Transcript CO poisoning - Lenox Hill Hospital

Carbon Monoxide
Poisoning
Joshua Rocker, MD
Pediatric Emergency Medicine
Schneider Children’s Hospital
The Basics
• CO is an odorless, tasteless, colorless, non-irritating
gas formed by organic (hydrocarbon) combustion
The Basics
• CO binds hemoglobin with a much greater affinity
then O2 (200-250x) forming carboxyhemoglobin
(COHb)
Sources
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Motor Vehicle Exhaust
Smoke from fires
Gas powered equipment
Non-electric heaters (kerosene, gas water)
Charcoal or Hibachi grills
Spray paint, solvents, methylene chloride,
degreasers and paint removers
Risks for exposure
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Riding in back of pickup trucks
Swimming behind motor boat
Industrial workers where combustion occurs
Personnel at fire scenes
Using combustion engines indoors
Using non-electric heating devices without proper
ventilation
Epidemiology
• 40,000 ER visits per year
• 5,000-6,000 deaths per year
• Accidental CO poisoning only responsible for
approximately 500 deaths annually
• Leading cause of accidental poisoning deaths in
America
Recent Trend
Data from the CDC
All U.S.A. Deaths from CO
Poisoning, 1979 – 1988
• Highest death rates among: males, blacks, the
elderly, and residents of northern states
• Motor vehicle exhaust caused 57% of
unintentional deaths
• 83% of deaths associated with stationary
automobiles
Cobb, N. & R.A. Etzel. (1991) Unintentional carbon monoxide-related deaths in the United States,
1979 through 1988. JAMA, 266, 659-663.
Age Distribution of cases
• <6 y/o- approximately 14%
• 6-19 y/o- approximately 16%
• >19 y/o- approximately 70%
Data for 1996 and 1997 from the Annual Report of the Am. Assoc. of Poison Control Centers, Toxic Exposure
Surveillance System (published in the American J. Emergency Medicine).
Symptoms
Symptoms
• Variable and nonspecific
• Cherry red lips or skin
• associated with high COHb, but rare
(2-3%) and insensitive
Symptoms
Fatigue
Headache
Frequency (%)
92
87
Dizziness
69
Sleep Disturbances
Cardiac Symptoms
Apathy
Nausea, vomiting
66
62
54
42
Memory Loss
Decreased Libido
Loss of Appetite
40
22
12
Symptoms
• Older child and adult symptoms are similar
• Symptoms of infant or young child may be more
vague and difficult to clarify
• Irritability, poor feeding
Symptoms loosely
associated with COHb level
Children Specific
• In theory children at higher risk of toxicity
• higher metabolic rate
• higher tissue oxygen demand
• Infants with high F-Hgb or other forms of anemias
may be at higher risk of deleterious effects
• Higher rate of lethargy and syncopy in children at
lower levels of COHb than expected
(Crocker,William: J Emerg Med, 1985.)
Be careful: Misdiagnoses
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Flu, viral syndrome
AGE
Migraine
Stroke
Alcohol Related Behavior
Psychiatric Disorder
CAD
Delayed Neuropsychiatric
Syndrome (DNS)
• Seen in up to 40% of those with significant
exposure
• Onset- 3-240 days after exposure
• Variable degrees of cognitive deficits,
personality changes, movement disorders or
focal neurological deficits
• In children may b/w difficulty in school
• May persist for years
DNS
• Cannot be reliably predicted
• Increased risk if patient presented with
LOC during acute phase
Pathophysiology
Pathophysiology
• Effects
• Oxygen delivery
• Total oxygen delivery diminished
• Oxygen utilization
• Asphyxia
Pathophysiology
• CO rapidly diffuses across pulmonary
capillary membrane and binds hemoglobin
forming COHb
• Once COHb is formed an allosteric change
occurs and the hemoglobin protein’s ability to
off-load the other 3 O2 is greatly diminished
TOTAL OXYGEN CONTENT DIMINSHED
Oxyhemoglobin
dissociation curve:
Left shift
Left shift- ↓ P50
↑ affinity
(↑ pH, ↓DPG, ↓temp,
CO, met-hgb,F-hgb)
Right shift- ↑ P50
↓ affinity
Pathophysiology
• CO also interferes with peripheral O2
utilization by impairing oxidative
phosphorylation in the mitochondria
ASPHYXIA
But…
• neither the transient hypoxemia nor the
transient asphyxia explains the symptoms in
full- especially the DNS.
