Download Carbon Monoxide Poisoning - MEDICINE DEPARTMENT of MMC

Carbon Monoxide Poisoning
Maria Rica P. Patawaran M.D.
Resident Grand Rounds
May 1, 2008
Objectives
1. To discuss the clinical features, diagnosis,
complications and treatment of CO
poisoning
2. Hyperbaric Oxygen Treatment
Case Presentation
•
•
•
•
•
•
B.A.
26 yo female
Single
Roman Catholic
Right-handed
No known co-morbidities
Case Presentation
CHIEF COMPLAINT:
Unresponsiveness
Case Presentation
4 mos PTA
• Voiced out relational
problems at work
• Noted to be indecisive;
difficulty concentrating;
more withdrawn, quiet and
had negative thoughts
2 weeks PTA
• More withdrawn and quiet
• Still had negative thoughts
• Evasive when asked about
reason for being depressed
Case Presentation
1 week PTA
• Went to a motel alone and
drank 1/8 bottle of
whiskey
• Advised psychiatric
consult but declined
2 weeks PTA
• Seen inside a their car
gasping with drooling of
the saliva.
• Also found unburnt
charcoals with thinner and
chinese herbal
medications for insomnia
MMC ER
Case Presentation
REVIEW OF SYSTEMS:
• No fever, no pallor
• No cough or colds,
dyspnea
• No chestpain,
orthopnea, PND
• No abdominal pain,
vomiting, no bowel
changes
• No dysuria, hematuria,
oliguria
• No bleeding diathesis
• No polyuria,
polydipsia, polyphagia
• No edema, cyanosis
Case Presentation
• Past Medical History: Unremarkable
• Family History: (+) Hypertension; Diabetes;
and Heart Disease
• Social History: Non-smoker and Nonalcoholic beverage drinker; Denies Illicit
drug use
Case Presentation
PE:
• Unconscious, GCS 5 (E1V2M2)
• BP:90/60 CR : 125 bpm, regular
RR: 16 cpm, regular T: 36.5C O2 sat 84%
• Pink palpebral conjucnctivae, anicteric
sclerae, (+) soot inside anterior nares
• Supple neck, no palpable cervical,
supraclavicular nor axillary LNs, neck veins
not distended, no carotid bruit
• SCE, no retractions, clear BS, no rales, no
wheezes
• Adynamic precordium, tachycardic, regular
rhythm, AB 6th LICS, MCL, no murmurs
• Flabby abdomen, normoactive bowel sounds,
soft, nontender, no hepatojugular reflux
• No edema, no cyanosis, full and equal pulses,
(+) soot stained fingertips
Case Presentation
Neurologic Examination:
• Mental Status: very drowsy; opens eyes to vigorous stimuli;
does not follow command
• Cranial Nerves:
CN: I – cannot be assessed
II – pupils 3-4mm ERTL
III,IV,VI – horizontal eye movements
V – not done
VII - grimaces to pain
VIII – XII – cannot be assessed
Case Presentation
Neurologic Examination:
• Sensory: LUE localizes to pain
RUE withdraws to pain
Both LE withdraws to pain
• Motor:
moves all extremities against resistance
• Pathologic Reflexes: Bilateral babinski; (+) ankle clonus (L)
• Meninges: supple neck
Case Presentation
Neurologic Examination
• Deep Tendon Reflexes
L
R
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++
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Case Presentation
• Salient Features:
 26 yo female
 No known Co-morbidities
 (+) Behavioral Changes
 unresponsive
 charcoals, thinner and chinese herbal medications
 (+) soot in the nares and fingertips
 GCS 5 (E1V2M2)
 (+) Babinski sign
Admitting Impression
• Inhalational Injury 2 to Carbon Monoxide
Poisoning
• Adjustment Disorder with Depressed
Features
Course in the Wards
At the ER
• Intubated with the ff MV settings:
FiO2 100%
vT 400
RR 20
PEEP 5
Peakflow 40L/min
• Referred to the ff services: Medico-legal and
Pulmonary Medicine
– Labs Requested: ABGs with CO Hb and Met Hb, CBC,
PT, PTT, CXR, 12L ECG, Spec 19, CBG
• IVF Started
• Immediately transferred to ICU
Course in the Wards
At the ICU
• Pulmonary Medicine:
– Antibiotics started: Co-amoxyclav 1.2 gms IV
q8
– Piracetam 1gm IV q8 hrs
• Referred to Neurology service
– Following tests requested:
• CT Scan - Normal
