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.

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Transcript 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.

NEAR DROWNING
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Objectives
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Definition
Incidence, epidemiology, causes
Prognosis
Interventions/managements
Opportunities that impact outcome
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
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~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
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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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Causes
Salt Water
1-2%
Fresh water
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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%
Causes
• Toddlers:
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Lapse of supervision
Afternoon/early evening-meal time
84% with responsible supervising adults
Only 18% of cases actually witnessed
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
aborted
Unexpected
Submersion
Aspiration &
Laryngospasm
Swallows
water
Laryngospasm
recurs
Stage I
(0-2 minutes)
aspiration
of
water (90%)
Stage II
(1-2 minutes)
anoxia, seizures
and death
without
aspiration (10%)
Stage III
Pathophysiology
• Part I
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Voluntary breath-holding
Aspiration of small amounts into larynx
Involuntary laryngospasm
Swallow large amounts
Laryngospasm abates (due to hypoxia)
Aspiration into lungs
Pathophysiology
• Part II
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Decrease in sats
Decrease in cardiac output
Intense peripheral vasoconstriction
Hypothermia
Bradycardia
Circulatory arrest, while VF rare
Extravascular fluid shifts, diuresis
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
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Occlusion of airways with water & particulate debris
Changes in surfactant activity
Bronchospasm
Right-to-left shunting increased
Physiologic dead space increased
Pathophysiology
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Cardiac arrhythmias
Hypoxic encephalopathy
Renal insufficiency
Pulmonary injury
Global brain anoxia & potential diffuse cerebral edema
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
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Increased permeability
Exudation of proteinaceous material in alveoli
Pulmonary edema
decreased compliance
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
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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
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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
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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
Prognosis
• Better outcomes associated with early CPR (bystander)
• C-spine protection:
• Transport
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Continue effective CPR
Establish airway
Remove wet clothes
Hospital evaluation
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
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• EKG
– Sinus tach, non spec STsegment & T-wave changes
– Resolved within hrs
– Ominous- vent arrhythmias,
complete heart block
• CXR
– May be nl initially
– Patchy infiltrate
– Pulm edema
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
ICU treatment: Respiratory
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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
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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)
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
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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
Submersion time
survival
Fatality
0-5 min
7/67
10%
6-9 min
5/9
56%
21/25
88%
4/4
100%
10-25 min
>25 min
• Prolonged resuscitation may increase the success of
resuscitation w/o normal neurologic recovery
 After 25 min of full but unsuccessful resuscitation, thin
“PROGNOSIS”
Effects of near drowning
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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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