Chief Complaint:
A well-established (to your office) 56 yo African American male braves an early winter snow fall
and presents to your family practice office at 7:30AM (anxious to be seen) with complaints of
headache x 2 weeks
HPI:
Headache:
Intermittently severe
Timing: in the evenings, nights, and weekends—consistently found x 2 weeks
Severity: 4-7/10
Duration: Continuously present
When present, nothing relieves pain
Medications: Ibuprofen for arthritis—does not resolve/alleviate headache better
No history of migraines
No aura or sensitivity to light
Occasional confusion, visual disturbances, but no loss of consciousness
Fatigue, dizziness, nauseated but no vomiting
No immediate history of other illness coryza, etc
No fever
No history of trauma
+ Other members of family have similar symptoms
Wears glasses—last eye exam 3 months ago; no change in corrective lens Rx
Past Medical history:
Arthritis x4 yrs. (takes ibuprofen)
Personal History:
Occupation: Salesperson –5 days a week; Monday through Friday; no weekends
Allergies: none
Not necessarily physically active—yard work on weekends in summer and fall, etc but
otherwise too busy.
Married, two children ages 16 and 17; living in same house
Family history:
Father died of lung cancer (smoker for 40 years); see HPI
Social history:
Smoker – ½ ppd
Occasional drink: social drinking (2/week)
Denies illicit drug use
Physical Exam
BP: 120/80
HR: 90 bpm
RR: 20
Temp: 98.7
Ht/Wt: 6’0 220 lbs (BMI 29.8) overweight
No nuchal rigidity—no meningitis
Heart—normal S1 and S2 heart sound; no murmurs, no rub; no distant heart sounds;
peripheral vascular normal
Lung—normal; vesicular sounds bilaterally; no pleural friction rub; no stridor, wheezes,
ronchi/rales
Eye—PERRLA; negative fundoscopic exam; Snellen visual acuity with glasses 20/20 on
exam today
Neuropsychiatric exam—normal/negative: Students should ask for a complete Neuro
exam!
Skin: normal (see note below)
Other systems:
Negative / Normal
FYI: Patients typically present with tachycardia and tachypnea, and may complain of
headache, nausea and vomiting. However, patients rarely have the classic findings of
cyanosis, retinal hemorrhage and cherry-red lips.—Shows up on boards so might cover
at end of case!
Symptom severity ranges from mild (constitutional symptoms) to severe (coma,
respiratory depression and hypotension) and is not associated with serum levels of
carboxyhemoglobin, although duration of exposure is an important factor. Not all
patients exhibit signs and symptoms immediately after exposure. In some patients,
neuropsychiatric symptoms, including cognitive and personality changes, may develop
anywhere from three days to eight months after exposure. The mechanism for these
conditions is unknown, but hypoxia alone is not sufficient to explain the observed
clinical manifestations.
Labs
CBC—look for anemia, infection, cancer—all normal; At the conclusion of the case, ask the
students if they would suspect a secondary polycythemia in a chronic exposure to carbon
monoxide? An acute exposure? Physiologically explain it.
-
WBC 7,000 (4-10,000); Hbg 18 (13-18); Hematocrit 62% (45-62) ;
RBC 6.1 million cells/mcL (4.7-6.1) ; platelet 150,000 (150-400,000)
MCV 88 (80-100); MCHC 35% (32-36); RDW 13 (11-15)
Arterial carboxyhemoglobin saturation slightly elevated. – 16% elevated.
Must have a degree of suspicion of carbon monoxide poisoning in order to know to
obtain this lab—they may go right past this…and have to come back to it in the end.
Arterial blood gas testing and pulse oximetry are not useful because they give falsely
normal Pao2 and oxyhemoglobin saturation determinations. A newer pulse oximetery
devise, the pulse CO-oximeter is capable of distinguishing oxyhemoglobin from
carboxyhemoglobin. The diagnosis of CO poisoning is based upon a compatible history
and physical exam in conjunction with an elevated carboxyhemoglobin level
measured by cooximetry of a blood gas sample. Nonsmokers may have up to 3 percent
carboxyhemoglobin at baseline; smokers may have levels of 10 to 15 percent. Levels
above these respective values are consistent with CO poisoning.
Once the diagnosis of CO intoxication is confirmed, it is recommended to obtain an
electrocardiogram (ECG); cardiac biomarker evaluation is warranted in patients with
ECG evidence of ischemia or a history of cardiac disease. Additionally, evaluation of
family members should be performed.
