ETIOLOGY

Tetanus is an acute, spastic paralytic illness historically called lockjaw that is

caused by the neurotoxin produced by Clostridium tetani
Motile, Gram-positive, spore-forming obligate anaerobe whose natural habitat
worldwide is soil, dust, and the alimentary tracts of various animals.
Tetanus spores can survive boiling but not autoclaving, whereas the vegetative
cells are killed by antibiotics, heat, and standard disinfectants.
C. tetani causes illness through the effects of a single toxin, tetanospasmin, more
commonly referred to as tetanus toxin.
Tetanospasmin is the second most poisonous substance known, surpassed in
potency only by botulinum toxin
 EPIDEMIOLOGY

Tetanus occurs worldwide and is endemic in approximately 90 developing

countries
The most common form, neonatal (or umbilical) tetanus, kills approximately
300,000 infants each year
In addition, an estimated 15,000-30,000 unimmunized women worldwide die each
year of maternal tetanus which results from postpartum, postabortal, or postsurgical
wound infection with C. tetani.
Most nonneonatal cases of tetanus are associated with a traumatic injury, often a
penetrating wound inflicted by a dirty object such as a nail, splinter, fragment of
glass, or unsterile injection.
The disease may also occur in association with animal bites, abscesses (including
dental abscesses), ear and other body piercing, chronic skin ulceration, burns,
compound fractures, frostbite, gangrene, intestinal surgery.
 PATHOGENESIS

Tetanus occurs after introduced spores germinate, multiply, and produce tetanus
toxin

Tetanus toxin binds at the neuromuscular junction and enters the motor nerve by
endocytosis, after which it undergoes retrograde axonal transport to the cytoplasm
of the α-motoneuron.

The toxin exits the motoneuron in the spinal cord and next enters adjacent spinal
inhibitory interneurons, where it prevents release of the neurotransmitters glycine
and γ-aminobutyric acid.

The autonomic nervous system is also rendered unstable in tetanus.

 CLINICAL MANIFESTATIONS

The incubation period typically is 2-14 days but may be as long as months
after the injury.
In generalized tetanus
Early symptoms :
◦ Headache
◦ restlessness
◦ irritability

Often followed by :
◦ stiffness
◦ difficulty chewing
◦ dysphagia
◦ neck muscle spasm
 CLINICAL MANIFESTATIONS (cont…)

Trismus (masseter muscle spasm, or lockjaw)

 CLINICAL MANIFESTATIONS
(cont…)

Risus sardonicus (sardonic smile of tetanus)

Wrinkling of the forehead and distortion of the eyebrows and
the corners of the mouth which results from intractable spasms
of facial and buccal muscles.
 CLINICAL MANIFESTATIONS (cont…)

Opisthotonos
extreme hyperextension of the body occur
When the paralysis extends to abdominal,
lumbar, hip, and thigh muscles, the patient
may assume an arched posture
 CLINICAL MANIFESTATIONS
(cont…)

Laryngeal and respiratory muscle spasm can lead to airway obstruction and
asphyxiation.
Because tetanus toxin does not affect sensory nerves or cortical function, the patient
unfortunately remains conscious
Dysuria and urinary retention result from bladder sphincter spasm
Forced defecation may occur.
Fever, occasionally as high as 40°C (104°F), is common because of the substantial
metabolic energy consumed by spastic muscles.
Notable autonomic effects include tachycardia, dysrhythmias, labile hypertension,
diaphoresis, and cutaneous vasoconstriction.
 CLINICAL MANIFESTATIONS
(cont…)

In extreme pain, and in fearful, anticipation of the next tetanic seizure.
The seizures are characterized by :
• Sudden, severe tonic contractions of the muscles,
• Fist clenching
• Flexion, and adduction of the arms
• Hyperextension of the legs.
The smallest disturbance by sight, sound, or touch may trigger a tetanic
spasm.

The tetanic paralysis usually becomes more severe in the 1st wk after
onset, stabilizes in the 2nd wk, and ameliorates gradually over the
ensuing 1-4 wk.
 CLINICAL MANIFESTATIONS
(cont…)

Neonatal tetanus
The infantile form of generalized tetanus, typically manifests within 3-12 days
of birth as progressive difficulty in feeding (sucking and swallowing), associated
hunger, and crying.
Characteristic feature :
◦ Paralysis
◦ diminished movement
◦ stiffness and rigidity to the touch
◦ spasms with or without opisthotonos
 CLINICAL MANIFESTATIONS (cont…)

Localized tetanus
Results in painful spasms of the muscles adjacent to the wound site and may precede generalized tetanus.

