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Tetanus, Pediatric


Basics


Description


  • Tetanus is characterized by muscle rigidity and spasms due to production of a neurotoxin in infected wounds by Clostridium tetani.
  • There are four clinical forms of tetanus: generalized, neonatal, localized, and cephalic.

Epidemiology


  • Tetanus remains a problem in certain countries but is rare in countries with widespread immunization (in the United States <40 cases/year).
  • Rare cases have been reported in patients with protective levels of antitetanus antibodies.
  • Generalized tetanus is the most common form of disease.
  • Neonatal tetanus is rare in the United States but is seen in countries in which mothers are not immunized and nonsterile care of the umbilical cord is practiced.

Risk Factors


  • Inadequate immunization
  • Neonate born to unimmunized mother
  • Elderly with declining immune status
  • Injection drug use
  • Chronic wounds
  • Acute traumatic injury
  • Foreign bodies
  • Nonsterile delivery conditions and practice of applying mud or feces to umbilical cord

General Prevention


  • All wounds should be cleaned with soap and water and foreign bodies should be removed.
  • Universal immunization with tetanus toxoid (for details and information on catch-up schedules, refer to CDC Web site)
  • Tetanus postexposure prophylaxis should be initiated at the time of injury:
    • For clean minor wounds:
      • If patient has had ≥3 prior doses of tetanus toxoid (DTaP, Tdap, or Td) and it has been <10 years since the last dose, no prophylaxis is indicated; if it has been ≥10 years since last dose, give tetanus toxoid.
      • If patient has had <3 prior doses of tetanus toxoids, give tetanus toxoid.
    • For all other wounds:
      • If patient has had ≥3 prior doses of tetanus toxoid and it has been <5 years since the last dose, no prophylaxis is indicated; if it has been ≥5 years since the last dose, give tetanus toxoid.
      • Patients with <3 prior doses of tetanus toxoid should receive tetanus immune globulin (TIG) and tetanus toxoid at separate sites.
      • Patients with HIV or severe immunodeficiency should receive TIG regardless of prior immunization history.
    • In neonates or infants <6 months of age who have not received 3 doses of DTaP, the decision to use TIG should be based on mother 's tetanus immunization status; if unknown or inadequate, should give TIG
    • Type of tetanus toxoid to use for prophylaxis:
      • For children <7 years old, use DTaP; if pertussis vaccine is contraindicated, use DT.
      • For a child 7 " “10 years old, use Tdap.
      • For an adolescent 11 " “18 years old who has not received Tdap, use Tdap; for those who have received Tdap or for those whom pertussis is contraindicated, use Td.
    • TIG dose is 250 U IM (regardless of age or weight); if TIG is unavailable, use IV immunoglobulin (IVIG) or tetanus antitoxin (TAT).
      • Because TAT is equine in origin, test patient for sensitivity prior to use.
      • TAT is no longer available in the United States.

Pathophysiology


  • C. tetani produces tetanospasmin, a powerful metalloprotease neurotoxin.
  • Tetanospasmin can be absorbed directly into skeletal muscles adjacent to the injury.
  • Tetanospasmin can travel to the CNS via retrograde axonal transport through peripheral nerves or via lymphocytes.
    • In the CNS, tetanospasmin prevents the release of gamma-aminobutyric acid (GABA) and glycine in inhibitory nerve terminals, resulting in sustained excitatory discharges (motor spasms and increased muscle tone) and autonomic instability; tetanospasmin does not directly affect cognitive processes.
    • In the peripheral nervous system, tetanospasmin may block inhibitory impulses to motor neurons.
    • Loss of regulation of adrenal catecholamine release precipitates tachycardia, hypertension, and sweating.
  • Infection does not confer immunity, and all patients need to be immunized during recovery.

Etiology


  • Tetanus is caused by C. tetani, a spore-forming, anaerobic Gram-positive bacillus.
  • C. tetani is found in soil, animal and human feces, house dust, and salt and fresh water.
  • Under anaerobic conditions, spores become vegetative and produce tetanospasmin; anaerobic conditions in wounds are promoted by extensive necrosis, foreign bodies, or other suppurative infections.

