Treatment of Tetanus
1
175 LEADING ARTICLES Treatment of Tetanus THE LANCET LONDON: SATURDAY, JULY 24, 1954 UNTIL a few years ago there seemed little reason to dispute the fatalistic view, first expressed by HIP- POCRATES, that no treatment availed against severe tetanus. Two developments have helped to change the picture. The first of these is the new-found ability to control the tone of voluntary muscle by muscle relaxants, which abolish muscle spasm without depressing the central nervous system. The second is the rapid growth in knowledge of how to handle patients with bulbar poliomyelitis, to which LASSEN 1 and IBSEN 2 have contributed so greatly. In tetanus the significance of these two developments is this : first, that administration of muscle relaxants may be * said to place the tetanic patient on a par with one who has bulbar poliomyelitis ; and secondly, that with improved treatment bulbar poliomyelitis has become much less commonly fatal. Dr. SHACKLETON’s article, on p. 155 of this issue, suggests that no patient with tetanus, however short the incubation period or however rapid the progress to convulsions, is necessarily doomed ; and at least his distress can be greatly mitigated. In this disease, as in bulbar poliomyelitis, most of the deaths are due to pulmonary infection and anoxia, though toxaemia, dehydration, and exhaustion are also important fac- tors. There is little doubt that the tetanus toxin ascends the regional nerve-trunks to the spinal cord and thence to the bulbar nuclei.3 The dorsal vagal nucleus is severely poisoned, and in consequence the pharynx, larynx, and oesophagus are affected 4 ; the larynx is no longer a watchdog for the lungs, which thus are readily invaded by secretions, gastric contents, and anything taken by,mouth. Coughing is ineffective and respiration is much impaired, partly because of the simultaneous action of agonists and antagonists, and partly because of closure of the larynx by the adductors of the vocal cords.5 Without treatment the result is pulmonary infection and anoxia. These can be averted by banning oral nutriment, by early tracheotomy, by frequent suction through the trache- otomy tube, and by postural drainage combined with assistance to respiration-by the very methods, that 1. Lassen, H. A. Lancet, 1953, i, 37. 2. Ibsen, B. Proc. R. Soc. Med. 1954, 47, 72. 3. Pavling Wright, G. Brit. med. Bull. 1954, 10, 59. 4. Baker. A. B. J. Neuropath. 1942, 1, 394. 5. Herzon, E., Killiam, E., Pearlman, S. J. Arch. Otolaryng., Chicago, 1951, 54, 143. is to say, which are now applied in treating bulbar poliomyelitis. In addition, tetanus antitoxin must be given, and muscle spasm should be continuously controlled with one or other of the muscle relaxants- . a short-acting one, such as succinylcholine, is probably best.6 Opiates and sedatives, since they depress the central nervous system, should be administered very sparingly. Fortunately the need has been greatly reduced by controlling muscle spasm and ensuring unembarrassed respiration. This scheme of treatment makes great demands on the hospital staff, and particularly on the anaesthetist. The dosage of relaxants has to be adjusted repeatedly, and in order to keep muscle spasm in abeyance it may have to be pushed to the point where artificial respiration must be maintained, either manually or mechanically, for days on end. This in turn raises perplexing problems of carbon-dioxide clearance and pH balance. The protection of the lungs and trachea calls for constant attention from laryngologist, physio- therapist, and nurses ; nutrition and fluid balance have to be carefully watched ; and many difficulties of nursing arise. Any lapse of vigilance, any wrong decision, may cost the patient’s life. No-one will grudge such attention if, as we have reason to believe, it relieves distress and restores to health some who otherwise would die. 6. Woolmer, R., Gates, J. E. Lancet, 1952, ii, 808. 7. Crampton Smith, A., Spalding, J. M. K., Russell, W. R. Ibid, 1954, i, 939. 8. Cecil, R. L., Nicholls, E. E., Stainsby, W. J. Amer. J. Path. 1930, 6, 619. 9. Waaler, E. Acta path. microbiol. scand. 1940, 17, 172. 10. Rose, H. M., Ragan, C., Pearce, E., Lipman, M. O. Proc. Soc. exp. Biol., N.Y. 1948, 68, 1. Serological Diagnosis of Rheumatoid Arthritis RHEUMATOID arthritis can usually be diagnosed confidently by clinical observation, supplemented if need be by radiography ; but sometimes a reliable laboratory test would be welcome. Formerly the streptococcal agglutination reaction first described by CECIL et al.8 came nearest to satisfying this need, though it was never widely adopted. Then, in 1940, WAALER 9 found that serum from a patient with rheumatoid arthritis produced brisk agglutination of sheep red cells previously " sensitised " by the addition of a small (non-agglutinating) dose of haemolytic amboceptor. The reaction was not caused by heterophile agglutinin, for it did not occur with unsensitised cells. WAALER next’tested sera from 77 cases ; but the reaction took place in only a third, and he concluded that it was of no diagnostic value. No further interest seems to have been taken in this property of rheumatoid-arthritis serum until 1948 when RosE et al.10 rediscovered it while setting up a complement-fixation test for rickettsialpox with serum from a patient convalescing from this disease and suffering also from rheumatoid arthritis. The patient’s serum agglutinated sheep cells sensitised with rabbit anti-sheep-cell amboceptor to a titre of 1 in 2048, whereas the titre against unsensitised cells was 1 in 16. This observation led ROSE et al. to devise a " differential agglutination test," in which the result was expressed as the quotient of the sensitised-cell titre divided by the unsensitised-cell titre. The
Transcript of Treatment of Tetanus
175LEADING ARTICLES
Treatment of Tetanus
THE LANCETLONDON: SATURDAY, JULY 24, 1954
UNTIL a few years ago there seemed little reason to
dispute the fatalistic view, first expressed by HIP-POCRATES, that no treatment availed against severetetanus. Two developments have helped to change thepicture. The first of these is the new-found abilityto control the tone of voluntary muscle by musclerelaxants, which abolish muscle spasm without
depressing the central nervous system. The second isthe rapid growth in knowledge of how to handle
patients with bulbar poliomyelitis, to which LASSEN 1and IBSEN 2 have contributed so greatly. In tetanusthe significance of these two developments is this :
first, that administration of muscle relaxants may be *
said to place the tetanic patient on a par with one whohas bulbar poliomyelitis ; and secondly, that withimproved treatment bulbar poliomyelitis has becomemuch less commonly fatal.