Cephalic tetanus
is a rare form of localized tetanus involving the bulbar musculature that occurs with wounds or foreign bodies in the
head, nostrils, or face. It also occurs in association with chronic otitis media.
Cephalic tetanus is characterized by
◦ Retracted eyelids
◦ Deviated gaze
◦ Trismus
◦ Risus sardonicus
◦ Spastic paralysis of the tongue and pharyngeal musculature.
 DIAGNOSIS
The picture of tetanus is one of the most dramatic in medicine, and the
diagnosis may be established clinically.
The typical setting is an unimmunized patient (and/or mother) who was
injured or born within the preceding 2 wk, who presents with trismus,
other rigid muscles, and a clear sensorium.
Results of routine laboratory studies are usually normal
The cerebrospinal fluid is normal
Neither the electroencephalogram nor the electromyogram shows a
characteristic pattern.
C. tetani is not always visible on Gram stain of wound material and is
 DIFFERENTIAL DIAGNOSIS

Infections
• Parapharyngeal abscess
• Retropharyngeal abscess
• Dental abscess
• acute encephalitis involving the brainstem

Rabies
Hypocalcemia
Epileptic seizures
Narcotic withdrawal
Strychnine poisoning may mimic generalized tetanus
 TREATMENT

Goal of Rx
◦ Eradication of C. tetani and
◦ The wound environment conducive to its anaerobic multiplication
◦ Neutralization of all accessible tetanus toxin
◦ Control of seizures and respiration
◦ Palliation
◦ Provision of meticulous supportive care
◦ Prevention of recurrences.
 TREATMENT (cont..)

MEDICATION (DRUGS)
Neutralization of unbound neurotoxin:
– Human TIG 3,000–6,000 U IM as a single dose.
Infiltration of TIG into the wound is now considered unnecessary.
– Administer prior to antibiotics and wound manipulation.
If TIG is not available:
IVIG 200–400 mg/kg may be used (IVIG contains 4-90 units/mL of TIG)
Equine or bovine-derived tetanus antitoxin (TAT) can be given in doses
of 50,000-100,000 units, with half given intramuscularly and half intravenously
 TREATMENT (cont..)

Antibiotics used to decrease the number of vegetative C. tetani that produce

tetanospasmin:
Penicillin G
100,000–200,000 U/kg/dIV in 4–6 divided doses. Treat for 10–14 days.

Metronidazole
(500 mg every 8 hr IV for adults) appears to be equally effective.
Metronidazole 30 mg/kg/d PO or IV in 4–6 divided doses. Maximum 4 g/d.

Erythromycin and tetracycline (for persons >8 yr of age) are alternatives for
penicillin-allergic patients.
 TREATMENT (cont..)

Sedation and muscle relaxation:

•Diazepam 0.1–0.2 mg/kg IV q3–6h.
•Magnesium sulfate, other benzodiazepines (midazolam), chlorpromazine,
dantrolene, and baclofen are also used.
•Carefully titrate sedation to desired effect and monitor for respiratory depression.
•Morphine has also proved useful.
•The highest survival rates in generalized tetanus are achieved with neuromuscular
blocking agents such as vecuronium and pancuronium, which produce a general
flaccid paralysis that is then managed by mechanical ventilation.
 TREATMENT (cont..)

General Measures
◦ 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 and removal of foreign bodies from the infected
wound is crucial.
 COMPLICATIONS

1. Most complications are related to the severe tetanic muscle

contractions:
• Rhabdomyolysis and hyperkalemia
• Vertebral body and other fractures
• Muscle hemorrhages
2. Respiratory failure from spasms of the upper airway or diaphragm is
the most common cause of death in acute phase.
3. Arrhythmias and myocardial infarctions are most common cause of
death later in disease.
4. Cerebrovascular hemorrhages may be seen in rare cases,
especially in neonatal tetanus.
 PROGNOSIS

Favorable prognosis is associated with

• A long incubation period
• Absence of fever
• Localized disease
Unfavorable prognosis is associated with
• Onset of trismus <7 days after injury and with
• Onset of generalized tetanic spasms <3 days after onset of trismus.
• Sequelae of hypoxic brain injury, especially in infants, include
o Cerebral palsy
o Diminished mental abilities
o Behavioral difficulties
 PROGNOSIS

Fatality rates :
Generalized tetanus are 5-35%

Neonatal tetanus they extend from <10% with intensive care treatment to
>75% without it.

Cephalic tetanus has an especially poor prognosis because of breathing and

feeding difficulties.
 PREVENTION

Active immunization
(DTaP) vaccine at 2, 4, 6 and 15-18 mo of age, with boosters at 4-6 yr (DTaP) and 11-12 yr (Tdap)
of age and at 10 yr intervals thereafter throughout adult life with tetanus and reduced diphtheria
toxoid (Td).
Prophylaxis in Routine Wound Management