drowning

1. DROWNING
DR NIRAV DHINOJA

2. DEFINITION
• “DROWNING IS THE PROCESS OF EXPERIENCING RESPIRATORY
IMPAIRMENT FROM SUBMERSION/IMMERSION IN LIQUID.”
• THE TERM DROWNING DOES NOT IMPLY THE FINAL OUTCOME,
DEATH OR SURVIVAL; THE OUTCOME SHOULD BE DENOTED AS
FATAL OR NONFATAL DROWNING.
• USE OF CONFUSING DESCRIPTIVE TERMS SUCH AS “NEAR,” “WET,”
“DRY,” “SECONDARY,” “SILENT,” “PASSIVE,” AND “ACTIVE” SHOULD

3. EPIDEMIOLOGY
• HIGHEST DROWNING DEATH RATES WERE SEEN IN CHILDREN AGED 1-4 YR AND
15-19 YR.
• IN CHILDREN, DROWNING IS SECOND ONLY TO MOTOR VEHICLE INJURY AS A
LEADING CAUSE OF DEATH FROM UNINTENTIONAL INJURY.
• CHILDREN YOUNGER THAN 1 YR :
• BATHTUB(71%)
• HOUSEHOLD BUCKETS(16%)
• CHILDREN 1-4 YR :
• POOL
• IRRIGATION DITCHES
• NEARBY PONDS & RIVERS.

4. • SCHOOL AGE CHILDREN
• SWIMMING OR BOATING ACTIVITIES.
• NATURAL WATER RESERVOIRS : LAKES, PONDS, RIVERS, CANALS.
• ADOLESCENT
• M : F = 10 : 1. (LIKELY DUE TO GREATER RISK TAKING BEHAVIOUR & ALCOHOL USE.)
• 70 % DEATHS DUE TO DROWNING IN NATURAL WATER RESERVOIRS.
• UNDERLYING CONDITIONS
• EPILEPSY
• LONG QT SYNDROME
• VENTRICULAR ARRHYTHMIAS
• ALCOHOL USE
• WATER SPORTS & RECREATIONAL ACTIVITIES

5. PATHOPHYSIOLOGY
• MOST OF DROWNING VICTIMS DROWN SILENTLY.
• VOCALIZATION IS PRECLUDED BY EFFORTS TO ACHIEVE MAXIMAL LUNG VOLUME
OR KEEP THE HEAD ABOVE THE WATER, OR BY ASPIRATION LEADING TO
LARYNGOSPASM.
• YOUNG CHILDREN CAN STRUGGLE FOR ONLY 10-20 SEC BEFORE BEING FINALLY
SUBMERGED.
• GLOBAL HYPOXIA IS THE INJURY, WITH THE SEVERITY OF INJURY DEPENDENT

6. ANOXIC-ISCHEMIC INJURY
Small amounts of water enter the hypopharynx, triggering
laryngospasm
Progressive decrease in arterial blood oxygen saturation
(Sao2), and the victim soon loses consciousness from
hypoxia
Profound hypoxia and medullary depression lead to
terminal apnea
The cardiovascular response leads to progressively
decreasing cardiac output and oxygen delivery.
By 3-4 min, the circulation abruptly fails because of
myocardial hypoxia

7. Ineffective cardiac contractions with electrical activity may
occur briefly, but there is no effective perfusion (pulseless
electrical activity).
Several hours after cardiopulmonary arrest, cerebral
edema may occur..
Severe cerebral edema can elevate intracranial pressure
(ICP), contributing to further ischemia.
Intracranial hypertension is an ominous sign of profound
CNS damage.

8. EFFECT OF HYPOXIC-ISCHEMIC INJURY ON
OTHER SYSTEM
• LUNG :
• ASPIRATION LEADS TO DAMAGE TO THE
PULMONARY VASCULAR ENDOTHELIUM
RESULTS IN ARDS.
• HEART :
• MYOCARDIAL DYSFUNCTION.
• ARTERIAL HYPOTENSION.
• DECREASED CARDIAC OUTPUT.
• ARRHYTHMIAS & CARDIAC INFARCTION.
• RENAL :
• ACUTE TUBULAR NECROSIS, CORTICAL
NECROSIS, AND RENAL FAILURE.
• VASCULAR ENDOTHELIAL INJURY MAY
INITIATE DIC, HEMOLYSIS, AND
THROMBOCYTOPENIA.
• GASTROINTESTINAL DAMAGE :
• BLOODY DIARRHEA WITH MUCOSAL
SLOUGHING.
• SERUM LEVELS OF HEPATIC
TRANSAMINASES AND PANCREATIC
ENZYMES ARE OFTEN ACUTELY
INCREASED.
• VIOLATION OF NORMAL MUCOSAL
PROTECTIVE BARRIERS PREDISPOSES
THE VICTIM TO BACTEREMIA AND

