to later pulmonary
complications, even in those without a history of loss
of consciousness, and thus care must be exercised in
the management of all patients with a history of
aspiration. Modell, Graves and Ketover reported
that in dogs, aspiration of as little as 2.2 ml/kg body
weight produced a decrease in
aP to approximately
8 kPa (60 mm Hg) within 3 min. Pulmonary
surfactant is altered locally by water in the alveoli
resulting in pulmonary shunting via either fluid-filled
(salt water) or atelectatic (fresh water) alveoli.
stated that within minutes after inhalation of
as little as 2.5 ml/kg body weight, the normal
intrapulmonary shunt of approximately 10% may
increase to as much as 75%. Even victims who are
conscious, alert and outwardly clinically normal after
a near-drowning incident may take several days to
revert to pre-immersion values.
After aspiration of
either fresh or salt water there may be delayed
outpouring of fluid into the alveoli, secondary to
pulmonary parenchymal damage with transuda-
tion of protein rich fluid, so called secondary
(Br. J. Anaesth. 1997; 79: 214–225).
Key words
Drowning. Hypothermia. Heart, cardiopulmonary bypass.
Heart, resuscitation. Immersion.
77 82
with consequent impairment of gas
exchange. Orlowski
cited several cases who
appeared normal on assessment in the emergency
department, even with normal chest x-rays, but who
developed fulminant pulmonary oedema as long as
12 h after the near-drowning incident.
While statistics on the incidence of drowning
deaths are available for most nations, there are no
precise data for near-drowning incidents, although
in the USA they are estimated to be 500–600 times
more common than their fatal counterpart.
Britain, a comprehensive hospital survey for the
years 1988–1989 by Kemp and Sibert
of 330
drowning and near-drowning incidents in children
reported 142 deaths and 188 survivors.
One of the great tragedies of drowning or near-
drowning is that the victims, frequently young, are
generally in good health before the unexpected event
which resulted in death or brain damage in a number
of survivors. In recent years increased public aware-
ness of the general principles of basic life support
and cardiopulmonary resuscitation (CPR) has
resulted in many more near-drowning victims
arriving in hospital in a state capable of being
resuscitated. The many contemporary reports in the
literature of apparently hopeless cases being success-
fully resuscitated, particularly after cold water
11 20–22 38 45 53 54 59 85 86 102
has led to
protracted resuscitative efforts by hospital personnel.
Drowning and near-drowning have been the
subject of many reviews.
15 64 66 74 78 88
While resuscita-
tion and the subsequent respiratory management of
the near-drowning patient is now well established
and largely non-controversial, the remaining major
therapeutic challenge is limitation of brain damage
in survivors with its associated consequent human
and economic costs. Although the success stories
tend to be reported, in the absence of full statistical
information it is difficult to obtain an overall picture
of the ratio of those who have been resuscitated and
left with or without residual brain damage.
The criteria used to identify those with a poor
prognosis needs to be refined. Some centres, based
on retrospective analysis, have reported their results
of various treatment regimens with suggested predic-
tive criteria for recovery without severe brain
34 53 68 74
Regrettably, these criteria are often
F. S
C. G
, M. J. T
Robens Institute, University of Surrey, Guildford, Surrey GU2
5XH. S
R. C. S
Royal Navy, RH Haslar, Gosport, Hants PO12 2AA.
Immersion, near-drowning and drowning 215
conflicting and thus of little real value other than to
act as a reminder that long-term complications occur
and caution should be exercised in discussing prog-
nosis with relatives in the early stages. One of the
problems appears to be that, although the protective
role of hypothermia is now generally recognized, it is
not always possible to determine from deep body
temperature on arrival at hospital what the cerebral
temperature was before severe hypoxia developed.
This review examines the physiological considera-
tions of accidental immersion and discusses the
factors which may influence outcome. The recom-
mended management of such victims is also
reviewed, with particular emphasis on the role of
cardiopulmonary bypass.
Physiological considerations
The physiological effects of immersion in
thermoneutral water have been reviewed previously
by Epstein.
In sum, changes which occur are
largely a consequence of the effects of the external
hydrostatic pressure on the resilient body tissues and
gas-containing body cavities during head-out
immersion. This results in physiological alterations
in the cardiovascular and respiratory systems, and in
the gastrointestinal tract. The increase in venous
return causes a 32–66% increase in cardiac output,
increase in right to left shunting as a result of a
combination of pulmonary pooling, cephalic move-
ment of the diaphragm and, to a lesser extent, minor
compression of the chest wall; overall there is a 65%
increase in the work of breathing. The central shift
in blood volume is sensed by the body as
hypervolaemia and results in diuresis, natriuresis
and kaliuresis.
From a practical viewpoint there is little evidence
that these changes cause respiratory or circulatory
embarrassment in a healthy individual.
during rescue, after protracted immersion in warm
water, or relative shorter immersion in cold water
when hypothermia may be present, circulatory
collapse and cardiac arrest may occur. This
phenomenon, which has been termed “circum-
rescue collapse” is considered to be outside the
scope of this article and has been reviewed
The increase in right atrial pressure, resulting from
reflex peripheral cold vasoconstriction after
immersion in cold water, is additive to the hydro-
static pressure effect described above and enhances
urinary output by as much as one-third.
of more importance to the accidental immersion
victim are a group of cardiorespiratory reflex
responses which can occur on sudden immersion in
cold water and last for approximately 2–3 min.
These responses, collectively known as the “cold-
shock” response, have been reviewed by Tipton.
They are initiated by a rapid decrease in skin
temperature and are probably responsible for the
majority of near-drowning incidents and drowning
deaths after accidental immersion in open waters in
the UK. Respiratory drive is enhanced on immersion
in water colder than 25 C
and is inversely related
to water temperature, reaching a maximum level
with immersion in water at 10 C.
The response
includes an initial “gasp” of 2–3 litre in an adult, fol-
lowed by uncontrollable hyperventilation which can
result in a 10-fold increase in minute ventilation
which significantly reduces
The inspiratory
shift in end-expiratory lung volume after cold water
immersion can result in tidal breathing within 1 litre
of total lung capacity, creating a sensation of
dyspnoea. This, coupled with the swim stroke/
respiration asynchrony caused by hyperventilation,
makes swimming very difficult, and is believed to be
one of the major causative factors in the mechanism
of cold-water swim failure.
The maximum breath-hold times of normally
clothed individuals are reduced to less than 10 s.
