Tetanus

1. Tetanus Dr.Vemuri Chaitanya

2. Tetanus Tetanos – a greek word – to strech First described by Hippocrates & Susruta A Neurological disease characterised by increased muscle tone & spasms. Caused by CLOSTRIDIUM TETANI An anaerobic, motile, gram positive rod that forms oval, colourless, terminal spores – tennis racket or drumstick shape.

3. It is found worldwide in soil, in inanimate environment, in animal faeces & occasionally human faeces.

5. Epidemiology Occurs sporadically Affects unimmunized, partially immunized & fully immunized who fail to maintain adequate immunity with booster doses of vaccine. Although it is an entirely preventable disease by immunization , the burden of disease worldwide is great.

6. As reporting is inaccurate & incomplete, particularly in devoleping countries, W.H.O considers reported cases to be an underestimate & takes case/death estimates to assess the burden of disease. In 2002, the estimated deaths in all age groups 2,13,000 of which 1,80,000 were attributable to neonatal tetanus. More common in areas where soil is cultivated, in rural areas, in warm climates, during summer, among males.

7. Pathogenesis Contamination of wounds with spores of C.tetani. Germination & toxin production – in wounds with low oxidation – reduction potential ( devitalized tissues, F.B, active infection ) Tetanospasmin ( neurotoxin ) Tetanolysin ( hemolysin )

8. Tetanospasmin ( exotoxin ) produced locally , released into bloodstream . Binds to peripheral motor neuron terminals & nerve cells of ant.horn of spinal cord The toxin after entering axon , transported to nerve cell body in brain stem & spinal cord – retrograde intraneuronal transport Toxin – migrates across synapse – presynaptic terminals- blocks the release of Glycine & GABA from vesicles.

9. The blocking of neurotransmitter release by Tetanospasmin involves cleavage of Synaptobrevin – essential for proper fn of synaptic vesicle release apparatus With diminished inhibition – resting firing rate of alpha motor neurons increases – rigidity Lessened activity of reflexes which limit polysynaptic spread of impulses, agonists & antagonists recruited - spasms

11. Loss of inhibition of preganglionic sym neurons – sympathetic hyperactivity

12. Mode of transmission Infection is acquired by contamination of wounds with tetanus spores. Range of injuries & accidents – trivial pin prick, skin abrasion, puncture wounds, burns, human bites, animal bites & stings, unsterile surgery, IUD, bowel surgery, dental extractions, injections, unsterile division of umbilical cord, compound #, otitis media, chr.skin ulcers, eye infections, gangrene NOT TRANSMITTED FROM PERSON TO PERSON

13. Types Traumatic Puerperal Otogenic Idiopathic Tetanus neonatorum PARK 19th Generalized Neonatal local HARRISON 17th

14. Clinical features May begin from 2 days to several weeks after the injury – USUALLY 1 WEEK Remember Shorter the incubation period More severe the attack Worse the prognosis

15. Clinical features GENERALIZED TETANUS Most common Increased muscle tone & generalized spasms Median time of onset after injury – 7 days Pt 1st notices increased tone in masseter ( Trismus, lock jaw ) Dysphagia Stiffness / pain in neck, shoulder, back muscles appear concurrently / or soon thereafter Rigid abd & stiff prox.limb muscles . Hands, feet spared.

16. trismus

17. Risus Sardonicus : Spasm of facial muscles ( frontalis & angle of mouth muscles ) producing grinning facies Opisthotonus : Painful spasms of neck, trunk and extremity. producing characteristic bowing and arching of back Some pts devolep paroxysmal, violent, painful, generalized muscle spasms – cyanosis . Spasms occur repetitively & may be spontaneous / provoked by slightest stimulation. Constant threat during gen.spasm is reduced ventilation, apnea / laryngospasm.

18. Risus sardonicus

21. Mild ds ( muscle rigidity , no / few spasms ) Moderate ds (trismus, dysphagia, rigidity, spasm) Severe ds ( freq explosive paroxysms ) Autonomic dysfn complicates severe cases - labile htn, hyperpyrexia, profuse sweating, peripheral vasoconstriction, raised catecholamines.

22. Neonatal Tetanus Usually fatal if untreated Children born to inadequately immunized mothers, after unsterile treatment of umbilical stump During first 2 weeks of life. Poor feeding ,rigidity and spasms

25. Local Tetanus Uncommon form Manifestations are restricted to muscles near the wound. Cramping and twisting in skeletal muscles surrounding the wound – local rigidity Prognosis – excellent

26. Cephalic Tetanus A rare form of local tetanus Follows head injury / ear infection Involves one / more facial cranial nerves Trismus and localised paralysis ,usually facial nerve, often unilateral. Incubation period : few days Mortality : high

28. Diagnosis Based entirely on clinical findings Examine all cases with wound infection & muscle stiffness Wound cultures – in suspected cases C.tetani can be isolated from wounds of pts without tetanus & freq cannot be isolated from wounds of those with tetanus Electromyograms – continous discharge of motor units, shortening / absence of silent interval seen after AP. Muscle enzymes – raised