• EEG - Normal
• Drug Tests
– Started Citicholine 1gm IV q12
Course in the Wards
6 - 8 hours post-admission
• Repeat labs requested:
•
•
•
•
Electrolytes
BUN and Creatinine
Total CPK, CK-MB
Repeat ABGs with COHb and MetHb
• FiO2 decreased to 60%
Course in the Wards
2nd Hospital Day:
• Patient noted to be more awake and follows commands
• Feeding started
• Repeat CXR
• Patient shifted to CPAP with PS 10, PEEP 5, FiO2 30%
• Repeat labs:
• Electrolytes
• Total CPK and CK-MB
• Repeat ABGs
• Started on CoQ10 1 tab 3x a day, Abixa 1 tab daily and
Clexane
• Referred to Psychiatry Service
Course in the Wards
3rd Hospital day
• Babinski sign now absent
• Mech vent settings adjusted: CPAP, PS 5,
PEEP 3, FiO2 28%  in-line neb via Tpiece
• Repeat ABGs done
Course in the Wards
4th Hospital Day
• Patient extubated and shifted to nasal
cannula
• Feeding per orem started
• Allowed to move around with assist
• Started on Serraline (Zoloft) ½ tab OD
Course in the Wards
5th Hospital Day
• O2 and clexane discontinued
• Regular diet given
Course in the Wards
6th Hospital Day
• Transferred out of the ICU to NP ward
The rest of the hospital stay was
unremarkable
DISCUSSION
Pathophysiology
• CO is a colorless, odorless, nonirritant gas
• Known as the “Silent Killer”
• CO is diffusion-limited. Amount of CO absorbed
is dependent on:
– Level of CO in the environment
– Minute ventilation
– Duration of exposure
Pathophysiology
• Rapidly absorbed across alveolarcapillary membrane
• Hemoglobin’s affinity for CO is 200 to
250 times its affinity for oxygen
O2 Dissociation Curve
• CO binding to hemoglobin
causes allosteric
modifications increasing
its affinity for oxygen
• Shift of O2 dissociation
curve to the left
• Decreased tension at
which O2 is released from
hemoglobin
• Less O2 delivery to the
cells
Pathophysiology
• CO exerts toxic effects by combination of
tissue hypoxia and inflammatory activity
• 3 mechanisms of hypoxia:
• Decrease O2 capacity of Hgb
• Decrease uptake of bound oxygen into
tissues
• Impairs mechanism of cellular
respiration
Pathophysiology
• Other mechanisms of toxicity:
– Binding to cytochrome oxidase
– Lipid peroxygenation
– Reperfusion injury
– Binding to myoglobin
Pathophysiology
• CO poisoning in pregnancy
–
–
–
–
endogenous fetal production
fetal hemoglobin has a higher affinity for CO
longer elimination half-life in fetus
fetal hypoxia worsened by maternal shift of O2
dissociation curve to the left
Epidemiology
• Incidence is underestimated
• Most common cause of poisoning death
• Death rates higher in males, blacks, ages 15
to 24 and the elderly
• Higher in northern and midwestern states
– North Carolina 18th (‘79 to ‘88)
• More common in winter months
Sources of Carbon Monoxide
• Tobacco smoke is the largest source of
inhaled CO
– independent of nicotine levels
– HbCO levels chronically elevated
•
•
•
•
0.5% for nonsmokers
1.9% for one ppd
3% for two ppd
other sources - 3% to 8% for “heavy smokers”
Sources of Carbon Monoxide
• Endogenous production
• Motor vehicles produce approximately 250
million tons per year, much is converted to
CO2 in the upper atmosphere
• “Clean” fuels such as propane, butane, etc.
can also be culprits
Sources of Carbon Monoxide
• Methylene chloride (CH2-Cl2) found in
paint removers
– absorbed through the skin or inhaled
– metabolized in the liver to CO
– longer half-life
Diagnosis - Symptoms
• Symptoms are numerous and nonspecific
• Acute CO toxicity often misdiagnosed as an
acute viral syndrome, in part because of
increased frequency in winter months
Diagnosis - Symptoms
• Most common Sx from 3 case series:
–
–
–
–
–
–
headache
dizziness
weakness
nausea
difficulty conc./confusion
shortness of breath
91%
77%
53%
47%
43%
40%
Diagnosis - Symptoms
• Common symptoms cont.
