Anaesthesia, 1976, Volume 31, pages 406-409 C A S E REPORT
A case of industrial carbon dioxide poisoning
PATRICK BRIGHTEN
Industrial carbon dioxide poisoning is a rare occurrence, but is alleged to occur in the brewing industry (apparently associated with subsequent drowning) and has been described in a worker in a maize silo’ and in a worker on a cargo ship carrying wine.’ The occurrence of a case of carbon dioxide poisoning in Bristol in December 1972 prompted a survey of the literature. This revealed no detailed report of a surviving case of poisoning, but two cases were reported of death from carbon dioxide asphyxia.”’ In the report of Jaulmes & Hamelle’ there were two survivals after intoxication in the rescuers but no details are given, and in Marcinkowski’s report’ the one rescuer felt faint and after a short time had difficulties in maintaining his balance, but no further details are given. The opportunity is taken here of describing a case of successful recovery from carbon dioxide intoxication in greater, if incomplete, detail. Case history
The patient, a 34-year-old male rig fitter who was otherwise in normal health, was assisting two other men in moving a large metal tank into a paint store through a doorway just wide enough to admit the tank. The paint store, because of its highly inflammable nature, was equipped with an automatic fire-extinguishing system consisting of several ‘sprinklers’ in the roof linked to a bank of carbon dioxide cylinders. The system was capable of being operated manually, and, for this purpose, a large two-way valve was mounted near the door which was the only means of access to the store. While the tank was actually blocking the door it appears that this valve was in some way knocked into the ON position; the effect was described by the patient as ‘like a cold, thick fog’ filling the paint store. The patient and two other men were in the store at the time and one of them was able to reach the safety of the top of the tank, and from there go back to rescue the patient. The third man was later retrieved but was found to be dead in spite of attempts to resuscitate him. The patient was given artificial respiration while awaiting the arrival of the Patrick Brighten, FFARCS, Senior Registrar in Anaesthetics, Basingstoke District Hospital, Basingstoke, Hampshire.
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Industrial carbon dioxide poisoning
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ambulance, and although deeply unconscious was breathing on his own in a very short time. On admission to the casualty department of the Bristol Royal Infirmary, within an estimated 15-20 minutes of the accident, the patient was deeply unconscious but was maintaining a free airway; he had a respiratory rate of 24 but he was grossly hyperpnoeic and was flushed and grossly vasodilated. The pulse was 120 beats per minute and the,blood pressure 130/60 mmHg. The chest was clear on percussion and auscultation and there was no clinical evidence of bony injury; there were some abrasions on the forehead and left cheek and there was mud in the left eye but there were no conjunctival abrasions. There were also abrasions on the left shin. An intravenous infusion of Ringer-lactate solution was set up and oxygen 8 litres/minute were administered by an M.C. mask. An arterial blood sample taken 10 minutes after arrival (an estimated 25-30 minutes after the accident) showed the following values: pH, 6.95; arterial carbon dioxide tension (Pco2), 17 mmHg; arterial oxygen tension (Po2),280 mmHg. The standard bicarbonate estimated using the Siggaard-Andersen nomogram and Astrup technique was 7.2 mEq/litre but the Base Excess could not be estimated using the nomogram since the point of intersection of the estimated buffer slope and the base excess curve, if extrapolated, would have been too far off the nomogram to have provided any meaningful result. These results did not accord with the clinical condition of the patient, who by this time (25 minutes later) was rousable, less hyperpnoeic and less vasodilated. A repeat arterial sample was taken with the patient breathing air, but only about a minute after discontinuing oxygen. This analysis showed: pH 7.15; Pco,, 30.5 mm/Hg; Po,, 135 mmHg; Standard bicarbonate, 12.2 mEq/litre and Base Excess, - 20 mEq/litre. The patient was transferred to the Intensive Care Unit for observation and on arrival there he was fully conscious and rational and complaining of severe frontal headache, nausea and stiffness all over the body, which he likened to the effects of having run several miles. Oxygen was continued at 4 litreslminute using the M.C. mask. By the following morning his arterial blood analysis was: pH, 7.38; Pco,, 32 mmHg.; Po,, 150 mmHg (on 4 litres/minute oxygen); Standard bicarbonate, 21 mEq/litre and Base Excess, - 4.5 mEq/litre. He was judged sufficiently recovered to return to a general medical ward, but the blood urea taken that morning was reported later in the day to be 74 mg/100 ml. He had passed no urine during that day, in spite of a normal oral fluid intake, and a repeat estimation of the blood urea was taken at 22.00 hr that night; this was reported as 104 mg/100 ml. He was therefore placed on a restricted fluid intake in accordance with accepted medical principles and his subsequent blood urea levels are shown graphically in Fig. 1. He developed a polyuria of 34 litres/day over the 8th and 9th days and he was discharged in good condition, in spite of a blood urea of 71 mg/100 ml on the 10th day following the accident. At follow up on the 23rd day he was back to normal with a blood urea of 28 mg/100 ml. Discussion In the following discussion three basic assumptions have been made. Since rapid unconsciousness can supervene after exposure to carbon dioxide levels above 15%, and the analyses of Marcinkowski’ and Jaulmes & Hamelle’ showed percentages of carbon dioxide of 26% and between 12 and 27% respectively, it has been
408
P. Brighten
23 Days
Fig. 1. Blood urea estimations. Day 1 was the day of the accident.