9. PULMONARY INJURY
• IN HUMANS, ASPIRATION OF SMALL AMOUNTS (1-3 ML/KG) CAN LEAD TO
MARKED HYPOXEMIA AND A 10-40% REDUCTION IN LUNG COMPLIANCE.
• ASPIRATED WATER DOES NOT OBSTRUCT AIRWAYS AND IS READILY MOVED INTO
THE PULMONARY CIRCULATION WITH POSITIVE PRESSURE VENTILATION.
• IT CAN WASH OUT SURFACTANT AND CAUSE ALVEOLAR INSTABILITY,
VENTILATION-PERFUSION MISMATCH, AND INTRAPULMONARY SHUNTING.

10. PULMONARY INJURY
• THE COMPOSITION OF ASPIRATED MATERIAL CAN AFFECT THE
PATIENT’S CLINICAL COURSE:
• GASTRIC CONTENTS, PATHOGENIC ORGANISMS, TOXIC CHEMICALS, AND
OTHER FOREIGN MATTER CAN INJURE THE LUNG OR CAUSE AIRWAY
OBSTRUCTION.
• CLINICAL MANAGEMENT IS NOT SIGNIFICANTLY DIFFERENT IN
SALTWATER AND FRESHWATER ASPIRATIONS, BECAUSE MOST

11. HYPOTHERMIA
• ACCORDING TO CORE BODY TEMPERATURE MEASUREMENT :
• MILD (34-36°C).
• MODERATE (30-34°C).
• SEVERE (<30°C).
• DROWNING SHOULD BE DIFFERENTIATED FROM COLD WATER IMMERSION
INJURY, IN WHICH THE VICTIM REMAINS AFLOAT, KEEPING THE HEAD ABOVE
WATER WITHOUT RESPIRATORY IMPAIRMENT.
• THE DEFINITION OF COLD WATER VARIES FROM 60 TO 70°F.

12. • HEAT LOSS THROUGH CONDUCTION AND CONVECTION IS MORE
EFFICIENT IN WATER THAN IN AIR.
• IF THE WATER IS COOL, HEAT PRODUCTION CANNOT BE MATCHED
BY THE BODY’S THERMOGENIC MECHANISMS.
• CHILDREN ARE AT INCREASED RISK FOR HYPOTHERMIA BECAUSE :
• RELATIVELY HIGH RATIO OF BODY SURFACE AREA TO MASS.
• DECREASED SUBCUTANEOUS FAT.
• LIMITED THERMOGENIC CAPACITY.
• HYPOTHERMIA MAY DEVELOP MORE QUICKLY WITH IMMERSION IN
FAST-FLOWING WATER AS A RESULT OF INCREASED CONVECTION.

13. • AS CORE TEMPERATURE DROPS TO <35°C, COGNITION,
COORDINATION, AND MUSCLE STRENGTH BECOME
PROGRESSIVELY IMPAIRED.
• WITH PROGRESSIVE HYPOTHERMIA, THERE MAY BE LOSS
OF CONSCIOUSNESS, WATER ASPIRATION, DECREASES IN
HEART RATE AND CARDIAC OUTPUT, INEFFECTIVE
BREATHING, AND CARDIAC ARREST.
• IMMEDIATE EFFECTS OF COLD WATER IMMERSION ARE
RESPIRATORY AND CARDIOVASCULAR.

14. • AFTER THE CHILD IS REMOVED FROM THE WATER, BODY
TEMPERATURE MAY CONTINUE TO FALL AS A RESULT OF COLD AIR,
WET CLOTHES, HYPOXIA, AND HOSPITAL TRANSPORT.
• HYPOTHERMIA IN PEDIATRIC DROWNING VICTIMS IS OBSERVED
EVEN AFTER DROWNING IN RELATIVELY WARM WATER AND IN
WARM CLIMATES.
• UNRECOGNIZED PROGRESSIVE HYPOTHERMIA CAN LEAD TO
FURTHER DECOMPENSATION.

