TETANUSSurgery Lecture on

WTetanushat is Tetanus?

▪ An infectious disease caused by contamination of wounds from the bacteria Clostridium tetani, or the spores they produce that live in the soil, and animal feces

▪ Greek words -“tetanosand teinein”, meaning rigid and stretched, which describe the condition of the muscles affected by the toxin, tetanospasmin, produced by Clostridium tetani

Sporulated Vegetative

Causes▪ Tetanus spores are found throughout the

environment, usually in soil, dust, and animal waste.

▪ Tetanus is acquired through contact with the environment; it is not transmitted from person to person.

Sponsored

Medical Lecture Notes – All Subjects

USMLE Exam (America) – Practice

Causes▪ The usual locations for the bacteria to enter the body:

▫ Puncture wounds (such as those caused by rusty nails, splinters, or insect bites.)

▫ Burns, any break in the skin, and IV drug access sites are also potential entryways for the bacteria.

Route of Entry▪Apparently trivial injuries▪Animal bites/human bites▪Open fractures▪Burns▪Gangrene▪In neonates usually via infected

umbilical stumps▪Abscess▪Parenteral drug abuse

Epidemiology

Tetanus is an international health problem, as spores are ubiquitous. The disease occurs almost exclusively in persons who are unvaccinated or inadequately immunized.

Tetanus occurs worldwide but is more common in hot, damp climates with soil rich in organic matter.More common in developing and under developing countries.

More prevalent in industrial establishment, where agricultures workers are employed.

Tetanus neonatorum is common due to lack of maternity ward care.

Incubation Period

▪Varies from 1 day to several months. It is defined as the time from injury to the first symptom.

Period of onset ▪It is the time from first symptoms to the

reflex spasm.

▪An incubation period of 4 days or less or

▪A period of onset of less than 48 hr is associated with the development of

severe tetanus !!!!

pathogenesis

1. C. tetani enters body from through wound.

3. Germinates under anaerobic conditions and begins to

multiply and produce tetnospasmin.

2. Stays in sporulated form until anaerobic conditions are

presented.

4. Tetnospasmin spreads using blood and lymphatic system, and

binds to motor neurons.

5. Travels along the axons to the spinal cord.

6. Binds to sites responsible for inhibiting skeletal muscle

contraction.

•Initially binds to peripheral nerve terminals •Transported within the axon and across synaptic junctions until it reaches the central nervous system. •Becomes rapidly fixed to gangliosides at the presynaptic inhibitory motor nerve endings, then taken up into the axon by endocytosis.

How the toxin acts?

Blocks the release of inhibitory neurotransmitters (glycine and gamma-amino butyric acid) across the synaptic cleft, which is required to check the nervous impulse.

If nervous impulses cannot be checked by normal inhibitory mechanisms, it leads to unopposed muscular contraction and spasms that are characteristic of tetanus.

Mechanism of Action of Tetanus Toxin

Tetanus prone wound

▪ A wound sustained more than 6 hr before surgical treatment.

▪ A wound sustained at any interval after injury which is puncture type or shows much devitalised tissue or is septic or is contaminated with soil or manure.

Signs and SymptomsOther symptoms include:▪Drooling▪Excessive sweating▪Fever▪Hand or foot spasms▪Irritability▪Swallowing difficulty▪Uncontrolled urination or defecation

Clinical features

▪ Risus sardonicus: Contraction of the muscles at the angle of mouth and frontalis

▪ Trismus (Lock Jaw): Spasm of Masseter muscles.▪ Muscle spasticity▪ OPISTHOTONUS: Spasm of extensor of the neck, back and

legs to form a backward curvature.▪ Prolonged muscular action causes sudden, powerful,

and painful contractions of muscle groups. This is called tetany. These episodes can cause fractures and muscle tears.

▪ If respiratory muscle is involved – apnoea.

Trismus of masseter muscles and risus sardonicus

Trismus of masseter muscles and risus sardonicus, contraction of muscles

Opisthotonos

Diagnosis▪ There are currently no blood tests that can be used

to diagnose tetanus. Diagnosis is done clinically.

Differential Diagnosis

▪ Masseter muscle spasm due to dental abscess▪ Dystonic reaction to phenothiazine▪ Rabies▪ Hysteria

Principle of Treatment

▪ 1. Neutralization of unbound toxin with Human tetanus immunoglobulin

▪ 2. Prevention of further toxin production by -Wound debridement -Antibiotics (Metronidazole)

▪3. Control of spasm - Nursing in quiet environment - Avoid unnecessary stimuli (sounds, bright

lights …. ) - Protecting the airway

▪4. Supportive care - Adequate hydration - Nutrition - Treatment of secondary infection - Prevention of bed sores.

Prevention

▪ Tetanus is completely preventable by active tetanus immunization.

▪ Immunization is thought to provide protection for 10 years.

▪ Begins in infancy with the DTP series of shots. The DTP vaccine is a "3-in-1" vaccine that protects against diphtheria, pertussis, and tetanus.

Prevention▪ Can be achieved by active immunization by tetanus toxoid

(5 doses – 0 day, 1 month, 6 month, 1 year).

▪ Older teenagers and adults who have sustained injuries, especially puncture-type wounds, should receive booster immunization for tetanus if more than 10 years have passed since the last booster.

▪ ! ! ! ! ! Clinical tetanus does not produce immunity to further attacks. Therefore, even after recovery patients must receive a full course of tetanus toxoid.

