Drowning management

1. Dr Abhijeet Deshmukh
Fellow in PICU & NICU

2. Definition
 Drowning as the process of experiencing respiratory
impairment from submersion/immersion in liquid.
(WHO)
 The definition implies that a drowning victim develops
an air-liquid interface that prevents the breathing of air.
 Terms Near drowning/secondary drowning etc are
abondoned

3. Types of drowning
 1. Wet drowning= primary drowning
 2. Dry drowning= 10-15%, laryngospasm, thick mucous foam
plug, panoramic views of past life, pleasant dreams without
distress.
 3. Secondary drowning= post immersion syndrome= near
drowning : Secondary drowning is death due to chemical or biological
changes in the lungs after a near drowning incident ; resuscitated and
survives for 24 hours, +/- conscious, hypoxemia brain damage,
electrolyte disturbances, pulmonary edema, hemoglobinuria, chemical
pneumonitis
 4. Immersion syndrome= hydrocution= submersion
inhibition; cold water n. endings +/ strike epigastrium +/
entering ear drums, nasal passages.
 Horizontal entry (dive) pressure on abdomen
 All these  Vagal inhibition Cardiac arrest death

4. Epidemiology
 30% Deaths from 1-4 years
 2nd leading cause of unintentional injury related
deaths in 1-14yrs.
 Two age groups <5years and >15 years
 Males>Females

5. Risk factors
 Age
- <5 year – d/t decreased supervision
(Bathtubs, buckets, toilets, swimming pools)
- >15 years- d/t risk taking beheviour
( Swimming, boating, alcohol/drug)

6.  Medical conditions :
 Seizure disorder - (7%) –Hyperventilation ppt seizures
 Long QT syndrome or other channelopathies•- Activation
of diving reflex and alters autonomic activity
 Use of alcohol or other substances (25%)
 Other conditions that less frequently predispose to
drowning:
Depression
Coronary artery disease
Cardiomyopathy
Hypoglycemia
Hypothermia

7. Pathophysiology

8. SEQUENCE OF EVENTS IN DROWNING
 1. SENSE OF PANIC
 Expressed by:
 Violent struggle
 Automatic swimming movements
 Usually followed by:
 2. PERIOD OF VOLUNTARY APNOEA
 Duration: 1-2 minutes.
 Hypoxemia, hypercapnia, R & M acidosis.

9.  3. ATTEMPT AT TAKING A BREATH
 WATER:
 May be freely inhaled
 Or, may cause glottic spasm due to impingement.
 In 10-15 % victims: glottic spasm severe asphyxia
water may not enter the lungs unless subcouncious.
Dry drowning
 In 85-90 % victims: water is swallowed inducing
vomiting, gasping & aspiration of water into lungs.
When expiratory effort is made: fine froth,
sometimes blood stained
Wet drowning

10.  2 major pathophysiological factors
- Hypoxemia
- Hypothermia
 Hypoxemia :
FRC is the only source of gas exchange in submerged
state, so depletion in FRC & Aspiration of water
aspiration of gastric contents
Laryngospasm (15%) k/a Dry drowning cause alveolar
hypoventilation compromise O2 uptake and co2
elemination

11.  Hypothermia :
- Two types
1. Primary hypothermia : Sudden submersion in Ice
cold water (<5 C).
- Excellent prognosis
> Decrease cerebral metabolic rate, O2 consumption,
ICP, cytotoxic edema, decrease in O2 free radicals
> activation of the diving reflex slows metabolism
and preserves some perfusion to the heart and brain.

12. 2. Secondary hypothermia :
Submersion in Tepid water (30 C)
- d/t radient skin loss

13.  Consequences of hypothermia :
- Flaccid paralysis and unconsciousness if temp <30
which facilitates aspiration.
- Shock
- Coagulopathy, Hemolysis, Platelet dysfunction
- Metabolic acidosis
-

14. Fresh water drowning

15. Freshwater moves rapidly across A.C.mb
into circulation
disrupts & denatures surfactant
Surface tension increased
compliance decreased
atelectasis

16. More liquid in the circulation
Hemodilution, decrease in Na+, Cl & Ca conc.
Liquid/ water goes inside RBCs
Hemolysis
Release of K+
Increase in K+ conc.

17.  Shift Acute hypervolemia
Increase in K+ irritates myocardium
Arrythmias (VF) occurs

18. Salt water drowning

19.  Pulmonary edema within minutes
 Shift Hypovolemia
Hypertonic liquid
Draws water out through alv capillary memb
Into pulmonary alveoli
Damage to basement mb + Dilution & washing out of Surfactant
compliance decreased

20.  Pulling out of water  Hemoconc. Inc. in Na, Cl
and Mg
 No hemolysis,
 Death within 5-12 minutes (later than freshwater)

21. Pulmonary edema X ray

22.  Aspiration of >11ml/kg of fluid is required to alter
blood volume
 Aspiration of >22ml/kg for electrolyte disturbances
 Most are Hypovolemic regardless the type of aspiration
fluid because of excessive capillary permeability d/t
asphyxia & loss of protein rich fluid in alveoli

