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traumatic injury, hypothermia and aspira- saemia have been reported following sub-
tion pneumonitis. Acute Respiratory mersion in the Dead Sea. Rhabdomyolysis
Distress Syndrome (ARDS) and Acute (11) may occur if the hypoxic insult to the
Lung Injury (ALI) pose management chal- muscles is extensive and the subsequent
lenges in the Intensive Care Unit (ICU). myoglobinaemia may precipitate acute
Hypoxia (7,9,10) is the principle mecha- tubular necrosis and consequent renal fail-
nism of injury in near drowning and occurs ure. Rhabdomyolysis (11) may occur if the
through several mechanisms. In the most hypoxic insult to the muscles is extensive
basic form submersion in water results in and the subsequent myoglobinaemia may
cessation of normal respiration and a sud- precipitate acute tubular necrosis and con-
den reduction in alveolar concentration of sequent renal failure.
oxygen. This causes the victim to gasp with
a subsequent intake of water. At first there
may be violent laryngospasm and bron-
chospasm, preventing ingress of water into
the lower airway, but as hypoxia supervenes,
the vocal cords relax and water enters the
lungs, exaggerating the hypoxia. Aspiration
leads to changes in pulmonary surfactant,
and here there is a difference between salt-
water and freshwater. In saltwater aspiration
acute pulmonary oedema occurs due to the
drainage of protein rich fluid from the
intravascular space into the alveoli; this is
because saltwater has 3-4 times the hyper-
tonicity of blood. In freshwater aspiration
Fig 1. Helicopter winching in action.
surfactant is inactivated resulting in alveolar
collapse (atelectasis), leading to an increase Circum-Rescue Collapse
in ventilation/perfusion mismatch (shunt) Circum-rescue circulatory collapse may
within the lungs. also occur following rescue from immersion
Pulmonary parenchymal damage occurs in water (7,9,12, 13). In the water, there is
due to the irritant effect of water within the an increased hydrostatic pressure around
lungs (7). As a consequence, a protein rich the victims legs and trunk which results in
transudate floods the alveoli further impair- an increase in venous return and hence an
ing gas exchange (secondary drowning) and increase in cardiac output. This increase in
this may occur up to 12 hours after the ini- central volume is sensed as hypervolaemia
tial event. 70% of submersion victims also by the body and thus a diuresis and salt loss
aspirate mud, algae and vomitus as well as (natriuresis) will occur. Peripheral vasocon-
water, which may cause an aspiration pneu- striction will occur due to the relative cold
monitis. Non-cardiogenic pulmonary oede- temperate of the water, even in temperate
ma may result from direct pulmonary climes, resulting in a further increase in
insult, surfactant loss, inflammatory con- venous return and exacerbating this
taminants and cerebral hypoxia. response. In this way the victim’s intravas-
Hypoxia is sensed by arterial chemore- cular volume becomes depleted. One sug-
ceptors, leading to activation of the auto- gested mechanism leading to circulatory
nomic nervous system (7). A subsequent collapse is that the myocardium becomes
bradycardia leads to a reduction of myocar- stressed due to increased venous and arteri-
dial oxygen consumption, and an increased al pressures resulting in increased cate-
tolerance to the hypoxic episode. cholamine release. Coupled with hypoxia,
Vasoconstriction to non-vital organs also the increase in circulating catecholamines
occurs (e.g. skin and splanchnic vessels), may provoke cardiac dysrythmias. A second
thus conserving available oxygen for the theory is that removal from the water caus-
heart and brain. This vasoconstriction may
be strong enough to decrease or obliterate
peripheral pulses, and this effect may be
exaggerated in the hypothermic victim.
Hypothermia is a concomitant hazard due
to prolonged immersion even in temperate
climes. Wind and surface spray over
exposed body surfaces, low water tempera-
tures, lack of insulation and alcohol inges-
tion are factors that will accelerate the drop
in core temperature.
Aspiration of water usually occurs in such
low volumes that it does not affect the
haemoglobin level or electrolyte balance,
although hypercalcaemia and hypermagn- Fig 2. Helicopter stretcher.
