Tetanus

Etiology and conditions of infection

The disease is caused by the bacterium Clostridium tetani. The infectious nature of the pathology, whose clinical picture was known as far back as Hippocrates, was first pointed out by the prominent surgeon N.I. Pirogov.

The entry gates for the infection are any wounds, as well as childbirth or abortions performed with a breach of asepsis rules. Agricultural and construction workers constitute a high-risk group. However, wound contamination alone does not guarantee the development of the disease. A number of conditions are necessary for the infectious process to start:

• Introduction of a sufficient quantity of a virulent pathogen.
• Presence of necrotic (non-viable) tissues and foreign bodies in the wound.
• Delayed primary surgical debridement.
• Tissue ischemia associated with hypothermia, anemia, or prolonged tourniquet application.
• Absence of specific anti-tetanus immunity in the patient.

Historically, the introduction of specific seroprophylaxis radically changed the epidemiology: whereas prior to the 20th century the incidence was 2.4–8 cases per 1,000 wounded, by the period of World War II this figure dropped to 0.1–0.6.

Pathogenesis: how the toxin acts

Multiplying under hypoxic conditions, the pathogen produces a complex exotoxin consisting of two components:

1. Tetanospasmin — a neurotoxic component that causes convulsive syndrome.
2. Tetanolysin — an enzyme that promotes the lysis of erythrocytes.

The toxin spreads through the body in two ways: neural (ascending via perineural and endoneural clefts to the motor centers of the spinal cord and medulla oblongata) and hematogenous (penetrating the central nervous system via the bloodstream). Fixation of the toxin in nerve cells occurs within 2–3 days, after which its neutralization becomes impossible.

Clinical presentation

The first signs develop during the prodromal period. Patients complain of general malaise, sweating, and difficulty swallowing. In the area of the wound, shooting, throbbing pains appear, radiating along the nerve trunks, along with burning, tingling, and increased muscle tone.

As tetanus progresses (descending or ascending form), full-blown symptoms develop against the background of high fever and tachycardia. In the late stage, the classic triad of symptoms appears:

• Trismus — pronounced spasm of the masticatory muscles, preventing the mouth from opening.
• Risus sardonicus — "sardonic smile" due to spasm of the facial muscles.
• Opisthotonos — a characteristic arched body posture due to hyperextension caused by tonic contraction of the back and neck muscles.

Spasms are excruciating, accompanied by severe muscle pain, and are triggered by the slightest external stimuli (bright light, sharp sound, touch). During a prolonged generalized seizure, respiratory arrest can occur, which, along with cardiac arrest, is the main cause of death.

Diagnostics

The diagnosis is established primarily based on physical examination and the identification of specific hyperreflexia. In patients, including those unconscious due to severe polytrauma, nuchal rigidity and the tone of the masticatory muscles are assessed.

Pathognomonic sign: if the patient's mouth is open and one lightly taps their chin with a finger, a sharp, convulsive closure of the jaw occurs. During dressings, touching the wound with a gauze sponge or tweezers also provokes local muscle twitching.

Complex treatment

Tetanus treatment requires immediate action and strict adherence to a supportive and protective regimen: the patient is placed in a quiet, isolated, darkened ward with round-the-clock monitoring.

1. Specific antitoxic therapy: Anti-tetanus serum (ATS) is administered at a daily dose of 100,000–150,000 IU (total course dose up to 350,000 IU), half of which is given intravenously by drip infusion. Tetanus immune globulin intramuscularly and tetanus toxoid (three doses of 0.5 ml at 5-day intervals) are also used.

2. Anticonvulsant therapy and mechanical ventilation: For local spasms, tranquilizers (diazepam) and antipsychotics are prescribed. In severe attacks, non-depolarizing muscle relaxants are indicated with mandatory transfer of the patient to mechanical ventilation via a tracheostomy. Mechanical ventilation may last from 7 to 30 days.

3. Maintenance of homeostasis: Massive detoxification with plasma-substituting fluids and electrolytes, and correction of acidosis are performed. Antibacterial therapy is mandatory, and adequate parenteral nutrition is provided at a rate of 2,000–2,500 kcal/day.

Class and exam questions

What else to study on this topic

• Clinical classification of tetanus by entry gate (wound, burn, cryptogenic, etc.)
• Forms of development of muscle rigidity: descending and ascending
• Strict indications for the use of muscle relaxants and transfer to mechanical ventilation
• Regimens for hyperbaric oxygenation (HBO) in combination therapy
• Features of the clinical presentation and course of neonatal tetanus

Other topics in "CHAPTER 10. GENERAL ISSUES IN TRAUMATOLOGY"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.