Computerized Tomographic Correlate of Carbon Monoxide Poisoning Louis R.
Nardizzi, MD,
PhD
\s=b\ A 44-year-old man was brought unconscious to the emergency room; he was believed to have suffered anoxic brain damage probably due to carbon monoxide poisoning. Computerized tomography with contrast enhancement helped establish the diagnosis and was correlated with the subsequent clinical improvement of the patient. (Arch Neurol 36:38-39, 1979)
serious physiological rp* hefeetmost of carbon monoxide
ef-
alveolar membranes and
re-
(CO) on humans is related to its propensity for competing with oxygen by diffusing across
versibly binding to one of the hemeproteins, hemoglobin, in the RBCs. Since the affinity of hemoglobin for CO is approximately 200 to 290 times its affinity for oxygen, exposure to
low concentrations of CO can result in clinically significant reductions in the oxygen-carrying capacity of the blood. A carboxyhemoglobin (COHg) concen¬ tration of 9% may be equivalent to a 46% reduction of arterial Po, or a lowering of venous PoL, by 4 to 6 mm Hg.' Furthermore, the presence of COHg shifts the oxyhemoglobin disso¬ ciation curve to the left, so that tissue oxygen tensions must fall to much lower levels before the remaining oxyhemoglobin can give up its oxyg¬ en. The inhalation of a 1% concentra¬ tion of CO is usually fatal to a resting man in 30 to 40 minutes and to a working man in ten minutes. Concen¬ trations of 0.01% produce light head¬
ache; 0.05%, severe headache, vertigo, weakness; 0.1%, acceleration of respiration and pulse; and 0.2%,
and
hemoglobin level; this should be repeated 12 to 16 hours after treat¬
ment. It has been shown that nonsmokers have an average COHg level of 1.2%, moderate smokers who inhale have average values of 5.9%, and inhalers of 40 or more cigarettes a day have an average COHg level of 6.9%.e Levels above 15% in healthy adults are associated with headaches, nausea, decreased manual dexterity, etc, and levels above 50% with coma and /or convulsions. Again, these figures vary considerably. Other laboratory tests include determination of blood gas measurements to assess the acid-base status, since acidosis frequently ac¬ companies CO poisoning. Screening toxicologie tests of serum and urine should be done because there is a high incidence of associated drug abuse with CO poisoning. Also, electrocardiography may show inverted waves and ST-wave depression.7 Cerebrospinal fluid pressure may occasionally be elevated or a few lymphocytes may be seen. More than 90% of patients have electroencephalographic abnormali¬ ties consisting of slow waves (two to five cycles per second) of low-voltage frequently with frontal preponder¬ ance.
The pathological effects of CO poisoning are present in almost all organs of patients who die from acute
intoxication. However, the most im¬ portant changes occur in the brain. These include marked venous and capillary dilation, which is found in both the meninges and in the vessels of the substance of the brain. Pete-
chial hemorrhages and frequently ear¬ necrosis of the basal ganglia, most often the globus pallidus, as well as the reticular zone of the substantia nigra, have been observed. The Purkinje cells of the cerebellar cortex and dentate nucleus are commonly in¬ volved, as are cortical cells, especially in levels II, III, and IV. Ammon's horn may also suffer ischemie necrosis, particular in the Somner sector and
ly
endplates.8
REPORT OF A CASE A 44-year-old engineer was admitted to a rural hospital in coma. The patient had been found unconscious by his wife at 5 pm on the front seat of his automobile in a closed garage. The automobile ignition switch was in the off position. The wife reported that he had been in good health, was not taking any medication, had no psychiatric problems, and earlier in the day had stated that he was going to work on his automobile engine that afternoon. On admission, the patient was uncon¬ scious. Temperature was 38.9 °C rectally; pulse rate, 100 beats per minute; respira¬ tions, 24/min; and blood pressure, 140/90 mm Hg. Examination of the head and neck disclosed no evidence of trauma. The left pupil was 5 mm in diameter and reacted sluggishly. The right pupil was 2 mm in diameter and reacted normally. There was no papilledema. The nose and posterior pharynx had a small amount of carbon-like particles. The neck was supple and without adenopathy. The carotids were normal and no jugular venous distention was present. The chest was clear; the heart and abdomi¬ nal examination were unremarkable. The patient exhibited decerebrate rigidity, and response to deep pain was elicited. Eye movement was elicited by rotation of the head. The muscle stretch reflexes were normal. There were sustained ankle clonus and Babinski's signs bilaterally. Lumbar puncture disclosed an opening CSF pres¬ sure of 200 mm , , glucose level was 95 mg/dl, no cells were present, and Gram stain was negative. Skull roentgenograms were unremarkable. Blood drawn while the patient was breathing room air demon¬ strated a pH of 7.42; Po, was 58 mm Hg;
The half-time of excretion of low concentrations is from two to four hours;' higher concentrations may take seven to ten days7' to be complete¬ ly eliminated. However, these figures vary, and depend on multiple factors. Laboratory tests can be of some help in CO poisoning. When the patient is first seen, blood should be drawn for determination of carboxycoma.-
'
Accepted
for publication Oct 24, 1977. From the Department of Internal Medicine, St Paul Hospital, Dallas. Reprint requests to Department of Internal Medicine, St Paul Hospital, 5909 Harry Hines Blvd, Dallas, TX 75235 (Dr Nardizzi).
