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Year : 1999  |  Volume : 53  |  Issue : 9  |  Page : 393-401

Tetanus : Study of 8697 cases*

King Edward VII Memorial Hospital, Bombay-400012., India

Correspondence Address:
J C Patel
King Edward VII Memorial Hospital, Bombay-400012.
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Source of Support: None, Conflict of Interest: None

PMID: 10710833

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How to cite this article:
Patel J C, Mehta B C. Tetanus : Study of 8697 cases*. Indian J Med Sci 1999;53:393-401

How to cite this URL:
Patel J C, Mehta B C. Tetanus : Study of 8697 cases*. Indian J Med Sci [serial online] 1999 [cited 2016 May 26];53:393-401. Available from:

Causes of high prevalence rate of tetanus in India have been men­tioned by us earlier.' Variations in the severity of the disease from case to case and the problems of evaluating any form of therapy have also been discussed. [2] Here are presented the results of our study of 8719 cases of tetanus.

 ¤ Material and Methods Top

Cases admitted to the tetanus ward of King Edward VII Memorial Hospital, Bombay during the period of 14 years form -november 1954 to october 1968 were studied. Alto­gather 10256 patients were admitt­ed. On examination, it was ob­served that 1220 patients were not suffering from tetanus. 339 pa­tients left the hospital against medical advice and are not includ­ed in the study. Records of 8697 patients are analysed here.

Method of grading the cases according to the severity, the rou­tine treatment and the mainte­nance of daily records have been described in detail earlier.' Teta­nus neonatorum has been known to have higher mortality. This group has, therefore, been considered separately in the analysis.

 ¤ Results Top

Disease was more common in males [Table 1].

Age incidence of tetanus and mortality in different age groups is shown in [Table 2].

Incubation period and its relation to mortality is shown in [Table 3].

 ¤ Discussion Top

Incidence of tetanus was higher in male than in female in both neo­natal and non-neonatal. groups, greater exposure to injuries may be the cause of higher incdence in male but the same cannot be said for the neonatal group. In the latter group, better attention to male newborns may result in theri being brought to the hospital more often than female children. Higher incidence in males has been ob­served by several workers.[3],[4],[5],[6] In non-neonatal group, mortality was higher in females than in males. This may be partly due to higher mortality in puerperal and post­abortion tetanus in females. Higher mortality has been reported in fe­males[7] as well as in males.[8],[9] In the neonatal group it was slightly higher in males than in females.

Nearly 70 per cent of cases are before age of 20 years. Nearly 56 per cent of cases were in the first decade of life. Even after exclud­ing neonaatal group, nearly 40% of cases are less than 10 years old. Itt seems that prophylactic immu­nization in childhood has yet not covered the class of children who attend the general hospital. This is an important field for work for the preventive medicine depart­ment. Mortality was highest in the neonatal group. In first two de­cades mortality increased with the age except the 3rd decade where ,t was considerably higher. Seve­ral workers [9] have reported lower mortality in children and young patients, while others' [2],[13] mention higher mortality in that group. When tetanus supervenes on a chronic pre-existing lesion e.g. otorrhea, bed sore, ulcer, gangrene etc. it is not possible to determine incu­bation period; this is also the case where the cause of tetanus is obs­cure i.e. idiopathic tetanus. In non-neonatal group incubation period could not be determined in 41.7% cases. Mortality was inver­sely related to the length of incu­bation period [Table 3]. Similar observations have been made by many workers. (6, 10, 11, 14-19).

In the non-neonatal group, 29.14% cases did not develop apasms; mortality in these c-ses was 2.14%. Comparatively in the neonatal group very few cases were spasm free (0.67% indicat­ing severity of disease in this age group). Amongst cases who deve­loped spasms, mortality was in­versely related to the length of period of onset in both neonatal and non-neonatal group. Many workers (6, 10, 11, 14, 16, 17, 19, ) have observed similar relation.

Temperature of 100°F or more within 24 hours of admission was recorded in 92.6% of neonates and 69.3% ff non-neonatales. Patients with fever had higher mortality than those without fever, the diffe­rence being much more in the non­neonatal group [Table 4]. Pyrexia increases the frequently and seve­rity of spasms which may exhaust the patient and bring about a fatal outcome."'

Patel and Joag suggested classifying tetanus cases into five grades according to presence or absence of five criteria e.g. lock jaw, incubation period of 7 days or less, presence of temperature of 100°F within 24 hours of admis­sion, presence of spasms and pe­riod of onset of 48 hours or less. Mortality in grade I is very 1w. Mor­tality increases as the grade of severity increases. Mortality in each grade is significantly different indi­cating the importance of grading the cases. Mortality in the same grade is higher for neonatal group as compared to non-neonatal group. Thus it is important to sepa­rate out these two groups as they differ in their severity and mortality.