Diagnosis


History


  • Incubation period is 3 " “21 days (usually 10 days) but varies, as inoculations distal to CNS are associated with longer incubation periods.
  • Generalized tetanus
    • "Lockjaw "  or trismus is initial symptom in 50 " “75% of cases.
    • Other early complaints include dysphagia, neck pain and stiffness, stiffness and pain in other muscle groups, urinary retention, restlessness, irritability, and headache.
    • More muscle groups involved as disease progresses
    • Noise, light, touch, and other stimuli can trigger painful spasms.
  • Neonatal tetanus (generalized tetanus during neonatal period)
    • Occurs following vaginal delivery to unimmunized mothers
    • Usually due to umbilical stump infections
    • Typically presents at around 1 week of life with irritability and poor feeding but progresses rapidly to generalized tetanic spasms
  • Local tetanus
    • Painful muscle contractions and stiffness limited to the area near the wound
    • Can persist for several weeks
    • Can progress to generalized tetanus
  • Cephalic tetanus (local tetanus of head/neck affecting cranial nerves)
    • Caused by C. tetani infections of head/neck including chronic infections of the head/neck (e.g., chronic otitis media)
    • Unlike generalized tetanus, flaccid CN palsies (especially CN VII) predominate; trismus may develop, however; if trismus is absent, could be confused with Bell palsy due to other etiologies

Physical Exam


  • Vital sign abnormalities
    • Severe, labile episodes of hypertension and tachycardia; hypotension is a late feature.
    • Initially, patients are afebrile but may develop hyperthermia with sustained contractions or from superinfections.
  • Trismus is often initial presenting sign.
  • Persistent trismus causes risus sardonicus, wrinkling of the forehead, and distortion of the eyebrows and the corners of the mouth.
  • With disease progression, other muscle groups develop tetanic contractions and spasms:
    • Can lead to a severe opisthotonic posture
    • Can mimic seizures
    • Can be extremely painful
    • Can be associated with laryngospasm and tetany of respiratory musculature
    • The anxiety and pain associated with these spasms may precipitate additional spasms.
  • Sweating can occur from autonomic instability.
  • Normal mental status is the norm.
  • In cephalic tetanus, CN palsies can be seen.
    • Look for underlying wounds or chronic infections of the face, scalp, neck, or ear.

Diagnostic Tests & Interpretation


Diagnostic Procedures/Other
  • Lab tests often yield little information; WBC is usually normal or mildly elevated and CSF studies are unremarkable, but serum calcium levels may help exclude hypocalcemic tetany.
  • Gram stain and anaerobic wound cultures yield C. tetani in <1/3 of cases.
  • Presence of protective tetanus antibody titer does not exclude possibility of disease.
  • EEG and EMG findings are nonspecific.

Differential Diagnosis


  • Infections
    • Dental infections, retropharyngeal and peritonsillar abscesses, poliomyelitis, viral encephalitis, and meningoencephalitis may present with trismus and/or CN findings.
  • Toxins and medications
    • Dystonic reactions to phenothiazine medications may resemble tetanus.
    • Strychnine poisoning may mimic generalized tetanus.
    • Malignant neuroleptic syndrome causes increased muscular rigidity resembling tetanic spasms.
  • Metabolic
    • Hypocalcemic tetany is usually not as severe as that seen in tetanus.
  • Stiff-man syndrome can result in fluctuating tonic contractions resembling tetanic spasms.
  • Bell palsy may resemble cephalic tetanus.

Treatment


Medication


First Line
  • Neutralization of unbound neurotoxin:
    • Human TIG 3,000 " “6,000 U IM as a single dose; part of the dose may be infiltrated around the wound.
    • Administer prior to antibiotics and wound manipulation.
  • Tetanus toxoid should be administered IM at a site contralateral to where TIG is given.
  • Antibiotics can decrease burden of vegetative C. tetani that produce tetanospasmin:
    • First line: metronidazole 30 mg/kg/24 h PO or IV in 4 " “6 divided doses; maximum 4 g/24 h
    • Alternative: parenteral penicillin G 1 " “200,000 U/kg/24 h IV in 4 " “6 divided doses; maximum 12,000,000 U/24 h
    • Treat for 10 " “14 days
    • Cephalosporins are not effective.
  • Sedation and muscle relaxation
    • Diazepam 0.1 " “0.2 mg/kg IV q4 " “6h
    • Phenothiazines, especially chlorpromazine, may be helpful.
    • Titrate sedation to desired effect and monitor for respiratory depression.
  • Nondepolarizing neuromuscular blockade and mechanical ventilation:
    • Use if spasms cannot be adequately controlled or if spasm of airway and respiratory musculature compromises ventilation:
    • Vecuronium 0.08 " “0.1 mg/kg IV followed by continuous infusion or hourly dosing
    • Avoid succinylcholine due to increased risk of hyperkalemia and arrhythmia.
  • Management of autonomic dysfunction
    • Beta-blockers (e.g., labetalol 0.4 " “1 mg/kg/h) can control hypertension or arrhythmias.
    • Magnesium sulfate can significantly reduce cardiovascular instability and act as an adjunctive agent to control muscle spasms.