Neuropathopysiology
• CO binds to cytochrome oxidase which
caused oxidative stress
• NO is released from platelets and endothelial
cells
• Form free radical peroxynitrite
• Damages the neural vascular endothelium
• END RESULT: lipid peroxidation of the brain
occurs during recovery
Lipid Peroxidation
• With perfusion of brain- leukocytes adhesion
and subsequent release of destructive
enzymes
• Excitatory AA exacerbation oxidative injury
Neuropathophysiology
• CO has predilection for the basal ganglia
• Explain movement abnormalities
• Autopsy results show involvement of: cerebral
cortex, hippocampus, cerebellum and
substantia nigra
• Explain the diverse neurological
abnormalities
Laboratory evaluation
• VBG/ABG, COHb, CPK, CBC, lytes and EKG
• Consider: tox screen, EtOH level and cardiac
enzymes
COHb
• Normal levels
• Non-smokers: 0-3
• Smokers: 3-5 (can be up to 10)
• Elevation does not always directly translate to
more symptoms or worse prognosis
Management
Management
#1- GET OUT!!!!!!
Management
• 1- Remove oneself from source of CO
• 2- Seek medical attention
• In ambulance- 100% non-rebreather
(NRB)
• In hospital- always …ABCs
Management
• 3. 100% NRB
• Half-life of COHb is 4-5 hours at RA
• Half-life is 40-80 minutes with NRB
• (Normobaric oxygen therapy- NBO)
Management
• 4. Hyperbaric Therapy
• Delivery 100% O2 at 2.5-3 atms of
pressure
• Alters the half life of COHb to less than 30
minutes.
Hyperbaric Therapy:
• Henry’s Law
• amount of an ideal gas dissolved in a
solution is directly proportional to its partial
pressure.
• Dissolved Plasma Oxygen Content:
• RA @ 1 atm- 0.3 ml/dl
• 100% O2 @ 1 atm- 1.5 ml/dl
• 100% O2 @ 3 atm- 6 ml/dl
• Sufficient to meet resting O2 demands
regardless of hgb-O2 supply
HBO
• Single place vs multi-place chambers
• Raise pressure to 2.5-3 atms
• Length of tx- 45-300 minutes
• Concerns:
• Can child tolerate alone- if single
• Deterioration in chamber- can’t open
immediately
HBO
• Complications:
• 20%- reversible myopia
• 3-20%- otic barotrauma
• pulmonary barotrauma
• pulmonary oxygen toxicity
• seizures
HBO
• Absolute contraindications:
• Untreated pneumothorax
• Relative contraindications
• URI, sinus disease, claustrophobia
• Hx of seizure d/o, pneumothorax or chest
surgery
HBO: how does it work??
• Decreasing the occurrence of DNS does not
seem to be solely based on the COHb
elimination but rather on the reduction of free
radical production and lipid peroxidation.
HBO: how does it work
• Thom, SR: Antagonism of CO-mediated brain
lipid peroxidation by HBO. Toxicol Appl
Pharmacol, 1990, 105: 340-344.
• Animal study which revealed that HBOT
accelerated the elimination of CO from
bound cytochrome oxidase, therefore
preventing oxidative brain injury.
HBO: how about in kids?
• Rudge: CO poisoning in infants. South Med J 1993, 86: 334-337
• Complete neurological recovery in 13 of 14
children < 2 y/o receiving HBO
• Crocker and Walker: Pediatric CO toxicity. J Emerg Med 1985,
3: 443-448.
