Tetanus

-Dr [Link], T
• Definition
• Microbiology
• Pathogenesis
• Forms
• Diagnosis and management
 Definition
• Tetanus is a nervous system disorder
characterized by muscle spasms that is caused by
the toxin-producing anaerobe, Clostridium tetani

• CDC defines tetanus as "the acute onset of

hypertonia or. . .painful muscular contractions
(usually of the muscles of the jaw and neck) and
generalized muscle spasms without other
apparent medical cause
• In 20% of cases of tetanus, no puncture entry
wound is found.

• Superficial abrasions to the limbs are the

commonest infection sites in adults.

• Deeper infections (e.g., attributable to open

fracture, abortion, or drug injection) are associated
with more severe disease and worse outcomes.
• An anaerobic, gram-positive, spore-forming
rod, motile bacteria
• Spores are highly resilient and can survive
readily in the environment throughout the
world.
• Spores resist boiling and many disinfectants.
• C. tetani spores and bacilli survive in the
intestinal systems of many animals, and fecal
carriage is common
• Transmission – puncture wounds, trauma,
human bites
• C. tetani produces two exotoxins: tetanolysin and
tetanospasmin.
Tetanolysin
• Related to the clostridial toxins and streptolysin,
Plays no role in the pathogenesis of the disease.
Tetanospasmin
• Generally referred to as "tetanus toxin,"
• Is the neurotoxin that causes the manifestations
of disease
• Very low concentrations of this highly potent
toxin can result in tetanus (minimum lethal
human dose, 2.5 ng/kg).
• Release of tetanospasmin from vegetative C.
Tetani --- toxin binds to peripheral motor
neuron terminals-----Retrograde intra-axonal
transport of toxin to the spinal cord and brain
stem----Blockade of inhibitory
neurotransmitters (glycine and GABA) release
in presynaptic terminal---
• the resting firing rate of motor neurons 
Rigidity  Simultaneous recruitment of agonist
and antagonistic muscles 20 to limited
glycinegic activity Spasm
• After reaching the spinal cord and brainstem
via retrograde axonal transport and binding
tightly and irreversibly to receptors at these
sites, tetanus toxin blocks neurotransmission
by its cleaving action on membrane proteins
involved in neuroexocytosis of inhibitory
neurotransmitters (glycine and GABA) release
in presynaptic terminals
The net effect
Disinhibit ion of neurons that modulate excitatory
impulses from the motor cortex.

Disinhibition of anterior horn cells and autonomic

neurons results in increased muscle tone, painful
spasms, and widespread autonomic instability
• Muscular rigidity in tetanus occurs though a
complex mechanism that involves an increase in the
resting firing rate of disinhibited motor neurons and
lack of inhibition of reflex motor responses to
afferent sensory stimuli

• Lack of neural control of adrenal release of

catecholamine induced by tetanus toxin produces a
hyper sympathetic state that manifests as sweating,
tachycardia and hypertension
 Clinical Features
• Forms of Tetanus:
– Generalized tetanus,
– Localized Tetanus
– Cephalic Tetanus
– Neonatal Tetanus
 Clinical Features
• Generalized Tetanus
– Most common presentation of tetanus
– Trismus (lockjaw) 20 to masseter muscle hyper
tonicity
– Neck shoulder and back muscle stiffness and pain
– Rigid abdomen and stiff proximal limb muscles
– Risus sardonicus, Arched back (Opisthotonus)
– Paroxysmal generalized muscle spasm apnea
/Cyanosis /laryngospasm (spontaneous or provoked)
– Hyperpyrexia with clear mentation
 Clinical Features
Mild tetanus Moderate Tetanus Severe Tetanus

- IP > 14 days - IP= 7-14 days - IP <7 days

- Onset time >7days - Period of onset > 3- - Period of onset <
- Mild trismus 6days 3days
- Localized spasm - Marked trismus - frequent explosive
and rigidity - Mild dysphagia spasms
- No autonomic - Rigidity and spasm - spontaneous spasm
dysfn - No autonomic dysfn - Asphyxia, dysphagia
- Autonomic
dysfunction
 Clinical Features
• Neonatal tetanus
– Generalized form of tetanus
– Develops in neonates born in unimmunized mothers after
unsterile treatment of the umbilical cord stump
– Occurs within 2 weeks of neonatal life
– Manifests with poor feeding, rigidity and spasm
– High rate of mortality
• Local tetanus
– Uncommon form of tetanus
– Manifests with localized muscle contraction near the wound
– good prognosis
 Clinical Features
• Cephalic tetanus
– Rare form of local tetanus
– Follows head injury or ear infection
– Manifests with trismus and CN palsy (often VII CN)
– High mortality
– Diagnosis: Entirely on clinical findings
– Spatula test – gag stimulation causes masseter
muscle spasm
 Differential Diagnosis
• Alveolar abscess,
• Strychnine poisoning*
• Dystonic drug reaction (phenothiazines,
metoclopramide),
• Hypocalcemic tetany,
• Rabies,
• Meningitis /encephalitis,
• Acute intraabdominal process
 Complications
• Aspiration pneumonia
• Vertebral fracture
• Muscle rupture
• DVT+PE (VTE)
• Decubitus ulcer
• Rhabdomyolysis (pigment-induced
nephropathy)
• Autonomic dysfunction - Labile or sustained
HTN, Tachycardia, Hyperpyrexia, Profuse
sweating, Bradycardia and hypotension
episodes, Sudden cardiac arrest
 Treatment