15. • IN HYPOTHERMIC VICTIMS, COMPENSATORY MECHANISMS USUALLY ATTEMPT
TO RESTORE NORMOTHERMIA AT BODY TEMPERATURES >32°C; AT LOWER
TEMPERATURES, THERMOREGULATION MAY FAIL AND SPONTANEOUS
REWARMING WILL NOT OCCUR.
• WITH MODERATE TO SEVERE HYPOTHERMIA, PROGRESSIVE BRADYCARDIA,
IMPAIRED MYOCARDIAL CONTRACTILITY, AND LOSS OF VASOMOTOR TONE
CONTRIBUTE TO INADEQUATE PERFUSION, HYPOTENSION, AND POSSIBLE
SHOCK.
• AT BODY TEMPERATURE <28°C, EXTREME BRADYCARDIA IS USUALLY PRESENT,
AND THE PROPENSITY FOR SPONTANEOUS VENTRICULAR FIBRILLATION (VF) OR
ASYSTOLE IS HIGH.
• CENTRAL RESPIRATORY CENTER DEPRESSION WITH MODERATE TO SEVERE
HYPOTHERMIA RESULTS IN HYPOVENTILATION AND EVENTUAL APNEA.

16. COLD WATER SHOCK
• IN HUMAN ADULTS, IMMERSION IN ICY WATER RESULTS IN INTENSE
INVOLUNTARY REFLEX HYPERVENTILATION AND TO A DECREASE IN
BREATH-HOLDING ABILITY TO <10 SECONDS, WHICH LEADS TO FLUID
ASPIRATION, CONTRIBUTING TO MORE RAPID AND DEEP HYPOTHERMIA.
• SEVERE BRADYCARDIA OCCURS IN ADULTS BUT IS TRANSIENT AND
RAPIDLY FOLLOWED BY SUPRAVENTRICULAR AND ECTOPIC
TACHYCARDIAS AND HYPERTENSION.

17. NEUROPROTECTION AND HYPOTHERMIA
• IT MAY BE POSSIBLE FOR THE BRAIN TO RAPIDLY COOL TO A
NEUROPROTECTIVE LEVEL, IF THE WATER IS COLD ENOUGH, THE
COOLING PROCESS IS QUICK, AND CARDIAC OUTPUT LASTS LONG
ENOUGH FOR SUFFICIENT HEAT EXCHANGE TO OCCUR.
• ONCE SUBMERSION-ASSOCIATED HYPOXIA, APNEA, AND
CARDIOVASCULAR COMPROMISE DECREASE BLOOD CIRCULATION,
THE EFFECT OF HYPOTHERMIA’S NEUROPROTECTION IS
MITIGATED.

18. MANAGEMENT
• PRE-HOSPITAL MANAGEMENT
• HOSPITAL BASED MANAGEMENT
• CARDIORESPIRATORY
• NEUROLOGICAL
• HYPOTHERMIA
• OTHER

19. PRE-HOSPITAL MANAGEMENT
• THE GOAL IS TO REVERSE THE ANOXIA FROM SUBMERSION AND PREVENT
SECONDARY HYPOXIC INJURY AFTER SUBMERSION.
• INITIAL RESUSCITATION MUST FOCUS ON RAPIDLY RESTORING OXYGENATION,
VENTILATION, AND ADEQUATE CIRCULATION.
• THE AIRWAY SHOULD BE CLEAR OF VOMITUS AND FOREIGN MATERIAL, WHICH
MAY CAUSE OBSTRUCTION OR ASPIRATION.
• ABDOMINAL THRUSTS SHOULD NOT BE USED FOR FLUID REMOVAL, BECAUSE
MANY VICTIMS HAVE A DISTENDED ABDOMEN FROM SWALLOWED WATER;
ABDOMINAL THRUSTS MAY INCREASE THE RISK OF REGURGITATION AND
ASPIRATION.