Fig 1 —Computerized admission.
tomographic scans without contrast enhancement eight days after
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ued to improve over the next three weeks, but his speech remained slow. He was disoriented to place and time, with poor recent memory. He could not remember the episode in his garage and he walked with a wide-based gait. A CT scan with contrast material (Fig 3) five weeks after admission showed evidence of anoxic dam¬ age in the same areas as in the earlier scan (Fig 2) but to a lesser degree. COMMENT
The differential diagnosis in this included head trauma, brain tumor, cerebrovascular accident, drug toxicity, CO poisoning, and other causes of hypoxia. Several laboratory tests and physical findings in the early phase of the illness ruled out most causes except for CO poisoning. The COHg level, drawn seven to ten hours after the insult in a pollutionfree environment, was moderately elevated at 4.5%; at 16 hours, it was 0.8%. These values extrapolate to an initial level in excess of 25%, assuming an exponential decay for CO elimina¬ tion on room air. The CT scans with¬ out contrast enhancement during the hospital course were normal. Howev¬ er, the CT scan with contrast enhance¬ ment on the eight hospital day demon¬ strated increased uptake in the basal ganglia and dentate nucleus (Fig 2), where it has been reported that necro¬ sis commonly occurs with CO encephalopathy/ A CT scan with contrast enhancement (Fig 3) five weeks after the insult demonstrates reduced up¬ take when compared to Fig 2 and correlated with the clinical improve¬ ment of the patient.
case
after
Fig 2.—Computerized tomographic
scans
with contrast enhancement
Fig 3.—Computerized tomographic
scans
with contrast enhancement five weeks after
Peo,, 30.9 mm Hg; 0, saturation, 91%; base excess, 2.5. No COHg measurement was available. Results of urinalysis and auto¬
graphie (CT) scan without contrast materi¬ al on the day after admission showed no abnormalities, but the posterior fossa could not be adequately evaluated due to motion. The patient continued to show improve¬ ment the next few days by standing and walking to the bathroom with assistance, as well as taking fluids by mouth and talking. On the fifth day, relapse with urinary incontinence and the patient was obtund-
eight days
admission.
admission.
mated 12-factor blood chemistry studies and serum electrolyte values were normal. Except for a WBCcount of 17,900/cu mm, complete blood cell count was normal. The patient was transferred to St Paul Hospital, Dallas, at 11 PM. A chest roentgenogram and ECG were normal. Serum and urine toxicology screening tests for amphetamines, barbiturates, benzodiazo-
pines, phenothiazides, salicylates, synthet¬ ic narcotics, tricyclic antidepressants, and alcohol were negative. An arterial blood
gas measurement
on room
air disclosed
a
pH of 7.47; Po, was 49.3 mm Hg; Pco„ 27 mm Hg; 0, saturation, 86.6%. The CÓHg concentration was 4.5%. The patient was placed on 100% oxygen by means of a rebreathing mask; this was tapered appro¬ priately over a period of 12 hours according to his blood gas measurements. The COHg
level 16 hours after admission was 0.8%. The patient was also given 4 mg of dexa¬ methasone intravenously every eight hours, with a tapering dose over the next ten days. Approximately 12 hours after being found by his wife, the patient became more responsive. He opened his eyes and demonstrated a wandering gaze. He would respond to verbal commands with motion of all extremities. However, bilateral ankle clonus and Babinski's signs were still evident. A computerized tomo-
puncture disclosed xanthochromic fluid, with 100 RBCs, no WBCs, and 25 mg/dl of protein. Another CT scan without contrast material showed enlarged third and lateral ventricles, but again the posterior fossa, was not well visualized. Posterior fossa angiography was normal. The patient was maintained on intrave¬ nous fluids and supportive care. On the eighth day, the patient could again follow simple commands, but his speech was slow and of low volume. At this time, a CT scan with and without contrast enhancement was performed with the patient sedated (Fig 1 and 2). The CT scan (Fig 1) without enhancement was again essentially nor¬ mal, but the CT scan (Fig 2) with contrast material clearly demonstrated increased uptake in the area of the basal ganglia and the dentate nucleus of the cerebellum. An EEG on the ninth hospital day was consis¬ tent with diffuse and bilateral cerebral dysfunction as found in anoxic or meta¬ bolic encephalopathy. The patient continent. Lumbar