–
–
–
–
–
visual changes
chest pain
loss of consciousness
abdominal pain
muscle cramping
25%
9%
6%
5%
5%
Diagnosis - Symptoms
• The Delayed Neuropsychiatric Syndrome
– Subacute manifestation (days to months)
– Occurs in spite of normal HbCO levels
– Broad variety of symptoms including cognitive
defects, personality changes, psychic akinesia,
parkinsonism, psychotic encephalopathy,
amnesia, incontinence, gait disturbances, etc.
Diagnosis - Symptoms
• The Delayed Neuropsychiatric Syndrome
– reported incidence varies widely, est. 10-30%
– can occur in initially asymptomatic patients
– symptoms can be subtle, often missed
• the Carbon Monoxide Neuropsychologic
Screening Battery consists of six subtests,
valuable for pre and post treatment and to
assess for later occurring Sx.
Diagnosis - Signs
• Physical exam signs are also generally
nonspecific
• tachypnea, tachycardia, vestibular signs
common
• cerebral edema if poisoning severe
• retinal hemorrhages uncommon but more
specific
Diagnosis - Signs
• Signs of smoke inhalation such as singed
nasal hairs, injured mucous membranes,
carbonaceous mucus discharge
• “Classic” findings of cherry-red lips, skin,
and mucus membranes are very rare
Diagnosis - Labs
• Carboxyhemoglobin
– measured with a co-oximeter
– arterial or venous blood sampling
– chronically elevated in smokers
– consider time of exposure to time of sampling
• Expired Carbon Monoxide
– monitor that measures CO in parts per million
then converts value to estimate HbCO
– gives rapid results and can be used at the scene
of suspected exposure
Diagnosis - Other
• Pulse Oximetry
– notoriously poor at detecting HbCO
– HbCO and HbO2 similar light absorbance, are
read as the same
– study of 25 CO exposed pts with measured
HbCO from 2.2-44% (mean of 16.1%), all had
simultaneous pulse-ox readings of 96-100%
Diagnosis - Labs
• Arterial Blood Gas
– may show metabolic acidosis
– normal to low normal PaO2
– HbO2 saturation is calculated from PaO2
• CK Levels
CPK and CK-MB Levels
CPK Levels
CK-MB Levels
Diagnosis - Other
• Other labs:
–
–
–
–
–
CBC
Electrolytes
BUN, Creatinine
Met-Hb
Toxicology screening
Diagnosis - Other
• Chest X-ray abnormalities in up to 30%, all
nonspecific and often related to associated
exposures or conditions
• Neuroimaging
– typically normal after acute exposure, used to
rule-out other pathology
– abnormalities in DNS sometimes seen on CT,
MRI, and SPECT, most often in deep white
matter and / or globus pallidus
Treatment
• First step is to remove victim from the
source of carbon monoxide
• High-flow 100% FiO2 continued until
HbCO levels have normalized
• Admission for underlying medical
conditions (cardiac pts) and assoc. injuries
• Screening of other possible victims at scene
Treatment
• Elimination of carbon monoxide is related
to minute ventilation, duration of exposure
to O2, and FiO2
• Half-life of HbCO:
– 4 to 6 hours breathing room air
– 40 to 80 minutes breathing 100% O2
– 15 to 30 minutes breathing hyperbaric O2
Tx – Hyperbaric Oxygen
• Defined as a treatment in which a patient
intermittently breathes 100% oxygen
• Expressed in Atmospheres (ATM)
• Treatment chamber is pressurized to a
pressure greater than sealevel
• Multiplace chambers - pressurized with air;
O2 given via face mask, hood tent, or ET
tube
• Monoplace chambers – pressurized with O2
Tx – Hyperbaric Oxygen
• Mechanism of Action:
1. Increase Oxygen delivery – using Henry’s
Law: P1/C1 = P2/C2
2. Reduction of bubble size – using Boyle’s law:
PV=K, where P = pressure and V= Volume;
K = constant
3. Antagonism of Carbon Monoxide.
4. Improved wound healing
Tx – Hyperbaric Oxygen
• Technique:
– Chamber pressure - between 2.5 and 3.0 atm
– DurationAcute therapy require only one or two
treatments, while chronic medical conditions
may warrant up to 30 or more sessions.
– : 45 to 300 minutes
– Pressures exceeding 2.8 to 3.0 atm - increase
the risk of both neurologic and pulmonary
oxygen toxicity
Tx. - Hyperbaric Oxygen
• Suggested Indications in CO poisoning
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–
–
–
–
–
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coma or any period of unconsciousness
Severe metabolic acidosis (pH < 7.1)
HbCO level >25 percent
pregnancy and HbCO level >20%
signs of cardiac ischemia or arrythmia
recurrent symptoms for up to three weeks
symptoms not resolved after 4-6 hr. of NBO
Tx – Hyperbaric Oxygen
• Contraindications:
– absolute: untreated pneumothorax.