20. • THE CERVICAL SPINE SHOULD BE PROTECTED IN ANYONE WITH
POTENTIAL TRAUMATIC NECK INJURY.
• THE NECK SHOULD BE MAINTAINED IN A NEUTRAL POSITION AND
PROTECTED WITH A WELL-FITTING CERVICAL COLLAR.
• IF THE VICTIM HAS INEFFECTIVE RESPIRATION OR APNEA,
VENTILATORY SUPPORT MUST BE INITIATED IMMEDIATELY(MOUTH-TO-
MOUTH OR MOUTH-TO-NOSE BREATHING).
• AS SOON AS IT IS AVAILABLE, SUPPLEMENTAL OXYGEN SHOULD BE
ADMINISTERED TO ALL VICTIMS.

21. • POSITIVE PRESSURE BAG-MASK VENTILATION WITH 100% INSPIRED
OXYGEN SHOULD BE INSTITUTED IN PATIENTS WITH RESPIRATORY
INSUFFICIENCY.
• IF APNEA, CYANOSIS, HYPOVENTILATION, OR LABORED
RESPIRATION PERSISTS, TRAINED PERSONNEL SHOULD PERFORM ET
INTUBATION AS SOON AS POSSIBLE.
• INTUBATION IS ALSO INDICATED TO PROTECT THE AIRWAY IN
PATIENTS WITH DEPRESSED MENTAL STATUS OR HEMODYNAMIC
INSTABILITY.
• HYPOXIA MUST BE CORRECTED RAPIDLY TO OPTIMIZE THE CHANCE
OF RECOVERY.

22. • SLOW CAPILLARY REFILL, COOL EXTREMITIES, AND ALTERED
MENTAL STATUS ARE POTENTIAL INDICATORS OF SHOCK.
• HEART RATE AND RHYTHM, BLOOD PRESSURE, TEMPERATURE, AND
END-ORGAN PERFUSION REQUIRE URGENT ASSESSMENT.
• CONTINUOUS MONITORING OF THE ECG ALLOWS APPROPRIATE
DIAGNOSIS AND TREATMENT OF ARRHYTHMIAS.

23. • CPR SHOULD BE INSTITUTED IMMEDIATELY IN PULSELESS,
BRADYCARDIC, OR SEVERELY HYPOTENSIVE VICTIMS.
• IV FLUIDS AND CARDIOACTIVE MEDICATIONS ARE REQUIRED TO
IMPROVE CIRCULATION AND PERFUSION.
• EPINEPHRINE IS USUALLY THE INITIAL DRUG OF CHOICE IN VICTIMS
WITH CARDIOPULMONARY ARREST.

24. HOSPITAL BASED MANAGEMENT
• PEDIATRIC DROWNING VICTIMS SHOULD BE OBSERVED FOR AT LEAST 6-8 HR,
EVEN IF THEY ARE ASYMPTOMATIC ON PRESENTATION.
• SERIAL MONITORING OF VITAL SIGNS AND REPEATED PULMONARY
EXAMINATION, AND NEUROLOGIC ASSESSMENT SHOULD BE PERFORMED IN ALL
DROWNING VICTIMS.
• MOST ALERT CHILDREN WITH EARLY RESPIRATORY SYMPTOMS RESPOND TO
OXYGEN AND, DESPITE ABNORMAL INITIAL RADIOGRAPHS, BECOME
ASYMPTOMATIC WITH A RETURN OF NORMAL ROOM AIR SAO2 AND PULMONARY
EXAMINATION BY 4-6 HR.
• SUBSEQUENT DELAYED RESPIRATORY DETERIORATION IS EXTREMELY UNLIKELY
IN SUCH CHILDREN.
• SELECTED LOW- RISK PATIENTS WHO ARE ALERT AND ASYMPTOMATIC WITH
NORMAL PHYSICAL FINDINGS AND OXYGENATION LEVELS MAY BE CONSIDERED

