Anatomy and Physiology

Gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous
system.

Pathophysiology
Tetanus toxin spreads through tissue spaces into the lymphatic and vascular systems. It enters the nervous
system at the neuromuscular junctions and migrates through nerve trunks and into the central nervous
system (CNS) by retrograde axonal transport by using dyeins.
Tetanus toxin causes violent spastic paralysis by blocking the release of gamma-aminobutyric acid.
Gamma-amiobutyric acid is a neurotransmitter that inhibits motor neurons

Case Presentation: Tetanus (Lockjaw)

Introduction

Pathophysiology
From our assessment, we have identified several predisposing and precipitating factors that we believe
have contributed to Pauls acquisition of tetanus. First, Pauls occupation, being a member of the
Philippine Army, exposes him to

Nursing Process Record

With Pauls current situation, we have decided to consider Risk for Injury as our nursing diagnosis.
Earlier it was mentioned that tetany, especially when left untreated, can complicate to fracture of the
bones.

Pathophysiology
1. Males are more susceptible to acquiring tetanus infections than females due to their adventurous
activities. Also, protection from tetanus infection is not ensured to individuals with incomplete
immunization. These factors increased Pauls susceptibility to acquiring tetanus infection.
2. Improper treatment of puncture wounds offers a favorable environment for the anaerobic bacteria
Clostridium tetani to enter and germinate on site.
3. With Pauls increased susceptibility and the presence of an improperly treated puncture into the
back of his knee, the anaerobic C. tetani is able to germinate.
4. C. tetani produces tetanolysin and tetanospasmin. Tetanolysin has no known effect while
tetanospasmin is known to cause the clinical manifestations of tetanus.\
5. Tetanospasmin (TeTx), by binding to gangliosides, transports via retrograde along the axon
towards the spinal cord (Rummel, 2003).
6. Tetanospasmin begins interrupting release of neurotransmitters, specifically GABA and glycine,
in the spinal cord (Collingridge, 1982; Cook, 2001).

Generalized tetanus is more common, however, and produces symptoms

Antitoxin levels decrease over time, however, and a booster should be given every 10 years.
Treating the Infection. The first two principles of tetanus treatment involve neutralizing the unbound toxin
and removing the source of infection. The unbound toxin is neutralized using human tetanus
immunoglobulin (HTIG). The source of infection must be eliminated in order to prevent the release of
more TeTx. Antibiotics must also be used to destroy any more C. tetani that may produce toxin.
Penicillin, metronidazole, erythromycin, tetracycline, chloramphenicol, and clindamycin are all
acceptable for use.
Treating the Symptoms. The three main categories of symptoms rigidity, muscle spasms, and autonomic
dysfunction must all be treated to avoid potentially fatal complications and to improve the general wellbeing of patients.
Muscle spasms and rigidity can often be controlled with the use of drugs that agonize GABAergic
neurons and systems. Drugs such as diazepam and midazolam have been used successfully to reduce
muscle spasms and induce sedation (Hsu, 2001; Cook, 2001). They bind to GABA receptors and facilitate
the binding of GABA, which helps increase the action of GABA on post-synaptic target neurons (Julien,
2008).
Collingridge, G. L., & Davies, J. (1982). The in vitro inhibition of GABA release by tetanus toxin.
Neuropharmacology, 21(9), 851-855.
Cook, T. M., Protheroe, R. T., & Handel, J. M. (2001). Tetanus: a review of the literature. BJA:
International Journal of Anaesthesia, 87(3), 477-487.
Hsu, S. S., & Groleau, G. (2001). Tetanus in the emergency department: A current review. Journal of
Emergency Medicine, 20(4), 357-365.
Julien, R. M. (2007). A Primer of Drug Action (Eleventh ed.). Worth Publishers.

Rummel, A., Bade, S., Alves, J., Bigalke, H., & Binz, T. (2003). Two Carbohydrate Binding Sites in the
HCC-domain of Tetanus Neurotoxin are required for Toxicity. Journal of Molecular Biology, 326(3), 835847.