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The Role of Catalytic Converters in Automobile Carbon Monoxide Poisoning*: A Case Report FREE TO VIEW

Bradley Vossberg, MD; Judah Skolnick, MD, FCCP
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*From the Frazier Rehab Center, Jewish Hospital Health Network, Louisville, KY.



Chest. 1999;115(2):580-581. doi:10.1378/chest.115.2.580
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Inhaling motor vehicle exhaust fumes is a common method used by people attempting to commit suicide; however, the decreased carbon monoxide concentrations found in the exhaust of late-model automobiles equipped with catalytic converters are changing the clinical presentation of exhaust inhalation.

Abbreviations: CO = carbon monoxide; CO2 = carbon dioxide; HbCO = carboxyhemoglobin; HBO = hyperbaric oxygen; MVEGE = motor vehicle exhaust gas emission; O2 = oxygen

Death resulting from carbon monoxide (CO) poisoning is the leading cause of poisonous deaths in the United States. The installation of catalytic converters in automobiles, prompted by the need to reduce environmental pollution from motor vehicle exhaust gas emission (MVEGE), has also lessened the likelihood of death resulting from the inhalation of exhaust fumes. The complications and sequelae of CO poisoning in patients after a failed suicide attempt are more likely to be seen by physicians today. Patient morbidity may not be related to carboxyhemoglobin (HbCO) levels, but rather to the length of exposure and other factors illustrated by this case.

A 56-year-old man, an orthopedic prosthesis salesman depressed at a decline in sales, was brought to the emergency room by ambulance after a friend smelled exhaust fumes in the patient’s house. The unconscious patient was found lying on his right leg against his car. The motor was running, and a hose attached to the exhaust pipe was emptying into the cab of the car. The patient had been in the garage for 8 to 10 h. When emergency medical service personnel arrived, the patient was alert and talking, although mildly confused, and complained of being unable to move his legs.

In the emergency room, the patient had an axillary temperature of 35.3°C, a BP of 148/110 mm Hg, a pulse rate of 115 beats/min, and a respiratory rate of 24 breaths/min. Global confusion was noted, and laboratory analysis of blood drawn after the patient had been on 100% oxygen (O2) for 1 h and 7 min revealed a HbCO level of 4.8%. Three and one half hours later, the HbCO level was 3.0%. An arterial blood gas analysis showed a pH of 7.4, a Po2 value of 175 mm Hg, a Pco2 value of 25 mm Hg, a serum bicarbonate value of 15.2 mmol/L, a base excess of −7 mmol/L, and an O2 saturation of 99.2% on a fraction of inspired oxygen of 100%. A toxicology screen (including alcohol) was negative. The CBC count revealed a WBC count of 22,400/mm3, hemoglobin of 18.3 g/dL, hematocrit of 52.7%, and a platelet count of 264,000/mm3. Serum chemistry levels were remarkable: potassium of 6.9 mEq/L, carbon dioxide (CO2) of 12.4 mEq/L, BUN of 19 mg/dL, creatinine of 2.1 mg/dL, anion gap of 28 mmol/L, uric acid of 15.6 mg/dL, lactate dehydrogenase of 6,001 U/L, serum glutamicoxaloacetic transaminase of 438 U/L, lactic acid of 9.6 mg/dL, and creatine phosphokinase of 131,805 IU/L. Myoglobin was not detected in the urine.

The ECG showed sinus tachycardia with left axis deviation. Physical findings included a right foot that was cool and cyanotic and a left foot that was warm and pink. Dorsalis pedis and posterior tibial pulses were palpable on the left foot. On the right foot, dorsalis pedis and posterior tibial pulses were present using Doppler ultrasound examination. The patient was unable to move either foot spontaneously; the left foot had diminished light touch sensation, and the right foot was anesthetic. The right calf was tense circumferentially. A CT scan without contrast of the head revealed mild ventricular dilation. A venous duplex scan demonstrated absent venous filling in the right calf consistent with a compartment syndrome. The patient underwent an urgent fasciotomy of the right lower extremity. All four compartments were found to be tense, with muscles appearing nonviable in the anterior and lateral compartments, but viable proximally in the posterior compartment. A significant improvement in blood flow in the right lower extremity was documented postoperatively.

