TETANUS

GUERRERO, DJAMEICA DANIELLE R.

TETANUS
Tetanus is an infectious disease caused by
Clostridium tetani which produces potent exotoxin with
prominent systemic neuromuscular efforts manifested
by generalized spasmodic contractions of the skeletal
musculator.
Tetanus is fata up to 60 percent of unimmunized
persons, usually within ten days of onset. When
symptoms develop within three days, the prognosis is
poor. (Longworth, 2000. Pp.304-305)
INCUBATION PERIOD
The incubation period is within three days
to three weeks in adult and three to thirty days
in Tetanus neonatorum.
ETIOLOGIC AGENT
The causative organism of the disease is Cl. Tetani with the
following characteristics:

1. Anaerobic, gram (+) with round terminal spore with slender body
giving a drumstick appearance
2. The organism comes with two forms, spore forming and the
vegetative form
3. The organism releases two types of toxin:
a. Tetanospasmin that is responsible for muscle spasm
b. Tetanolysin that is responsible for destruction of RBC
MODE OF TRANSMISSION
Normally, the mode of transmission is through punctured wound
that is contaminated by dust, soil, or animal excreta containing Cl.
Tetani.

1. Rugged traumatic wounds and burns

2. Umbilical stump in new born especially for babies delivered at
home with faulty cord dressing; babies delivered to mothers
without tetanus toxoid immunization
3. Unrecognized wounds (cleaning of the ears with sharp materials)
4. Dental extraction, circumcision, ear piercing
PATHOGENESIS
1. After Cl. Tetani enters the body, it causes local infection and extensive tissue
destruction
2. Local multiplication of microorganisms occurs more frequently when the wound
is healed. While reproducing, they also release toxins that are absorbed by the
bloodstream and the lymphatics or through the peripheral motor nerves. These
eventually spread into the central nervous study.
3. The toxin (tetanospasmin) has a great affinity to the central nervous system
tissues and the spinal motor ganglia, inducing hyper excitability of the motor
neurons by interfering with the release of an inhibitory transmitter.
4. Other tissues reflect the effects of asphyxia convulsions, toxic degeneration,
inanition, and non- specific complications
CLINICAL MANIFESTATIONS
1. Neonate
a. New born infants have feeding and sucking difficulty.
b. The infant may cry excessively, most of the time voiceless crying.
c. An attempt to suck result in spasm and cyanosis.
d. There is fever due in infection and dehydration.
e. The jaw becomes so stiff that the baby cannot suck or swallow.
f. Tonic or rigid muscular contraction, spasm or convulsions provoked by stimuli.
g. Mild, short, voiceless cry
h. Cyanosis and pallor
i. May end with flaccidity, exhaustion, and finally, death
2. Older children and adult
a. If tetanus remains localized, signs of onset are spasm and increased
muscle tone near the wound.
b. If it becomes systematic or generalized, indications include:
- Hyper tonicity, hyperactive deep tendon reflexes, tachycardia, profuse
sweating, low grade fever, and painful involuntary muscle contractions.
- Neck and facial muscle rigidity (trismus)
- Grinning expression (risus sardonicus)- considered as pathognomonic to
the disease
- Board- like abdomen/ abdominal rigidity
- Opisthotonos
 - Intermittent tonic convulsions lasting for several minutes which may
result in cyanosis and sudden death due to asphyxiation
- In severe cases, laryngospasm followed by the accumulation of
secretions in the lower airway resulting to respiratory distress due to
involvement of respiratory muscles.
- Fracture of the vertebrae may occur during severe spasm, yielding to
coma and death.
c. In mild cases, after a period of weeks, spasm gradually diminishes in
frequency and severity with trismus being the last symptom to disappear.
d. In fatal cases, death usually occurs during the first 10 days of the disease.
COMPLICATIONS

1. Resulting from laryngospasm and involvement of respiratory muscle

a. Hypostatic pneumonia
b. Hypoxia due to laryngospasm and decreased oxygen
c. Atelectasis, pneumothorax
d. Traumatic glossitis and microglassia
2. Changes related to symphatic nervous system
a. Transitory hallucinosis
b. Hypersalivation, diaphoresis, unusual tachycardia, especially with the
use if aerosolized bronchodilators
c. Cardiac standstill and bradycardia (high mortality)
3. Due to trauma
a. Laceration of tongue and bucal mucosa
b.Intramuscular hematoma
c. Fracture of the spine and ribs
4. Septicemia
MODALITIES OF TREATMENT
1. Specific
a. Within 72 hours after a punctured wound, the patient should
receive ATS, TAT, or TIG especially if the patient does not have
any previous immunization
b. Tetanus toxoid, .5cc IM give in standard schedule
c. Pen G Na to control infection
d. Muscle relaxant to decrease muscle rigidity and spasm
2. Nonspecific
a.Oxygen inhalation
b.Feed thru NGT
c.Tracheostomy
d.Adequate fluid, electrolyte, and caloric intake
e. Good nursing care
- Maintain adequate airway
- Provide cardiac monitoring
- Maintain an IV line for medication and emergency care if necessary
- Carry out efficient wound care
- Avoid stimulation
- Avoid contractures and pressure sores
- Watch out for urinary retention
- Close monitoring of vital signs and muscle tone
- Provision of optimum comfort measures
PROGNOSIS
 Highest fatality rates occur at the extremes of life.
 Local tetanus usually offers favourable prognosis, except in dysphagic
form of cephalic tetanus.
 Absence of convulsions favors the prognosis especially in patients 20
years old and below.
 Apnea occurs after a prolonged spasm and is a critical factor in sudden
death
 Acute respiratory obstruction and over sedation may lead to early
death. Response to anticonvulsant therapy is relevant to prognosis.
PREVENTION AND CONTROL

1.Active immunization with Tetanus toxoid

for adults
2.DPT for babies and children