29. Serum Anti toxin levels >= 0.1 IU/ml – protective & makes tetanus unlikely .

30. Differential diagnosis Cond producing trismus : alveolar abscess, strychnine poisoning, dystonic drug reactions, hypocalemic tetany Meningitis/encephalitis Marked increased tone in central muscles , with superimposed generalized spasms & relative sparing of hands & feet – sugg tetanus

31. Treatment – general measures Goal is to eliminate the source of toxin, neutralize the unbound toxin & prevent muscle spasm & providing support - resp support Admit in a quiet room in ICU Continuous careful observation & cardiopulmonary monitoring Minimize stimulation Protect airway Explore wounds – debridement

32. NEUTRALIZE TOXIN : Inj.Human Tetanus Immunoglobulin 3000 – 6000 units IM, usually in divided doses as volume is large. ANTIBIOTIC THERAPY : Although of unproven value , antibiotics adm to eradicate vegetative cells – the source of toxin IV Penicillin 10 -12 million units daily for 10 days IV Metronidazole 500mg Q 6 hrly / 1gm Q 12 hrly Allergic to Penicillin : consider Clindamycin & Erythromycin

33. Control of Spasms Nurse in a quiet dark room Avoid noise & other stimuli IV Diazepam / Lorazepam / Midazolam Barbiturates & Chlorpromazine –2nd line drugs Continued spasms : intubate & ventilate Propofol, dantrolene, intrathecal baclofen, succinylcholine & magnesium sulfate can be tried

34. Management of autonomic dysfn Labetalol Continuous infusion of esmolol Clonidine / verapamil

35. Additional measures Pts recovering from tetanus should be actively immunized Hydration Nutrition Physiotherapy Prophylactic anticoagulation Bowel, bladder, back care Treatment of intercurrent infection

36. Prevention – Active Immunization For partially immunized, unimmunized and recovering from tetanus It stimulates production of protective antitoxin 2 prep : combined vaccine : DPT monovalent vaccine : plain / formol toxoid tetanus vaccine , adsorbed

37. Combined vaccine According to National Immunization, 3 doses of DPT – at intervals of 4-8 wks, starting at 6 wks age, followed by booster at 18 months age 2nd booster (only DT) at 5-6 yrs 3rd booster ( only TT) after 10 yrs age

38. Monovalent vaccines Purified tetanus toxoid ( adsorbed ) supplanted the palin toxoid – higher & long lasting immunity response Primary course of immunization – 2 doses Each 0.5 ml , injected into arm given at intervals of 1-2 months The longer the interval b/w two doses, better is the immune response 1st booster – 1 yr after the initial 2 doses 2nd Booster : 5 yrs after the 1st booster ( optional ) Freq boosters to be avoided

39. Passive immunization Temp protection – human tetanus immunoglobulin /ATS Human Tetanus Hyperimmunoglobulin : 250-500 IU Does not cause serum sickness Longer passive protection compared to horse ATS( 30 days / 7 -10 days )

40. Passive immunization ATS ( EQUINE ) : 1500 IU s/c after sensitivity testing 7 – 10 days High risk of serum sickness It stimulates formation of antibodies to it , hence a person who has once received ATS tends to rapidly eliminate subsequent doses.

41. Active & Passive Immunization In non immunized persons 1500 IU of ATS / 250-500 units of Human Ig in one arm & 0.5 ml of adsorbed tetanus toxoid into other arm /gluteal region 6 wks later, 0.5 ml of tetanus toxoid 1 yr later , 0.5 ml of tetanus toxoid

42. Prevention of neonatal tetanus Clean delivery practices 3 cleans : clean hands, clean delivery surface, clean cord care Tetanus toxoid protects both mother & child Unimmunized pregnant women : 2 doses tetanus toxoid 1st dose as early as possible during pregnancy 2nd dose – at least a month later / 3 wks before delivery

43. Immunized pregnant women : a booster is sufficient No need of booster in every consecutive pregnancy

44. Prevention of tetanus after injury All wounds should be thoroughly cleaned soon after injury Remove all foreign bodies, soil, dust, necrotic tissue A – completed course of toxoid/booster < 5 yrs ago B- completed course of toxoid / booster >5 yrs ago & < 10 yrs ago C- completed course of toxoid / booster >10 yrs ago D- not completed course of toxoid / immunity status unknown

45. Wounds < 6hrs, clean, non penetrating & negligible tissue damage Immunity Category A B C D Treatment Nothing more required Toxoid 1 dose Toxoid 1 dose Toxoid complete course

46. Other Wounds Immunity Category A B C D Treatment Nothing more required Toxoid 1 dose Toxoid 1 dose + Human Tetanus Ig Toxoid complete course + Human Tetanus Ig

47. Thank You