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Tetanus is an acute toxemia caused by the action of exotoxin (tetanospasmin) produced by the bacteria Clostridium tetani. The toxin is produced by the vegetative forms of the microorganism at the place of its penetration into the tissues of the body, and then enters the central nervous system and is fixed there.

Etiology. The causative agent of tetanus is an obligate anaerobic, a thin, gram-positive, movable, unencapsulated stick, forming terminal spores that give it a resemblance to a drum stick. Spores are very resistant to external influences, tolerate boiling, but are destroyed by autoclaving. In soil, spores protected from sunlight can remain viable for many years. They are found in house dust, earth, salt and fresh water, feces of many animal species. Both spores and vegetative forms of the pathogen can be found in the human intestines.

Vegetative C. tetani are sensitive to heat and the effect of disinfectants.

Tetanus bacilli themselves are safe, their pathogenic effect is associated with two toxins they produce: tetanospasmine and tetanolysin. Several types of tetanus bacilli, different in their antigenic structure, produce tetanospasmin identical in immunological parameters. Neurotoxic and responsible for the clinical symptoms of the disease, the toxin is considered the most powerful organic poison after botulinum toxin. Its lethal dose for humans is 130 mcg.

Epidemiology. Tetanus disease is ubiquitous, but the incidence in different geographical areas is not the same and is associated with the characteristics and level of injury, the state of active immunity of the population, the development of the health care system, etc. Tetanus is characterized by seasonality, with a peak in May-October.

Sources of infection are animals and humans, in the intestines of which tetanus bacillus saprophytes, which, with animal feces, enters the soil and disperses in the environment.

Tetanus is a wound infection, the disease occurs when the pathogen enters the body through the wound surface. In newborns, the umbilical wound, infected with violation of aseptic and antiseptic rules, can serve as the entrance gate. Mostly 3–7 years old children and newborns suffer from tetanus.

Tetanus is not transmitted from person to person.

Pathogenesis. The disease develops after tetanus spores that have fallen into damaged tissues begin to sprout, multiply and produce tetanospasmin. Germination and reproduction of spores occurs at the site of entry of infection and only with a decrease in the level of oxygen in the tissues. The place of persistent infection may be the gastrointestinal tract or crypts of the tonsils. Sometimes tetanus can develop after the introduction of contaminated serum, a vaccine, or enter the body along with suture material.

From the place of the entrance gate, the infection spreads throughout the body:

1) on the surrounding tissues;

2) in the lymphatic system;

3) along the nerve trunks.

Tetanospazmin can penetrate the central nervous system by being absorbed in the neuromuscular synapses and spreading along the perineural spaces along the large nerve trunks, as well as with the help of lymphocytes.

Tetanospazmin acts on the endings of motor nerves in myoneural synapses, on the spinal cord and brain, and on the sympathetic nervous system. In neuromuscular synapses, the toxin inhibits the destruction of acetylcholine, causing disturbances in the processes of neuromuscular transmission. In the spinal cord, its action causes disturbances in the system of polysynaptic reflexes. In the central nervous system, tetanospasmin binds to gangliosides and affects motor and insertion neurons, removing the inhibition of motor neurons and facilitating the spread of excitation processes throughout the spinal cord. Violation of inhibitory mechanisms in the spinal cord itself significantly reduces the inhibitory effect from the higher sections of the central nervous system. The toxin causes an increase in the activity of the sympathetic nervous system: tachycardia, unstable hypertension, arrhythmias, peripheral vascular spasms, profuse sweating, hypercarbia and increased excretion of catecholamines in the urine.

Tetanospazmin, adsorbed in tissues, binds strongly to them, subsequently it is not destroyed and is not neutralized by antitoxin. Tetanus antitoxin can prevent tetanospasmin binding in the central nervous system if the latter is in the peripheral nerve trunks. The antitoxin does not affect the germination of spores of C. tetani and the propagation of vegetative forms of the pathogen in tissues.

Pathomorphology. C. tetani infection remains localized and causes minimal inflammatory changes in damaged tissues. Local pathological changes are secondary. Pneumonia, which develops in patients, is caused by other pathogens and is associated with difficulties in expectoration of sputum. Often there is degeneration of striated muscles, including diaphragmatic, intercostal, rectus abdominis, etc. The essence of the changes is the disappearance of transverse striation, lysis and death of myofibrils. Hemorrhages in muscle fibers and their rupture are observed. Degenerative changes in the diaphragmatic and intercostal muscles can lead to ventilation failure, as well as to myasthenia gravis, which can develop during the period of convalescence. Fractures of the spine can be the result of seizures.