assumed that the percentage in the inspired atmosphere could have been between 15 and 30% (PICO, 125-250 mmHg). It could have been higher given that the gas was being delivered at high pressure. As a consequence of the increased inspired carbon dioxide (FIco,) the calculated inspired oxygen (FIo,)would drop to between 14 and 17% (Pro, 105-127 mmHg, or PAO, 58-80 mmHg). The patient could not have been inside the paint store for longer than 5-10 minutes, and it has been assumed that he was rescued in 1-5 minutes, since Marcinkowski,’ reported placing a cat in the maize silo and stated that the cat ‘was asphyxiated almost instantly and died very rapidly’. Using intracerebral electrodes Metzger et al.’ showed that the time constant for oxygen changes in the brain tissue was 0.2 seconds and that for carbon dioxide changes was 0.3 seconds. This would suggest that the brain was in this case saturated with sufficient carbon dioxide within a few seconds to cause unconsciousness and cessation of respiration. The intracerebral Po, would also have fallen rapidly and it is likely that the patient suffered convulsions during his time in the paint store. He was also described as having a weak but palpable pulse on being rescued and these factors, taken together, would suggest that an initial severe respiratory acidosis rapidly became a combined respiratory and metabolic acidosis due to the effects of hypoxia, a poor peripheral circulation, and possibly clonic muscle activity. On resuscitation, initially with air and later with added oxygen, the carbon dioxide was presumablyeliminated as rapidly as it had been taken up and thereafter the patient’s symptoms were probably due to hyperventilation giving a low Paco, and therefore poor cerebral circulation helping to maintain the low intracerebral pH4 and also lactic acid production by the muscles of respiration helping to maintain a metabolic acidosis. The combination of a short period of hypoxia and hypotension, followed by a period of at least half an hour of severe acidosis and hypocapnia, would be sufficient to explain the patient’s pre-renal uraemia and the rapid spontaneous recovery of renal function would suggest a fairly short exposure to these factors.
Industrial carbon dioxide poisoning
409
Summary A case of poisoning by carbon dioxide from an overhead fire-extinguishing apparatus is reported, and the subsequent rapid reversal of blood-gas and acid-base changes during the recovery phase described. A possible explanation of these changes is discussed.
References 1. MARCINKOWSKI, T. (1900) L'intoxication par C 0 2 dans un silo. Acta Medicinae Legalis et Socialis (LiPge), 19, 151. 2. JAULMES,P. & HAMELLE, G. (1968) Asphyxie par le gaz carbonique ti bord d'un bateau-citerne. M2decine LPgale et Dommage Corporel, 1, 216. 3. METZGER, H., ERDMANN, W.&THEWS, G. (1971) Effect of short periods of hypoxia, hyperoxia and hypercapnia on brain O2 supply. Journal of Applied Physiology, 31,751. 4. GRANHOLM, L. & SIESJO, B.K.(1969) The effects of hypercapnia and hypocapnia upon the cerebro-
spinal fluid lactate and pyruvate concentrations and upon the lactate, pyruvate, ATP, ADP, phosphocreatine and creatine concentrations of cat brain tissue. Acta Physiologica Scandinavica, 75, 257.