As a consequence, on immersion in choppy or
turbulent water where the airway may be intermit-
tently submerged, there is a significant chance of
aspiration during the first few minutes. Breath-
holding to facilitate escape from a submerged vehicle
may be equally difficult and result in entrapment
and drowning, or possibly near-drowning in
those who manage to escape or are rescued before
a lethal volume of water is aspirated, approximately
22 ml kg
Thus in healthy young people, who may be
competent swimmers but unhabituated to cold, the
initial respiratory responses to immersion in cold
water may cause short-term incapacitation which
could prevent them from relaxing and swimming a
short distance to save their lives. In turbulent water,
or if escape from a submerged vehicle is necessary,
the inability to breath-hold for more than 10–20 s
may result in aspiration and near-drowning, or even
The initial cardiovascular responses to cold
immersion include an immediate intense reflex
peripheral vasoconstriction, 42–49% increase in
heart rate and 59–100% increase in cardiac output,
with a resulting increase in arterial and venous
pressures. These responses significantly increase the
workload of the myocardium and, coupled with the
concomitant increased catecholamine response,
5 16 48
may induce undesirable cardiac arrhythmias.
Additionally, in middle-aged or elderly people
with heart disease, hypertension or vascular disease,
the initial cardiovascular responses to immersion in
cold water may precipitate a cardiovascular accident.
It is considered that this mechanism as a cause of
incapacitation resulting in drowning is probably
underestimated. The eyewitness reports of the
sudden cessation of movement in some drowning
is more suggestive of sudden circulatory
malfunction. The fact that aspiration may occur
subsequent to a cardiovascular incident may
mislead some into concluding that drowning was
the only problem requiring treatment or the cause of
Given the above, it is perhaps less surprising
to discover that 60% of the annual open water
216 British Journal of Anaesthesia
immersion deaths in the UK occur within 3 m of a
safe refuge, and two-thirds of those who die were
regarded as “good swimmers”.
Hypothermia”, defined as a deep body temperature
:35 C,
is an inevitable consequence of protracted
immersion in cold water and appears to play an
important role in the successful outcome of those
who have survived prolonged submersion. The
mechanism of how deep body temperature is
reduced so rapidly in some of these victims is less
The rate of change of core temperature in an
immersed body is dependent on the inter-relation-
ship of several physical and physiological factors
such as water temperature, relative movement of
water adjacent to the skin, body surface area to mass
ratio, insulation, peripheral circulation, metabolism
or conditions which may affect any of these factors
(e.g. injury, intoxication, etc).
With continued body cooling, consciousness
becomes progressively impaired until it is lost at a
deep body temperature of approximately 30 C.
Cerebral blood flow decreases in proportion to the
reduction in metabolism,
while Stone, Donnelly
and Frosbese
reported a 6–7% reduction for each
decrease in core temperature of 1 C; cerebral
activity is abolished at brain temperatures less than
22 C.
However, these data relate to anaesthetized
patients in whom shivering was controlled. In
victims of accidental immersion in cold water whose
airway is being maintained clear of the water by a life
jacket, shivering is pronounced with a resulting
increased production of carbon dioxide, at least in
the early stages, until body temperature decreases to
approximately 29 C. Should ventilation be impaired
however, shivering is depressed or even absent while
hypercapnia produces cerebral vasodilatation which
increases cerebral perfusion.
With further cooling, in spontaneous breathing
adults, cardiac arrest from ventricular fibrillation
(VF) may occur at a deep body temperature :28 C,
or asystole at approximately 24–26 C.
with surface cooling, when core temperatures
decrease to 35–33 C, skeletal muscle temperatures
are usually at or below 28 C when neuromuscular
performance is significantly impaired, making swim-
ming or other actions necessary for survival
extremely difficult.
Therefore, it is likely that most
immersion victims, excepting those wearing a life
jacket with a “spray hood”,
aspirate water as con-
sciousness becomes impaired (i.e. as core tempera-
ture decreases to less than 34 C) and thus well
before significant protection from cerebral hypoxia is
In spite of the ability of cold water to extract heat
from the immersed body, hypothermia per se is
unlikely to be a problem within 30 min of head-out
immersion for a healthy, clothed adult, even in water
as cold as 5 C. The normal physiological responses
to cold reduce heat transfer by mass flow (circula-
tion) to the surface from the deeper tissues and
increase shivering heat production by as much as
As a general rule, however, in spite of
these responses, during head-out immersion in
laboratory conditions, deep body temperature of the
average adult wearing outdoor clothing has fallen to
35 C after approximately 1 h in water at 5 C, 2 h in
water at 10 C, and 3–6 h in water at 15 C.
In open
water however, because of the rich supply of blood
vessels to the scalp which do not vasoconstrict in the
cold, heat loss from the unprotected head may be
enhanced by forced convection and evaporation
thereby increasing the rate of body cooling consider-
ably. Similarly, if the head is immersed the rate of
body cooling is significantly faster.
Because of their greater surface area to mass ratio
and reduced subcutaneous fat content, cooling rates
of immersed children are also significantly faster
than those seen in adults. However, with surface
cooling alone, even in children, rates for decrease in
body temperature are too slow to cool the brain suf-
ficiently to protect it from the hypoxia encountered
in drowning asphyxia. In anaesthetized naked
infants, being surface cooled for surgery with ice
packs and ice cold water, rectal temperatures
decreased by as little as 2.5 C in the first 10 min of
the procedure, and it took 32.5 min for it to reduce
to 24–25 C.
Thus if cerebral hypothermia is the
mechanism through which some children can
survive protracted submersion without sustaining
lasting hypoxic neurological damage, an alternative
method of heat exchange to surface cooling alone
must be found.
To date it has been postulated by several
23 29 33 59 71 78 86
that the “mammalian diving
response”, either alone or in combination with
may be the explanation.
The diving response, characterized by apnoea,
generalized marked peripheral vasoconstriction and
18 23
is initiated reflexly by stimulation of
the ophthalmic division of the trigeminal nerve on
immersion of the face in cold water. It plays a
powerful role in oxygen conservation in diving
animals, enabling some to remain submerged for
periods in excess of 30 min. The response is
enhanced by both anxiety and cold water. The
magnitude of the diving response found in humans is
qualitatively similar to that found in diving
mammals, but quantitatively less marked, with the
cold-shock response predominating in the majority
of normally clothed adults.
Nevertheless about
15% of people do show a profound reaction
this percentage increases with the use of specialist
protective clothing, such as immersion “dry” suits,
which prevent rapid cooling of the cutaneous
thermal receptors of the majority of the body, but
leave those of the face exposed to the cold stimulus.
Tipton, Kelleher and Golden
have reported that in
such circumstances, where the cold-shock and
diving responses are stimulated in roughly equal pro-
portions, the resulting fluctuation in the competing
parasympathetic and sympathetic chronotropic
influences to the heart frequently (in 31 of 36
immersions) caused a variety of cardiac arrhythmias
Immersion, near-drowning and drowning 217
(predominantly supraventricular) just after the
cessation of breath-holding in cold water.
The diving response is also reported to be more
marked in infants than adults.