– Relative contraindications:
•
•
•
•
•
obstructive lung disease
upper respiratory or sinus infections
recent ear surgery or injury
fever
claustrophobia
Tx. - Hyperbaric Oxygen
• Side effects
– reversible myopia
– pain in tympanic membrane (rupture), cranial
sinuses, teeth, and/or lungs due to rapid
changes in pressure
– rarely can precipitate generalized seizures
– reversible tracheobronchial Sx and decreased
pulmonary function assoc. with multiple Tx.
– claustrophobia
Summary
• CO poisoning is common and is often
misdiagnosed
• Toxic effects mainly cardiac and CNS
• Main sources are tobacco smoke and
automobile exhaust
• Neuro Sx can appear late when HbCO level
is normal
Summary
• PE, labs, CXR, pulse-ox normal or
nonspecific
• HbCO levels don’t correlate well with Sx
• Tx with normobaric vs hyperbaric oxygen
• HBO quickens elimination of HbCO and
shortens acute Sx, but long-term benefits
unproven and controversial
• No adequate PRCT of HBO vs NBO
Acknowledgements
• Dr. Ruth Divinagracia
• Dr. Paul Tan
• Dr. Glenn Michael
Ramos
• Dr. Daryl De Ramos
• Nel (my sweetypie!)
Thank You for your kind attention
Arterial Blood Gas
10/6/07
12:19
370.6
10/6/07
19:29
254.7
10/7/07
pO2
10/6/07
10:20
440.6
10/8/07
20:00
114.0
10/9/07
105.3
10/8/07
14:15
107.8
pH
7.38
7.37
7.419
7.45
7.40
7.44
7.44
pCO2
30.0
31.0
30.0
29.9
38.8
34.8
36.0
HCO3
17.7
17.6
19.0
20.6
23.9
23.4
24.1
O2 sat
99.8
99.1
99.3
98.1
98.0
98.3
98.0
B.E.
-5.9
-6.1
-2.0
-0.6
+0.1
+0.5
Total CO2
18.6
21.6
25.1
24.5
25.2
CO Hb
(N.V. 0 –
0.8)
Met Hb
(NV 0.2 –
0.6)
FiO2
100%
Mode
AC Mode
104.8
4.4%
0.6
-
-
-
-
0.5%
0.9
-
-
-
-
100%
100%
30%
28%
30%
28%
CPAP
CPAP
In-line neb
via T piece
In-line neb
via T piece
Complete Blood Count
10/6/07
Hemoglobin
Hematocrit
RBC
WBC
Segmenters
Lymphocytes
Monocytes
Eosinophils
Platelet Count
15.8
53
27,860
88%
5%
5%
2%
427,000
10/6/07
17:23
13.2
39.5
4.1
29,000
83%
10%
6%
1%
245,000
10/8/07
10.8
32.8
3.5
12,160
85%
10%
5%
198,000
10/6/08
2030
145
10/7/07
1017
143
10/7/07
2031
141
10/8/07
10/9/07
Na
10/6/07
1100
140
140
140
K
3.8
4.3
3.3
3.3
3.4
4.1
BUN
23
16
13
Crea
1.5
0.9
0.8
0.8
0.6
Glu
135
1.14
1.18
162
325
321
241
CK-MB
7.5
8.4
2.5
0.8
Mg
1.8
1.9
1.9
iCa
TCPK
103
SGOT
31
SGPT
73
LDH
147
Alk Phos 70
CO2
19
TP
6.9
Albumin
3.6
Globulin
3.3
1.9
Toxicology Report
Drug/Metabolit
e
Amphetamine/
Metamphetami
ne
Barbiturates
Cannabinoids
Cocaine
Results
Cut-off Level
30.88 ng/mL
NEGATIVE
1000 ng/Ml
3.44 ng/mL
4.78 ng/mL
12.49 ng/mL
NEGATIVE
NEGATIVE
NEGATIVE
200 ng/mL
50 ng/mL
300 ng/mL
CXR
10/6/07
10/07/07
10/8/08
 Clear lungs and  Blunting of the left  Mild
basal
normal
vascular
hilum
pulmonary
markings
 Heart and the rest
congestion.
 Heart and the rest
of
the
chest  The rest of the
of
the
chest
structures
are
lungs are clear
structures
are
unremarkable
 No
other
unremarkable
 ET is in place
remarkable
 ET is in place
findings
 ET still in place