23. Organ specific effects
 Pulmonary effects
- FRC (the only source of gas exchange in submerged
state is reduced) Hypoxia and Hypercarbia
- Severe laryngospasm/ Aspiration  Alv
hypoventilation Incr PaCO2 & decr PaO2
- Fresh water aspiration  destruction of surfactant
atelectasis.
- Sea water  Mitochondrial swelling, disruption of
pulmonary capillary endothelium., Osmolar effects
heavy water filled lungs

24. - Exudation of proteinaceous material in alveoli,
pulmonary edema, decreased compliance, increased
airway resistance.
- ARDS is hallmark of delayed pulmonary insufficiency
d/t aspiration.
- Neurogenic pulmonary edema may contribute to
deficits in gas exchange and lung function.

25. - Contaminated water  pneumonia Fungal,
bacterial
- Aspiration of gastric contents (acid injury) & mud,
algae alter gas exchange
- Low VT at low FRC vicious cycle of atelectasis,
decreased compliance & further decrease in VT.
- Hypoxemia if not immediately reversed  vicious
cycle of capillary leak, surfactant damage, collapses,
V/Q mismatch, raised pulmonary vascular resistance.

26. - ARDS can cause either d/t Aspiration or as
consequence of Hypoxic ischemic insult (Shock lung)

27.  CNS effects :
- Most imp cause of death and neurological morbidity
- HIE results in cytotoxic cerebral edema, raised ICT.
- The combination of hypoxemia and low-flow states
results in a host of pathologic processes, including
energy failure, lipid peroxidation, production of free
radicals, inflammatory responses, and release of
excitotoxic neurotransmitters.

28.  Conns criteria (Extent of cerebral hypoxia) :
A : Awake
B : Blunted conciousness
C : Comatose

29.  The vascular end zones are particularly vulnerable
 Watershed area•infarctions may be appreciated on CT
scan with ground glass appearance.

30.  CVS Effects :
- Hypoxemia  life-threatening dysrhythmias such as
ventricular tachycardia, ventricular fibrillation, and
asystole.
- The two determinants of oxygen delivery, namely
cardiac output and arterial O2 content, can be
adversely affected by the submersion event.
- Decrease in arterial O2 content decrease in
myocardial oxygen deliveryworsening cardiac output
and decreased myocardial perfusion pressure.

31.  Cytosolic calcium overload and oxygen-derived free
radicals myocardial injury
 Cardiogenic shockhypoxic damage to the
myocardium.
 Hallmark of cardiovascular dysfunction with
submersion injury is shock
 Metabolic acidosis may further impair myocardial
performance

32.  Right ventricular afterload is also increased by
structural pulmonary microvascular damage and
humoral inflammatory mediators involved in ARDS

33.  Other organ systems :
- Multisystem failure resulting from prolonged
ischemic-hypoxic state, sepsis,
- Renal and hepatic insufficiency, disseminated
intravascular coagulation, gastrointestinal injury, and
metabolic abnormalities

34.  Fluid & Electrolyte disturbance :
- Mild-to-moderate hyponatremia of victims who
drowned in fresh water and moderate hypernatremia
and hyperchloremia in those who drown in salt water.
- Hypermagnesemia has been described in seawater
drowning, probably a result of both aspiration and
ingestion
- Fresh-water-associated hemodilution and
hypervolemia are generally mild.
- Hypovolemia after saltwater drowning may be seen
in severe cases, usually in victims who do not survive.

35. Management
 At the scene
- Remove victim from the water as soon as possible.
-Airway, breathing, and circulation.
- The aim of resuscitation at the scene is to prevent irreversible
tissue injury from prolonged hypoxia and ischemia.
- Mouth-to-mouth breathing should be performed even while in
the water if it can be accomplished.
- The stability of the cervical spine
- Avoid prolonged attempts to remove water from the lungs
- Most drowning victims aspirate relatively small amounts of
water, the Heimlich maneuver can not remove aspirated fresh
water or pulmonary edema fluid

36. Emergency room

38. Prognosis
 Success of resuscitative measures at the scene of injury.
 Patients who are successfully resuscitated and who are
conscious on arrival at the hospital have an excellent
chance of intact survival.
 Related to the extent of cerebral injury.
 Poor prognostic signs include an unwitnessed event,
prolonged time to resuscitation, the need for
cardiopulmonary resuscitation at the scene and in the
emergency department

39.  Neurologic prognosis is poor if the patient arrives
comatose in the emergency department, whether or
not they receive aggressive “brain resuscitation.
 Absence of cognitive function 72 hours after the
hypoxic episode is strongly associated with either
death or survival in a persistent vegetative state
 Need for continued CPR at the hospital > 25 minutes,
 fixed and dilated pupils, seizures, flaccidity, Glasgow
Coma Scale of 5 or less, and decreased cerebral blood
flow suggest poor prognosis

40. Thank You !
 References
 Zimmerman –Pediatric critical care (4th ed)
 Rogers Textbook of pediatric critical care.