Gooden, in his
excellent review,
argued that while the diving
response alone is unlikely to explain the reported
survival of those cases of protracted submersion in
cold water, it does play a contributory role together
with hypothermia. He hypothesized that survival
from prolonged near-drowning appears to depend
on a specific interplay between the diving response
and hypothermia, resulting in a protective state of
“hypometabolism”. Peripheral vasoconstriction,
associated with both the diving response and cold,
depresses tissue metabolism and thus reduces body
oxygen requirements. Gooden postulated that
immediately on face immersion the diving response
apnoea prevents water aspiration into the lungs.
Even if water does enter the larynx he postulated that
reflex glottal spasm prevents further penetration into
the lungs. The associated bradycardia and selective
redistribution of blood conserves oxygen stores
thereby protecting the brain from hypoxia during the
initial minutes of immersion. Gradually, with surface
cooling, hypothermia develops so that by the time
oxygen stores are depleted, cerebral metabolism
has been reduced to a level which confers some
protection from hypoxia.
While to some extent this hypothesis is plausible
there are several questions that remain to be
answered. First, why is it that in most cases of pro-
longed submersion who survived, sufficient water
was aspirated to cause near-drowning? It is possible
that aspiration, when it did occur, was a relatively
terminal event when the diving response, or
laryngospasm, could no longer be maintained
because of profound hypoxia. However, from our
understanding of surface cooling, discussed above, it
is probable that profound hypoxia is present before
significant brain cooling has occurred in this circum-
stance. Second, does the cold-shock response over-
ride the diving response in children as it does in
41 92
The only evidence in the literature
relating to children in this context is that of Ramey,
Ramey and Hayward
who found that children
could not hold their breath long enough for a diving
response to occur; in their experiment however, the
temperature of the water was 29 C, above that
normally associated with the initiation of the most
powerful diving response. Skin temperature of
children already playing in water is at or in the region
of the water temperature and thus, if they become
accidentally submerged, should not exhibit a cold-
shock response. However, those children who fall
into water without prior wetting should display a
cold-shock response. Finally, another factor mitigat-
ing against the “hypometabolism” hypothesis is the
large discrepancy in the rates of cooling reported
(varying from 10 C in 10 min in ice water
75 102
3.5 C in 6 min in a young adult
). Such rates of
cooling are not compatible with either surface cool-
ing alone or in combination with a diving response.
Thus while not ruling out entirely the participa-
tion of the diving response in the early stages of some
of these remarkable survival stories, it is considered
that the rapid rates of cerebral cooling encountered
may be largely dependent on pulmonary heat
exchange after aspiration.
After submersion, the victim may attempt to breath-
hold for as long as possible before neurogenic
afferents from the respiratory muscles or cutaneous
thermoreceptors build to an intolerable level, forcing
the individual to take a breath.
It has been shown
that voluntary breath-holding can be extended by
movements of the respiratory muscles, and swallow-
ing, against a closed glottis.
This may be the
explanation for the large amounts of water reported
to have been found in the stomach of some drowning
11 27 67 78
but not in others
(i.e. ingestion of
water is only likely to be found in those who
attempted to extend voluntary breath-holding).
Depending on the volume and temperature of the
water swallowed, heat exchange between the blood
and gastric wall could contribute significantly to
blood cooling, especially in children. When
continued breath-holding is impossible, aspiration of
water into the airways and alveoli occurs with
inspiration and possibly reflex coughing, provided
reflex laryngeal spasm does not supervene.
Regardless of the method of entry of cold water
into the core of the body, be it lungs, stomach, or
both, it precipitates a decrease in deep body
temperature. The magnitude of this decrease is
directly proportional to the volume of water
aspirated, its temperature differential with the body
and state of the circulation. However, to protect the
brain from hypoxic damage it would be necessary to
cool the brain very rapidly, at least 7 C in 10 min.
This doubles cerebral hypoxia survival time
even colder brain temperatures are required for
longer survival periods.
argues that, to explain some of the
remarkable survival stories reported, such a
mechanism of cooling lacks quantitative evidence.
On simple thermal physical principles of “methods
of mixtures”, he points out that “a (normal) person
would need to ingest an amount of ice-cold water
equivalent to 20% of body mass in order to reduce
the average body temperature to 30 C. Thus a child
weighing 20 kg would need to ingest approximately
4 litre of ice-cold water”. Such volumes of aspirated
water are not compatible with resuscitation
are they usually encountered in near-drowning
stated that it is unusual to
aspirate more than 200 ml but it is unclear how this
estimation has been determined, particularly as it
has been shown experimentally
that aspirated fresh
water is quickly absorbed and redistributed within
the body.
Gooden’s calculation, however, appears to be
based on the requirement for the entire body mass to
be cooled to 30 C. Using the same simple methods
of mixtures, the volume of ice water necessary to
cool the blood volume of a 20-kg child (approxi-
mately 1.6 litre) to 30 C would be approximately
300 ml. It is accepted that this is a gross over
simplification as the actual amount required to be
218 British Journal of Anaesthesia
aspirated to cool the brain would need to be in
excess of this because of the dynamic heat exchange
that would occur with the perivascular tissues and
perfused organs; in addition, pulmonary heat
exchange is reduced because of pulmonary shunting.
Nevertheless, given that a large proportion of the
cardiac output in a child in such circumstances (i.e.
with generalized peripheral vasoconstriction) is
diverted to the cerebral circulation, it is conceivable
that selective cooling of the brain occurs some time
before the general body mass equilibrates. Thus
aspiration of cold water may play a critical role in the
production of cerebral hypothermia and brain
survival in the submerged child or young adult of
relatively small body mass.
At first sight the volume of water required to be
aspirated would appear to be in conflict with
Modell’s conclusion that volumes in excess of 22 ml
are usually incompatible with life. This would
allow a maximum aspiration of 440 ml for a child
with a body mass of 20 kg. While this is more than
the theoretical 300 ml to cool the blood, as stated
above, larger volumes would in reality be required to
negate dynamic heat exchange with the perivascular
tissues and perfused organs. However, during the
drowning process, aspiration of water is unlikely to
occur in one single bolus but is more likely to be a
dynamic process with flushing of small volumes of
cold water in and out of the lung. Fainer, Martin and
demonstrated in dogs that rapid violent
respiratory movement continued for about 70 s after
submersion. It is proposed that with each tidal
volume of water aspirated, heat is exchanged but the
total volume retained in the lungs when respiration
ceases is significantly less than the total volume of
water which has entered and exited the lungs up to
that time.
This hypothesis is supported by a recent animal
experiment by Conn and colleagues
showed that aspiration of cold water produces
extremely rapid blood cooling; in lightly anaes-
thetized dogs, the mean carotid artery temperature
decreased by approximately 8.0 C in the first 2 min
of drowning, but only by 0.8 C in a control head-out
group of similarly shaved dogs; rectal temperature
lagged “considerably behind”. Regrettably the
experimental method did not make it possible to
estimate how much fluid had been aspirated in those
2 min. When the animals were killed after 10 min of
submersion, the volumes aspirated, estimated from
post-mortem weight changes, were considerably in
excess of the accepted lethal level of 22 ml kg
Incidentally, it is quite difficult to find the origin of
the value of 22 ml kg
quoted frequently by Modell
and others; in the original report by Modell and
the value appears to be 20 ml lb
, with
death caused by VF rather than irreversible
pulmonary damage.