Electrolytes normal
Arterial Acid Base Normal
EKG normal—too early to have students interpret; however, ask them why they might be
interested in obtaining one when diagnosis established. End organ disease secondary to
ischemia…
Kidney function tests—normal; BUN 14 (7-18) R/O End organ disease secondary to ischemia…
Computed tomography (CT) of the head is usually helpful only to rule out other causes of
neurologic decompensation.
Conclusion
The most important interventions in the management of a CO-poisoned patient are prompt
removal from the source of CO – correlate symptoms of “while home, patient has symptoms;
while at work, no symptoms.”
Institution of 100 percent oxygen by nonrebreathing face mask or endotracheal tube. We
recommend initial treatment with 100 percent normobaric oxygen for all suspected victims of
CO poisoning, regardless of pulse oximetry or arterial PO2
Determination of the mechanism of exposure is critical in cases of accidental poisoning in order
to limit the risk to others. Evaluate functioning of furnace/ ensure no use of kerosene heaters
in enclosed spaces, functioning stoves, heaters, etc. “emphasize use of furnace (onset of use
with correlation of symptoms)
Evaluation of family members should be performed.
Installation of carbon monoxide detectors are inexpensive and widely available, but there are
no standard recommendations regarding their use in the home or the workplace.
Consider follow up appointments to switch arthritis medication to: consider Acetaminophen for
arthritis and Encourage lifestyle modifications:-- exercise, stop smoking.
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Because carbon monoxide poisoning has no pathognomonic signs or symptoms, a high level of
suspicion is needed to confirm the diagnosis. Measuring the level of carbon monoxide in the
exhaled air of a patient can be diagnostic, but a blood sample should be obtained to measure
carboxyhemoglobin levels and any coexisting acidosis. A detailed neurologic examination,
including psychological testing, is recommended to document any abnormal findings, which are
often subtle.
The most important steps in treatment are removing the patient from the source of poisoning
and administering 100 percent oxygen. Oxygen should be given until the patient's
carboxyhemoglobin level returns to normal. Hospitalization should also be considered for
patients with severe poisoning or serious underlying medical problems. Indications for
hyperbaric oxygen therapy are not clear, except that it is undisputedly indicated in unconscious
patients.
Carbon monoxide (CO) is an odorless, tasteless, colorless, nonirritating gas formed by
hydrocarbon combustion. About 600 accidental deaths from carbon monoxide poisoning occur
each year, making it one of the most common causes of morbidity from poisoning in the United
States. About five to 10 times as many intentional deaths from carbon monoxide are reported.
Smoke inhalation is responsible for most inadvertent cases of CO poisoning. Other potential
sources of CO include poorly functioning heating systems, improperly vented fuel-burning
devices (eg, kerosene heaters, charcoal grills, camping stoves, gasoline-powered electrical
generators), and motor vehicles operating in poorly ventilated areas (eg, ice rinks, warehouses,
parking garages). Exposure occurs from a variety of sources, particularly motor vehicle exhaust.
The number of accidental deaths caused by carbon monoxide poisoning from motor vehicle
exhaust is higher in the North and peaks during the winter months.
PATHOPHYSIOLOGY — Carbon monoxide (CO) diffuses rapidly across the pulmonary capillary
membrane and binds to the iron moiety of heme (and other porphyrins) with approximately
240 times the affinity of oxygen. The degree of carboxyhemoglobinemia (COHb) is a function of
the relative amounts of CO and oxygen in the environment, duration of exposure, and minute
ventilation.
Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline; smokers may have
levels of 10 to 15 percent. Severe chronic obstructive pulmonary disease can cause a modest
but significant elevation in carboxyhemoglobin levels, even among patients without exposure
to tobacco smoke. The mechanism and clinical significance of this finding is unclear.
Once CO binds to the heme moiety of hemoglobin, an allosteric change occurs that greatly
diminishes the ability of the other three oxygen binding sites to off-load oxygen to peripheral
tissues. This results in a deformation and leftward shift of the oxyhemoglobin dissociation
curve, and compounds the impairment in tissue oxygen delivery.
CO also interferes with peripheral oxygen utilization. Approximately 10 to 15 percent of CO is
extravascular and bound to molecules such as myoglobin, cytochromes, and NADPH reductase,
resulting in impairment of oxidative phosphorylation at the mitochondrial level. The half-life of
CO bound to these molecules is longer than that of COHb. The importance of these
nonhemoglobin-mediated effects has been best documented in the heart, where mitochondrial
dysfunction due to CO can produce myocardial stunning despite adequate oxygen delivery
Because of their higher oxygen utilization and higher minute ventilation, young children may
develop signs and symptoms of carbon monoxide poisoning before older children and adults
who experience the same exposure (eg, family members living in a house with a faulty furnace).
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