• The patient with tetanus requires

simultaneous attention to several concerns
 Treatment
• A. Assess airway and ventilation. If necessary,
perform endotracheal intubation
• B. Obtain samples for antitoxin level, strychnine
and dopamine antagonist assays, electrolytes,
blood urea nitrogen, creatinine, creatine kinase,
and urinary myoglobin determination
• [Link] the portal of entry, incubation
period, period of onset, and immunization history
 Treatment
• D. Administer benztropine (1 to 2 mg, intravenously) or
diphenhydramine (50 mg, intravenously) to rule out a
dystonic reaction to a dopamine blocking agent

• E. Administer a benzodiazepine intravenously* to control

spasm and decrease rigidity.
– Initially, employ a dose that is adequate to produce sedation and
minimize reflex spasms.
– If this dose compromises the airway or ventilation, intubate using
a short-acting neuromuscular blocking agent.
– Transfer the patient to a quiet, darkened area of the intensive
care unit
 Treatment
• Control of spasms
– Spasms are controlled by heavy sedation using
benzodiazepines.

– Chlorpromazine or phenobarbital are commonly

used worldwide, and IV magnesium sulfate has been
used as a muscle relaxant.

– Infusions of propofol have also been used

successfully to control spasms and provide sedation
 Treatment
• Antitoxins: should be given early in an attempt
to deactivate any circulating tetanus toxin and
prevent its uptake into the nervous system.
– Two preparations are available: human tetanus
immune globulin (TIG) and equine antitoxin (TAT)
– TIG is the preparation of choice as it is less likely to
be associated with anaphylactoid reactions.
– Standard therapy is 3000–6000 IU of TIG or 10,000–
20,000 U of equine antitoxin as a single IM dose*
 Treatment
• Wound management & Antibiotics
– If possible, the entry wound should be identified,
cleaned, and debrided of necrotic material in order to
remove anaerobic foci of infection and prevent further
toxin production.
– Metronidazole (400 mg rectally or 500 mg IV every 6 h
for 7 days) is the preferred antibiotic.
• An alternative is penicillin (100,000–200,000 IU/kg per day),
although this drug theoretically may exacerbate spasms.
– Failure to remove pockets of ongoing infection may
result in recurrent or prolonged tetanus.
 Treatment
• Control of Autonomic disturbance
– Cardiovascular instability in severe tetanus is notoriously
difficult to treat.

– Rapid fluctuations in blood pressure and heart rate can

occur.

– Cardiovascular stability is improved by

• Increasing sedation with IV magnesium sulfate (plasma
concentration, 2–4 mmol/L), morphine, or other sedatives.
• Drugs acting specifically on the cardiovascular system (e.g.,
esmolol, calcium antagonists, and inotropes) may be required*.
 Treatment
• Prevention of VTE

– In some centers, prophylaxis against deep-vein

thrombosis and thromboembolism is routine
 Complications of Treatment
• Thrombophlebitis associated with diazepam
injection,

• Ventilator-associated pneumonia,

• Central-line infections, and

• Septicemia.
 Active Immunization
• Tetanus is one of the few bacterial diseases that does
not confer immunity following recovery from acute
illness

• All patients with tetanus should receive active

immunization with a total of three doses of tetanus and
diphtheria toxoid (Td) spaced at least two weeks apart,
commencing immediately upon diagnosis
– It should be assumed that anyone who is not adequately
vaccinated or protected against tetanus is also inadequately
protected against diphtheria
 Active Immunization
• The tetanus-diphtheria-acellular pertussis vaccine (TdaP)
may be used instead of Td, but if used, recommendations
are for this formulation to be used only once in adults

• Subsequent tetanus doses, in the form of Td, should be

given at 10-year intervals throughout adulthood.

• Tetanus toxoid alone should be given only to those

patients with documented allergy or untoward reactions
to diphtheria toxoid
 Active Immunization
Clean and minor wound All other woundsΔ
Previous
doses of Tetanus toxoid-
tetanus Human tetanus TT-containing Human
containing
toxoid* immune globulin vaccine◊ TIG§
vaccine◊
<3 doses or
unknown Yes¥ No Yes¥ Yes

Only if last dose Only if last dose

≥3 doses given ≥10 years No given ≥5 years No
ago ago‡
 Prognosis
• Case-fatality rates for non-neonatal tetanus in
developing countries range from 8 to 50
percent, whereas the majority of patients with
tetanus recover when modern supportive care
is available
 Prognosis
Factors associated with Poorer Prognosis
Adult Tetanus
Age >70 years
Incubation period <7 days
Short time from first symptom to admission
Puerperal, IV, postsurgery, burn entry site
Period of onseta <48 h
Heart rate >140 bpmb
Systolic blood pressure >140 mmHgb
Severe disease or spasmsb
Temperature >38.5°Cb
• Harrison’s 19th edd
• Tintinalis emergency 10th edd
• Dr. brook alemayehu harrsion’s notes