The theory of water flushing in and out of the lung
rather than absorption of water as the primary cause
of the rapid cooling of blood on submersion is sup-
ported further by data from Conn and colleagues.
The marked decrease in carotid artery blood temp-
erature in dogs (average weight 9.2 kg) was 8.5 C
after 2 min in fresh water at 4 C and 7.5 C in salt
water; while over the remaining 8 min of the experi-
ment, mean carotid temperature decreased by
another 2.4–10.9 C in fresh water and by
3.1–10.6 C in salt water. Body mass increased by
1.5 kg (fresh) and 0.6 kg (salt) in the 10 min.
Although Conn and colleagues
reported that all
animals were tachypnoeic on immersion, the study
did not state when respiration ceased. In an earlier
experiment by Fainer, Martin and Ivy,
using 160
dogs, it was reported that violent respiratory
movement lasted approximately 71 s and thereafter
respiratory movement was limited to the occasional
agonal movement. Thus it would be fair to assume
that, in the experiment by Conn and colleagues,
most of the aspiration had taken place during the
2-min period showing the greatest decrease in
carotid temperature. Furthermore, if one assumes
no, or little, absorption in the salt water group in this
time, it suggests that in the equivalent fresh water
group, 7.5 C of the 8.5 C decrease in blood
temperature in the initial 2 min was caused by
flushing and 1.0 C by absorption of approximately
900 ml of fresh water.
Increasingly, hypothermia has been recognized as a
favourable prognostic indicator. However, the rate
of onset of hypothermia is clearly critical; to be of
benefit it must occur rapidly before profound
hypoxia develops.
Exposure to cold ambient conditions during
resuscitative procedures, while awaiting the arrival
of the ambulance, facilitates continued cooling if
adequate insulation is not provided. Furthermore,
thermoregulation in the hypoxic individual is likely
to be severely compromised. This, combined with
high evaporate heat loss from wet clothing and
increased conductive heat loss to the ground beneath
the supine patient, cause deep body temperature to
continue to decrease. By the time the victim arrives
at hospital, body temperature, in a patient with
intact circulation, may have decreased significantly.
Unless such a decrease occurs quickly, and before
hypoxia becomes severe, little useful cerebral
protection is provided.
Thus cooling which occurs during rescue and
transport to hospital is of little benefit and may
render deep body temperature on arrival in hospital
an unreliable prognostic indicator.
Rescue and treatment
Advice on rescue lies more correctly with rescue
organizations but a few important principles are
offered for consideration:
At all times it is important to ensure the safety of
the rescuer in addition to the casualty.
! Landing a casualty should never be delayed to
enable attempts at in-water resuscitation.
! Where possible, casualties wearing life jackets
whose airway is clear of the water should be
recovered in a horizontal attitude.
Immersion, near-drowning and drowning 219
! The possibility of cervical spine trauma should be
considered in unconscious victims rescued from
shallow water and appropriate measures and
techniques used.
Out-of-hospital management
It should be presumed that all near-drowning
victims rescued from UK open waters are hypoxic,
acidotic and hypothermic.
The primary aims of treatment of the near-
drowned are listed below in order of priority:
! Effective immediate relief of hypoxia. The speed
of achieving this has the greatest influence on
73 87
! Restoration of cardiovascular stability.
! Prevention of further heat loss.
! Speedy evacuation to hospital.
Airway patency and adequate ventilation should
be achieved rapidly. There is a significant risk of
regurgitation and aspiration of gastric contents
during resuscitation.
Tracheal intubation, if
indicated, should be carried out at the earliest oppor-
High fractional inspired oxygen
should be delivered using a self-inflating bag and
reservoir; if available, a positive end-expiratory
pressure (PEEP) valve set to 5 cm H
O should also
be used. Application of cricoid pressure during
EAR, or bag and mask ventilation, reduce the risk of
regurgitation and aspiration.
The use of the Heimlich manoeuvre in near-
drowning has been considered by the Emergency
Cardiac Care Committee of the American Heart
Association and is not recommended.
There is
insufficient evidence to support the claims that it is
effective in removing aspirated liquid. Additionally,
the manoeuvre itself may delay early intubation,
aggravate visceral or spinal injury, cause confusion
among rescuers with yet another procedure to
induce vomiting
and increase the risk of
precipitating an undesirable cardiac arrhythmia in
the hypothermic casualty rescued from cold water.
In the hypothermic near-drowning casualty,
because of the marked cold-induced peripheral vaso-
constriction, characteristically low volume and pro-
found bradycardia, peripheral pulses are notoriously
difficult to feel. Accordingly, the carotid artery
should be palpated gently for at least 1 min.
37 74
Extreme caution must be taken not to precipitate VF
by rough handling.
VF responds poorly to defibril-
lation at core temperatures less than 28 C; at this
temperature, Purkinje tissue looses its conduction
advantage over normal ventricular muscle fibres.
Nevertheless, it may be worth attempting, especially
in children, as some successes have been
88 100
However, even when sinus rhythm is
achieved at these temperatures it tends to be
unstable and revert easily to VF. If attempts at
defibrillation at less than 28 C are not immediately
successful they should be discontinued until cardiac
temperature increases to greater than 29 C.
The casualty should be insulated against further
heat loss and transported to the nearest emergency
department as rapidly as gentle handling allows.
Any life-support measures instituted at the scene
should be continued during transportation.
authors advocate immediate transfer of all severely
hypothermic and clinically lifeless patients to
the nearest facility with cardiopulmonary bypass
11 60
Hospital management
Near-drowning is an emergency: even those victims
who appear normal on arrival at hospital can
deteriorate rapidly.
An accurate, rapid initial
assessment of the victim is essential. A suggested
algorithm for subsequent management, based on
the classification by Simcock of near-drowning
is shown in figure 1.
Survival figures for victims of near-drowning are
very encouraging for those with a minimal reduction
in the Glasgow coma score (GCS) but much less
favourable for those with low scores.
34 74
Figure 1 A suggested algorithm for management of near-drowning, based on the classification by Simcock of near-
drowning victims.
ALS:Advanced life support.
220 British Journal of Anaesthesia
which have been associated with favourable outcome
are listed in table 1, but none, either individually or
in combination, has been shown to have absolute
predictive significance.
Therefore, full resuscitative
efforts should be attempted in all near-drowning
patients arriving in emergency departments.
Patients with no evidence of aspiration
Victims of near-drowning who appear normal in the
emergency department can deteriorate unexpect-
edly. All should be admitted to a general ward for a
period of observation, generally accepted to be a
minimum of 6 h.
Other authors, however, consider
it prudent to admit the victim for 24 h because of the
risk of late onset pulmonary and cerebral oedema.