Clinical manifestations. The incubation period for tetanus is 3-14 days after injury, less often - from 1 day to several months.

Three clinical forms of tetanus are distinguished: 1) local tetanus, manifested by pain, prolonged rigidity and muscle spasm proximal to the site of damage, which can persist for several weeks and disappear without a trace. In some cases, they precede the development of a generalized form of the disease. Local and easily occurring common tetanus is sometimes observed in children with chronic otitis media. The causative agent can be found in the discharge from the middle ear. Lethal outcomes with a localized form of the disease occur in 1% of cases;

2) a common tetanus, usually beginning imperceptibly, but trismus can be detected in 50% of patients. Chewing muscle spasm is often combined with stiff neck muscles and difficulty swallowing. Early symptoms include anxiety, irritability, headaches. A spasm of the facial muscles causes a sardonic smile. Short tonic contractions of different muscle groups appear. The lumbar and abdominal muscle groups become rigid, spasms of the back muscles begin, leading to opisthotonus. Tetanus convulsions are characterized by the sudden appearance of tonic contractions of different muscle groups, causing flexion and adduction of arms, clenching of the hands, and extension of the legs. At first, cramping can be mild, lasting seconds and alternating with periods of relaxation. Subsequently, convulsions become stronger, longer and exhaust the patient. Attacks of convulsions provoke almost any visual, auditory or tactile stimulus. During the entire period of the illness, the victim retains consciousness, he experiences severe pain. At the same time, a pronounced sense of fear is noted. Cramps in the muscles of the pharynx and respiratory tract can lead to closure of the respiratory tract, cause cyanosis, asphyxiation. Dysuria, or urinary retention, develops a second time in connection with a spasm of the sphincter of the bladder. Involuntary urination, bowel movements may occur. Excessively violent cramps often lead to compression fractures of the vertebral bodies and muscle hemorrhages. Sometimes weakness of certain muscle groups and loss of sensation caused by peripheral neuropathy can be observed. During electrophysiological studies in the initial period, conduction disorders along the nerve trunks are revealed. Full or partial recovery occurs in a few weeks and even months.

The body temperature in patients usually rises slightly, increasing it to 40 ° C is explained by increased energy expenditure during seizures. Patients have excessive sweating, tachycardia, hypertension, arrhythmia. During the first 3–7 days, the symptoms of the disease increase, over the next 2 weeks the patient’s condition stabilizes, and only after that his gradual improvement is observed. Full recovery occurs after 2-6 weeks;

3) head tetanus. This is an unusual manifestation of the disease. The incubation period is 1-2 days. The disease is usually caused by otitis media, injuries of the head, face and foreign bodies in the nasal cavity. The most characteristic symptoms of the disease include impaired function of III, IV, VII, IX, X, and XI pairs of cranial nerves. Most often, the VII pair (facial nerve) is involved in the process. Following the cranial brain, a generalized form of tetanus may also develop.

Tetanus of newborns usually begins in a child aged 3-10 days and proceeds as a generalized form.
At first, the sucking act is violated in the child, anxiety and severe crying appear. Soon, swallowing disorders join, muscle stiffness appears, cramps begin. Opistotonus may be absent.

Complications Adequate therapy and careful care reduce the frequency and severity of complications that develop with tetanus. Aspiration pneumonia, atelectasis, mediastinal emphysema, and tetanus pneumothorax are caused by impaired pulmonary ventilation due to respiratory muscle spasm, laryngospasm and accumulation of discharge in the bronchi. Mediastinal emphysema and pneumothorax are most common after tracheostomy. Biting of the tongue and mucous membrane of the cheek, vertebral fractures, intramuscular hematomas are the result of severe seizures. With prolonged convulsions, dehydration of the body and general exhaustion occurs.

Diagnosis and differential diagnosis. Diagnosis of tetanus is based on clinical data. The results of routine laboratory tests are not of particular diagnostic significance. The determination of tetanus bacilli in smears from a separable wound or their growth on culture media confirms the diagnosis of tetanus only with anamnestic and clinical data characteristic of tetanus. The mere detection of tetanus sticks in a wound does not mean that a person is ill with tetanus or that he will develop later.

Tetanus in newborns is differentiated with birth injuries and purulent meningitis, spasmophilia, paratonsillar abscess and other inflammatory diseases in the lower jaw, in which there may be a spasm of the masticatory muscles, as well as with strychnine poisoning.

In older children, tetanus is differentiated with hysteria, rabies.