Postoperative neurological diagnoses were compressive neuropathies, including compartment syndrome in the right lower extremity and bilateral sciatica resulting from pressure palsies. Physical therapy was recommended and initiated; however, the patient developed fever and was found to be septic from a right lower extremity source. Despite being given IV antibiotics, the patient’s condition worsened rapidly. Before an above-knee amputation could be performed, he died, 5 days after admission.

This case is notable because after 8 to10 h of breathing exhaust fumes in a closed garage, the patient’s HbCO level was only 4.8%. The half-life of CO at 100% O2 at sea level is 80 min. Using extrapolation, this patient’s HbCO level at the scene would have been < 10%, well below the toxic level of 20%. The automobile in this case was a 1995 model equipped with a catalytic converter.

Closed-environment exposure to MVEGE from automobiles not equipped with catalytic converters can result in death within 30 min. The introduction of catalytic converters beginning with 1975 new-car models dropped CO emission rates to 6.00 g/min. By 1989, the average new-car CO emission at idling was 0.22 g/min. The catalytic conversion process removes CO, hydrocarbons, and nitrogen oxide; the resultant emission is a more desirable mixture of nitrogen, CO2, and water. Contemporary three-way catalytic converters eliminate > 99% of CO emissions. The overall catalytic reactions that are important for controlling exhaust emissions are given by the following stoichiometric equations1:

Common morbidity from CO poisoning involves myocardial and/or neurologic injury. Acute mortality from CO appears to result from ventricular dysrhythmias, which may either occur without warning or be preceded by ECG changes including T-wave inversion of electrocardiographic wave segment depression consistent with myocardial ischemia. This is caused by the hypoxic stress precipitated by the preferential affinity hemoglobin has for CO, which is over 200 times its affinity for O2.

Neurologic sequelae of CO poisoning are common and include cerebrovascular accidents, peripheral neuropathies, acute psychosis, cortical blindness, and decreased memory. Neuroimaging studies suggest that the perivascular zone is the primary site of CO injury in the CNS, and that the focal pathology may be a result of secondary hemorrhagic necrosis.2Although most neurological damage occurs within the first 6 h of exposure to toxic CO levels, delayed neurological signs can occur up to 40 days after exposure. Manifestations of delayed neurological sequelae include disorientation, bradykinesia, gait disturbances, aphasia, apraxia, incontinence, and cogwheel rigidity.3

Other complications from CO poisoning include rabdomyolysis from crush injury secondary to unconsciousness with compartment syndrome, myoglobinuria, and acute renal failure as demonstrated in this report. In cases of MVEGE intoxication from automobiles with catalytic converters, one must think of the pathophysiology of poisoning related to hypoxia from the catalytic converter utilizing and displacing O2. Also, because of the nitrogen generated by the catalytic conversion process, methemoglobinemia should be considered. Hypoxia cannot explain all of the deleterious effects of CO poisoning. CO impairs electron transport and affects leukocytes, platelets, and the endothelium, thereby inducing a cascade of events resulting in an oxidative injury.3 There is also a reperfusion ischemia type injury linked to WBC and endothelium adherence, and β2-integrins irreversibly binding WBCs to the membrane. CO also interferes with cytochrome A3.