75 87
It is recommended that the investigations listed
in table 2 are considered. Hypothermic patients who
are conscious and cooperative can be rewarmed in a
bath of warm water (40 C) until rectal temperature
has increased to 36 C. Arterial blood-gas values,
obtained while breathing air, and core temperature
must be normal before discharge. Signs of aspira-
tion, which may become manifest later, include
cough, tachypnoea, retrosternal discomfort, audible
crackles on auscultation of the chest, abnormal
arterial oxygen tension with the patient breathing air,
abnormal chest x-ray and fever.
Infection after immersion is common; usually this
is confined to the chest, although there are reports of
intracerebral abscess and septicaemia.
the benefits of prophylactic antibiotic therapy have
been questioned.
It is generally agreed that anti-
biotic therapy should be withheld until bacterio-
logical studies, or clinical examination, indicate
active infection.
Patients should be informed of the
potential seriousness of any pyrexial illness which
develops within a few days of discharge. They should
be advised to attend either their general practitioner
or return to the A&E department in such an event.
Patients with evidence of aspiration but without
ventilatory compromise
These patients may develop pulmonary oedema and
deteriorate precipitously. Accordingly, they should
be admitted to a high dependency (HDU) or inten-
sive care unit (ICU). Monitoring should include
continuous pulse oximetry and frequent arterial
blood-gas analysis. The onset of pulmonary oedema
is usually within a few hours of aspiration of water,
either fresh or salt, and can be rapidly progressive.
Continuous positive airways pressure (CPAP) sup-
port provided by a mask or nasal cannula (in infants
who are obligate, nasal breathers),
should be
offered in the first instance. The aim is to achieve an
arterial oxygen partial pressure
(a)P of more than 8
kPa with an
less than 0.5. If this is unsuccessful
the facility for tracheal intubation and intermittent
positive pressure ventilation (IPPV) with PEEP must
be available immediately.
Patients with ventilatory compromise or hypothermia,
or both
Patients who have clinical or investigative evidence
of inadequate ventilation must undergo tracheal
intubation and ventilatory support with PEEP.
This should be maintained at 8–10 kPa or at 10–12
kPa in those with ischaemic heart disease. Ideally,
F should be less than 0.5 and PEEP provided at
the lowest pressure consistent with minimizing
intrapulmonary shunt and achieving these aims.
74 87
All victims of near-drowning who are hypothermic
should be rewarmed in an ICU with continuous
Those who are cardiovascularly stable
may be warmed slowly but actively, at a controlled
rate of approximately 1 C h
. This can be achieved
using warmed humidified inspired gas, warmed i.v.
fluids, warming mattress/blanket or wrapping
exposed areas in dry woollen blankets. It is advisable
to consider rapid rewarming for any patient whose
core temperature is less than 28 C because of the
perilous state of the myocardium and its propensity
for ventricular arrhythmias below this temperature.
Patients who have an unstable cardiovascular system
or are in cardiopulmonary arrest should be warmed
more aggressively with consideration given to extra-
corporeal rewarming (ECR) using haemofiltration or
cardiopulmonary bypass (CPB).
47 98
Methods used to rewarm rapidly without ECR
include bladder irrigation, gastric lavage,
oesophageal heat interchanger,
pericardial lavage,
peritoneal dialysis,
thoracotomy and pleural
The easiest way to accomplish this in
most hospitals is peritoneal dialysis.
The dialysate
Table 1
Favourable prognostic indictors for near-drowning
Children 3 yr
Water temperature
Duration of submersion
5 min
10 min
No aspiration
Time to effective basic life support
10 min
Rapid return of spontaneous cardiac output
Spontaneous cardiac output on arrival in emergency
Core temperature
Minimum blood pH
Blood glucose
11.2 mmol litre
GCS: no coma on admission
Pupillary responses: present
Table 2
Suggested investigations for near-drowning patients
Arterial blood gas analysis
Urea and creatinine
Total creatinine kinase
Coagulation studies
Blood and tracheal aspirate for aerobic and anaerobic culture
Chest radiograph
Rectal temperature measured at least 15 cm from the anal
Drugs screen for overdose of:
Aspirin, etc
Immersion, near-drowning and drowning 221
(2 litre of potassium free) is warmed to 54 C so that
it enters the peritoneal cavity at 43.5 C, and hourly
cycles are preferred.
The advantages of ECR are rapid restoration of
normothermia up to 10.7 C h
reduction of high
blood viscosity found in hypothermia and, most
importantly, when bypass is used, there is reinstitu-
tion of perfusion regardless of cardiac rhythm
avoidance of “rewarming shock”. An additional
benefit is the ability to rapidly off-load ultrafiltrate in
the presence of overwhelming pulmonary oedema;
Norberg and colleagues removed 2300 ml in 1 h to
facilitate withdrawal from CPB.
Those in cardiopulmonary arrest
Full resuscitation must be attempted in accordance
with the Resuscitation Council (UK) guidelines and
an attempt made to rewarm the casualty to 33 C.
This may cause manpower problems when pro-
longed external chest compressions (ECC) are
required. Successful manual massage maintained for
a period of 4.5 h has been demonstrated,
Ireland and colleagues reported success after 5.5 h
using a “Thumper” cardiopulmonary resuscitator
system (Michigan Instruments Inc., Grand Rapids,
MI, USA) mechanical device.
The advantage of a
mechanical device is to ensure consistent effective
compression during rewarming thus maintaining an
adequate circulation to meet metabolic demands
and facilitate regular emptying of the heart during
Jones and Swan also recommend the use of
such devices in prolonged resuscitation.
Cardiopulmonary bypass
Rewarming by institution of emergency CPB has
been used with dramatic effect in severely hypo-
thermic casualties who were in full arrest,
11 43 47 49 98
many after submersion in cold water.
50 60 72 99
most notable of these was the neurologically intact
survival of a 2.5-yr-old girl who was trapped under
ice for 66 min.
The majority of reports describe partial bypass
from the femoral artery to femoral vein.
11 43 49 98
Norberg and colleagues described conversion to full
bypass to achieve faster flow rates and decompres-
sion of a dilating asystolic heart in a 7-yr-old boy
with a successful outcome.
Letsou and co-workers
suggested that full bypass using median sternotomy
is the method of choice.
There is also a report of
successful resuscitation in one of two hypothermic
adult casualties using a modified dilatational/
Seldinger technique to apply percutaneous CPB via
the femoral veins, with a portable pump and
paediatric oxygenator.