Dr. SHACKLETON’s article, on p. 155 of this issue,suggests that no patient with tetanus, however shortthe incubation period or however rapid the progressto convulsions, is necessarily doomed ; and at leasthis distress can be greatly mitigated. In this disease,as in bulbar poliomyelitis, most of the deaths are dueto pulmonary infection and anoxia, though toxaemia,dehydration, and exhaustion are also important fac-tors. There is little doubt that the tetanus toxinascends the regional nerve-trunks to the spinal cordand thence to the bulbar nuclei.3 The dorsal vagalnucleus is severely poisoned, and in consequence thepharynx, larynx, and oesophagus are affected 4 ; the
larynx is no longer a watchdog for the lungs, whichthus are readily invaded by secretions, gastric contents,and anything taken by,mouth. Coughing is ineffectiveand respiration is much impaired, partly because ofthe simultaneous action of agonists and antagonists,and partly because of closure of the larynx by theadductors of the vocal cords.5 Without treatmentthe result is pulmonary infection and anoxia. Thesecan be averted by banning oral nutriment, by earlytracheotomy, by frequent suction through the trache-otomy tube, and by postural drainage combined withassistance to respiration-by the very methods, that1. Lassen, H. A. Lancet, 1953, i, 37.2. Ibsen, B. Proc. R. Soc. Med. 1954, 47, 72.3. Pavling Wright, G. Brit. med. Bull. 1954, 10, 59.4. Baker. A. B. J. Neuropath. 1942, 1, 394.5. Herzon, E., Killiam, E., Pearlman, S. J. Arch. Otolaryng.,
Chicago, 1951, 54, 143.
is to say, which are now applied in treating bulbarpoliomyelitis. In addition, tetanus antitoxin must begiven, and muscle spasm should be continuouslycontrolled with one or other of the muscle relaxants- .a short-acting one, such as succinylcholine, is probablybest.6 Opiates and sedatives, since they depress thecentral nervous system, should be administered verysparingly. Fortunately the need has been greatlyreduced by controlling muscle spasm and ensuringunembarrassed respiration.
This scheme of treatment makes great demands onthe hospital staff, and particularly on the anaesthetist.The dosage of relaxants has to be adjusted repeatedly,and in order to keep muscle spasm in abeyance it
may have to be pushed to the point where artificialrespiration must be maintained, either manually ormechanically, for days on end. This in turn raises
perplexing problems of carbon-dioxide clearance andpH balance. The protection of the lungs and tracheacalls for constant attention from laryngologist, physio-therapist, and nurses ; nutrition and fluid balancehave to be carefully watched ; and many difficultiesof nursing arise. Any lapse of vigilance, any wrongdecision, may cost the patient’s life. No-one will
grudge such attention if, as we have reason to believe,it relieves distress and restores to health some whootherwise would die.
6. Woolmer, R., Gates, J. E. Lancet, 1952, ii, 808.7. Crampton Smith, A., Spalding, J. M. K., Russell, W. R. Ibid,
1954, i, 939.8. Cecil, R. L., Nicholls, E. E., Stainsby, W. J. Amer. J. Path.
1930, 6, 619.9. Waaler, E. Acta path. microbiol. scand. 1940, 17, 172.
10. Rose, H. M., Ragan, C., Pearce, E., Lipman, M. O. Proc. Soc.exp. Biol., N.Y. 1948, 68, 1.
Serological Diagnosis of RheumatoidArthritis
RHEUMATOID arthritis can usually be diagnosedconfidently by clinical observation, supplemented ifneed be by radiography ; but sometimes a reliable
laboratory test would be welcome. Formerly thestreptococcal agglutination reaction first described byCECIL et al.8 came nearest to satisfying this need,though it was never widely adopted. Then, in 1940,WAALER 9 found that serum from a patient withrheumatoid arthritis produced brisk agglutinationof sheep red cells previously " sensitised " by theaddition of a small (non-agglutinating) dose ofhaemolytic amboceptor. The reaction was not caused
by heterophile agglutinin, for it did not occur withunsensitised cells. WAALER next’tested sera from 77cases ; but the reaction took place in only a third,and he concluded that it was of no diagnostic value.No further interest seems to have been taken in this
property of rheumatoid-arthritis serum until 1948when RosE et al.10 rediscovered it while setting up acomplement-fixation test for rickettsialpox withserum from a patient convalescing from this diseaseand suffering also from rheumatoid arthritis. The
patient’s serum agglutinated sheep cells sensitisedwith rabbit anti-sheep-cell amboceptor to a titre of1 in 2048, whereas the titre against unsensitised cellswas 1 in 16. This observation led ROSE et al. to devisea " differential agglutination test," in which the result
was expressed as the quotient of the sensitised-celltitre divided by the unsensitised-cell titre. The