Though accidental injury was the single commonest cause of tetanus, over 50% of cases of tetanus did not have injury as a cause of tetanus. In about 22.0 cases tetanus supervened upon otorrhea. Similar high incidence of otogenic tetanus has been report­ed. [2],[12] 2 Mortality in otogenic teta­nus was significantly lower than in other groups. Reasons for this have been discussed by us earlier.'

In about 18.3% cases, history and examination failed to reveal the mode of infection. This group has been labelled as idiopathic tetanus. Mortality in this group was similar to the overall mortality.

Infection gained entry through the genital tract in 3.6% cases. Tetanus was seen more often after abortion than after delivery; mor­tality was higher in the former group than in the latter. Abortion was often induced by unqualified people using crude contaminated materials and medical aid was sought at a late stage in the disease. These account for higher incidence and higher mortality in post-abortal tetanus as compared to puerperal tetanus. Mortality in puerperal tetanus was not much different from post-operative teta­nus.

Small pox vaccination was fol­lowed by tetanus in 190 cases (2.64%). Inadequate care of vaccinated part and application of contaminated materials on pustules are most likely causes of infection. Mortally in this group was 42.1%. Such cases of tetanus have been reported by a few workers.[8],[10]

Infection gained entry along the intramuscular injection of some drug in 114 cases. Sources of in­fection may be contaminated drugs, syringes, needles or injection site which has been inadequately pre­pared prior to injection. Mortality in this group was very high (80.7%) approaching that of neo­natal group. High mortality in post­injection tetanus has been reported by several workers. [8],[10],[23] Post­ operative tetanus occurred in 94 cases with mortality of 43.62% which was not much different from overall mortality.

Penetrating injury was followed by tetanus in 1021 cases. Morta­lity in this group was also a little higher than overall mortality. Other workers [8],[9] have also found pene­trating injury as the commonest in­jury in cases of tetanus. Super ficial abrasions were followed by tetanus in 804 cases. Thus minor nature of injury or absence of se­condary infection at site of injury is no guarantee against tetanus. Mortality in this group was how­ever, lower (33.54%) than overage mortality (40.18%). Contused lacerated and incised wounds were also common with mortality simi­lar to overall mortality.

Lower limb was the commonest site of infection followed by upper limb, head and face and trunk in that order. Cases of otogenic, puer­peral and neonatal tetanus are not considered in this group. In 94 cases there were multiple sites through which infection could have gained entry. Mortality was high in cases with trunk as site of in­fection and low in cases with head and face as site of infection. Diffe­rent workers have found different correlations with the site of infec­tion and mortality. (8, 9, 11, 13)

Gases were treated with different doses of antitetanus serum (ATS). Some cases were treated without any ATS. Tetanus immune globu­lin (human) - 250 units were given to 127 cases. In cases treat­with 5,000, 10,000, 20,000 and 60,000 i.u. A.T.S. and tetanus irn­mune globulin, mortality was low and comparable whereas cases re­ceiving higher or lower dose of A.T.S. or no A.T.S. had higher mor­tality. Results of various control trials to evaluate serum therapy in tetanus have been reported by us earlier .[24],[25]

Respiratory spasm was the most frequent cause of death accounting for 59.43% deaths. Res­piratory failure was the cause of death in over one-fifth of cases. Various pulmonary complications, e.g. pulmonary edema, pulmonary embolism and bronchopneumonia were responsible for deaths in about 7.5% cases.

 ¤ Summary Top

Records of 8,697 cases of teta­nus seen over a period of 14 years are analysed. Overall mortality was 48.0%. Mortality in neo!: ital group was 86.38% whereas that in non-neonatal group it was 40.18%.

Disease was seen more fre­quently in male than in female. Mortality in male was lower than in female. Incidence was highest in the first decade of life. Mor­tality was lowest (about 33%) in first two decades (excluding neo­natal group). Mortality in neonatal group was highest (86.38%).

Mortality was inversely related to length of incubation period. In cases with incubation period of 7 days or less, mortality was 58.26% in non-neonates and 94.15% in neonates.

Mortality was very low (2.14%) in 2,100 cases who did not deve­lop spasms. In cases with spasms mortality was inversely related to the length of period of onset. Tem­perature of 100'F wihin first 24 hours of admission was an adverse factor and these cases had higher mortality.

Cases were divided into five grades according to the severity. Mortality in each grade was signi­ficantly different from that in the other.

Mortality was lower in otogenic tetanus while it was higher in post­abortion and post-injection teta­nus. Tetanus following penetrat­ing injury carried higher mortality whereas tetanus following abra­sions had lower mortality. With head and face as the site of infec­tion, mortality was low while it was high when the site of infec­tion was a trunk.

