TETANUS

1. TETANUS

2. INTRODUCTION Greek word-tetanos - taut and stretched First described by Hippocrates & Susruta Tetanus is an acute, toxin-mediated disease caused by Clostridium tetani Only vaccine preventable disease that is infectious but not contagious

3. CAUSATIVE AGENT Caused by CLOSTRIDIUM TETANI Anaerobic Motile Gram positive bacilli Oval, colourless, terminal spores – tennis racket or drumstick shape. It is found worldwide in soil, in inanimate environment, in animal faeces & occasionally human faeces.

5. Clostridium tetani Gram Stain NOTE: Round terminal spores give cells a “drumstick” or “tennis racket” appearance.

6. EPIDEMIOLOGY • Entirely preventable disease by immunization • Tetanus occurs worldwide but is more common in hot, damp climates with soil rich in organic matter. • More common in developing and under developing countries. • More prevalent in industrial establishment, where agricultural workers are employed. • Tetanus neonatorum is common due to lack of MCH care.

7. India • Tetanus is endemic infection in India. • Causative factors • Hand washing • Delivery practices • Traditional birth customs • Interest in immunization • Prior to the national immunization programme estimated 3.5 lakh children were dying annually. • 70,000 cases continue to occur largely in the states – Orissa, Bihar, MP, Aasam, Rajasthan, UP ,where TT immunization coverage is less than national coverage(70%) .

8. TRANSMISSION :

9. Host Factors • Age : It is the disease of active age (5-40 years), New born baby, female during delivery or abortion • Sex : Higher incidence in males than females • Occupation : Agricultural workers are at higher risk • Rural –Urban difference: Incidence of tetanus in urban areas is much lower than in rural areas • Immunity : Herd immunity does not protect the individual • Environmental and social factors: Unhygienic custom habits,Unhygienic delivery practices

10. ROUTE OF ENTRY Apparently trivial injuries Animal bites/human bites Open fractures Burns Gangrene In neonates usually via infected umbilical stumps Abscess Parenteral drug abuse

11. TETANUS PRONE WOUND A wound sustained more than 6 hr before surgical treatment. A wound sustained at any interval after injury which is puncture type or shows much devitalised tissue or is septic or is contaminated with soil or manure.

12. Sporulated Vegetative • Spores that gain entry can persist in normal tissue for months to years under anaerobic conditions. • When the oxygen levels in the surrounding tissue is sufficiently low, the implanted C. tetani spore then germinates into a new, active vegetative cell that grows and multiplies and most importantly produces tetanus toxin - tetanospasmin and tetanolysin. • Tetanolysin is not believed to be of any significance in the clinical course of tetanus. • Tetanospasmin is a neurotoxin and causes the clinical manifestations of tetanus.

13. The toxin migrates across the synapse (small space between nerve cells critical for transmission of signals among nerve cells) where it binds to presynaptic nerve terminals and inhibits or stops the release of certain inhibitory neurotransmitters (glycine and gamma-amino butyric acid). • Loss of inhibition of preganglionic sym neurons – sympathetic hyperactivity • These neurons become incapable to release neurotransmitter. The neurons, which release gamma-aminobutyric acid (GABA) and glycine, the major inhibitory neurotransmitters, are particularly sensitive to tetanospasmin, leading to failure of inhibition of motor reflex responses to sensory stimulation.

14. This results in generalized contractions of the agonist and antagonist musculature characteristic of a tetanic spasm. • The shortest peripheral nerves are the first to deliver the toxin to the CNS, which leads to the early symptoms of facial distortion and back and neck stiffness. • Once the toxin becomes fixed to neurons, it cannot be neutralized with antitoxin. Recovery of nerve function from tetanus toxins requires sprouting of new nerve terminals and formation of new synapses.

15. Mechanism of Action of TetanusToxin

16. 1. C. tetani enters body from through wound. 2. Stays in sporulated form until anaerobic conditions are presented. 4. Tetnospasmin spreads using blood and lymphatic system, and binds to motor neurons. 3. Germinates under anaerobic conditions and begins to multiply and produce tetnospasmin. 5. Travels along the axons to the spinal cord. 6. Binds to sites responsible for inhibiting skeletal muscle contraction.

18. Spores are extremely stable,although immersion in boiling water for 15 minutes kills most spores. Exposure to saturated steam under 15 lbs.of pressure for 15-20 minutes at 121°c is highly effective against spores . • Dry heat is slower than by moist heat (1 -3 hrs at 160 °C),but it is also effective against spores. • Ethylene oxidesporocidal. • Autoclaving at 121°C for 15min kills the spores readily. • Iodine(1% aqueous soon) and H2O2 (10 volume) kills spores within few hours.

