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Tetanus

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Tetanus Tetanus Presentation Transcript

  • TETANUS DR. ABHAY MANGE
  •  A 60 yrs old houeswife ,uanabai thakur r/o katedhara M.P. admitted on 24/9/13 in micu with c/o  1.difficulty in swallowing since 5 days  2. difficulty in opening mouth since 5 days
  •  H/o pain in both ears since 15 days  No h/o injury  No h/o fever / convulsion  No h/o consumption of any substance  Not taking any medication  No h/o similar complaints in past  No HT/DM/IHD in past  Non tobacco chewer
  • On examination  Afebrile  Pulse -110/min  Bp -150/90 mmhg  Resp -24/min, intermittent spasms +  Risus sardonicus +  Neck stiffness +  Trismus +  Oral cavity – wnl  No external injury
  • On examination  CNS :-Conscious ,oriented Power gr 4+ ul/ll Sensation –wnl DTR + Planters – flexor b/l  P/A:- Ant .abdominal wall Rigidity +  RS :- wnl  CVS:-wnl
  • PROVISIONAL DIAGNOSIS  Cephalic Tetanus
  • Investigations  Routines investigations - wnl  Fundus- wnl  ENT opinion:- s/o b/l safe csom
  • Final diagnosis  B/L CSOM (safe) with Cephalic tetanus
  • Treatment   Tetanus human immunoglobulin 2750 U Antibiotcs –inj C/P 2 MU 4 hrly inj metronidazole 500 mg tds inj cefotaxime 1 gm tds inj robinex tdS inj pantoprazole 40 mg bd  Day 2 -Tracheostomy done  Day 3- spasms increased,bp 200/100 mmhg , HR- 140/MIN So put on mechanical ventilation with knock down by inj atracuronium +midazolam infusion,tab labetolol 200mg bd started 
  • Treatment  Day 5- patient febrile so inj meropenam added ,culture sent  Day 10- patient weaned from mechanical ventilation, tracheal culture – pseudomonas aregionosa s/t imepenam  Day 12 – patient transferred to IDH
  • Treatment  Day 18 –  Put on non-cuffed TT  Antibiotics continued  Nutrition  Physiotherapy
  • DISCUSSION
  • Historical perspective  The word tetanus comes from the Greek tetanos, which is derived from the term teinein, meaning to stretch.  During World War I, tetanus occurred in 1.47 per 1000 British wounded and in 12.5 per 1000 persons involved in the Peninsular campaign.  Nicolaier discovered Clostridium tetani in 1885 .  In 1889, Koch's pupil, Kitasato, obtained the bacillus of tetanus in pure culture .  introduction of tetanus toxoid vaccination by Behring and Knorr in 1886.
  • Problem  Although it is an entirely preventable disease by immunization , the burden of disease worldwide is great.  W.H.O considers reporting is inaccurate & incomplete, particularly in devoleping countries,  In 2008 16628 cases 0f tetanus other than neonatal and 6658 cases reported to who worldwide !  in 2009 Govt. of India reported (other than NT) 2051 cases and 160 death.there were 889 NT cases and 31 deaths!!  In 2009 maharastra reported 392 (other than NT) cases and 1 death.while 57 NT cases and 0 death !!! (park 21)
  • The Organism  Clostridium tetani is a gram positive, obligately anerobe, spore forming bacillus, which give it a characteristic drumstick or a tennis racket appearance.  distributed in soil and in intestine of horses, sheep, cattle, dogs, cats, rats, chickens and nearly 10% of humans.   Hot and damp climate with soil rich in organic matter Spores are especially resistant to heat, usual antiseptics and chemical agents but are destroyed by autoclaving at 1200C for 15 minutes or boiling for atleast 4 hours.
  • Pathogenesis  Disease Occurs sporadically ,Affects unimmunized, partially immunized & fully immunized who fail to maintain adequate immunity with booster doses of vaccine  The incubation period ranges from 3-14 days, Although can as short as one day to as long as several months have been reported  IP have prognostication and correlates with the severity of disease,  Tetanus usually follows a recognized injury.  It can complicate burns, ulcers, gangrene, necrotic snakebites, middle ear infections, septic abortions, childbirth, intramuscular injections, and surgery.  Up to 50% of cases the injury not considered serious enough to seek medical treatment.  In 15-25% of patients, there is no evidence of a recent wound
  • 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 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.
  • Pathogenesis    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
  • Clinical presentation  Four clinical forms of this disease are recognized depending upon the extent and location of neurons involved.  Generalized  Neonatal  Cephalic  local.
  • Clinical presentation Generalized tetanus  Commonest form and is characterized by increased muscle tone and generalized spasms.  Usually, the first symptom is trismus or lock jaw. Dysphagia, stiffness and pain in neck, shoulder and back muscles appears.  Rigidity of abdomen and facial grimacing, popularly known as  „Risus sardonicus‟ ,opsthotonus.  Appearance of generalized muscle spasms, occurring spontaneously or due to minor stimuli  Spasms may lead to respiratory compromise necessitating respiratory support.  Spasms can cause compressive fractures of the spine, rupture of muscles, rhabdomyolysis and renal failure. These are maximum during the first two weeks of illness and decrease thereafter in frequency and intensity. 
  • Clinical presentation  Autonomic Disturbances Seen in Tetanus  Sustained or labile hypertension Progressive and refractory hypotension Peripheral vasoconstriction Tachycardia (episodic commonly) Bradycardia and asystole Arrythmias Fever Profuse diaphoresis, salivation Increased bronchial secretions Gastric stasis and ileus Urinary retention          
  • Clinical presentation Localised tetanus  This is a relatively uncommon and benign form of the  Disease process in which patients have persistent contraction of muscles in same anatomic area as the injury preceding the tetanus.  Local tetanus might generalize over time but overall mortality is about 1%.  The most important indicator for poor prognosis was the progression to secondary generalization (27%).
