NEAR DROWNING

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NEAR DROWNING Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta

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NEAR DROWNING. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. Objectives. Definition Incidence, epidemiology, causes Prognosis Interventions/managements Opportunities that impact outcome. Definition. - PowerPoint PPT Presentation

Transcript of NEAR DROWNING

Page 1: NEAR DROWNING

NEAR DROWNING

Pediatric Critical Care MedicineEmory University

Children’s Healthcare of Atlanta

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Objectives• Definition• Incidence, epidemiology, causes• Prognosis• Interventions/managements• Opportunities that impact outcome

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Definition• Drowning: die within 24 hours of a submersion

incident• Near Drowning: survive at least 24 hrsafter a

submersion incident

» 2002 World Congress: all victims to be labeled as drowning

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Incidence/Epidemiology• CDC 2012 for 2005-2009 for US

– ~3,880 fatal drowning, 2X treated in ER for non-fatal drowning

– Leading cause of injury death among children 1-4 yrs, highest rate

– 2nd leading cause of all accidental deaths <14 yr (MVC 1st)

– Fatality: male>female (42.07:0.54/100,000– African-American

» 1.3X higher than Caucasian» 3.4X higher in 5-14 yo age group

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Incidence• For every 1 death

– 4 others hospitalized a– 14 seen in the ER

• incidence: holidays, weekends and warm weather

• Children <5 pools; older kids and adults in open water• Fatality: 35%; 33% with neurological

impairment; 11% severe neurologic sequelae

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CausesSalt Water 1-2%

Fresh water 98%

swimming pools: public 50%

swimming pools: private 3%

lakes, rivers, streams, storm drains 20%

bathtubs 15%

buckets of water 4%

fish tanks or pools 4%

toilets 1%

washing machines 1%

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Causes• Toddlers:

– Lapse of supervision– Afternoon/early evening-meal time– 84% with responsible supervising adults– Only 18% of cases actually witnessed

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Causes• Recreational boating

– 90% of deaths due to drowning» Vast majority are not wearing life jackets

– 1,200/yr– Small, open boats– 20% of deaths

» Too few or no floatation devices!

• Diving – 700-800/yr– 1st drive in unfamiliar water– 40-50% alcohol related

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Causes• Spas, hot tubs

– Entrapment in drains, covers

• Buckets drowning– males/>females– African-Americans>caucasians– Warm months>cold

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Causes• Epilepsy:

– 1.5-4.6 % had pre-existing seizure disorder– >5 yr, drown in bathtub, not be supervised

• Long QT syndrome:– Swimming may be a trigger for LQTS– Near drowning may be first presentation– Specific gene KVLQT1 mutation associated w/swimming

trigger & submersion

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Laryngospasm

recurs

Unexpected

Submersion

Aspiration &

Laryngospasm anoxia, seizures

and death without

aspiration (10%)

Laryngospasm

aborted

aspirationof

water (90%)

Stage I(0-2 minutes)

Stage II(1-2 minutes)

Swallows

water

Stage III

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Pathophysiology• Part I

– Voluntary breath-holding– Aspiration of small amounts into larynx– Involuntary laryngospasm– Swallow large amounts– Laryngospasm abates (due to hypoxia)– Aspiration into lungs

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Pathophysiology• Part II

– Decrease in sats– Decrease in cardiac output– Intense peripheral vasoconstriction– Hypothermia– Bradycardia– Circulatory arrest, while VF rare– Extravascular fluid shifts, diuresis

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Pathophysiology• Diving reflex

– Bradycardia, apnea, vasoconstriction– Relatively quite weak in humans

» better in kids

– Occurs when the face is submerged in very cold water (<20°C)

– Extent of neurologic protection in humans due to diving reflex is likely very minimal

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Pathophysiology• Asphyxia, hypoxemia, hypercarbia, & metabolic

acidosis• Fresh water vs salt water - little difference

(except for drowning in water with very high mineral content, like the Dead Sea)

• Hypoxemia– Occlusion of airways with water & particulate debris– Changes in surfactant activity– Bronchospasm– Right-to-left shunting increased– Physiologic dead space increased

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Pathophysiology• Cardiac arrhythmias• Hypoxic encephalopathy• Renal insufficiency• Pulmonary injury• Global brain anoxia & potential diffuse cerebral

edema

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Pathophysiology – Cerebral edema

• Initial hypoxia• Post resuscitation cerebral hypoperfusion

– Increased ICP – Cytoxic cerebral edema:

» BBB remains intact: derangement in cellular metabolism resulting in inadequate functioning of the Na & K pump

– Excessive accumulation of cytosolic calcium causing cerebral arterial spasm

• Lance-Adams syndrome – with sign hypoxia– Post hypoxic (action) myoclonus, often mistaken for sz– Happens more often with coming out of sedation– Must be differentiated from myoclonic status (poor prognosis)

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Pathophysiology – Pulmonary Injury