19. CLINICAL FEATURES: IP : Time from injury to the first symptom.The median incubation period is 7 days, and, for most cases (73%), incubation ranges from 3-21 days. Period of onset : It is the time from first symptoms to the reflex spasm. In general the further the injury site is from the central nervous system, the longer the incubation period. The shorter the incubation period, the higher the chance of death.

20. Triad of muscle rigidity, spasms & autonomic dysfunction Early symptoms are neck stiffness, sore throat and poor mouth opening. Patients with generalized tetanus present with trismus (ie, lockjaw) in 75% of cases. Other presenting complaints include stiffness, neck rigidity, dysphagia, restlessness, and reflex spasms. Spasms usually continue for 3-4 weeks. Subsequently, muscle rigidity becomes the major manifestation. Rigid Abdomen. Muscle rigidity spreads in a descending pattern from the jaw and facial muscles over the next 24-48 hours to the extensor muscles of the limbs – stiff proximal limb muscles & relatively sparing hand & feet.

21. Risus sardonicus: Sustained contraction of facial musculature produces a sneering grin expression known as risus sardonicus. • Contraction of the muscles at the angle of mouth and frontalis

22. Trismus (Lock Jaw): Spasm of Masseter muscles.

23. Opisthotonus: Spasm of extensor of the neck, back and legs to form a backward curvature. • Muscle spasticity

24. Poor cough, • inability to swallow, • gastric stasis all increase the risk of aspiration. Respiratory failure continues to be a major cause of mortality in developing countries. • whereas severe autonomic dysfunction causes most deaths in the developed world.

25. Dysphagia occurs in moderately severe tetanus due to pharyngeal muscle spasms. Reflex spasms triggered by minimal external stimuli such as noise, light,or touch. The spasms last seconds to minutes; become more intense; increase in frequency with disease progression; and can cause apnea, fractures, dislocations, and rhabdomyolysis. Laryngeal spasms can occur at any time and can result in asphyxia.

26. AUTONOMIC DYSFUNCTION Tetanospasmin has a disinhibitory effect on the autonomic nervous system (ANS) due to increased release of catecholamines it causes : Hyperpyrexia Sweating Peripheral vasoconstriction Labile/Sustained Hypertension Episodic tachycardia, dysrhythmias and cardiac arrest Occasionally period of bradycardia & hypotension

27. Other symptoms include: • Drooling • Fever usually absent • Mentation unimpaired • Hand or foot spasms • Irritability • Uncontrolled urination or defecation • Duration of illness — Tetanus toxin-induced effects are long-lasting because recovery requires the growth of new axonal nerve terminals. The usual duration of clinical tetanus is four to six weeks.

28. SEQUENCE OF EVENTS Lock Jaw Stiff Neck Difficulty Swallowing Muscle Rigidity Spasms

29. THANK YOU

30. TYPES OF TETANUS Generalied vs Local Cephalic Traumatic Otogenic Idiopathic Puerperal Tetanus neonatorum

31. Maternal tetanus • Tetanus occurring during pregnancy or within 6 weeks after any type of pregnancy termination, is one of the most easily preventable causes of maternal mortality. • It includes postpartum or puerperal tetanus • (i) postpartum or puerperal tetanus, usually resulting from septic procedures during delivery, • (ii) postabortal tetanus, following septic maneuvers during induced abortion • (iii) Tetanus during pregnancy, generally resulting from inoculation through a nongenital portal of entry

32. NEONATAL TETANUS Tetanus neonatorum (8th day disease) 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 It is easily preventable by 2 tetanus toxoid injections and ‘5 cleans’ while conducting deliveries.

35. 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

36. 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. Involvement of cranial nerves VI,III, IV, and XII may also occur either alone or in combination with others Incubation period : few days Mortality : high

38. Ophthalmoplegic tetanus is a variant that develops after penetrating eye injuries and results in CN III palsies and ptosis.

39. DIAGNOSIS www.medicalgeek.com • There are currently no blood tests that can be used to diagnose tetanus. Diagnosis is done clinically based on the presence of trismus, dysphagia, generalized muscular rigidity, and/or spasm. • Laboratory studies may demonstrate a moderate peripheral leukocytosis. • An assay for antitoxin levels is not readily available. However, a level of 0.01 IU/mL or greater in serum is generally considered protective, making the diagnosis of tetanus less likely. • Cerebrospinal fluid (CSF) study findings are usually within normal limits.

40. DIRECT SMEAR Show Gram-positive bacilli with drum-stick appearance. Morphologically indistinguishable from similar nonpathogenic bacilli.

41. CULTURE Done in blood agar under anaerobic condition or in Robertson’s cooked meat medium. Produces swarming growth after 1-2 days of incubation. In contaminated specimen heat at 80°C for 10mins before culture to destroy non-sporing organisms.

