Carbon Monoxide Headquarters





Chronic CO Poisoning:

Lumio Chronic Carbon Monoxide Study (Cont.):

B. Results of Carbon Monoxide Poisoning Investigations (Literature Review):

The aspect of CO poisoning was treated in the literature long ago. Already at the end of the 17th century the literature mentioned dizziness as a result of CO poisoning, although naturally no scientific investigations of the matter were at that time presented. Kayser published the first scientific investigation on otological symptoms caused by CO poisoning in 1893. Holm (1890) and Sibelius (1903) were the first Finnish investigators who issued publications on the matter. Neither of them, however, treated the poisoning from an otological point of view.

1. Vestibular Symptoms of Carbon Monoxide Poisoning:

In spite of the fact that CO poisoning has already for a long time been a well-known disease, earlier only acute CO poisoning was spoken of. The name chronic CO poisoning was instead seldom heard before the latest world war and most of the investigations on the matter were made in Germany. In the United States very little attention bas been paid to chronic CO poisoning. Kunkel (1888) was perhaps the first investigator who wrote about dizziness as a result of chronic CO poisoning. Spirtoff (1926) as the first one published anatomico-pathological investigations based on an obduction find. He namely found centres of softening in the brain especially in the thalamus opticus. Lowy (1926) likewise paid attention to vertigo present in connection with chronic CO poisoning, which he found to be clearly labyrinthogenic. He was of the opinion that chronic CO poisoning is a much more common disease than gencrally believed. It is rarely observed owing to the fact, that it is difficult to diagnose correctly. Lowy supported the standpoint that labyrinthogenic vertigo is a primary symptom of this disease and hence vertigo is an exceedingly important factor in the investigation. The question has had less significance in America, but may it be mentioned, however, that Apfelbach and Hayhurst (1926) found vertigo which was caused by CO, to be otogenic. As previously mentioned, only a few separate publications appeared before the latest world war (WW II). A systematic and vast investigation on chronic CO poisoning was not begun until after 1939 and then especially in the Northern Countries.

In the general survey at the beginning of this work we mentioned, that the investigators in Sweden had the first opportunity to investigate chronic CO poisoning and its prophylaxis. Radmark, Nylen and Nyman are the most important investigators of this branch of medical science. Radmark particularly carried out an exceptionally vast research work. The oto-neurological research method used in examining chronic CO poisoning is mainly developed by him. He also classified the patients suffering from chronic CO poisoning according to different reaction types. As the vestibulary reactions caused by chronic CO poisoning are the most manifest reaction types it is justified to describe them more accurately in this connection. May it be mentioned that the oto-neurological research method used in Finland and explained in this work is entirely based on the rescarch method used and developed by Radmark.

2. Results of Cochlear Investigations of Carbon Monoxide Poisoning:

The literature has only a few reports of the effects on the function of the cochlea produced by CO. Meagre reports of only one case only or at the most a few cases have been published on the matter. Neither have the cases, with one exception, been examined with an audiometer. Only the hearing for conversation and for whisper were tested and the usual tuning-fork investigations were performed. The test with Struycken's tuning-fork series was not performed either. In spite of the fact that the cases were individual ones it is justified to consider them more closely. They namely offer a picture of the nature of the hearing defect caused by CO, although no conclusion can, on their basis, be drawn as to the frequency of this type of defects. The hearing losses presented have still one common characteristic: the cases have arisen as a result of acute CO poisoning. Accurate knowledge of the possible function of disturbances of the cochlea caused by chronic CO poisoning has never been presented.

Kayser in 1893 mentioned in his investigation, that CO poisoning impairs hearing. He did not, however, give any results of accurate investigation. Alt (1915) was the first investigator to present a case in which hearing was impaired after an acute CO poisoning. Results of vestibular investigation were missing from his studies also. Apparently this was due to war. Instead, he presented pathologic anatomical changes which CO poisoning causes in the inner ear. He came to the conclusion, that the degenerative changes in the acoustic nerve and the minor hemorrhages in the labyrinth are the causes of defective hearing in CO poisonings. Kayser was the first investigator who found that hearing losses were due to thc decrease of bone conduction, hence, to inner ear defects.

Ruttin (1918, 1922, 1934, 1936) performcd investigations on hearing losses, which resulted from acute CO poisoning. ln one of his papers he published three cases simultaneously. They are as follows:

-1. A lighting gas poisoning owing to which the patient was found unconscious in his bed in the morning. After recovering he complained of headache, giddiness and ringing in the ears. When testing the hearing for conversation and for whisper it proved to be quite normal, but the Schwabach had decreased. One ear did not respond to caloric stimulation at all.
-2. A worker received acute CO poisoning caused by petrol. The effect produced by fuel oil gases is chiefly due to the CO contained therein. The patient was unconscious for a longer time and after awaking he complained of headache and impaired hearing in both ears. In the right ear, the tympanic membrane was slightly dull, otherwise nothing special. Hearing of speech at 2-3 meters. The *Schwabach was considerably decreased, the upper limit c3. The caloric reaction was weak. In the left ear the tympanic membrane was somewhat retracted, otherwise nothing unusual. The ear was completely deaf to speech as well as to tuning-forks and the caloric reaction was weak. The follow-up performed after half a year disclosed the condition of the patient to be practically unchanged.
-3. A young girl earlier healthy, who after an acute CO poisoning lost hearing completely. In the tests she heard neither speech nor tuning-forks. A caloric reaction was not obtained from either ear. Ruttin published the above-mentioned cases in 1918.
Later on he also treated the effect of CO on the cochlea in another connection. At that time he reported two cases of poisoning. One patient had a severe, acute CO poisoning. At the examination the hearing was normal but, instead, neither of the ears responded to caloric stimulation. In the rotatory test a reaction was obtained from one ear but not from the other. Follow-ups were performed during three months and hearing impaired slowly during this time. The caloric tests finally gave some kind of reactions which, however, were weaker than normally. No changes were observed at the rotatory reaction performed in the follow-ups. The other case: a previously healthy man, who worked for 6 hours under thc influence of air polluted by carbolineum. Immediately after coming home he had attacks of vertigo and vomiting, which lasted 2-1/2 hours and then gradually weakened. The examinations proved hearing to be normal; III degree spontaneous nystagmus, neither of the ears responded to caloric stimulation. After 8 days, the hearing seemed to have improved slightly; the III degree spontaneous nystagmus had become a II degree nystagmus, caloric reaction was still fully negative. The condition of the patient was followed for 2-1/2 months during which time the hearing was weaker than normally. A weak caloric reaction was finally obtained although after a long period of latency. Ruttin was of the opinion that hoth of the cases had a retrolabyrinthine injury. He came to this conclusion on the basis of the following: hearing was fully normal, the caloric reaction was negative on both sides, the rotatory reaction on one side. According to Ruttin, namely the peripheral labyrinth is affected as follows: either all the reactions stop abruptly and simultaneously or gradually in the following order: first hearing, then the caloric reaction and finally the rotatory reaction.

Urbantschitsch (1927) also published a case, in which the patient lost the hearing of both ears completely after an acute lighting gas poisoning. The patient was a woman, previously perfectly healthy. She lay in a room in which the gas tap was open for 23 hours. When brought to the hospital she was absolutely unconscious, no reactions to light were observable in the pupils even. After having regained consciousness the patient was found to be deaf, but no vestibular symptoms were observed. Complete deafness lasted 2 weeks after which time hearing showed signs of improvement. The patient was hospitalized because of the poisoning for 2 months. On leaving the hospital severely impaired hearing was the only symptom she had: speech with the right ear ad concham and whispering 0. Speech with the left ear 0.5 and whispering 0.1.

Tanturri (1936) mentioned in his investigation published in 1926 that two of the cases of hypacusis lacunaris which he examined was in all probability caused by CO poisoning. The hearing deficiency appeared then at C5. The defect was, according to Tanturri, a result of the toxic effect directed to the cochlea and he was of the opinion that the defect is peripheral, hence, quite contrary to the conclusion of Ruttin.

The only report on audiometric investigations mentioned in the literature is the one presented by Wirth (1937). He observed in his evaluation of audiograms, one case of acute lighting gas poisoning: the hearing of the patient impaired suddenly and when testing with thc audiometer the hearing was to be at its best at 1,000 Hz. When the vibration rate increased beyond this, hearing impaired rapidly; the upper limit was 3,000 Hz. In addition there was a small hearing island left at the point of 8,000 Hz. Unfortunately, no other investigation results, not even of speech and whispering were given.

Rutenburg (1944) verified hearing disturbances in the form of impaired hearing and decreased bone conduction in five patients out of fifteen who had suffered from CO poisoning.

Although Alt's investigation hereinabove mentioned is partly incomplete, we shall consider it more particularly: he reported two cases: one was a mate who had got severe CO poisoning aboard a ship. He complained of impairment of hearing and he heard speech with both ears at a distance of 1-1/2 m but whispering not in the least. The patient was followed for a long time but no improvement was observable. The other case was a slight CO poisoning which did not cause absolute unconsciousness. The patient heard speech at a distance of 2.5 - 3.0 m and whispering 0.1 m. The follow-up disclosed that healing had improved slightly. In both cases the Swabach had decreased considerably.

Although chronic CO poisoning has during and after the latest war been investigated very eagerly also from an oto-neurological point of view, surprisingly little attention has been paid to the investigation of hearing. Radmark only mentions briefly, that hearing is in the cases usually normal.

In spite of the fact, that all the above-presented observations were chiefly separate cases we can, however, on basis of them secure a schematic picture of the defective hearing caused by CO poisoning. The most significant observation is that the hearing loss always was of an inner ear type. The fact that the loss almost always appears together with vestibular symptoms in both ears is also an important fact. With the exception of one case, the defect improved slightly only or not at all. At least three investigators (Wirth, Ruttin, Tanturri) found the loss of hearing to be in the area of the upper tones. Wirth, particularly, noticed that the deficiency of hearing increases in the area above 1,000 Hz. These general characteristics shall later on have their own significance when comparing the research results of this study with those of the earlier investigations presented in the literature.

From: Lumio, J.S. (1948) Hearing deficiencies caused by carbon monoxide (generator gas). Acta Otolaryngol., Suppl. 71, 1-112.

................... Schwabach test - A test for hearing using 5 tuning forks, each of a different tone.


...... last changed 03/14/02


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