• Aspiration as little as 1-3 cc/kg can cause significant effect on gas exchange– Increased permeability– Exudation of proteinaceous material in alveoli– Pulmonary edema– decreased compliance

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Pathophysiology – fresh vs. salt

• Both forms wash out surfactant– Damaged alveolar basement membrane pulmonary

edema, ARDS

• Theoretical changes not supported clinically– Salt water: hypertonic pulmonary edema– Fresh water: plasma hypervolemia, hyponatremia– Unless in Dead Sea

• Humans (most aspirate 3-4cc/kg) – Aspirate > 20cc/ kg before significant electrolyte

changes– Aspirate > 11cc/kg before fluid changes

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Pathophysiology• Findings at autopsy

– Wet, heavy lungs– Varying amounts of hemorrhage and edema– Disruption of alveolar walls– ~70% of victims had aspirated vomitus, sand, mud, and

aquatic vegetation– Cerebral edema and diffuse neuronal injury– Acute tubular necrosis

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Pathophysiology – Pulmonary edema

• Findings at autopsy– Wet, heavy lungs– Varying amounts of hemorrhage and edema– Disruption of alveolar walls– ~70% of victims had aspirated vomitus, sand, mud, and

aquatic vegetation– Cerebral edema and diffuse neuronal injury– Acute tubular necrosis

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Signs & Symptoms• 70% develops sxs within 7 hrs• Alertness agitation coma• Cyanosis, coughing & pink frothy sputum (pulm

edema)• Tachypnea, tachycardia• Low grade fever• Rales, rhonchi & less often wheezes• Signs of associated trauma to the head & neck

should be sought

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Prognosis• Better outcomes associated with early CPR

(bystander)• C-spine protection:• Transport

– Continue effective CPR– Establish airway– Remove wet clothes– Hospital evaluation

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Labs & Tests • Min electrolyte changes• Increase WBC• Hct & HgB normal

initially– Fresh water: Hct falls due

to hemolysis– Inc. in free HgB w/o a

change in Hct

• DIC occasionally• ABG – metabolic

acidosis & hypoxemia

• EKG– Sinus tach, non spec

ST-segment & T-wave changes

– Resolved within hrs– Ominous- vent

arrhythmias, complete heart block

• CXR– May be nl initially– Patchy infiltrate– Pulm edema

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Treatment • ED eval• Admit if: CNS or respiratory symptoms• Observe for 4-6 hours if

– Submersion >1min– Cyanosis on extraction– CPR required

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Treatment: ED discharge • ED eval• Admit if: CNS or respiratory symptoms• Observe for 4-6 hours if

– Submersion >1min– Cyanosis on extraction– CPR required

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Predicting Ability for ED Discharge

• Several studies support selected ED discharge• Child can safely be discharged home if at 6 hours

after ED presentation:– GCS > 13– Normal physical exam/respiratory effort– Room air pulse oximetry oxygen saturation > 95%

-Causey et al., Am J Emerg Med, 2000

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ICU treatment: Respiratory• PPV• Treatment of bronchospasm• Steroids: no benefits• Bronchoscopy• Prophylactic abx: no benefits• Surfactant: no beneficial

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ICU treatment: Cardiovascular• Re-warming • CBF decrease 6-7% / ºC drop

– LOC 34ºC– Pupil dilate at 30ºC– V-fib 28ºC– EEG isoelectris 20ºC

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ICU treatment: CNS• ICP monitoring - not indicated, typically irreversible

hypoxic cellular injury• Brain CT – not indicated, unless TBI suspected• Mild hyperventilation?• Osmotherapy – not indicated• Corticosteroids (dexamethasone) - no proven benefit• Seizures - treat aggressively• Shivering or random, purposeless movements can

increase ICP• Hypothermia and barbiturate coma - highly

controversial & unlikely to benefit the patient (31 comatose kids, J Modell, NEJM 1993) -

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ICU treatment: Others• Antibiotics: no benefit or prophylaxis, may

increase superinfection• Fulminant strep pneumo sepsis has been

described after severe submersion• Steroids – no demonstrated benefit

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Prognosis predictors• Poor outcomes

– Age < 3yrs– Submersion time: >10 min– Time to BLS >10 min– Serum pH: <7.0– CPR >25 min– Initial core temp <33ºC– GCS <5

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Prognosis predictors

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Prognosis predictors

• Prolonged resuscitation may increase the success of resuscitation w/o normal neurologic recovery

After 25 min of full but unsuccessful resuscitation, thin “PROGNOSIS” -

Submersion time survival Fatality

0-5 min 7/67 10%

6-9 min 5/9 56%

10-25 min 21/25 88%

>25 min 4/4 100%

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Effects of near drowning• Divorce• Sibling psychosocial maladjustment• 100,000 yrs of productive life lost• $4.4 million/yr in direct health care costs• $350-450 million/yr in direct costs

– $100,000/yr to care for the neurologically impaired survivor of a near drowing

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