Treatment. Intramuscular injections of large doses (100 000-150 000) of antitoxic antitetanus serum are employed.

To reproduce active immunity, 2 ml of toxoid is administered two hours before injecting the serum; the same dose of toxoid is repeated within 5-6 days.

The best result is produced by gamma-globulin obtained from the blood of humans immunized against tetanus.

Anticonvulsant therapy includes intramuscular injections of 25 per cent solutions of magnesium sulphate, administration of diplacine, condelphine, aminazine, pipolphen or andaxine and chloral hydrate introduced in enemas.

Uninoculated persons are subjected to active and passive immunization. This is achieved by injecting 0.5 ml of toxoid and 3.000 units of Antitoxic Serum and then 5 days later, another 0.5 ml of toxoid. The tetanus antitoxin is also introduced into previously inoculated individuals suffering from a severe wound. Injection of the total dose of antitoxin is preceded by an intracutaneous test for body sensitivity to horse protein. This is carried out by introducing 0.1 ml of antitoxin, previously diluted 1 :100, into the front part of the forearm. If the intracutaneous test proves negative, 0.1 ml of whole antitoxin is injected subcutaneously and if no reaction is produced in 30 minutes, the total immunization dose is introduced.

The complex of prophylactic measures includes adequate surgical treatment of wounds.

The organisms are sensitive to penicillin, but the antibiotic has no effect on the neutralization of the toxin. However, after surgical cleansing of the wound, antibiotic therapy can be helpful in preventing any additional growth of the organisms.

Prophylaxis is ensured by prevention of occupational injuries and traumas in everyday life. Active immunization is achieved with tetanus toxoid. It is injected together with a tetravalent or polyvalent vaccine or maybe a component of an associated adsorbed vaccine.

The pertussis-diphtheria-tetanus vaccine and associated diphtheria-tetanus toxoid are employed for specific tetanus prophylaxis in children.

Immunization is carried out among all children from 5-6 months to 12 years of age.

Causative agents of Anaerobic Infection

The organisms responsible for anaerobic infections are: (1) C. perfringens, (2) C. novyi, (3) C. septicum, (4) C. histolyticum, and (5) C. sordellii.

C. chauvoei, C. fallax, and C. sporogenes are pathogenic for animals. C. aerofoetidum and C. tertium are non-pathogenic organisms which have significance in the pathogenesis of anaerobic infections only in association with pathogenic bacteria.

Anaerobic infections are called "gas gangrene"Pathogens:

C. Perfringens - Gas forming clostridiaC. Edematiens - Clostridium edemaC. Histolyticum - melted tissuesC. Septicum - septic vibrio

ANAEROBES

➢ Obligate anaerobes are bacteria that cannot survive in the presence of a high oxidation- reduction potential (redox potential) / high oxygen content.

➢ During metabolism bacteria can produce toxic bi-products from oxygen (including superoxide radicals and hydrogen peroxide).

Clostridia may also be involved in milder non-necrotizing wound infections, often in combination with other pathogens, e.g., diabetic foot infections, leprous wounds

Forms of clostridial infections

1. Emphysematous (classical)2. Edematous (toxic)3. Mixed4. Putrid5. Phlegmonous

Early signs of local - have a phase character- Arching pain in the woundreduction of discharge from wounds- Color change wounds - Grey- Swelling proximal to the wound

The incubation period of from several hours up to 2-3 weeks on average 1-7 days

Local signs are phase character

- Limited by gas phlegmon- Gas phlegmon (clinic, X-ray)- Gangrene

In the absence of timely treatment - the spread of necrosis, anaerobic sepsis, death

Laboratory diagnosis▪ To cultivate anaerobes, the specimen should not

be exposed to air

Сommon signs of early period

- Weakness- Anxiety, agitation, and later depression- The temperature of the low-grade-Tachycardia, not corresponding to the temperature

- Color wound becomes dark brown - Muscles in the wound look like boiled meat

- Foul-smelling wound

- With the development of myonecrosis the state becomes dramatically heavier

- Body temperature rises to 38-40º- Severe intoxication- Depression- Yellowness of the sclera- Dry coated tongue- Tachycardia- Drop in blood pressure- Leukocytosis- Progressive anemia- Oliguria, anuria

Engelbert Schröpfer, Stephan Rauthe and Thomas Meyer, Wikimedia Commons

Management of gas gangrene▪Surgical debridement of all devitalized

tissues (remove the anaerobic/necrotic focus)

▪Widespread tissue dissection, and sometimes to the bone

▪Separation of muscle , necrectomy▪In the absence of a pulse at the distal

arteries - high. amputation. ▪The wounds are not closed▪Draining wounds

Hyperbaric oxygenation

Hyperbaric oxygen may be useful

Hyperbaric oxygenation

- Penicillin and other beta-lactam antibiotics are effective but not sufficient

- Antitoxins are not effective

- Patients require strict isolation !!

- Personnel protection !!!

- Disinfection of premises !!!

To the development of anaerobic infection in the wound predispose:

- Wounds of the lower extremities with extensive crush and tissue

- Injury and injuries contamination earth, pieces of clothing;

- Circulatory disorders resulting from injury, tourniquet, ligation of large vessels.

- Factors that reduce the overall resistance: shock, anemia, starvation, hypothermia, lack of transport immobilization of the damaged limb.

- Depending on the pathogen in the wound prevail or toxic edema, or gas formation, which exacerbate poor circulation of the damaged organ.

- Compression of vascular edema, gases, and necrotic tissue changes lead to gangrene of the extremities