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Drowning Dr Abhijeet Deshmukh Fellow in PICU & NICU

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Drowning

DrowningDr Abhijeet DeshmukhFellow in PICU & NICU

DefinitionDrowning as the process of experiencing respiratory impairment from submersion/immersion in liquid. (WHO)The definition implies that a drowning victim develops an airliquid interface that prevents the breathing of air.

Terms Near drowning/secondary drowning etc are abondoned

Types of drowning1. Wet drowning= primary drowning2. 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 pneumonitis4. Immersion syndrome= hydrocution= submersion inhibition; cold water n. endings +/ strike epigastrium +/ entering ear drums, nasal passages. Horizontal entry (dive) pressure on abdomenAll these Vagal inhibition Cardiac arrest death

Epidemiology30% Deaths from 1-4 years

2nd leading cause of unintentional injury related deaths in 1-14yrs.Two age groups 15 yearsMales>Females

Risk factorsAge -15 years- d/t risk taking beheviour ( Swimming, boating, alcohol/drug)

Medical conditions :Seizure disorder - (7%) Hyperventilation ppt seizuresLong QT syndrome or other channelopathies - Activation of diving reflex and alters autonomic activityUse of alcohol or other substances (25%)Other conditions that less frequently predispose to drowning:DepressionCoronary artery diseaseCardiomyopathyHypoglycemiaHypothermia

Pathophysiology

SEQUENCE OF EVENTS IN DROWNING1. SENSE OF PANICExpressed by:Violent struggleAutomatic swimming movementsUsually followed by:

2. PERIOD OF VOLUNTARY APNOEADuration: 1-2 minutes.Hypoxemia, hypercapnia, R & M acidosis.

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3. ATTEMPT AT TAKING A BREATHWATER:May be freely inhaledOr, may cause glottic spasm due to impingement.In 10-15 % victims: glottic spasm severe asphyxia water may not enter the lungs unless subcouncious.Dry drowningIn 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

2 major pathophysiological factors- Hypoxemia- HypothermiaHypoxemia :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

Hypothermia :- Two types1. Primary hypothermia : Sudden submersion in Ice cold water ( 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.

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

Consequences of hypothermia :- Flaccid paralysis and unconsciousness if temp 11ml/kg of fluid is required to alter blood volumeAspiration of >22ml/kg for electrolyte disturbancesMost are Hypovolemic regardless the type of aspiration fluid because of excessive capillary permeability d/t asphyxia & loss of protein rich fluid in alveoli

Organ specific effectsPulmonary 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

- 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.

- 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.

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

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.

Conns criteria (Extent of cerebral hypoxia) :A : AwakeB : Blunted conciousnessC : Comatose

The vascular end zones are particularly vulnerableWatershed area infarctions may be appreciated on CT scan with ground glass appearance.

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 deliveryworsening cardiac output and decreased myocardial perfusion pressure.

Cytosolic calcium overload and oxygen-derived free radicals myocardial injury Cardiogenic shockhypoxic damage to the myocardium. Hallmark of cardiovascular dysfunction with submersion injury is shockMetabolic acidosis may further impair myocardial performance

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

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

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.

ManagementAt 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

Emergency room

PrognosisSuccess 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

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 stateNeed 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

Thank You !ReferencesZimmerman Pediatric critical care (4th ed)Rogers Textbook of pediatric critical care.