• No m and m among 16 children who
received HBO vs 25% developed DNS in
those receiving NBO.
• Kim and Coe: Clinical study on CO intoxication in children.
Yonsei Med J 1987, 28:266-273.
• 29.4% vs 19.4% (NBO vs HBO) with
neurological sequelae
•BUT…
HBO: controversy
• Tibbles and Perrotta: Treatment of Carbon
Monoxide poisoning: a critical review of
human outcome studies comparing NBO with
HBO. Ann Emerg Med, 1994.
• "no randomized, controlled, blinded clinical
trial demonstrated a clear advantage of
HBO over NBO in reducing morbidity and
mortality in carbon monoxide poisoning."
Criteria for HBO:
Although controversial, these are general
accepted
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Syncopy
Acutely severe neurological symptoms
MI
Cardiac Dysrhythmias
Persistent neuro symptoms
Pregnancy if >COHb15
Severe acidemia
Criteria to consider HBO
• COHb >20-25%
• <6 months with symptoms
• Children with underlying disease for whom
hypoxia may be deleterious
• > 60 y/o
Further Management
• Treat other issues…
• Hypotension- 2º to myocardial damage
• Hypoglycemia
• Cardiac Ischemia
• Smoke inhalation injuries
• Burns
• Seizures
• Rhabdomyolysis
Prevention
• Careful behavior
• Proper ventilation
• CO monitors
• “To protect against carbon monoxiderelated deaths, New York State
implemented a new law requiring carbon
monoxide detectors in all one- and twofamily houses, condominiums and co-ops
built on or after December 1, 2002.”
New York City Department of Health and Mental Hygiene
Miscellaneous
• Pulse oximetry may read normal or even
over-estimate the arterial hemoglobin oxygen
saturation
Hampson, NB. Pulse oximetry in severe carbon monoxide poisoning.
Chest, 1998; 114:1036-1041
Questions
A family of 5 presents to the ER. The 5 and 7 years old
children present with headaches and abdominal pain. The 6
month old is refusing feeds and is having diarrhea. Their
vitals are WNL. The mother passed out at home. What
should you do first?
• A. Call Jacobi and see if they will receive these
patients
• B. Call 1-800-POISONS
• C. Obtain COHb levels on all the children
• D. Put 100% NRB on the older children and give
20cc/kg NS bolus to the youngest
• E. Place all the children on 100% NRB
• ABCs
• 100% NRB to all
• Secondary survey may reveal a dehydrated
child which can be addressed but it is
secondary.
• HBO may be necessary but institute first line
therapy first.
• Yes, draw the levels- after O2.
A 9 yr old girl is brought to the ER because she is lethargic.
The mother returned home to find her minimally responsive.
The mother suffers from chronic lower back pain and has
medications in the home. The child is on winter vacation from
school. There home is heated with an old coal furnace. On
exam she is obtunded. Her vitals are: 36.8 C, HR 100, RR-8,
BP- 80/40. O2 sat is- 95%. With 100% NRB her sats increase
to 100%. Her skin is normal color. Her lungs are clear. Her
pupils are miotic. What is the most likely confirmatory study?
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A. CXR
B. Methemoglobin level
C. COHb level
D. Urine tox
E. LP
• CXR
• no respiratory distress only depression
• Methgb
• toxin-induced from ingestion or dermal exposure
to an oxidizing agent
• aniline
• dapsone,
• local anesthetics
• phenazopyridine
• nitrates/nitrites
• naphthalene
• Genetic
• dietary (eg, well water nitrates),
• idiopathic causes (acidosis).
• Patients usually present with cyanosis not
responsive to oxygen administration.
• COHb
• Right season
• right risk factors- indoor furnace
• right symptom- obtunded, but… miotic,
hypotensive and experiencing respiratory
depression. Still treat and w/u.
• Urine tox
• Where the money is. Mom with meds at
home and patient with signs of opiate tox.
• LP
• No fever, respiratory and BP involved.
Unlikely, but if else negative encephilitis is
possiblity.
QUESTIONS???