The amount of CO uptake depends on the ventilatory rate, length of exposure, and concentrations of CO and O2 in the enclosed space. A longer exposure is associated with a greater risk for CO sequelae than a shorter exposure, even when both exposures terminate with the same HbCO levels.4Other complication risk factors include a period of unconsciousness, pre-existing cardiovascular disease, and an age of > 60 years.5

The deleterious effects of CO poisoning may be ameliorated by treatment with hyperbaric oxygen (HBO) initiated within 6 h of exposure.6HBO therapy can reduce the half-life for HbCO elimination from 5 h and 20 min in room air at 1 atmosphere absolute to 23 min with 100% O2 at 2.5 atmosphere absolute. HBO therapy increases the O2 dissolved in blood by a factor of 20, thereby making O2 available to tissues with an adequate vascular supply, and enabling O2 to diffuse 2 to 3 times longer distances to ischemic cells.7 HBO has also been shown to prevent CO-mediated oxidative brain injury in animals by inhibiting leukocyte adherence to the microvascular endothelium, which is a required step in CO pathogenesis.8

Given the increased efficiency of modern catalytic converters, patients presenting with closed-environment MVEGE exposure may have much lower HbCO levels than would have been previously expected; in some cases, the HbCO level may be normal. Other important factors to be considered are the role of supplemental O2 given at the scene and the time taken to obtain the HbCO level.

The percentage of HbCO correlates poorly with the severity of intoxication or prognosis,5 and the length of exposure has been shown to be associated with an increased risk for injury from CO poisoning. In those patients where HBO therapy may be indicated, the decision to treat must not rest solely on the HbCO level. The clinical approach to patients presenting with MVEGE exposure must be broadened to take into account the role of the catalytic converter.

For related comment see page 322.

Correspondence to: Bradley Vossberg, MD, Frazier Rehab Center, Jewish Hospital Health Network, 220 Abraham Flexner Way, Louisville, KY 40202-1887

Taylor, KC (1984)Automobile catalytic converters.,12-14 Springer-Verlag. New York:
 
Silverman, CS, Brenner, J, Murtagh, FR Hemorrhagic necrosis and vascular injury in carbon monoxide poisoning: MR demonstration.AJNR1993;14,168-170. [PubMed]
 
Hardy, KR, Thom, DR Pathophysiology and treatment of carbon monoxide poisoning.Clin Toxicol1994;32,613-629. [CrossRef]
 
Bogusz, M, Cholewa, L, Pach, J, et al A comparison of two types of acute carbon monoxide poisoning.Arch Toxicol1975;33,141-149. [PubMed]
 
Choi, IS Delayed neurologic sequelae in carbon monoxide intoxication.Arch Neurol1983;40,433-435. [PubMed]
 
Thom, SR, Taber, RL, Mendiguren, II, et al Delayed neurological sequelae following carbon monoxide poisoning.Ann Emerg Med1994;23,612-613
 
Kindwall, EP, Goldmann, RW Hyperbaric Medicine Procedures.1995,172-185 Aurora Health Care. Milwaukee, WI:
 
Thom, SR Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats.Toxicol Appl Pharmacol1993;123,248-256. [PubMed]
 

Figures

Tables

References

Taylor, KC (1984)Automobile catalytic converters.,12-14 Springer-Verlag. New York:
 
Silverman, CS, Brenner, J, Murtagh, FR Hemorrhagic necrosis and vascular injury in carbon monoxide poisoning: MR demonstration.AJNR1993;14,168-170. [PubMed]
 
Hardy, KR, Thom, DR Pathophysiology and treatment of carbon monoxide poisoning.Clin Toxicol1994;32,613-629. [CrossRef]
 
Bogusz, M, Cholewa, L, Pach, J, et al A comparison of two types of acute carbon monoxide poisoning.Arch Toxicol1975;33,141-149. [PubMed]
 
Choi, IS Delayed neurologic sequelae in carbon monoxide intoxication.Arch Neurol1983;40,433-435. [PubMed]
 
Thom, SR, Taber, RL, Mendiguren, II, et al Delayed neurological sequelae following carbon monoxide poisoning.Ann Emerg Med1994;23,612-613
 
Kindwall, EP, Goldmann, RW Hyperbaric Medicine Procedures.1995,172-185 Aurora Health Care. Milwaukee, WI:
 
Thom, SR Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats.Toxicol Appl Pharmacol1993;123,248-256. [PubMed]
 
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