Deadly Air
Case
23 yo F BIBEMS s/p suicide attempt.
Patient was found unconscious in bathtub after
making comments about suicidal ideation.
She was foaming at the
mouth, with empty bottles
of Advil PM and Tylenol
PM, and a charcoal grill lit
nearby.
Family members report recent EtOH use.
EMS Report
EMS reports patient is confused but able to move
all extremities and follow commands.
SpO2 measured in the
field to be 90%.
Carboxyhemoglobin level
measured at 50%.
Patient was given 100% O2 at 15
LPM by NRB and transported to
Elmhurst hospital.
Initial Hospital Workup
Carboxyhemoglobin level measured at 1:30 am
at Elmhurst hospital to be 44%.
Measured again
45 mins later to be
11.7%.
Patient was
transferred to Jacobi
Hospital by EMS,
arrived at 4:30 am.
History
Patient did not remember events leading up to her
arrival at Jacobi, and did not want to talk about
what she did remember from earlier.
Pt only c/o some mild SOB.
Pt denied any chest pain, headache, body aches,
dizziness or nausea.
History
PmHx: TMJ
PsHx: none
Meds: metformin (self-prescribed)
All: NKDA
FamHx: breast cancer, DM, Alzheimer’s
SocHx: occ EtOH, pt denies smoking, drug use
Vitals
Temp: 98.3° F
HR: 69
RR: 20
BP: 121/84
SpO2: 94%
With an SpO2 of 94%, is she fine?
Carbon monoxide diffuses rapidly across the pulmonary
capillary membrane and binds to the iron component of
hemoglobin with 240x the affinity of oxygen.
The standard pulse oximeter
cannot distinguish between
carboxyhemoglobin and
oxyhemoglobin, and will measure
a falsely elevated level.
Physical Exam
Gen: Pt awake & alert in bed,
slightly confused, NAD
HEENT: NCAT, PERRL, EOMI, MMM,
anicteric sclera, clear conjunctivae
CV: RRR, normal S1/S2, no chest
wall tenderness, no M/R/G
LUNGS: slightly shallow breathing,
CTA bilat, no wheezes/crackles,
equal respiratory effort
Physical Exam
ABD: soft, NT/ND, +BS, no organomegaly
EXT: 2+ pulses x4, no track marks, no edema
Neuro: A&Ox3, but no memory
of events leading up to incident,
able to recall 3/3 words, CN IIXII grossly intact, no facial
droop, EOMI, no gait
abnormalities, reflexes 2+ in all
extremities
Labs
13.4
226
17.2
44
141 109
Calcium: 7.8
troponin I: 5.164
CK: 1133
91 57
EtOH level: < 10
ASA level: < 1
Tylenol level: < 10
51
PT: 9.8
PTT: 20.1
INR: 1.0
βhcG: neg
13
4.3 23.5 0.7
89
6.4 3.9
0.3
Complications of CO Poisoning
Acute myocardial injury is common in cases of CO
poisoning, and is associated with an increased long-term
mortality.
In a 2005 cohort study by Satran et al, 230 patients exposed to
varying levels of carbon monoxide showed ischemic changes on
EKGs in 30%, biomarkers diagnostic of myocardial injury in 35%
and in-hospital mortality in 5% (12 patients, 8 from anoxic brain
injury).
Ten year follow-up in 2006 showed an overall mortality of 24%
in these patients, with myocardial injury (as determined by
elevated biomarkers or ischemic EKG changes) being a
significant predictor of mortality (adjusted hazard ratio of 2.1).
Complications of CO Poisoning
Neurologic sequelae are the most frequent form of morbidity in
CO poisoning, from hypoxic brain injury and white matter
demyelination. Necrosis of the globus pallidus is the most
common site of injury.
Delayed neurologic sequelae have been seen weeks to months
after apparent recovery, marked by cognitive deficits, personality
changes, movement disorders and focal neurologic deficits.
(Lo et al. 2007)
Unenhanced CT scan about 16 hours after injury
shows bilaterally symmetric low attenuation
lesions in the cerebellum (blue arrows), globus
pallidus (red arrows) and caudate nuclei (white
arrows). The patient was in a house fire.