References 1. Permutt S, Farhi L: Tissue Hypoxia and Carbon Monoxide in Effects of Chronic Exposure to Low Levels of Carbon Monoxide on Human Health, Behavior and Performance. Washington DC, National Academy of Sciences and National Academy of Engineering, 1969, pp 18-24. 2. Stewart RD: The effect of carbon monoxide on humans. Ann Rev Pharmcol 2:409-423, 1975. 3. Ginsburg R, Romano J: Carbon monoxide encephalopathy: Need for appropriate treatment. Am J Psychiatry 133:317-320, 1976. 4. Goldsmith JR, Landaw SD: Carbon monoxide and human health. Science 162:1352-1359, 1968. 5. Smith JS, Brierly H, Brandon S: A kinetic mutism with recovery after repeated carbonmonoxide poisoning. Psychol Med 1:172-174, 1971. 6. Stewart RD, Baretta ED, Platte LR, et al: Carboxyhemoglobin levels in American blood donors. JAMA 229:1187-1195, 1974. 7. Aronow WS, Isbell MW: Carbon monoxide effects on exercise induced angina pectoris. Ann Intern Med 79:392-395, 1973. 8. Blackwood W, McMenemey W, Neyer A, et al: Greenfield's Neuropathology, ed 2. Baltimore, Williams and Wilkins Co, 1963, pp 240-244. 9. Garland H, Pearce J: Neurological complications of carbon monoxide poisoning. Q J Med 144:445-455, 1967.
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Nardizzi, MD,
PhD
\s=b\ A 44-year-old man was brought unconscious to the emergency room; he was believed to have suffered anoxic brain damage probably due to carbon monoxide poisoning. Computerized tomography with contrast enhancement helped establish the diagnosis and was correlated with the subsequent clinical improvement of the patient. (Arch Neurol 36:38-39, 1979)
serious physiological rp* hefeetmost of carbon monoxide
ef-
alveolar membranes and
re-
(CO) on humans is related to its propensity for competing with oxygen by diffusing across
versibly binding to one of the hemeproteins, hemoglobin, in the RBCs. Since the affinity of hemoglobin for CO is approximately 200 to 290 times its affinity for oxygen, exposure to
low concentrations of CO can result in clinically significant reductions in the oxygen-carrying capacity of the blood. A carboxyhemoglobin (COHg) concen¬ tration of 9% may be equivalent to a 46% reduction of arterial Po, or a lowering of venous PoL, by 4 to 6 mm Hg.' Furthermore, the presence of COHg shifts the oxyhemoglobin disso¬ ciation curve to the left, so that tissue oxygen tensions must fall to much lower levels before the remaining oxyhemoglobin can give up its oxyg¬ en. The inhalation of a 1% concentra¬ tion of CO is usually fatal to a resting man in 30 to 40 minutes and to a working man in ten minutes. Concen¬ trations of 0.01% produce light head¬
ache; 0.05%, severe headache, vertigo, weakness; 0.1%, acceleration of respiration and pulse; and 0.2%,
and
hemoglobin level; this should be repeated 12 to 16 hours after treat¬
ment. It has been shown that nonsmokers have an average COHg level of 1.2%, moderate smokers who inhale have average values of 5.9%, and inhalers of 40 or more cigarettes a day have an average COHg level of 6.9%.e Levels above 15% in healthy adults are associated with headaches, nausea, decreased manual dexterity, etc, and levels above 50% with coma and /or convulsions. Again, these figures vary considerably. Other laboratory tests include determination of blood gas measurements to assess the acid-base status, since acidosis frequently ac¬ companies CO poisoning. Screening toxicologie tests of serum and urine should be done because there is a high incidence of associated drug abuse with CO poisoning. Also, electrocardiography may show inverted waves and ST-wave depression.7 Cerebrospinal fluid pressure may occasionally be elevated or a few lymphocytes may be seen. More than 90% of patients have electroencephalographic abnormali¬ ties consisting of slow waves (two to five cycles per second) of low-voltage frequently with frontal preponder¬ ance.