CPB provides fast
rewarming of the core, maintains tissue perfusion
and oxygenation while assisting the cold and
inefficient heart to regain normal electromechanical
The advocates of median sternotomy claim that
exposure and cannulation of the aorta and right
atrium is faster than dissection and cannulation of
the femoral vessels in the pulseless patient, and that
flow rates are faster. There may also be advantage in
having access to the heart for massage, defibrillation
and decompressive venting of a cold and dilating
A survey of members of the American
Association of Thoracic Surgeons and the Southern
Thoracic Surgical Association in the early 1980s
produced evidence of 174 cases of hypothermia
rewarmed with CPB with a survival rate of 45%.
review of the literature in 1994
analysed data from
68 hypothermic patients undergoing CPB. In
reports describing attempted resuscitation of two or
more cases the survival rate was 50%; if case reports
and singletons were included the rate improved to
60%. VF was associated with greater survival than
asystole, but the difference (73% vs 52%) was not
significant. Walpoth and colleagues also noted that
documented VF had a favourable outcome with
CPB in hypothermia.
Eighty percent of survivors
returned to their previous level of function. The
recommendations of that review were that CPB
resuscitation is advised for hypothermic patients in
arrest and for those with core temperatures less than
25 C, irrespective of rhythm; patients in a stable
rhythm of 25–28 C can be treated with CPB or con-
ventional warming methods.
The maxim nobody
is dead until warm and dead” should always be
borne in mind.
Cessation of resuscitative efforts
Hyperkalaemia in severely hypothermic patients is
usually indicative of asphyxial cardiac arrest before
significant cooling occurred.
A potassium concen-
tration in excess of 10 mmol litre
is not compatible
with successful resuscitation
39 84
and is advocated for
use in the triage of avalanche victims.
Hypoxic encephalopathy is probably the most
debilitating of the consequences of near-drowning.
The majority of flaccid, comatose victims admitted
to the ICU suffer either severe cerebral injury or
cerebral death. Early prediction of outcome requires
accurate determination of the nature and extent of
neurological injury; it is also fundamental for patient
management. In children, there are four distinct
outcomes: full recovery, neurologically impaired
survival, persistent vegetative state and death.
Cerebral resuscitative efforts to reverse the changes
of hypoxic damage and reperfusion injury have rarely
been successful.
66 74
Poor outcomes are especially
likely when ICP 920 and CPP :60 mm Hg, despite
One USA source
cited by Orlowski
that one-third of all near-drowning survivors were
moderately to severely brain damaged. The progno-
sis for children in the UK appears to be similar: of
188 hospital resuscitations of near-drowning
patients reported by Kemp and Sibert,
33 had
fixed dilated pupils on admission to hospital; of these
13 died, 10 had severe residual neurological defects
(spastic quadriplegia) and 10 recovered fully. A
recent report from Seattle
found an unfavourable
outcome in patients who were comatose on admis-
sion: of 72 admissions there were 38 deaths, 14 in a
222 British Journal of Anaesthesia
vegetative state, three with dependent neurological
impairment, six with mild neurological impairment
and 11 discharged normal. The Australian experi-
ence was similar: 31 admissions with cardiac arrest
of whom 17 died and six survived with severe spastic
This could be related to the warmer
waters found in the Brisbane area. This view is
supported by the Canadian experience
prolonged in-hospital resuscitation and aggressive
treatment of near-drowning victims who initially had
absent vital signs and were not hypothermic
(933 C), resulted either in eventual death or an
increase in the number of survivors with a persistent
vegetative state.
A prognosis score for paediatric near-drowning
victims has been derived by Orlowski.
It is based
on five indicators: age younger than 3 yr, maximum
submersion estimated longer than 5 min, post-
rescue delay in resuscitation for greater than 10 min,
coma at time of admission to hospital and initial pH
less than or equal to 7.1.
Neurological classification of 101 paediatric
drowning and near-drowning victims based on the
level of consciousness, as assessed by GCS, has been
used for prognostic purposes.
GCS:5 predicted a
high-risk group of patients with 80% mortality or
permanent neurological sequelae. In general, 2–6 h
after the accident, patients who remain decorticate,
decerebrate or flaccid fair poorly; patients who are
improving at this time, but remain unresponsive,
have a 50% chance of doing well, while those who
are showing definite signs of improvement (alert,
stuporous or obtunded but responding to painful
stimuli) generally do well and most have a normal or
near normal outcome.
A recent article by Kreis and
suggested that the most accurate
method of predicting neurological outcome is by
magnetic resonance spectroscopy (MRS): their
spectroscopic prognosis index distinguished between
good (n:5) and poor (n:11) outcome, with one
false negative after a borderline MRS result, and no
false positive results (100% specificity).
It is generally agreed that hypothermia is neuro-
logically protective, especially in children, although
Kruus and co-workers concluded that a core
temperature of less than 30 C is indicative of pro-
longed immersion and therefore of more severe brain
In reports where rapid reversal of the
hypoxic state was achieved, in combination with
ICU support, often with ECR and occasionally with
control of intracranial pressure (ICP), there was
complete or near-complete return of neurological
function with time.
11 85 86 102
Many studies assessing predictive factors have
analysed data from near-drownings in warmer
waters than are usually found in the UK.
Therefore, it may be inappropriate to assess
immersion victims using the same criteria, as the
presence of hypothermia may offer some cerebral
In addition to the complications already described
(pulmonary oedema, infection, hypothermic cardiac
arrhythmia, hypoxic encephalopathy and cerebral
oedema), disseminated intravascular coagulation
(DIC) has been described in near-drowning,
as has
Rhabdomyolysis complicated by acute renal
failure has been reported in two normothermic
casualties of near-drowning in cold (14 C and
17 C) surf.
One victim who was retrieved in cardio-
pulmonary arrest and was alert, lucid and apparently
normal 1 h later, had a plasma creatinine concentra-
tion of 2106 mol litre
3 h after immersion. He
required support with peritoneal dialysis for 11 days
and forced saline diuresis to avert oliguria. The
second patient discharged 2 h after the event, re-
presented 24 h later complaining of weakness,
myalgia and dark urine. His serum creatinine
concentration was 359 mol litre
, and forced
saline/frusemide diuresis avoided the need for dialy-
sis. Excessive or sustained muscle exercise and heat
stress are well recognized causes of rhabdomyolysis;
cold stress is a significantly less common trigger.
However, in view of the potential consequence of
acute renal failure, it would seem prudent to
measure total creatinine kinase activity in addition to
serum electrolytes and simple urinalysis in survivors
of near-drowning.
Peripheral neurological sequelae may be manifes-
tations of traumatic or even “non-freezing cold
injury” to peripheral nerves rather than hypoxic
damage from near-drowning. One should also be
mindful of the near-drowning patient having a pre-
disposing injury or medical condition, while the
possibility of there being a drug-related condition
should also be borne in mind.
Other treatment modalities
Artificial surfactant (Exosurf
) has been used success-
fully in the management of a 9-yr-old victim of near-
drowning with a rectal temperature of 30.3 C who
was acidotic (pH 6.95).