Results were similar with dose of A.T.S. ranging between 5,000 and 60,000 i.u. and tetanus immune globulin, whereas mortality was high with higher and lower dose of A.T.S. or with no A.T.S.

Respiratory spasms, respiratory failure, respiratory complications and circulatory failure were the common causes of death.

 ¤ Acknowledgements Top

We are thankful to he Dean, King Edward VII Memorial Hospital, Bombay, for permission to publish the paper.[25][Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11]

 ¤ References Top

1.Patel JC, Mehta BC, Goodluck PL. Tetanus. Experience with 4718 cases. Proceedings of First Inter­national Conference on Tetanus, Study Group of Tetanus, Bombay, 1965, p.l.  Back to cited text no. 1    
2.Patel JC, Mehta BC, Modi KN. Prognosis in Tetanus ibid, p. 181.  Back to cited text no. 2    
3.Cole L. The Prevention and Treat­ment of Tetanus. BMJ 1955:1:150­152..  Back to cited text no. 3    
4.Gordon JE, Singh S, Wyon JB. Tetanus in Villages of Punjab. An Epidemiologic Study. J Ind Med Assn 1961;37:157-161.  Back to cited text no. 4    
5.Matveyev MP, Paul SS. Study of Tetanus Cases. Ind J Child Hlth 1959;8:181-194.  Back to cited text no. 5    
6.Srivastav SP, Chatterji GG. Teta­nus J Ind Med Assn 1961:36:289­285.  Back to cited text no. 6    
7.Vener HL, Bower AG. Clinical Tetanus. JAMA 1941:116:1627-1637_  Back to cited text no. 7    
8.Moore RM, Singleton AO. Tetanus at the John Sealy Hospital. Surg Gyn Obst 1939;69:146-154.  Back to cited text no. 8    
9.Vinnard RT. Three Hundred and Fifty-two cases of tetanus. Surgery 1945;18:482-492.  Back to cited text no. 9    
10.Bhatt AN, Anwikar AK. Tetanus J Indian Med Assn 1962;38:71-75.  Back to cited text no. 10    
11.Cole L. The Prognosis of Tetanus. Lancet 1940;5:164-167.  Back to cited text no. 11    
12.Diaz Rivera RS, Deliz LR. Berio­Suarez J. Pencillin in Tetanus. A clinical analysis of 59 cases JAMA 1948:138:191-194.  Back to cited text no. 12    
13.Topley and Wilsons;: Principles of Bacteriology and Immunology. Ed­ward Arnold (Publishers) Ltd., Ed. IV. Vol. II, P:1957.  Back to cited text no. 13    
14.Altemier WAJ. Pancillin in Tetanus. JAMA 19461 - 130;67-71.  Back to cited text no. 14    
15.Diaz Rivera RS, Raniirez E, Eduardo RP, Mercedes VT Management of Tetanus. JAMA 1957;147:1635-1641.  Back to cited text no. 15    
16.Patel JC, Joag GG. Grading of Tetanus to Evaluate Ind J Med Sc 1959;13:834-840.  Back to cited text no. 16    
17.Vakh BJ, Tulpule TH, Verkey CC. Chlorpromazine in the Management of Tetanus. J Ass Phys Ind 1955:7: 303-309.  Back to cited text no. 17    
18.Yodh BB. Observations on treat­ment of tetanus. BMJ 1932;2:589­592.  Back to cited text no. 18    
19.Yodh BB. Further observations on treatment of tetanus. BMJ 1937;1: 855-857.  Back to cited text no. 19    
20.Patel JC, Sardesai HV, Bhatia KC. The Prognostic Value of Fever in Tetanus. Ind J Med Sc 1959;13:831­833.  Back to cited text no. 20    
21.Barua AR. A study of 280 conse­cutive cases of Tetanus. J Ind Med Assn 37;  Back to cited text no. 21    
22.Shah RM, Shah LJ, Damany SJ. Treatemnt of Tetanus. Comparison of two different dosage Schedules of Antitoxin Serum. Ind J Med Sc 1962:16:867-872.  Back to cited text no. 22    
23.Perlstein MA. Control of Tetanus Spasm by Administration of Mepro­bamate. JAMA 1959;170:1902-1908.  Back to cited text no. 23    
24.Jatel JC, Rao SS, Mehta BC, Good­luck PL. Requirement of ATS in non-neonatal Tetanus, ibid, p. 346.  Back to cited text no. 24    
25.Patel JC, Mehta BC. Serum re­quirements in Tetanus. Principles on Tetanus. Proceedings of hte Second International Conference on Tetanus. Bern Hans Huber Pub­lishers, Bern 1967 p. 471.  Back to cited text no. 25    


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11]

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