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es a sudden release in the hydrostatic pres- foetal position. This is said to reduce the
sure around the abdomen and legs, with a incidence of circum rescue collapse following
consequent venous pooling in the lower prolonged immersion (9), which occurs due
limbs and reduced venous return to the to the sudden release of the protective hydro-
heart. The resultant acute decrease in coro- static pressure around the victim’s legs and
nary perfusion may provoke ventricular fib- trunk. Primary survey immediately follows
rillation or acute myocardial ischaemia, the rescue phase. Submersion injury alone
causing death. without traumatic injury is not an indication
for C-spine immobilization (14). However,
Prehospital Management diving and surfing incidents in which there
Prehospital care commences with the rescue has been shallow water impact, significantly
phase during which the victim is safely and increase the risk of cervical spine injury due
rapidly removed from the water. ‘Scene safe- to the axial load onto the vertebral column,
ty’ is paramount and there are a myriad of and in these cases there must be a low
examples where would-be rescuers have threshold for full spinal immobilisation.
become secondary victims through failure to The airway should be cleared, suctioned as
appreciate the hazards posed by the environ- necessary and maintained with assisted ven-
ment. Extraction from the water should ide- tilation as required. Supplemental oxygen
ally be on a long spinal board or in a purpose should be administered at the highest possi-
designed litter (Figs 1 & 2). Cervical and ble concentration available (in absence of
spinal immobilisation should be employed saturation monitoring), or at a rate to main-
when injury has occurred, although the need tain saturations (SpO2) above 92% when
for continued spinal precautions should be conservation of oxygen supply is an issue. In
actively reviewed once the rescue phase is cardiac arrest the victim should be intubated
complete. Variations in body position may without drugs. In the unconscious and
provoke dysrythmias in the severely hypoxic, but self-ventilating victim, skilled
hypothermic victim. This is because the car- providers may undertake rapid sequence
diovascular system cannot cope with fluid intubation (RSI) and provide intermittent
shift changes brought about by being moved positive pressure ventilation (IPPV) with
from the supine to the vertical position for positive end-expiratory pressure (PEEP).
instance. For this reason hypothermic vic- This will secure the airway, treat hypoxia,
tims should be managed supine, preferably prevent atelectasis and optimise gaseous
in a litter. Some search and rescue (SAR) exchange. However, the provider must con-
helicopters employ a double strop to winch sider concomitant barotrauma resulting in
victims from the water. One strop passes pneumothorax / tension pneumothorax,
around the trunk beneath the axillae, the especially in diving incidents, and be pre-
other around the leg beneath the knees, pared to site an intrapleural drain. If the
allowing the victim to be winched in the patient is hypotensive or tachycardic then
judicious use of (warmed) intravenous crys- arrival in the emergency department, with
talloid fluid boluses will be required. subsequent management in the ICU. Ideally
In cases of cardiac arrest cardiopulmonary mechanical ventilation should potentiate
resuscitation (CPR) should be commenced alveolar recruitment and optimise intra pul-
and continued through to the hospital facili- monary gas distribution. Inappropriate ven-
ty as hypothermia may be a confounding fac- tilator management may exacerbate respira-
tor making the detection of vital signs diffi- tory failure. Ventilator – associated lung
cult in the field. Remember the adage that injury (VALI) may occur with ‘traditional’
hypothermic victims are not dead until they high tidal volume (TV) – low PEEP ventila-
are ‘warm and dead’. tor settings. In the submersion victim further
Any secondary survey must concentrate on parenchymal lung damage may occur due to
life and limb threatening injuries only, and in the overdistension of aerated lung (stretch)
any case must not delay onward transport to and the repeated opening and closing of the
definitive care.The correct disposition is to a collapsed, derecruited lung (shear) (14).This
hospital with 24-hour ICU facilities. may disrupt the normal alveolar integrity
and perpetuate the inflammatory response
Definitive Care (14). Critical care may begin at the point of
This phase focuses on continued resuscita- rescue in the hands of skilled providers; oth-
tion, correction of respiratory failure and erwise it must begin in the emergency
management of concomitant injuries. All department with the employment of ventila-
patients require the following investigations: tor management that is effective and does no
- full blood count (FBC) and coagulation further harm to the patient.