25. CARDIORESPIRATORY MANAGEMENT
• ADEQUATE OXYGENATION AND
VENTILATION IS A PRE-REQUISITE TO
IMPROVING MYOCARDIAL FUNCTION.
• FLUID RESUSCITATION AND INOTROPIC
AGENTS ARE OFTEN NECESSARY TO
IMPROVE HEART FUNCTION AND RESTORE
TISSUE PERFUSION.
• FOR PATIENTS WITH PERSISTENT
CARDIOPULMONARY ARREST ON ARRIVAL
AFTER NON–ICY WATER DROWNING, THE
DECISION TO WITHHOLD OR STOP
RESUSCITATIVE EFFORTS CAN BE
ADDRESSED BY REVIEW OF THE HISTORY
AND THE RESPONSE TO TREATMENT.
• DEATH OR SEVERE NEUROLOGIC
SEQUELAE ARE QUITE LIKELY IN
PATIENTS WITH
• DEEP COMA.
• APNEA.
• ABSENCE OF PUPILLARY RESPONSES.
• HYPERGLYCEMIA.
• SUBMERSION DURATIONS >10 MIN.
• FAILURE OF RESPONSE TO CPR
GIVEN FOR 25 MIN.

26. NEUROLOGICAL MANAGEMENT
• DROWNING VICTIMS WHO PRESENT TO THE HOSPITAL AWAKE AND ALERT USUALLY
HAVE NORMAL NEUROLOGIC OUTCOMES.
• COMATOSE DROWNING PATIENTS ARE AT RISK FOR INTRACRANIAL HYPERTENSION.
• ICP MONITORING AND THERAPY TO REDUCE INTRACRANIAL HYPERTENSION WOULD
SEEM LIKELY TO PRESERVE CEREBRAL PERFUSION AND PREVENT HERNIATION, BUT
THERE IS LITTLE EVIDENCE THAT THESE MEASURES IMPROVE OUTCOMES FOR
DROWNING VICTIMS.
• CONVENTIONAL NEUROLOGIC INTENSIVE CARE THERAPIES, SUCH AS FLUID
RESTRICTION, HYPERVENTILATION, AND ADMINISTRATION OF MUSCLE RELAXANTS,
OSMOTIC AGENTS, DIURETICS, BARBITURATES, AND STEROIDS, HAVE NOT BEEN
SHOWN TO BENEFIT THE DROWNING VICTIM, EITHER INDIVIDUALLY OR IN
COMBINATION.

27. • EEG MONITORING HAS ONLY LIMITED VALUE IN THE MANAGEMENT
AND IS GENERALLY NOT RECOMMENDED, EXCEPT TO DETECT
SEIZURES OR AS AN ADJUNCT IN THE CLINICAL EVALUATION OF
BRAIN DEATH.
• SEIZURES SHOULD BE TREATED IF POSSIBLE, ALTHOUGH THEY TEND
TO BE VERY REFRACTORY.
• THERE IS NO EVIDENCE THAT TREATMENT OF SEIZURES AFTER
DROWNING IMPROVES OUTCOME.
• FOSPHENYTOIN OR PHENYTOIN LOADING DOSE FOLLOWED BY
MAINTENANCE DOSING MAY BE CONSIDERED.IT MAY HAVE SOME
NEUROPROTECTIVE EFFECTS AND MAY MITIGATE NEUROGENIC
PULMONARY EDEMA.

28. • WITH OPTIMAL MANAGEMENT, MANY INITIALLY COMATOSE
CHILDREN CAN HAVE IMPRESSIVE NEUROLOGIC IMPROVEMENT,
BUT USUALLY DO SO WITHIN THE 1ST 24-72 HR.
• ALMOST HALF OF DEEPLY COMATOSE DROWNING VICTIMS
ADMITTED TO THE PICU DIE OF THEIR HYPOXIC BRAIN INJURY OR
SURVIVE WITH SEVERE NEUROLOGIC DAMAGE.
• MANY CHILDREN BECOME BRAIN DEAD.
• DEEPLY COMATOSE DROWNING VICTIMS WHO DO NOT SHOW
SUBSTANTIAL IMPROVEMENT ON NEUROLOGIC EXAMINATION
AFTER 24-72 HR AND WHOSE COMA CANNOT BE OTHERWISE
EXPLAINED SHOULD BE SERIOUSLY CONSIDERED FOR WITHDRAWAL
OF SUPPORT.

