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Pathophysiology of Tetanus

A 18-year-old male presented with tetanus after a dental infection. Clostridium tetani entered through the wound where anaerobic conditions allowed spore germination and toxin production. The toxins were disseminated through blood and lymphatics to the nervous system. Specifically, tetanospasmin was transported into central nervous system neurons. This interfered with neurotransmitter release, blocking muscle relaxation and leading to unopposed muscle contraction and spasm. Without intervention, the spasms could cause respiratory failure, autonomic dysfunction, and death.

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Anitha Supriono
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456 views2 pages

Pathophysiology of Tetanus

A 18-year-old male presented with tetanus after a dental infection. Clostridium tetani entered through the wound where anaerobic conditions allowed spore germination and toxin production. The toxins were disseminated through blood and lymphatics to the nervous system. Specifically, tetanospasmin was transported into central nervous system neurons. This interfered with neurotransmitter release, blocking muscle relaxation and leading to unopposed muscle contraction and spasm. Without intervention, the spasms could cause respiratory failure, autonomic dysfunction, and death.

Uploaded by

Anitha Supriono
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOC, PDF, TXT or read online on Scribd
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V.

Pathophysiology

PREDISPOSING FACTOR Tetanus PRECIPITATING FACTOR


o lifestyle
Age : 18 years old
Dental infection
Sex: Male

Clostridium tetani enters body through a wound

Anaerobic conditions allow germination of spores


and production of toxins

Toxins are produced and disseminated via blood and lymphatic

Tetanospasmin enters the nervous system peripherally at the myeoneural junction and is transported
centripetally into neurons of CNS
Sx:
Interferes with neurotransmitter release to block inhibitors
Lockjaw
Leads to unopposed muscle contraction and spasm o BP
Stiffness
temperature
Neck rigidity
sweating
Dysphagia
Without Intervention Restlessness
o Reflex spasms
o SEIZURE
o opisthotonos

Toxins acts at the synapse of Spasms of the vocal cords or


interneurons of inhibitory muscles involved in breathing
Cardiovascular complications
pathways and motor neurons

Obstructions(by secretions,
Hyperactivity of the
exhaustionand pulmonary
Blockage of spinal inhibition sympathetic nervous system
aspiration)

General Muscle Rigidity


Respiratory Failure Sx:
o Tachycardia
Uninhibited afferentstimuli Sweating
Facial muscle spasm Fever
entering CNS

Sx:
Severe Vasoconstriction
Lock jaw
o Seizure(as an effect of Difficulty swallowing
the toxin in the brain ) Hypertension

Aspiration Pneumonia
Increasedbasal sympathetic activity and
episodesof sympathetic over activity
Progressive muscle spasm

o Sx:Reflex Spasms
o Sx:opisthotonos

Autonomic Dysfunction
Legend:
Manifested by the
Death
patient
o NotFracture
manifested by the
client
(Bones to break and joints to dislocate) Bad Prognosis
Sx Sign And Symptoms

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