Tetanus

Reviewed and revised 9 February 2014

OVERVIEW

  • potentially lethal condition characterised by muscular rigidity and spasms, caused by the tetanospasmin toxin produced by Clostridium tetani, that may lead to life-threatening respiratory failure and autonomic dysregulation in severe cases
  • rare in the developed world, but accounts 1 million deaths worldwide each year

TYPES

  • cephalic
  • local
  • generalised
  • neonatal (50% of tetanus deaths worldwide)

CAUSE

Clostridium tetani

  • caused by toxin from Clostridium tetani -> able to survive in the environment as highly resistant spores
  • anaerobic spore forming gram positive bacillus
  • once in a suitable environment -> spores germinate -> bacteria multiply -> toxins released (tetanospasmin and tetanolysin)

Tetanospasmin

  • taken up by motor nerves or haematogenous spread to CNS
  • disrupts synaptic transmission by preventing release of neurotransmitters (zinc endopeptidase)
  • preferentially prevents discharge from GABA inhibitory interneurons in spinal cord and brainstem
    -> unrestricted motor nerve activity and autonomic instability

CLINICAL FEATURES

Clinical triad of rigidity, muscle spasms and, if severe, autonomic dysfunction

  • contaminated wound (may be trivial) or umbilical stump in neonates
  • incubation period: 3-14d (1-60 at the extremes) = time to first symptom
  • onset time: 1-7d = time from first symptom to first spasm
  • rigidity (persists > 2 weeks)
    — trismus, dysphagia, increased tone in trunk muscles – greater on side of injury initially
  • spasms (reduce after 2 weeks)
    — spontaneous or provoked by physical or emotional stimuli, laryngospasm, risus sardonicus, opisthotonos (severe spasm in which the back arches and the head bends back and heels flex toward the back)
  • autonomic disturbance (onset after spasms, lasts 1-2 weeks)
    — tachycardia and hypertension may alternate with bradycardia and hypotension, dysrhythmia, cardiac arrest
    — salivation, bronchial secretions
    — gastric stasis, ileus, diarrhoea
  • respiratory compromise
    — chest wall rigidity
    — laryngospasm
    — aspiration
    — retained secretions

DIFFERENTIAL DIAGNOSIS

Diagnosis of tetanus is made clinically

  • strychnine poisoning
  • trismus due to orofacial infection
  • stiff person syndrome
  • acute dystonic reaction
  • seizure disorder
  • hypocalcaemic tetany
  • psychogenic
  • meningism

Neonatal tetanus may resemble:

  • Seizures
  • meningitis
  • sepsis

INVESTIGATIONS

  • urinary strychnine to exclude this as a cause
  • CK, UEC, CMP for rhabdomyolysis and to rule out low Ca
  • ABG (respiratory failure)

MANAGEMENT

Resuscitation

A – intubate as requires large doses of sedatives to control muscle spasm and to overcome laryngospasm
B – at risk of aspiration and have copious bronchial secretions requiring frequent suctioning, often ventilated for 2-3 weeks until spasms subside
C – autonomic dysfunction necessitate monitoring in a critical care environment, fluctuant haemodynamics so use short acting agents; fluid loading
D – benzodiazepines in large doses (up to 100mg/h diazepam) -> non-depolarsing NMBD

Specific Therapy

  • metronidazole (first choice); penicillin is used throughout most of the world but is a GABA antagonist
  • anti-tetanus immunoglobulin: 100-300IU/kg of human Ig IM
  • benzodiazepines; adjuncts include barbiturates, propofol, chlorpromazine
  • Mg to 2-4mmol/L as useful in spasm treatment and limits autonomic instability
  • consider dantrolene (unproven)
  • consider intrathecal baclofen

Treat underlying cause and complications

  • clean and debride wounds (source control)
  • immunize (infection does not confer immunity) – Q10 yearly

Supportive care and monitoring – usual cares with emphasis on:

  • calm environment
  • cardiac monitoring
  • nutrition e.g. enteral feeding
  • often require tracheostomy
  • prevention of pressure sores and GI stress ulcers

COMPLICATIONS

Respiratory

  • Aspiration
  • Laryngospasm/obstruction
  • Sedative-associated obstruction
  • Respiratory apnoea
  • Type I (atelectasis, aspiration, pneumonia) and type II respiratory failure (laryngeal spasm, prolonged truncal spasm, excessive sedation)
  • ARDS
  • Complications of prolonged assisted ventilation (e.g. pneumonia)
  • Tracheostomy complications (e.g. tracheal stenosis)

Cardiovascular

  • Tachycardia, hypertension, ischaemia
  • Hypotension, bradycardia, asystole
  • Dysrhythmias
  • Cardiac failure

Renal

  • High output renal failure
  • Oliguric renal failure
  • Urinary stasis and infection

GI

  • Gastric stasis
  • Ileus
  • Diarrhoea
  • Haemorrhage

Other

  • Dehydration
  • Weight loss
  • Thromboembolus
  • Sepsis and multiple organ failure

Musculoskeletal

  • Fractures of vertebrae during spasms
  • Tendon avulsion during spasms
  •  rhabdomyolysis

PROGNOSIS

Mortality

  • untreated: >50% (usually due to respiratory failure)
  • high level ICU care available: 10-25% (usually due to autonomic failure)

Survivors

  • severe cases usually require 3-5 weeks in ICU
  • often make full recovery

Indicators of poor prognosis

1. incubation of < 7 days
2. period of onset < 48 hours
3. portal of entry from umbilicus, uterus, burns, open fracture or IM injection
4. presence of spasms
5. temperature > 38.4
6. HR > 120 (adults), > 150 (neonates)


References and Links

LITFL

Journal

  • Cook TM, Protheroe RT, Handel JM. Tetanus: a review of the literature. Br J Anaesth. 2001 Sep;87(3):477-87. Review. PubMed PMID: 11517134.
  • Dingli K, Morgan R, Leen C. Acute dystonic reaction caused by metoclopramide, versus tetanus. BMJ. 2007 Apr 28;334(7599):899-900. PMC1857743.
  • Farrar JJ, Yen LM, Cook T, Fairweather N, Binh N, Parry J, Parry CM. Tetanus. J Neurol Neurosurg Psychiatry. 2000 Sep;69(3):292-301. Review. PubMed PMID: 10945801; PubMed Central PMCID: PMC1737078.

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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