A case of industrial carbon dioxide poisoning
PATRICK BRIGHTEN
Industrial carbon dioxide poisoning is a rare occurrence, but is alleged to occur in the brewing industry (apparently associated with subsequent drowning) and has been described in a worker in a maize silo’ and in a worker on a cargo ship carrying wine.’ The occurrence of a case of carbon dioxide poisoning in Bristol in December 1972 prompted a survey of the literature. This revealed no detailed report of a surviving case of poisoning, but two cases were reported of death from carbon dioxide asphyxia.”’ In the report of Jaulmes & Hamelle’ there were two survivals after intoxication in the rescuers but no details are given, and in Marcinkowski’s report’ the one rescuer felt faint and after a short time had difficulties in maintaining his balance, but no further details are given. The opportunity is taken here of describing a case of successful recovery from carbon dioxide intoxication in greater, if incomplete, detail. Case history
The patient, a 34-year-old male rig fitter who was otherwise in normal health, was assisting two other men in moving a large metal tank into a paint store through a doorway just wide enough to admit the tank. The paint store, because of its highly inflammable nature, was equipped with an automatic fire-extinguishing system consisting of several ‘sprinklers’ in the roof linked to a bank of carbon dioxide cylinders. The system was capable of being operated manually, and, for this purpose, a large two-way valve was mounted near the door which was the only means of access to the store. While the tank was actually blocking the door it appears that this valve was in some way knocked into the ON position; the effect was described by the patient as ‘like a cold, thick fog’ filling the paint store. The patient and two other men were in the store at the time and one of them was able to reach the safety of the top of the tank, and from there go back to rescue the patient. The third man was later retrieved but was found to be dead in spite of attempts to resuscitate him. The patient was given artificial respiration while awaiting the arrival of the Patrick Brighten, FFARCS, Senior Registrar in Anaesthetics, Basingstoke District Hospital, Basingstoke, Hampshire.
406
Industrial carbon dioxide poisoning
407
ambulance, and although deeply unconscious was breathing on his own in a very short time. On admission to the casualty department of the Bristol Royal Infirmary, within an estimated 15-20 minutes of the accident, the patient was deeply unconscious but was maintaining a free airway; he had a respiratory rate of 24 but he was grossly hyperpnoeic and was flushed and grossly vasodilated. The pulse was 120 beats per minute and the,blood pressure 130/60 mmHg. The chest was clear on percussion and auscultation and there was no clinical evidence of bony injury; there were some abrasions on the forehead and left cheek and there was mud in the left eye but there were no conjunctival abrasions. There were also abrasions on the left shin. An intravenous infusion of Ringer-lactate solution was set up and oxygen 8 litres/minute were administered by an M.C. mask. An arterial blood sample taken 10 minutes after arrival (an estimated 25-30 minutes after the accident) showed the following values: pH, 6.95; arterial carbon dioxide tension (Pco2), 17 mmHg; arterial oxygen tension (Po2),280 mmHg. The standard bicarbonate estimated using the Siggaard-Andersen nomogram and Astrup technique was 7.2 mEq/litre but the Base Excess could not be estimated using the nomogram since the point of intersection of the estimated buffer slope and the base excess curve, if extrapolated, would have been too far off the nomogram to have provided any meaningful result. These results did not accord with the clinical condition of the patient, who by this time (25 minutes later) was rousable, less hyperpnoeic and less vasodilated. A repeat arterial sample was taken with the patient breathing air, but only about a minute after discontinuing oxygen. This analysis showed: pH 7.15; Pco,, 30.5 mm/Hg; Po,, 135 mmHg; Standard bicarbonate, 12.2 mEq/litre and Base Excess, - 20 mEq/litre. The patient was transferred to the Intensive Care Unit for observation and on arrival there he was fully conscious and rational and complaining of severe frontal headache, nausea and stiffness all over the body, which he likened to the effects of having run several miles. Oxygen was continued at 4 litreslminute using the M.C. mask. By the following morning his arterial blood analysis was: pH, 7.38; Pco,, 32 mmHg.; Po,, 150 mmHg (on 4 litres/minute oxygen); Standard bicarbonate, 21 mEq/litre and Base Excess, - 4.5 mEq/litre. He was judged sufficiently recovered to return to a general medical ward, but the blood urea taken that morning was reported later in the day to be 74 mg/100 ml. He had passed no urine during that day, in spite of a normal oral fluid intake, and a repeat estimation of the blood urea was taken at 22.00 hr that night; this was reported as 104 mg/100 ml. He was therefore placed on a restricted fluid intake in accordance with accepted medical principles and his subsequent blood urea levels are shown graphically in Fig. 1. He developed a polyuria of 34 litres/day over the 8th and 9th days and he was discharged in good condition, in spite of a blood urea of 71 mg/100 ml on the 10th day following the accident. At follow up on the 23rd day he was back to normal with a blood urea of 28 mg/100 ml. Discussion In the following discussion three basic assumptions have been made. Since rapid unconsciousness can supervene after exposure to carbon dioxide levels above 15%, and the analyses of Marcinkowski’ and Jaulmes & Hamelle’ showed percentages of carbon dioxide of 26% and between 12 and 27% respectively, it has been
408
P. Brighten
23 Days
Fig. 1. Blood urea estimations. Day 1 was the day of the accident.