Despite circulatory and
ventilatory support (
F 1, minute volume 230 ml
, PEEP 5 cm H
O, peak ventilator airway pres-
sure 40 cm H
O) acidosis persisted and there was
severe and progressive respiratory distress (pH 6.87,
aP 7.6 kPa,
aP 12.4 kPa, base excess 917.5
mmol litre
). Four hours after admission artificial
surfactant was instilled slowly via the tracheal tube.
Within 5 min there was an improvement in gas
exchange (
aP 11.5 kPa,
aP 9.5 kPa) and a
decrease in peak pressure to 30 cm H
O, with no
change in ventilator settings. His trachea was
extubated 3 days later and he was discharged
neurologically intact.
Animal models of near-drowning have failed to
demonstrate any improvement in pulmonary
function after the use of exogenous surfactant,
4 7 76
although damage to the alveolar capillary
membranes is reduced. This disappointing finding
may be a result of using volumes of surfactant which
were too large and instilled too soon after injury,
causing documented severe hypoxia (i.e. a second
major insult). The use of smaller volumes, instilled
or nebulized at different times, with additional
PEEP, have not been reported.
Immersion, near-drowning and drowning 223
A study on the effect of corticosteroid therapy on
survival and blood-gas exchange in dogs after
aspiration of fresh water drowning demonstrated no
beneficial effect.
Their value in the management
of pulmonary injury has not been proved
probably should not be used.
The rapid onset of cerebral hypothermia would
appear to be the essential mechanism by which some
submerged victims, in particular children, appear to
be able to withstand protracted periods of asphyxia
without suffering irreversible neurological damage.
For this protective mechanism to be effective, brain
cooling must be established rapidly, before severe
hypoxia occurs. Such rates of cooling are unlikely to
be achieved through surface cooling alone, or in
combination with the diving reflex. It is postulated
that rapid selective brain cooling is achieved through
pulmonary heat exchange by repeated flushing of the
lungs with cold water during the drowning process
before cardiorespiratory arrest supervenes.
Successful treatment depends on speedy recovery
and the immediate institution of CPR if indicated.
All near-drowning victims, even those who appear to
be ostensibly clinically well, should be transferred to
hospital for pulmonary screening. Although some
successful resuscitations of victims in cardiac arrest
who are flaccid with fixed dilated pupils have been
reported, the great majority would appear to have a
poor prognosis. The prognosis is better for those
with profound hypothermia but rewarming may
be difficult in the absence of a good circulation.
Accordingly, consideration should be given to trans-
ferring all profoundly hypothermic patients who are
in cardiac arrest to a centre where cardiopulmonary
bypass facilities are available, sooner rather than
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... The DR, with its elevated activation of vagal cardiac nerves, long has been acknowledged as a treatment for paroxysmal atrial tachycardia (Wildenthal et al., 1975;Gooden, 1982) by normalizing sinus rhythm. Moreover, cases of "cold water drowning" in humans, where children lie submerged underwater for prolonged periods, but recover basically unharmed, have been documented numerous times (Hayward et al., 1984;Golden et al., 1997;Xu et al., 1999;Giesbrecht, 2000). Thus, perhaps in these cases, a DR induces a persistent apnea, saving these victims from inhaling water and drowning. ...
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The mammalian diving response (DR) is a remarkable behavior that was first formally studied by Laurence Irving and Per Scholander in the late 1930s. The DR is called such because it is most prominent in marine mammals such as seals, whales, and dolphins, but nevertheless is found in all mammals studied. It consists generally of breathing cessation (apnea), a dramatic slowing of heart rate (bradycardia), and an increase in peripheral vasoconstriction. The DR is thought to conserve vital oxygen stores and thus maintain life by directing perfusion to the two organs most essential for life—the heart and the brain. The DR is important, not only for its dramatic power over autonomic function, but also because it alters normal homeostatic reflexes such as the baroreceptor reflex and respiratory chemoreceptor reflex. The neurons driving the reflex circuits for the DR are contained within the medulla and spinal cord since the response remains after the brainstem transection at the pontomedullary junction. Neuroanatomical and physiological data suggesting brainstem areas important for the apnea, bradycardia, and peripheral vasoconstriction induced by underwater submersion are reviewed. Defining the brainstem circuit for the DR may open broad avenues for understanding the mechanisms of suprabulbar control of autonomic function in general, as well as implicate its role in some clinical states. Knowledge of the proposed diving circuit should facilitate studies on elite human divers performing breath-holding dives as well as investigations on sudden infant death syndrome (SIDS), stroke, migraine headache, and arrhythmias. We have speculated that the DR is the most powerful autonomic reflex known.
... It has been reported that, in this case, microvascular circulation fails, capillary insufficiency develops, alveolar fluid flow increases, and, eventually pulmonary edema develops 3,5 . Adrenergic discharge, depending on anxiety with hypoxia, makes the case even worse 6,7 . In its etiology, croup, epiglottitis, previous oropharyngeal surgery, short neck, obesity, foreign materials, tumors, non-viscous tracheal secretions are also taken into consideration. ...
In this paper we describe two cases with negative pressure pulmonary edema (NPPE). Excessive negative airway pressures against an obstructed airway has been reported to cause fluid filtration into alveoli and lung edema. The patients are generally young adults without any medical problems. The condition involves central interstitial area of both lungs and is treated by nonnvasive mechanical ventilation and corticosteroids.
Thermal physiology research is entirely dependent on the ability to measure temperature, and that could not happen until the invention of the thermometer by Santorio Santorio in 1612. However, it was not until 1724 that Daniel Gabriel Fahrenheit devised an accurate scale of temperature measurement, followed by the Swedish scientist, Anderss Celsius in 1742, who invented the centigrade (Celsius) scale. It was much later, in 1867, that Sir Thomas Allbutt invented the first practical medical thermometer, and soon after James Joule (1850) demonstrated the relationship between thermal energy and mechanical work. However, with some exceptions (e.g. Blagden, 1775), scientific observations on the physiology of temperature regulation did not really begin in the UK until the end of the eighteenth century. Anyone entering the field of human thermal physiology could adopt the principle of not exposing others experimentally to conditions to which they have not exposed themselves. In preparation, read the well-known heroic tale of how the UK physician and scientist Charles Blagden (Fig. 1.1) exposed himself and other volunteers (including a dog) to air temperatures up to 127 °C, much hotter than modern saunas (see Chap. 4) and enough to cook a steak alongside him, as he demonstrated, and found, to his relief, that sweating kept the deep-body temperatures in the low forties.
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Celem niniejszego opracowania jest przedstawienie szerokiego spektrum działania poszczególnych służb w systemie PRM, KSRG oraz podmiotów z nimi współpracujących. Autorzy dokonali analizy przepisów prawnych, możliwości współpracy w ramach istniejącego systemu, wysunęli propozycje zmian i omówili interesujące zagadnienia praktyczne z zakresu medycyny cywilnej i wojskowej.