  • Clinical presentation Cephalic tetanus :  This involves cranial nerves and has an overall incidence of 6%.  It commonly results from middle ear infections and head injuries.  Facial muscles are most commonly affected, followed by 6th, 3rd, 4th and 12th cranial nerves in the order of frequency.  Trismus may be present but usually follows other cranial nerve deficits in 42% of patients.  Although, overall mortality described is high (15-30%), many cases with a milder disease have been reported from India.
  • Clinical presentation Neonatal tetanus  This form of tetanus still has a high incidence and mortality in the developing countries  The common age of onset is between 5 and 15 days following birth.  Common presenting complaints are rigidity, spasms, failure to suck, trismus, fever and seizures.  Due to lack of inhibiting influences from higher centers in newborns, the anterior horn cells react more violently, resulting in more spasms.  Overall mortality is around 70% and most patients with severe disease die.
  • Opisthotonus Neonatal Tetanus
  • Risus sardonicus Trismus
  • Ablett Classification of the Severity of Tetanus  I Mild- Mild to moderate trismus; general spasticity; no respiratory embarrass - ment; no spasms; little or no dysphagia  II Moderate -Moderate trismus; well-marked rigidity; mild to moderate but short spasms; moderate respiratory embarrassment with an increased respiratory rate greater than 30, mild dysphagia  III Severe -Severe trismus; generalized spasticity; reflex prolonged spasms; respiratory rate greater than 40; apnoeic spells, severe dysphagia; tachycardia > 120.  IV Very severe- Grade III and violent autonomic disturbances involving the cardiovascular system. Severe hypertension and tachycardia alternating with relative hypotension and bradycardia, either of which may be persistent
  • Diagnosis   Tetanus is diagnosed by clinical observation. Electromyographic studies are occasionally useful in questionable cases.  Antitetanus antibodies are undetectable in most tetanus patients, “protective” concentration of 0.01 IU/L.  Rare patients apparently develop antibodies that are not protective.  Attempts to culture C. tetani from wounds are not useful in diagnosis  „Spatula test‟ to aid in diagnosis with a sensitivity of 94% and specificity of 100%. (Apte and Karnad )`
  • Differential diagnosis  Strychnine poisoning,  Dystonic reactions to neuroleptic drugs or other central dopamine. Treatment with anticholinergic agents (benztropine or diphenhydramine) is rapidly effective against dystonic reactions.  Dental infections can produce trismus, and should be sought, but they do not cause the other manifestations of tetanus.
  • Management  Management of tetanus patients involves a team approach.  The defined goals of treatment include the following :  a) halting production of toxin within the wound, b) neutralization of unbound toxin, c) control of muscle spasms, d) management of autonomic instability, e) supportive therapy, f) management of complications, g) prevention      
  • Management Halting the production of toxin      Wound management eradicate spores and change conditions for germination, thereby preventing further elaboration and absorption of the neurotoxin. Antibiotic therapy : Penicillin still remains a standard therapy in many parts of the world, although metronidazole seems to be replacing it and is being considered as a drug of choice by. The usual dose of penicillin is 100,000 – 200,000 IU/kg/day given intravenously or intramuscularly. Metronidazole is used at a dose of 500 mg every 6 hours intravenously or per orally and 400 mg rectally every 6 hours, for 7-10 days.
  • Management Neutralization of the unbound toxin  This is achieved through passive immunization with either human or equine tetanus immunoglobulin. should be undertaken as early as possible since the toxin becomes inaccessible once it is bound to the nerve terminus.  The usual dose of equine preparation is 500- 1000 IU/kg given intravenously or intramuscularly.  The dose of HTIG is 5000-8000 IU intramuscularly.  Usual dose for prophylaxis is1500-3000 IU of equine and 250-500 IU of human preparation.
  • Management Control of muscle spasms  Sedatives : Diazepam-.Midazolam,Propofol,  Neuromuscular blocking agents :  Magnesium sulfate  Baclofen  Methacarbamol  Dantrolene Management of dysautonomia  Sedatives- benzodiazepenes, Morphine  Adrenergic blockers Labetolol, Esmolol, Clonidine,  Magnesium sulfate  Intrathecal baclofen
  • Supportive Management  Secure airway/tracheostomy/ventilatory support  Pts recovering from tetanus should be actively immunized  Hydration  Nutrition  Physiotherapy  Prophylactic anticoagulation  Bowel, bladder, back care  Treatment of intercurrent infection
  • 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  
  • 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
  • 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  
  • Passive immunization  • • •  • • • • Human Tetanus Hyperimmunoglobulin : 250-500 IU Does not cause serum sickness Longer passive protection compared to horse ATS( 30 days / 7 -10 days 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.
  • 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
  • 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     Immunized pregnant women : a booster is sufficient No need of booster in every consecutive pregnancy
  • 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
  • Wounds < 6hrs, clean, non penetrating & negligible tissue damage  Immunity Category  Treatment • A B C D • Nothing more required Toxoid 1 dose Toxoid 1 dose Toxoid complete course • • • • • •
  • Other Wounds  Immunity Category  Treatment • • • A B C • D • Nothing more required Toxoid 1 dose Toxoid 1 dose + Human Tetanus Ig Toxoid complete course + Human Tetanus Ig • • •
  • Thank You!