1 / 16

Neonatal tetanus

Neonatal tetanus. DR AUDU LAMIDI CHIEF CONSULTANT PAEDIATRICIAN. Introduction. Acute non contagious infection A non - communicable/infectious disease that causes sustained muscular s pasm ,  contraction as a result of toxins

amandae
Download Presentation

Neonatal tetanus

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Neonatal tetanus DR AUDU LAMIDI CHIEF CONSULTANT PAEDIATRICIAN

  2. Introduction • Acute non contagious infection • A non - communicable/infectious disease that causes sustainedmuscular spasm, contraction as a result of toxins • Released by the causative organism Clostridium tetani : a large , Gram positive, rod shaped, spore forming, anaerobic bacteria, • Found in soil, especially heavily manured soils, intestine and faeces of animals (animal dung)

  3. Pathogenesis • Human pathogenicity derives from release of a potent protein toxin from spores; TETANOSPASMIN • Also produces tetanolysin which has no clinical relevance • Spores gain access to wounds, germinate into vegetative forms multiply locally but symptoms appear remote from site of infection • Tetanospasmin is one of 3 known most powerful biologic toxins( Diphtheria and botulism). Estimated lethal human dose is 2.5 ngm/kg

  4. Pathogenesis • Toxin binds to peripheral nerve ending, transported along the axon and across synaptic junctions and ends in the CNS. • Fixes rapidly to gangliosides at the presynaptic inhibitory motor nerve endings and gets transported into the axon by endocytosis • Blocks release of inhibitory neurotransmitters (glycine gama-amiobutyric acid) required to check nervous impulse • Nervous impulses can no longer be checked by normal inhibitory mechanisms resulting in unopposed muscular contractions and spasms.

  5. Transmission • Enters the body through contaminated object: • blades, scissors, knives etc used to ligate umbilical cord as well as for traditional uvulectomy, circumcision and tribal marks, ear piercing ect • cow dung applied on cord, • Affected babies are usually those whose mothers were not immunized against tetanus in pregnacy

  6. Clinical presentation • Incubation period 3-21 days; may be shorter • Onset time: interval between appearance fo first sign and onset of spasm • Usually generalized • Trismus • Risussardonicus • Abdominal rigidity • Generalized spasms: provoked or unprovoked • Inability to feed • Sweating and fever • Neck retraction/retrocolis and opistotonus

  7. Clinical phothograph

  8. Neck retraction

  9. Diagnosis • Usually clinical • History is suggestive • Examination reveals signs listed above • Laboratory investigation not useful as Clostridium is rarely cultured fron site of infection • Investigations are often done to rule out differential diagnosis eg meningitis, strychnine poinsoning

  10. Treatment • Antibiotics to clear residual Clostridium penicillin G:50000IU/kg/day • Tetanus immune globulin to neutralize circulating toxins500 IU im stat • Sedatives to stop and control spasms; phenobarbitone, chlorpromazine, diazepam • Muscle relaxation with Diazepam may be required • Spasm chart should be kept • NGT for feeding • Avoid provoking sounds/noise • May require muscle paralysis, endotracheal intubation and mechanical ventilation. • Immunization following recovery with tetanus toxoid

  11. Complication • Laryngeal spams • Apnea: may be recurrent • Aspiration pneumonitis • Skeletal fractures • Autonomic dysfunction: tachycardia bradycardia • Respiratory failure is the most common cause of death. • Brain damage can occur in infants from recurrent hypoxia (apnoic episodes)

  12. Poor prognostic features • Short incubation period • Short onset time • Delay in treament • Frequent unprovoked spasms • Death is usually due to respiratory or cardiac failure. • Intensive medical care improves the prognosis.

  13. Prevention • Maternal immunization with TT:This protects the mother and – and through a transfer of tetanus antibodies to the fetus – also her baby. • Avoidance of unsterile instrument in the care of cord. • Cord care with chlorhexidine gel only • Discourage unhealthy traditional practices • Health education

  14. Points to note • Neonatal tetanus is a significant problem in developing countries due to poor umbilical stump hygiene and lack of maternal immunization. • Neonatal tetanus requires treatment in a medical facility, often in a referral hospital. • Acute condition requiring intensive care • Prevention is by immunization

  15. End • Thank You

More Related