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Thiazoline-related innate fear-eliciting compounds (tFOs) orchestrate hypothermia, hypometabolism, and anti-hypoxia, which enable survival in lethal hypoxic conditions. Here, we show that most of these effects are severely attenuated in transient receptor potential ankyrin 1 ( Trpa1 ) knockout mice. TFO-induced hypothermia involves the Trpa1 -mediated trigeminal/vagal pathways and non- Trpa1 olfactory pathway. TFOs activate Trpa1 -positive sensory pathways projecting from trigeminal and vagal ganglia to the spinal trigeminal nucleus (Sp5) and nucleus of the solitary tract (NTS), and their artificial activation induces hypothermia. TFO presentation activates the NTS-Parabrachial nucleus pathway to induce hypothermia and hypometabolism; this activation was suppressed in Trpa1 knockout mice. TRPA1 activation is insufficient to trigger tFO-mediated anti-hypoxic effects; Sp5/NTS activation is also necessary. Accordingly, we find a novel molecule that enables mice to survive in a lethal hypoxic condition ten times longer than known tFOs. Combinations of appropriate tFOs and TRPA1 command intrinsic physiological responses relevant to survival fate.
Even though many patients complaining of fever in emergency department (ED) have infection as an underlying disease, fever in some other patients is caused by non-infectious causes. Non-infectious conditions eliciting fever and related pulmonary abnormalities and becoming the cause of ED visit can be identified in two different conditions besides infection and they are connective tissue disease (CTD) and malignant condition such as leukemia and related condition capillary leak syndrome and lymphoma. Other conditions that cause pulmonary emergency without infection include drug-related pneumonitis (DRP), radiation pneumonitis, cardiogenic or renal and neurogenic pulmonary edema (PE), diffuse alveolar hemorrhage (DAH), adult respiratory distress syndrome (ARDS) and acute interstitial pneumonia (AIP), fat embolism, acute eosinophilic pneumonia (AEP), organizing pneumonia (OP) and acute fibrinous organizing pneumonia (AFOP). Diffuse alveolar damage pattern with diffuse or wide patchy areas of parenchymal opacity is the key feature and is seen in most diseases. Pattern approach is most important in differential diagnosis.
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Children diagnosed with autism have the right to access evidence-based practices that are necessary for their education and welfare. Oftentimes, parents of these children are not satisfied with the education provided by the State and they challenge education or health authorities in tribunals. Usually, these tribunal hearings revolve around the inclusion/exclusion of the science called Applied Behaviour Analysis (ABA) in directing evidence-based practice. Given that the number of these tribunals is rising, this paper addresses why it is important for judges and lawyers to be informed correctly about (1) the nature of ABA, (2) the reasons why parents petition for evidence-based practices to be grounded in ABA, (3) why education and health authorities petition against ABA, and (4) the combined influences of these issues on decision making.
We describe two patients who suffered prolonged (greater than four minutes) submersion in cold water (25 minutes, 32 s, and six minutes, respectively), with complete neurologic recovery. We postulate that hypothermia served to protect the brain from hypoxic injury. These cases also serve to emphasize the need for vigorous on-the-scene resuscitative efforts. We review the problems associated with the treatment of hypothermia and drowning. (Arch Intern Med 140:775-779, 1980)
Hospital records of 91 consecutive near-drowning victims were studied retrospectively. Eight-one (89 percent) of these patients survived. Patients who were alert on arrival at the emergency room survived, but those who were comatose and had fixed dilated pupils died. Other states of consciousness were unreliable predictors of survival. All patients with a normal chest roentgenogram on admission survived; however, values for arterial oxygen tension (PaO2) did not necessarily correlate with the chest roentgenograms. Values for arterial blood gas tensions and pH varied widely, as follows; PaO2, 25 to 465 mm Hg; arterial carbon dioxide tension (PaCO2), 17 to 100 mm Hg; pH, 6.77 to 7.50; and arterial bicarbonate level, 6.6 to 29.7 mEq/L. The ratio of PaO2 to the fractional concentration of oxygen in the inspired gas (FIo2), which was calculated to standardize PaO2 data for varying concentrations of inspired oxygen, ranged from 30 to 585 mm Hg. Only one patient with a ratio of PaO2/FIo2 greater than 150 mm Hg on admission subsequently died; this was a neurologic rather than a pulmonary death. Serum electrolytic concentrations and values for hemoglobin level and hematocrit reading neither predicted survival nor indicated that a threat to life existed. Steroid and prophylactic antibiotic therapy did not appear to increase the chance of survival. Observations on these patients are discussed in light of previous experiments in animals, and an approach to therapy is suggested.
A 2 1/2year-old girl had a good neurologic recovery after submersion in cold water for at least 66 minutes; as far as we know, this is the longest time ever reported. Cardiopulmonary resuscitation was maintained for more than two hours before the initiation of extracorporeal rewarming in this child who had a core temperature of 19°C. To our knowledge, this is the first successful use of extracorporeal rewarming in a child suffering from accidental hypothermia. Extension of this technique to children offers rapid rewarming and cardiovascular support for pediatric victims of severe hypothermia. We emphasize the importance of a coordinated response by the entire emergency medical system integrated with hospital-based personnel. Where it is geographically feasible, regionalization of triage and care for the pediatric victim of severe accidental hypothermia should be considered. (JAMA 1988;260:377-379)
Cardiopulmonary resuscitation and rewarming were successful in a 5-year-old boy who had been submerged for 40 minutes in ice-cold fresh water. Severe metabolic acidosis was corrected by intravenous infusion of sodium bicarbonate solution before spontaneous circulation could be re-established. Fulminant pulmonary œdema developed after re-establishment of spontaneous circulation. This was efficiently reversed by positive-end-expiratory-pressure ventilation. During 2 days of treatment on a respirator the patient gradually regained consciousness; the endotracheal tube was then removed and the patient immediately started talking intelligently. The patient went through a period of slow cerebration and motor dysfunction but recovered rapidly, and on examination 13 months after the accident all findings were normal.
When hypothermic patients appear to be dead, the decision to resuscitate may be difficult due to lack of reliable criteria of death. To discover useful prognostic indicators, we reviewed the hospital charts of nine hypothermic victims of snow avalanches (group A: median value of rectal temperature, 29.6°C; range, <12°C to 34°C) and of 15 patients with hypothermia following acute drug intoxication and/or cold exposure (group B: 28.8°C; range, 25.5°C to 32°C. In group A, plasma potassium level on admission was extremely high (14.5 mmol/L; range, 6.8 to 24.5 mmol/L) compared with that obtained in group B (3.5 mmol/L; range, 2.7 to 5.3 mmol/L). All patients in group A were in cardiorespiratory arrest. None could be successfully resuscitated despite effective rewarming by cardiopulmonary bypass or peritoneal lavage. In contrast, all of the patients in group B recovered from hypothermia, including two in cardiorespiratory arrest. Thus, extreme hyperkalemia during acute hypothermia appears to be a reliable marker of death. It might be used to select those patients in whom heroic resuscitation efforts can be useful.