29. HYPOTHERMIA MANAGEMENT
• DAMP CLOTHING SHOULD BE REMOVED FROM ALL DROWNING VICTIMS.
• THE GOAL IS TO PREVENT OR TREAT MODERATE OR SEVERE HYPOTHERMIA.
• REWARMING MEASURES ARE GENERALLY CATEGORIZED AS PASSIVE, ACTIVE
EXTERNAL, OR ACTIVE INTERNAL.
• PASSIVE REWARMING MEASURES CAN BE APPLIED IN THE PRE-HOSPITAL OR
HOSPITAL SETTING.
• THEY INCLUDE THE PROVISION OF DRY BLANKETS, A WARM ENVIRONMENT, AND
PROTECTION FROM FURTHER HEAT LOSS.
• REWARMING MEASURES SHOULD BE INSTITUTED AS SOON AS POSSIBLE FOR
HYPOTHERMIC DROWNING VICTIMS WHO HAVE NOT HAD A CARDIAC ARREST.

30. • FULL CPR WITH CHEST COMPRESSIONS IS INDICATED FOR
HYPOTHERMIC VICTIMS IF NO PULSE CAN BE FOUND OR IF
NARROW COMPLEX QRS ACTIVITY IS ABSENT ON ECG.
• WHEN VF IS PRESENT IN SEVERELY HYPOTHERMIC VICTIMS (CORE
TEMPERATURE <30°C), UP TO 3 DEFIBRILLATION ATTEMPTS
SHOULD INITIALLY BE DELIVERED, BUT FURTHER DEFIBRILLATION
ATTEMPTS SHOULD BE HELD UNTIL THE CORE TEMPERATURE IS
≥30°C, AT WHICH TIME SUCCESSFUL DEFIBRILLATION MAY BE
MORE LIKELY.

31. • THERE IS SIGNIFICANT CONTROVERSY REGARDING THE
DISCONTINUATION OF PROLONGED RESUSCITATIVE EFFORTS IN
HYPOTHERMIC DROWNING VICTIMS.
• VICTIMS WITH PROFOUND HYPOTHERMIA MAY APPEAR CLINICALLY
DEAD, BUT FULL NEUROLOGIC RECOVERY IS POSSIBLE, ALTHOUGH
RARE.
• BODY TEMPERATURE, WHETHER THE WATER WAS ICY OR THE
COOLING WAS VERY RAPID WITH FAST-FLOWING COLD WATER
SHOULD BE TAKEN INTO ACCOUNT BEFORE RESUSCITATIVE

32. • REWARMING EFFORTS SHOULD USUALLY BE CONTINUED UNTIL THE TEMPERATURE IS
32-34°C.
• IF THE VICTIM CONTINUES TO HAVE NO EFFECTIVE CARDIAC RHYTHM AND REMAINS
UNRESPONSIVE TO AGGRESSIVE CPR, THEN RESUSCITATIVE EFFORTS MAY BE
DISCONTINUED.
• COMPLETE REWARMING IS NOT INDICATED FOR ALL ARREST VICTIMS BEFORE
RESUSCITATIVE EFFORTS ARE ABANDONED.
• DISCONTINUING RESUSCITATION IN VICTIMS OF NON–ICY WATER SUBMERSION WHO
REMAIN ASYSTOLIC DESPITE 30 MINUTES OF CPR IS PROBABLY WARRANTED.
• ONCE A DROWNING VICTIM HAS UNDERGONE SUCCESSFUL CPR AFTER A CARDIAC
ARREST, TEMPERATURE MANAGEMENT SHOULD BE CAREFULLY CONSIDERED, AND

33. • VICTIMS IN WHOM RESUSCITATION DURATION HAS BEEN LONGER ARE MORE
LIKELY TO REMAIN COMATOSE; TEMPERATURE MANAGEMENT IN THESE
INDIVIDUALS IS AN AREA OF CONTROVERSY.
• FEVER COMMONLY DEVELOPS WITHIN THE 1ST 24-48 HR OF DROWNING.
• FEVER OR HYPERTHERMIA (CORE BODY TEMPERATURE >37.5°C) IN COMATOSE
DROWNING VICTIMS RESUSCITATED FROM CARDIAC ARREST SHOULD BE
PREVENTED AT ALL TIMES IN THE ACUTE RECOVERY PERIOD (AT LEAST THE 1ST
24-48 HR).
• HYPERTHERMIA AFTER DROWNING MAY INCREASE THE RISK OF MORTALITY AND
EXACERBATE HYPOXIC-ISCHEMIC CNS DAMAGE.