The pathological effects of CO poisoning are present in almost all organs of patients who die from acute
intoxication. However, the most im¬ portant changes occur in the brain. These include marked venous and capillary dilation, which is found in both the meninges and in the vessels of the substance of the brain. Pete-
chial hemorrhages and frequently ear¬ necrosis of the basal ganglia, most often the globus pallidus, as well as the reticular zone of the substantia nigra, have been observed. The Purkinje cells of the cerebellar cortex and dentate nucleus are commonly in¬ volved, as are cortical cells, especially in levels II, III, and IV. Ammon's horn may also suffer ischemie necrosis, particular in the Somner sector and
ly
endplates.8
REPORT OF A CASE A 44-year-old engineer was admitted to a rural hospital in coma. The patient had been found unconscious by his wife at 5 pm on the front seat of his automobile in a closed garage. The automobile ignition switch was in the off position. The wife reported that he had been in good health, was not taking any medication, had no psychiatric problems, and earlier in the day had stated that he was going to work on his automobile engine that afternoon. On admission, the patient was uncon¬ scious. Temperature was 38.9 °C rectally; pulse rate, 100 beats per minute; respira¬ tions, 24/min; and blood pressure, 140/90 mm Hg. Examination of the head and neck disclosed no evidence of trauma. The left pupil was 5 mm in diameter and reacted sluggishly. The right pupil was 2 mm in diameter and reacted normally. There was no papilledema. The nose and posterior pharynx had a small amount of carbon-like particles. The neck was supple and without adenopathy. The carotids were normal and no jugular venous distention was present. The chest was clear; the heart and abdomi¬ nal examination were unremarkable. The patient exhibited decerebrate rigidity, and response to deep pain was elicited. Eye movement was elicited by rotation of the head. The muscle stretch reflexes were normal. There were sustained ankle clonus and Babinski's signs bilaterally. Lumbar puncture disclosed an opening CSF pres¬ sure of 200 mm , , glucose level was 95 mg/dl, no cells were present, and Gram stain was negative. Skull roentgenograms were unremarkable. Blood drawn while the patient was breathing room air demon¬ strated a pH of 7.42; Po, was 58 mm Hg;
The half-time of excretion of low concentrations is from two to four hours;' higher concentrations may take seven to ten days7' to be complete¬ ly eliminated. However, these figures vary, and depend on multiple factors. Laboratory tests can be of some help in CO poisoning. When the patient is first seen, blood should be drawn for determination of carboxycoma.-
'
Accepted
for publication Oct 24, 1977. From the Department of Internal Medicine, St Paul Hospital, Dallas. Reprint requests to Department of Internal Medicine, St Paul Hospital, 5909 Harry Hines Blvd, Dallas, TX 75235 (Dr Nardizzi).
Fig 1 —Computerized admission.
tomographic scans without contrast enhancement eight days after
Downloaded From: http://archneur.jamanetwork.com/ by a UNIVERSITY OF SYDNEY LIBRARY User on 06/09/2015
ued to improve over the next three weeks, but his speech remained slow. He was disoriented to place and time, with poor recent memory. He could not remember the episode in his garage and he walked with a wide-based gait. A CT scan with contrast material (Fig 3) five weeks after admission showed evidence of anoxic dam¬ age in the same areas as in the earlier scan (Fig 2) but to a lesser degree. COMMENT
The differential diagnosis in this included head trauma, brain tumor, cerebrovascular accident, drug toxicity, CO poisoning, and other causes of hypoxia. Several laboratory tests and physical findings in the early phase of the illness ruled out most causes except for CO poisoning. The COHg level, drawn seven to ten hours after the insult in a pollutionfree environment, was moderately elevated at 4.5%; at 16 hours, it was 0.8%. These values extrapolate to an initial level in excess of 25%, assuming an exponential decay for CO elimina¬ tion on room air. The CT scans with¬ out contrast enhancement during the hospital course were normal. Howev¬ er, the CT scan with contrast enhance¬ ment on the eight hospital day demon¬ strated increased uptake in the basal ganglia and dentate nucleus (Fig 2), where it has been reported that necro¬ sis commonly occurs with CO encephalopathy/ A CT scan with contrast enhancement (Fig 3) five weeks after the insult demonstrates reduced up¬ take when compared to Fig 2 and correlated with the clinical improve¬ ment of the patient.