(learningradiology.com)
Now What?
Initial Management of CO Poisoning:
Prompt removal of patient from environment
ABCs, consider intubation
High-flow O2
Management of co-ingestion
+/- Hyperbaric oxygen treatment
Hyperbaric Oxygen
Hyperbaric oxygen therapy exposes patients to 100% oxygen
under supra-atmospheric pressure.
This decreases the half-life of COHb from approx 90 mins on
100% O2 to 30 mins on hyperbaric O2.
Indications for initiation of hyperbaric therapy:
COHb level > 25%
evidence of ongoing end-organ ischemia
loss of consciousness
pregnant women with COHb > 20% of evidence of fetal distress
Greatest benefit is seen when treatment is given early, no benefit
has been shown when patients are treated > 12hrs after
exposure
Hyperbaric Oxygen
Weaver L, Hopkins R, Chan K, et al. Hyperbaric oxygen for acute
carbon monoxide poisoning. New England Journal of Medicine
2002; 347(12): 1057.
Single-center, double-blind trial that randomly assigned 152 patients
symptomatic acute carbon monoxide poisoning to either three hyperbaric
oxygen treatments or one normobaric oxygen treatment plus two sessions of
normobaric room air.
Neuropsychological tests were administered immediately after the sessions and
2 weeks, 6 weeks, 6 months and 1 year later. The primary outcome measured
was cognitive sequelae 6 weeks after treatment.
The trial was stopped early, with 76 patients in each group. Cognitive sequelae
were less frequent in the hyperbaric oxygen treatment group (25.0% vs 46.1%).
Hyperbaric Oxygen
5 ½ hours after exposure, the
patient was given 2.8 ATM for
46 minutes, given in two dives
of 23 minutes each.
After the treatments, she
reported improved breathing,
with less difficulty taking deep
breaths.
Remaining Hospital Course
Labs improved:
repeat WBC at 6:30 am: 9.4
repeat cardiac enzymes:
5:30 pm:
Troponin I: 4.200
CK: 428
2:15 am:
Troponin I: 1.419
Pt was admitted to the burn unit at 8:00 am.
Labs continued to trend down, and she was transferred to
the psych unit two days later.
Take-Home Points
•
Carbon monoxide diffuses rapidly across the
pulmonary capillary membrane and binds to
hemoglobin with very high affinity, decreasing its
ability to transport oxygen.
•
Clinical findings of carbon monoxide poisoning are largely
nonspecific but sequelae may include myocardial ischemia and
delayed cognitive deficits.
•
Obtain a COHb level whenever CO poisoning is suspected,
because SpO2 will give a falsely elevated level.
•
The most important interventions are airway control, prompt
administration of O2 +/- hyperbaric oxygen treatment.
References
Clardy P, Manaker S, Perry H. Carbon monoxide poisoning. UpToDate, Traub S, UpToDate, 2013.
Crawford Mechem C, Manaker S. Hyperbaric oxygen therapy. UpToDate, Traub S, UpToDate 2013.
Henry S, Satran D, Lindgren B, et al. Myocardial injury and long-term mortality following moderate to severe
carbon monoxide poisoning. JAMA 2006; 295(4): 398-402.
Juurlink D, Buckley N, Stanbrook M, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane
Database Syst Rev 2005; :CD002041.
Kwon OY, Chung SP, Ha YR, et al. Delayed postanoxic encephalopathy after carbon monoxide poisoning. Emerg
Med J 2004; 21:250.
Lo C, Chen S, Lee K, et al. Brain injury after acute carbon monoxide poisoning: early and late complications.
Neuroradiology 2007; 189(4): W205-11.
Satran D, Henry CR, Adkinson C, et al. Cardiovascular manifestations of moderate to severe carbon monoxide
poisoning. J Am Coll Cardiology 2005. 45(9): 1513-6.
Weaver L, Hopkins R, Chan K, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. New England
Journal of Medicine 2002; 347(12): 1057.
Weaver L, Valentine K and Hopkins R. Carbon monoxide poisoning: risk factors for cognitive sequelae and the
role of hyperbaric oxygen. American Journal of Respiratory and Critical Care Medicine 2007; 176(5):491-7.