Precipitating Factors: Environmental Contaminated/Punctured Wound Lack of Immunization Bacterial Infection

Lack/Insufficient tetanus toxoid immunization

Stepped a contaminated wire cause of cuts

Presence of puncture

Spores of ''Clostridium tetani'' enter damaged tissue

Presence of anaerobic condition (oxidation-reduction potential, such as those with dead or devitalized tissue)

Spores transform into rod-shaped bacteria and germinate

Hypertermia Excessive sweating

Produce the 2 exotoxins

Tetanolysin

Tetanospasmin

This substance is a hemolysin with no recognized pathologic activity

It is synthesized as a 150-kd protein consisting of a 100-kd heavy chain and a 50kd light chain joined by a disulfide bond

It mediates binding of tetanospasmin to the presynaptic motor neuron and also creates a pore for the entry of the light chain into the cytosol

The light chain is a zincdependent protease that cleaves synaptobrevin

Toxin amplifies the chemical signal from the nerve

Headache

After the light chain enters the motor neuron, it travels by retrograde axonal transport from the contaminated site to the spinal cord in 2-14 days

Localized Mild Case

Generalized Severe Case

develops when only the nerves supplying the affected muscle are involved

Develops when the toxin released at the wound spreads through the lymphatics and blood to multiple nerve terminals. The blood-brain barrier prevents direct entry of toxin to the CNS.

dysfunction in the interneurons that inhibit the alpha motor neurons of the affected muscles

The brain receives blood with toxins from the internal carotid arteries, which arise at the point in the neck where the common arteries bifurcate.

Lock Jaw Stiffneck

If treated:

If Not treated:

-tetanus immune globulin IV or IM -metronidazole IV for 10 days -diazepam -tetanus vaccination -tetanus shots -tetanus digestion

Toxin reaches the spinal cord, it enters central inhibitory neurons. The light chain cleaves the protein synaptobrevin,

Synaptobrevin, which is integral to the binding of neurotransmitter containing vesicles to the cell membrane.

Gamma-aminobutyric acid (GABA)-containing and glycine-containing vesicles are not released

Good Prognosis

loss of inhibitory action on motor and autonomic neurons

Autonomic hyperactivity as well as uncontrolled muscle contractions (spasms) in response to normal stimuli.

Leads to unopposed muscle contraction and spasm

Drooling Dysphagia Excessive sweating

Back Pain Hand/Foot Spasm Body Weakness Seizure

If treated:

If not treated:

Severity muscle spasms -Require admission to intensive care -maintenance of an airway and proper nutrition are required -An intake of 3500-4000 calories, and at least 150 g of protein per day, is often given in liquid form through a tube directly into the stomach -This high-caloric diet maintenance is required because of the increased metabolic strain brought on by the increased muscle activity -Full recovery takes 4 to 6 weeks because the body must regenerate destroyed nerve axon terminals. Painful Contraction Uncontrolled /involuntary muscular contraction of the vocal cords Interferes breathing Breathin g foreign materials

Fractures in spinal cord

Laryngospas m Paralysis

Lack of Oxygen receives

Pneumon ia

Bad Prognosis ?Medications: -human tetanus immunoglobulin injected intrathecally -tracheostomy and mechanical ventilation for 3 to 4 weeks,

-magnesium, as an intravenous (IV) infusion, to prevent muscle spasm,

-diazepam (known under the common name Valium) as a continuous IV infusion,

Good Prognosis

Blockage of the main artery of the lung or one of its branches by a blood clot that has travelled from elsewhere in the body through the bloodstream

flow of blood to the heart becomes restricted, causing the muscles of the heart to become damaged.

muscle tissues are broken down, causing a protein called myoglobin to leak into the

Pulmonary embolism

Respiratory Failure rhabdomyolysis

Cardiac Arrest

acute kidney failure

DEATH