Gas (clostridial) infection
The disease causes severe intoxication up to toxic-infectious shock with a drop in temperature and loss of consciousness. Local manifestations depend on the form of the lesion.
- Clostridial myositis. Muscle tissue becomes dull, loses elasticity, tears easily with forceps, and bulges from the wound. Gas actively penetrates the muscles, dissecting them (which is clearly visualized on radiographs). A characteristic crepitus sign may appear far from the wound hours later.
- Clostridial cellulitis. Massive edema comes to the foreground. Due to vascular compression, the skin becomes bloodless, shiny, tense, and white («white erysipelas» sign).
- Mixed form. All soft tissues are involved in the process. Purple-cyanotic spots appear on the pale skin, the epidermis detaches with the formation of blisters filled with brownish or yellow exudate. There is no local hyperthermia or hyperemia, and the wound is covered with a dirty-gray coating with almost no discharge.
Treatment must be immediate. An absolute indication is wide surgical dissection of tissues down to the bone («lamprey incisions») and removal of non-viable muscles. The wound is managed open and washed with oxygen-active solutions (hydrogen peroxide, potassium permanganate). Hyperbaric oxygenation (HBO) is used. In severe cases, only guillotine amputation without suture of the stump can save a life. Conservative treatment involves administering huge doses of penicillin and 150,000 IU of polyvalent anti-gangrene serum.
Putrefactive infection
Most frequently develops with extensive tissue crushing, animal bite wounds, and urinary phlegmon against the background of pelvic fractures. Causative agents include Pseudomonas aeruginosa, Escherichia coli, Proteus, and Streptococcus. Intoxication caused by microbial waste products leads to chills, dyspepsia, and meningeal symptoms.
Unlike clostridial flora, putrefactive infection spreads more slowly. Necrosis extends persistently, without the body attempting to delimit the focus (no demarcation occurs). Tissues undergo breakdown, accompanied by a fermentation process, release of foul-smelling gas, and hemorrhagic exudate.
Key difference from gas infection: muscles remain intact, and gas accumulation is observed exclusively in the subcutaneous adipose tissue. A dangerous complication is erosive hemorrhage upon the melting of major vessel walls.
Treatment: radical necrotomy and opening of fascial spaces with active drainage. The wound is never sutured. If the process cannot be controlled and extends beyond the wound, amputation is indicated.
Tetanus
The disease is caused by Clostridium tetani — an anaerobic gram-positive rod. The entry gates are any skin injuries: from microtraumas to the epidermis detached by burns. The bacterium secretes two exotoxins: tetanospasmin (causes spasms) and tetanolysin (destroys red blood cells). Mortality reaches 30–40% due to asphyxia, pulmonary complications, and cardiac arrest.
The incubation period lasts from 4 to 14 days, but can be fulminant (<24 hours) or delayed (after wound healing).
Clinical stages:
- Prodromal period. Sweating, insomnia, headache. Pain and muscle twitching appear in the area of the healed wound.
- Primary manifestations. Classic triad: spasm of the masticatory muscles (trismus), swallowing disorder (dysphagia), and nuchal rigidity. These symptoms are frequently mistaken for trigeminal neuralgia or tonsillitis.
- Period of full development. Facial spasms form the «risus sardonicus». Tonic and clonic seizures occur in response to any stimulus (light, sound). Due to tetanic spasm of the back muscles, the trunk arches (opisthotonos). Laryngeal and diaphragmatic spasms lead to fatal asphyxia.
Briefly: answers to topical questions
What does the emergency specific tetanus prophylaxis scheme for injuries include?
The emergency specific tetanus prophylaxis scheme for injuries includes passive immunization, active-passive prophylaxis, and emergency revaccination. The choice of a specific method depends on the availability of documented vaccination records and the nature of the injury.
- Passive immunization — human tetanus immunoglobulin (HTIG) or tetanus antitoxin (TAT) is used.
- Active-passive prophylaxis — simultaneous administration of HTIG (or TAT) and tetanus toxoid into different anatomical sites.
- Emergency revaccination — administration of tetanus toxoid or diphtheria-tetanus toxoid with a reduced antigen content (Td-toxoid) to stimulate already existing immunity.
The classic early triad of tetanus — TDR: Trismus (inability to open the mouth), Dysphagia (inability to swallow), Rigidity of the neck (inability to bend the neck).
Class and exam questions
How to differentiate a putrefactive infection from anaerobic gas gangrene?
In putrefactive infection, the process proceeds more slowly, gas accumulates only in the subcutaneous tissue, and muscle tissue remains preserved (intact).
What is the ligature sign used for?
It is used to assess the rate of edema progression in gas gangrene. A thread is tied loosely around the limb; if it deeply embeds into the skin within 2–4 hours, it means the edema is progressing rapidly.
What is the main cause of death in tetanus?
Patients most frequently die from asphyxia, which develops against the background of laryngospasm, diaphragmatic paralysis, and total spasm of the respiratory muscles.
What else to study on this topic
- Rationale for the technique of lamprey incisions and guillotine amputation.
- Application of hyperbaric oxygenation (HBO) in purulent surgery.
- Differential diagnosis of trismus and trigeminal neuralgia.
- Mechanism of action of tetanospasmin at the synaptic level.
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