Treatment and patient care. The main goal of treatment for tetanus is to eliminate the source of the formation of tetanospasmin, neutralize the toxin circulating in the blood and conduct maintenance therapy until the tetanospasmin fixed by the nervous tissue is destroyed. Maintenance therapy should be carried out quite intensively and thoroughly.

Human specific immunoglobunal (SIG) is administered as early as possible at a dose of 3000-6000 IU intramuscularly. Intravenous administration is contraindicated. There are no allergic reactions after the introduction of SIG, and the level of antitoxin in the blood is created higher than after the administration of immunoglobulins obtained from animals. Repeated administration of SIG is not required. Anti-tetanus immunoglobulin does not cross the blood-brain barrier and does not affect the toxin fixed in the nervous tissue. Its therapeutic effect boils down only to the neutralization of tetanospasmine circulating in the blood.

In the absence of SIG and unchanged patient reactivity in accordance with the data of the intradermal test with tetanus antitoxin (CAT), it is recommended to administer the latter at a dose of 50,000-100,000 units: half the dose intramuscularly and the other half intravenously. In the case of a reaction to a foreign protein, desensitization is carried out according to the usual scheme.

Surgical measures for the treatment of wounds are carried out after the introduction of antitoxin and sedatives. Necrotic tissue and foreign bodies are removed from the wound. Wound surfaces are left open.

Antibiotic therapy helps eliminate vegetative forms of tetanus bacillus located in dead tissue. Typically, large doses of penicillin G are prescribed intravenously in 6 doses for at least 10 days and try to ensure sufficient penetration of it into the lesion. With penicillin intolerance, tetracycline is prescribed. Careful care includes ensuring a quiet and peaceful environment, the absence of exposure to the patient of any auditory and visual stimulus, adequate breathing, the introduction of oxygen, aspiration of the bronchial secretion and caring for the tracheostomy tube.

Muscle relaxants must be administered to all tetanus patients. Diazepam (sibazon) is effective in reducing the increased muscle tone and prevents cramps. You can enter chlorpromazine or mefenesin, but their effect is less pronounced. Preparations of neuromuscular blocking action contribute to the reduction of seizures while maintaining spontaneous breathing or to completely shut down muscle function when switching to artificial ventilation.

After the introduction of sedatives and muscle relaxants, patients should be on artificial ventilation and under constant monitoring. It is necessary to control the adequacy of ventilation, systematically aspirate the secret from the bronchi and prevent deep depression of the respiratory center.

It is necessary to weigh patients daily, carefully monitor the amount of fluid taken and released, maintaining electrolyte and caloric balance. Enteral nutrition is possible only in some patients, in most cases it is necessary to resort to intravenous infusions and the introduction of food through a gastric tube. Sometimes you have to make a gastrostomy. Particular attention should be paid to caring for the skin, oral cavity and monitor the function of the bladder and intestines.

Particular problems are associated with artificial ventilation, sedative treatment and maintaining adequate hydration in newborns. Their treatment should be carried out as actively as possible with the help of tracheal intubation, muscle relaxation and assisted ventilation. If it is impossible to carry out all these activities, they fully resort to the enteral administration of sedatives and muscle relaxants. Every 6 hours, children are given to drink syrup with chlorpromazine, an elixir with phenobarbital or mefenesin. Diazepam is administered intravenously, repeatedly depending on the severity of the seizures. The additional purpose of pyridoxine has a beneficial effect, contributing to an increase in the production of gamma-aminobutyric acid formed in the region of nerve endings, weakening their sensitivity and reducing spasms. Dissection of the umbilical cord is not currently recommended.

Forecast. The death rate from tetanus averages 45–55%, in newborns - 60% or more.

The outcome depends on many factors. In infants and the elderly, the disease usually ends fatally, in adolescence and youth, recovery most often occurs. Among patients aged 10-19 years, death occurs in only 20% of cases. Adverse symptoms include widespread damage to muscle tissue, high body temperature, short intervals between the time of injury and the development of clinical signs of tetanus, or between the time of the onset of trismus and the development of seizures. In severe cases, tetanus ends in death usually within the first week. Intensive and supportive therapy to a large extent determines the outcome of tetanus.

In surviving children after tetanus, paresis, central type paralysis, and mental development disorders may remain. Causes of brain damage are prolonged states of apnea and anoxia during prolonged cramping.

Persons who have been ill with tetanus do not have stable immunity, therefore, even those who have suffered it must subsequently be actively immunized.