42. ANIMAL INOCULATION To demonstrate toxigenicity. Positive case : test animal develops stiffness & spasm of tail & inoculated hind limb within 12-24hrs which spreads to rest of the body. Death occurs in 1-2 days.

43. Procedures: • The spatula test is one diagnostic bedside test. • This simple test involves touching the oropharynx with a spatula or tongue blade. • This test typically elicits a gag reflex, and the patient tries to expel the spatula (ie, a negative test result). • If tetanus is present, patients develop a reflex spasm of the masseters and bite the spatula (ie, a positive test result). • Sensitivity of 94% and a specificity of 100%.[2] • No adverse sequelae (eg, laryngeal spasm) from this procedure were reported

44. DIFFERENTIAL DIAGNOSIS Drug induced Dystonic Reactions e.g. Phenothiazines Strychnine poisoning Neuroleptic Malignant Syndrome, Serotonin syndrome Trismus d/t Peritonsillar Abscess/Dental infection Stiff person syndrome Acute abdominal emergencies Dislocations, Mandible Encephalitis, Meningitis Hysteria Hypocalcemia Rabies Seizure disorder (partial or generalized) Spider Envenomations, Widow Stroke, Hemorrhagic Stroke, ischemic (cephalic tetanus) Subarachnoid Hemorrhage

45. PRINCIPLE OF TREATMENT 1. Neutralization of unbound toxin -HTIG/ATS 2. Prevention of further toxin production -Wound debridement & antibiotics 3. Antibiotics 4. Control of spasm -Anticonvulsants, Sedatives, Muscle relaxants etc. 5. Management of autonomic dysfunction -MGSO4, Betablockers etc. 6. Supportive care -Physiotherapy, Nutrition, Thromboembolism prophylaxis ABC etc…

46. 1. NEUTRALIZATION OF UNBOUND TOXIN www.medicalgeek.com • A single intramuscular dose of 3000-5000 units (100U/kg-half in each buttocks) is generally recommended for children and adults, with part of the dose infiltrated around the wound if it can be identified. • The WHO recommends TIG 500 units by IM/IV (depending on the available preparation) as soon as possible; in addition, administer age-appropriate TT-containing vaccine (Td, Tdap, DT, DPT, DTaP, or TT depending on age or allergies), 0.5 cc by intramuscular injection at separate site with HTIG. • TIG can only help remove unbound tetanus toxin, but it cannot affect toxin bound to nerve endings. • 250 U/vial available in our hospital, so 10 vial in each buttock is usual dose.

47. PRINCIPLE OF TREATMENT Admit patients to the intensive care unit (ICU). Because of the risk of reflex spasms, maintain a dark and quiet environment for the patient. Avoid unnecessary procedures and manipulations. Attempting endotracheal intubation may induce severe reflex laryngospasm; prepare for emergency tracheostomy.  Seriously consider prophylactic tracheostomy in all patients with moderate-to-severe clinical manifestations. Intubation and ventilation are required in 67% of patients. Tracheostomy has also been recommended after onset of the first generalized seizure.

48. 2. PREVENTION OF FURTHER TOXIN PRODUCTION • Debridement of Wound to remove organisms and to create an aerobic environment. • The current recommendation is to excise at least 2 cm of normal viable-appearing tissue around the wound margins. • Incise and drain abscesses. • Delay any wound manipulation until several hours after administration of antitoxin due to risk of releasing tetanospasmin into the bloodstream.

49. 3. ANTIBIOTICS • Theoretically, antibiotics may prevent multiplication of C tetani, thus halting production of toxin. Penicillin G was the drug of choice initially but now Metronidazole is preffered drug. • Penicillin G aqueous : (10-12 MU IV in 2-4 divided doses- 2-4 MU IV every 4 to 6 hrs) • A 10- to 14-d course of treatment is recommended • Metronidazole: (5oomg 6 hrly or 1gm 12 hrly) • A 10- to 14-d course of treatment is recommended. Some consider this the DOC since penicillin G is also a GABA agonist, which may enhance effects of the toxin. • Doxycycline, Clindamycin and Erythromycin are alternative for penicillin allergic patients who can not tolerate metronidazole.

50. 4. Control of spasm - Nursing in quiet environment, avoid unnecessary stimuli, Protecting the airway. • Drugs used to treat muscle spasm, rigidity, and tetanic seizures include sedative-hypnotic agents, general anesthetics, centrally acting muscle relaxants, and neuromuscular blocking agents. • Anticonvulsants • Sedative-hypnotic agents are the mainstays of tetanus treatment. Benzodiazepines are the most effective primary agents for muscle spasm prevention and work by enhancing GABA inhibition. • Diazepam : • Mainstay of treatment of tetanic spasms and tetanic seizures. Depresses all levels of CNS, including limbic and reticular formation, possibly by increasing activity of GABA, a major inhibitory neurotransmitter.