34. THERAPEUTIC HYPOTHERMIA
• FOR DROWNING VICTIMS WHO REMAIN COMATOSE AFTER SUCCESSFUL CPR,
MORE IMP ISSUES INCLUDE:
• REWARMING OF HYPOTHERMIC VICTIMS.
• CONTROLLED APPLICATION OF THERAPEUTIC HYPOTHERMIA.
• HYPOTHERMIC DROWNING VICTIMS WHO REMAIN UNRESPONSIVE BECAUSE OF
HYPOXIC-ISCHEMIC ENCEPHALOPATHY AFTER RESTORATION OF ADEQUATE
SPONTANEOUS CIRCULATION SHOULD NOT BE ACTIVELY REWARMED TO
NORMAL BODY TEMPERATURES.
• ACTIVE REWARMING SHOULD BE LIMITED TO VICTIMS WITH CORE BODY
TEMPERATURES <32°C, BUT TEMPERATURES 32-37.5°C SHOULD BE ALLOWED
WITHOUT FURTHER REWARMING EFFORTS.

35. • THE 2002 WORLD CONGRESS ON DROWNING RECOMMENDED
THAT HYPOTHERMIA (32-34°C) BE INSTITUTED AS SOON AS
POSSIBLE AFTER RESUSCITATION AND SUSTAINED FOR 12-24 HR.
• THESE PATIENTS SHOULD BE INTUBATED, MECHANICALLY
VENTILATED, AND TREATED WITH SEDATIVES AND/OR ANALGESICS
(WITH OR WITHOUT NEUROMUSCULAR BLOCKING AGENTS) AS
NECESSARY TO PREVENT SHIVERING AND MAINTAIN
HYPOTHERMIA.
• REWARMING AFTER THIS PERIOD SHOULD BE VERY GRADUAL.

36. • A SPECIFIC RECOMMENDATION FOR THERAPEUTIC HYPOTHERMIA,
ESPECIALLY IN CHILDREN, IS NOT YET GENERALLY ACCEPTED.
• THE ADVANCED LIFE SUPPORT TASK FORCE OF THE
INTERNATIONAL LIAISON COMMITTEE ON RESUSCITATION (2002)
DID NOT RECOMMEND THERAPEUTIC HYPOTHERMIA IN CHILDREN
RESUSCITATED AFTER CARDIOPULMONARY ARREST.

37. OTHER MANAGEMENT ISSUES
• ACUTE RENAL FAILURE :
• DIURETICS,
• FLUID RESTRICTION.
• DIALYSIS IF REQUIRED.
• PROFUSE BLOODY DIARRHEA AND
MUCOSAL SLOUGHING :
• BOWEL REST.
• NASOGASTRIC SUCTION.
• GASTRIC PH NEUTRALIZATION.
• FEVER :
• ALMOST HALF OF DROWNING
VICTIMS HAVE A FEVER DURING THE
1ST 48 HR AFTER SUBMERSION.
• HYPERTHERMIA IS USUALLY NOT DUE
TO INFECTION AND RESOLVES
WITHOUT ANTIBIOTICS IN
APPROXIMATELY 80% OF PATIENTS.
• PROPHYLACTIC ANTIBIOTICS ARE
NOT RECOMMENDED.

38. PROGNOSIS
• THE OUTCOMES FOR DROWNING VICTIMS ARE REMARKABLY BIMODAL.
• MAJORITY OF VICTIMS EITHER HAVE A GOOD OUTCOME (INTACT OR MILD
NEUROLOGIC INJURY) OR A BAD OUTCOME (PERSISTENT VEGETATIVE STATE OR
DEATH).
• FINNISH STUDY OF PEDIATRIC DROWNING SHOWED SUBMERSION DURATION WAS
THE BEST PREDICTOR OF OUTCOME.

39. • THE GCS SCORE HAS SOME LIMITED UTILITY IN PREDICTING
RECOVERY.
• IMPROVEMENT IN THE GCS SCORE DURING THE FIRST SEVERAL
HOURS OF HOSPITALIZATION MAY INDICATE A BETTER PROGNOSIS.
• NEUROLOGIC EXAMINATION AND PROGRESSION DURING THE 1ST
24-72 HR ARE CURRENTLY THE BEST PROGNOSTIC INDICATORS OF
LONG-TERM CNS OUTCOME.

40. THANK
YOU