Prevention Active immunization is the best method of tetanus prophylaxis. It is preferable to immunize women before pregnancy, and unvaccinated vaccinations immediately after childbirth.

Children 6 years of age and older are immunized according to the recommended method for adults. Tetanus and diphtheria toxoids are administered intramuscularly in 3 doses. The main immunization should be with a tetanus toxoid. The introduction of at least 4 doses provides a sufficient level of immunity to tetanus.

Preventive measures after an injury are determined by the patient’s immune status and the nature of the lesion itself. Surgical treatment of the wound should be carried out immediately and thoroughly. Patients who have not been actively immunized or which was incomplete, must be administered intramuscularly human tetanus immunoglobulin at a dose of 250-500 units. Предварительное проведение кожных аллергических проб необязательно, так как СИГ не вызывает сывороточной болезни. При отсутствии СИГ внутримышечно вводят столбнячный антитоксин в дозе 3000—5000 ЕД, предварительно проведя реакцию на чувствительность к чужеродным белкам. Введение поддерживающих доз анатоксина показано при получении ребенком травмы через 5 лет и более после полного курса активной иммунизации.

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    Столбняк - это острое инфекционное заболевание, вызванное действием токсина, выделяемого бациллой Николаера (Clostridium tetani), микроорганизмом, который может долгие годы сохранять жизнеспособность, находясь в грунте. Эта бацилла легко проникает в организм человека через рану, особенно если в рану попадает грязь. См. статью СУДОРОГИ, учитывая при этом, что метафизическое значение столбняка
    Столбняк [греч. — Tetanus (отверждение); English — Lockjaw] — остро протекающая, неконтагиозная раневая токсикоинфекционная болезнь млекопитающих животных, птиц и человека, характеризующаяся повышенной рефлекторной возбудимостью, судорожными тоническими судорогами мышц тела под воздействием токсина возбудителя (см. цв. вклейку). Историческая справка, рспространение, степень опасности и ущерб.
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    Столбняк - острая раневая инфекционная болезнь животных и человека, характеризующаяся поражением нервной системы, рефлекторной возбудимостью и судорожным сокращением мышц тела без нарушения сознания. Etiology. Возбудитель столбняка широко распространен в природе, его много в почве садов и огородов, в навозе. Имеются сведения о том, что он размножается в кишечнике животных, с их калом
  5. Столбняк
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  6. Столбняк
    Объем обследования 1. Столбняк — острое инфекционное заболевание, характеризующееся токсическим поражением нервной системы, проявляющееся тоническими судорогами. Возбудителем заболевания является анаэробная спорообразующая палочка Clostridium tetani. 2. Входными воротами являются раны или другие повреждения кожи и слизистых, в том числе — ожоги, отморожения, потертости, криминальные аборты,
  7. Столбняк
    ЭТИОЛ. Clostridium tetani. ФП: экзотоксин (тетаноспазмин – нейротоксин и тетаногемолизин). ИСТ: почва, фекалии травоядн. жив. и людей. ВОР: раны, ожоги, отморожения, при родах, абортах. П-З. необх. усл. – отсутсв О2. Входн. ворота – 1) тетаноспазмин – двиг. волокна периф. нервов + гематогенно – НС – паралич встав. нейр. полисинаптич. рефл. дуг – наруш. проц. торможения – судороги. 2)
  8. Столбняк
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    Столбняк - острая раневая токсикоинфекция животных, вызываемая Clostridium tetanus и характеризующаяся поражением нервной системы, рефлекторной возбудимостью и судорожным сокращением мышц без нарушения сознания. Возбудитель обитает в основном в почве, содержащей навоз. Есть данные, что патогенные клостридии, размножаясь в кишечнике животных, выделяются во внешнюю среду вместе с фекалиями.
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    Столбняк (тетанус) – острое инфекционное заболевание, обусловленное воздействием на организм экзотоксина столбнячной палочки с преимущественным поражением нервной системы, характеризующееся тоническими и судорожными сокращениями поперечно-полосатых мышц. Этиология: Clostridium tetani – во внешней среде существует в виде чрезвычайно устойчивых спор, которые при благоприят-ных анаэробных
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    Столбняк — острое заболевание с явлениями интоксикации центральной нервной системы, тоническими и клоническими мышечными судорогами. Epidemiology. Возбудитель — столбнячная палочка, строгий анаэроб; вегетативная форма продуцирует сильнейший экзотоксин. Вне организма образует споры, устойчивые к физическим и химическим факторам: в почве сохраняются до 10 лет, при кипячении погибают только
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