case
after
Fig 2.—Computerized tomographic
scans
with contrast enhancement
Fig 3.—Computerized tomographic
scans
with contrast enhancement five weeks after
Peo,, 30.9 mm Hg; 0, saturation, 91%; base excess, 2.5. No COHg measurement was available. Results of urinalysis and auto¬
graphie (CT) scan without contrast materi¬ al on the day after admission showed no abnormalities, but the posterior fossa could not be adequately evaluated due to motion. The patient continued to show improve¬ ment the next few days by standing and walking to the bathroom with assistance, as well as taking fluids by mouth and talking. On the fifth day, relapse with urinary incontinence and the patient was obtund-
eight days
admission.
admission.
mated 12-factor blood chemistry studies and serum electrolyte values were normal. Except for a WBCcount of 17,900/cu mm, complete blood cell count was normal. The patient was transferred to St Paul Hospital, Dallas, at 11 PM. A chest roentgenogram and ECG were normal. Serum and urine toxicology screening tests for amphetamines, barbiturates, benzodiazo-
pines, phenothiazides, salicylates, synthet¬ ic narcotics, tricyclic antidepressants, and alcohol were negative. An arterial blood
gas measurement
on room
air disclosed
a
pH of 7.47; Po, was 49.3 mm Hg; Pco„ 27 mm Hg; 0, saturation, 86.6%. The CÓHg concentration was 4.5%. The patient was placed on 100% oxygen by means of a rebreathing mask; this was tapered appro¬ priately over a period of 12 hours according to his blood gas measurements. The COHg
level 16 hours after admission was 0.8%. The patient was also given 4 mg of dexa¬ methasone intravenously every eight hours, with a tapering dose over the next ten days. Approximately 12 hours after being found by his wife, the patient became more responsive. He opened his eyes and demonstrated a wandering gaze. He would respond to verbal commands with motion of all extremities. However, bilateral ankle clonus and Babinski's signs were still evident. A computerized tomo-
puncture disclosed xanthochromic fluid, with 100 RBCs, no WBCs, and 25 mg/dl of protein. Another CT scan without contrast material showed enlarged third and lateral ventricles, but again the posterior fossa, was not well visualized. Posterior fossa angiography was normal. The patient was maintained on intrave¬ nous fluids and supportive care. On the eighth day, the patient could again follow simple commands, but his speech was slow and of low volume. At this time, a CT scan with and without contrast enhancement was performed with the patient sedated (Fig 1 and 2). The CT scan (Fig 1) without enhancement was again essentially nor¬ mal, but the CT scan (Fig 2) with contrast material clearly demonstrated increased uptake in the area of the basal ganglia and the dentate nucleus of the cerebellum. An EEG on the ninth hospital day was consis¬ tent with diffuse and bilateral cerebral dysfunction as found in anoxic or meta¬ bolic encephalopathy. The patient continent. Lumbar
References 1. Permutt S, Farhi L: Tissue Hypoxia and Carbon Monoxide in Effects of Chronic Exposure to Low Levels of Carbon Monoxide on Human Health, Behavior and Performance. Washington DC, National Academy of Sciences and National Academy of Engineering, 1969, pp 18-24. 2. Stewart RD: The effect of carbon monoxide on humans. Ann Rev Pharmcol 2:409-423, 1975. 3. Ginsburg R, Romano J: Carbon monoxide encephalopathy: Need for appropriate treatment. Am J Psychiatry 133:317-320, 1976. 4. Goldsmith JR, Landaw SD: Carbon monoxide and human health. Science 162:1352-1359, 1968. 5. Smith JS, Brierly H, Brandon S: A kinetic mutism with recovery after repeated carbonmonoxide poisoning. Psychol Med 1:172-174, 1971. 6. Stewart RD, Baretta ED, Platte LR, et al: Carboxyhemoglobin levels in American blood donors. JAMA 229:1187-1195, 1974. 7. Aronow WS, Isbell MW: Carbon monoxide effects on exercise induced angina pectoris. Ann Intern Med 79:392-395, 1973. 8. Blackwood W, McMenemey W, Neyer A, et al: Greenfield's Neuropathology, ed 2. Baltimore, Williams and Wilkins Co, 1963, pp 240-244. 9. Garland H, Pearce J: Neurological complications of carbon monoxide poisoning. Q J Med 144:445-455, 1967.
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