assumed that the percentage in the inspired atmosphere could have been between 15 and 30% (PICO, 125-250 mmHg). It could have been higher given that the gas was being delivered at high pressure. As a consequence of the increased inspired carbon dioxide (FIco,) the calculated inspired oxygen (FIo,)would drop to between 14 and 17% (Pro, 105-127 mmHg, or PAO, 58-80 mmHg). The patient could not have been inside the paint store for longer than 5-10 minutes, and it has been assumed that he was rescued in 1-5 minutes, since Marcinkowski,’ reported placing a cat in the maize silo and stated that the cat ‘was asphyxiated almost instantly and died very rapidly’. Using intracerebral electrodes Metzger et al.’ showed that the time constant for oxygen changes in the brain tissue was 0.2 seconds and that for carbon dioxide changes was 0.3 seconds. This would suggest that the brain was in this case saturated with sufficient carbon dioxide within a few seconds to cause unconsciousness and cessation of respiration. The intracerebral Po, would also have fallen rapidly and it is likely that the patient suffered convulsions during his time in the paint store. He was also described as having a weak but palpable pulse on being rescued and these factors, taken together, would suggest that an initial severe respiratory acidosis rapidly became a combined respiratory and metabolic acidosis due to the effects of hypoxia, a poor peripheral circulation, and possibly clonic muscle activity. On resuscitation, initially with air and later with added oxygen, the carbon dioxide was presumablyeliminated as rapidly as it had been taken up and thereafter the patient’s symptoms were probably due to hyperventilation giving a low Paco, and therefore poor cerebral circulation helping to maintain the low intracerebral pH4 and also lactic acid production by the muscles of respiration helping to maintain a metabolic acidosis. The combination of a short period of hypoxia and hypotension, followed by a period of at least half an hour of severe acidosis and hypocapnia, would be sufficient to explain the patient’s pre-renal uraemia and the rapid spontaneous recovery of renal function would suggest a fairly short exposure to these factors.
Industrial carbon dioxide poisoning
409
Summary A case of poisoning by carbon dioxide from an overhead fire-extinguishing apparatus is reported, and the subsequent rapid reversal of blood-gas and acid-base changes during the recovery phase described. A possible explanation of these changes is discussed.
References 1. MARCINKOWSKI, T. (1900) L'intoxication par C 0 2 dans un silo. Acta Medicinae Legalis et Socialis (LiPge), 19, 151. 2. JAULMES,P. & HAMELLE, G. (1968) Asphyxie par le gaz carbonique ti bord d'un bateau-citerne. M2decine LPgale et Dommage Corporel, 1, 216. 3. METZGER, H., ERDMANN, W.&THEWS, G. (1971) Effect of short periods of hypoxia, hyperoxia and hypercapnia on brain O2 supply. Journal of Applied Physiology, 31,751. 4. GRANHOLM, L. & SIESJO, B.K.(1969) The effects of hypercapnia and hypocapnia upon the cerebro-
spinal fluid lactate and pyruvate concentrations and upon the lactate, pyruvate, ATP, ADP, phosphocreatine and creatine concentrations of cat brain tissue. Acta Physiologica Scandinavica, 75, 257.