Second Line
If TIG is not available: ‚  
  • IVIG 200 " “400 mg/kg may be used (not FDA approved for this use)
  • TAT can be given in doses of 1,500 " “3,000 U IM or IV (to achieve a serum concentration of 0.1 IU/mL) but only after a negative skin test or desensitization:
    • TAT is not available in the United States.
    • Anaphylactic reactions can occur with varying severity in up to 20% of patients.

Additional Therapies


General Measures
  • Tetanus is not a transmissible disease.
  • Keep patient in a quiet, darkened room with minimum stimulus.
  • Monitor cardiac and respiratory status closely.
  • Be prepared to perform a tracheotomy to prevent fatal laryngospasm.
  • Monitor for and treat urinary retention and constipation.
  • Parenteral nutrition is usually required to maintain adequate nutrition and hydration.
  • Monitor for and correct electrolyte abnormalities, especially hyperkalemia.

Surgery/Other Procedures


Aggressive surgical debridement of wounds and removal of foreign bodies is critical. ‚  

Inpatient Considerations


Initial Stabilization
  • Prompt recognition of clinical signs of tetanus and initiation of emergency care are crucial.
  • All suspected cases of tetanus should be rapidly transferred to a tertiary care center capable of providing ventilatory and cardiovascular support in an intensive care setting.
  • In the emergency department, treatment with TIG should be initiated to neutralize unbound neurotoxin; however, supportive care including aggressive airway management, ventilatory support, and pharmacologic interventions (sedation, muscle relaxation) are also critical to ameliorate the effects of bound neurotoxin.

Ongoing Care


Prognosis


  • Signs and symptoms usually progress for ¢ ˆ ¼1 week, then plateau for ¢ ˆ ¼1 week, and gradually improve over the next 2 " “6 weeks.
  • Overall mortality rates have decreased with advances in the ability to provide respiratory support in an intensive care setting.
  • Mortality rates vary from 1 " “18% for localized tetanus, 15 " “30% for cephalic tetanus, 45 " “55% for generalized tetanus, to 50 " “100% for neonatal tetanus.
  • Children and young adults have a better prognosis than older individuals or neonates.
  • A more rapid onset and progression of disease from trismus to generalized spasms is associated with a more severe course.
  • In the absence of complications, survivors usually recover fully without sequelae.

Complications


  • Most complications are related to the severe tetanic muscle contractions:
    • Rhabdomyolysis and hyperkalemia
    • Vertebral body and other fractures
    • Muscle hemorrhages
  • Respiratory failure from spasms of the upper airway or diaphragm is the most common cause of death in acute phase, whereas arrhythmia and myocardial infarction are most common cause of death later in disease.
  • Cerebrovascular hemorrhages may be seen in rare cases, especially in neonatal tetanus.
  • Pneumonia, including aspiration, can occur.

Additional Reading


  • Brook ‚  I. Tetanus in children. Pediatr Emerg Care.  2004;20(1):48 " “51. ‚  [View Abstract]
  • Hassel ‚  B. Tetanus: pathophysiology, treatment, and the possibility of using botulinum toxin against tetanus-induced rigidity and spasms. Toxins.  2013;5(1):73 " “83. ‚  [View Abstract]
  • Rhee ‚  P, Nunley ‚  MK, Demetriades ‚  D, et al. Tetanus and trauma: a review and recommendations. J Trauma.  2005;58(5):1082 " “1088. ‚  [View Abstract]
  • Thwaites ‚  CL, Farrar ‚  JJ. Preventing and treating tetanus. BMJ.  2003;326(7381):117 " “118. ‚  [View Abstract]

Codes


ICD09


  • 037 Tetanus
  • 771.3 Tetanus neonatorum

ICD10


  • A35 Other tetanus
  • A33 Tetanus neonatorum

SNOMED


  • 76902006 Tetanus (disorder)
  • 43424001 tetanus neonatorum (disorder)
  • 240434007 Generalized tetanus
  • 240429008 Localized tetanus

FAQ


  • Q: What types of wounds are tetanus-prone?
  • A: Punctures, avulsion wounds, crush injuries, burns, wounds from frostbite or missiles, and wounds contaminated with saliva, soil, or feces
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