profile, urea and electrolytes (U&E), serum
glucose and creatine phosphokinase (CPK), Recommendations For
arterial blood gas estimation (ABG), electro- Ventilation (15)
cardiograph (ECG), chest X-ray (CXR) and These are based upon the ‘open lung tech-
urinalysis (MSU) for myoglobinuria. A toxi- nique’, which aims to optimise lung mechan-
cology screen may be useful in differentiating ics and to limit iatrogenic damage caused by
the unconscious victim.Tetanus immunosta- mechanical ventilation.
tus should be checked and a booster or 1. Manual ventilation. When ventilating by
course of treatment given as necessary (6, reservoir – bag, e.g. prehospital, each
11, 12). breath should be administered so that the
Patients can be divided into two sub- chest is seen to just rise and fall.This pre-
groups: - The first group is those who are vents excess volume and pressure. Aim
self-ventilating and who have a normal level for an Sp02 of 93 – 97% and end-tidal
of consciousness - these patients only require carbon dioxide (ETCO2) of 4.5 – 6.0kPa
supplemental oxygen to maintain their SpO2 (35 – 45mmHg)
>94%. Nebulised bronchodilotors may be 2. PEEP. Set PEEP at >10 cm H2O initially.
required to control bronchospasm. They Most alveolar derecruitment occurs in
require hourly observations to detect post supine patients at PEEP levels between
immersion syndrome or aspiration pneu- 10 – 15 cm H2O. Extensive parenchymal
monitis, either on a general ward or in a High injury will require increased PEEP.
Dependency Unit (HDU) setting (see Hypotension suggests under-filling, indi-
Figure 3) (11). If a patient’s respiratory func- cating further fluid replacement or
tion deteriorates, but they are alert, unlikely inotropic support.
to vomit and can comply with mask therapy 3. Oxygenation. PEEP or mean airway pres-
then they should be considered for non-inva- sure should be increased to maintain the
sive ventilatory assistance (NIVA). Those highest possible PaO2 / FiO2 ratio. Aim for
who do not meet these criteria, or who dete- PaO2 of 60 – 80mmHg (8 – 10kPa) using
riorate further, should undergo RSI and be the lowest possible oxygen concentration.
managed as detailed below. Patients man- High oxygen concentrations have been
aged in the ward or HDU setting must be shown (paradoxically) to increase at
observed for a minimum period of six hours, atelectasis and to cause toxic parenchy-
and prior to discharge the patient must have mal damage through free radical forma-
documented normal blood gases and a nor- tion (15).
mal core temperature and be advised to 4. Peak/Plateau airway pressure.This should
return if they suffer any deterioration in be limited to <35cm H2Oto minimise
symptoms or if they develop a fever within VALI.This can be achieved by decreasing
the subsequent few days. TV, decreasing respiratory rate and
The second group of patients are those increasing inspiratory time. Change to
patients who have inadequate ventilation sec- pressure mode ventilation +/- inverse
ondary to decreased conscious level or due ratio ventilation on advanced ventilators.
to the initial pulmonary injury. Patients with 5. Tidal Volume. Limit TV at 6 – 8ml/kg.
significant submersion injury are at very high Volutrauma may result from high TVs
risk for compounding their respiratory fail- causing over distension, or from high
ure through ALI or ARDS. These patients PEEP without a corresponding limitation
require early controlled ventilation upon in TV.
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3. Royal Society for Prevention of Accidents Accident 15. McCunn M, Sutcliffe A, Mauritz W + ITACCS
Statistics- Brief Overview Feb 2005 Available at: Critical Care Committee – Guidelines for manage-
www.rospa.com/factsheets/accidents_overview.pdf. ment of mechanical ventilation in critically injured
4. Telegraph newspaper Race to save mini-sub trapped patients. Available at: www.itacc.com/move/ventita-
in nets. Available at: www.telegraph.co.uk/news/ tion.htm
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5. Telegraph newspaper 116 Russians trapped in sub- expanding role for cardiopulmonary bypass in trau-
marine. Available at: www.telegraph.co.uk/news/ ma. Canadian Journal of Surgery 2002;45(2):95-103.
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Notes