THEME OF THE LESSON:

BOTULISUM. URGENT CONDITIONS. TETANUS.

Botulism.

The Activator: Clostridium botulinium - it is strict anazerobic sporogenous bacillus producing strongest in a nature neutrotropic exotoxin. Distinguish 7 types of baccillus and toxin: A, B, C, D, E, F and G. In conditions of an environment clostridias form spores. Spores do not produce botulotoxin, for this purpose they should sprout in vegetative forms, appearing in anaerobic conditions. Toxin causes disease at hit in an organism of the person, in the basic through a digestive path (with food), and also in respiratory ways (its application in the sprayed condition as the bacteriological weapon).

Epidemiology Vegetative forms of clostridias are found out in clinic of domestic and wild

animals, a waterfowl, fishes. In ground, silt of lakes and ponds of clostridias are long kept as spores. For occurrence of food botulism the combination of the following characteristics of foodstuff is necessary:

Pollution of a product by the ground or water and its insufficient machining; Insufficient thermal processing of a product; Creation of anaerobic conditions during storage; Storage of products without refrigerating chambers; Usage of the given product without preliminary chemical processing.

As the factor of pollution serve vegetable, fish or a canned meat, mainly domestic preparation. A sign of infection of canned food by clostridias is bombage of covers of thermally closed jars. Meat and fish products become soft, break up. At the use of the infected products by many people only those from them who used the portions containing colonies of a microbe and impregnated with toxin fall ill.

Pathogenesis The basic mechanism of the disease is the poisoning with the toxin contained in a

product and steady against action of gastric juice. Toxin is resorpted through a mucous membrane in lymph, in blood and will penetrate into various organs and CNS, strongly communicates with nervous cells, causes lesions of the bulbar part of a brain and development of bulbar symptoms. Alongside with it, mononeurons of forward horns of a spinal medulla aredamaged, nervous - muscular transfer of excitabilities, and innervation of muscles is broken. Paresises and paralyses arise. Functions of oculomotor muscles, pharynx, larynx are suppressed. In result of paresis of ingestional muscles (intercostal and diaphragm) acute ventilating insufficiency is developed. It is a principal cause of death at botulism. Lesion of nerve ganglions of a heart with its sudden stop serves as the second reason of death of patients. Duplication of the activator in intestines with development of new portions of toxin strengthens intoxication.

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Immunity after a botulism does not develop, because necessary for formation of antitoxic antibodies the quantity of toxin is lethal.

Clinic The Clinic of botulism does not depend on type of toxin. The incubatory period

makes more often 12-24 hours, less often 2-8 days. Than the doze of the toxin which has got in an organism is more, than the incubatory period is more shortly and disease proceeds more hardly. It begins in most cases sharply by plural symptoms, arising quickly one by one: an indisposition, communicating muscular slackness, a headache. At 2/3 patients nausea, vomiting of 4-5 times and 2-4 multiple stool are observed, there can be pains in an abdomen. Dyspepsia keeps 1-2 days and it is replaced by constipation and meteorism. Simultaneous occurrence of myoneurological symptoms is typically.

One of the first complaints of the majority of patients is disturbance of vision: occurrence of “fog” or “grid” before eyes, a vagueness of contours and doubling of subjects. At objective research restriction of movement of eyeballs in all sides, expansion of pupils (midriasis), slackness of pupillar reactions, ptosis of eyelids are defined. It is the ophthalmologic syndrome caused by lesion of a ciliary muscle with change of curvature of a crystalline lens and a paralysis of accommodation, lesion of sphincter of an iris of the eye, lesion of external muscles of an eye with disturbance of convergence and ptosis of eyelids.

Early symptom is disorder of swallowing. It appears by feeling of “clot” in a throat, difficulty at swallowing of the firm, dry food, connected with disorder of secretion of saliva and slime in result of atropinoliked actions. The cavity of a mouth, a pharynx, nasal courses dries up. Reception of a liquid does not satisfy the thirst. At progressing process swallowing both soft, and liquid food is broken. In result of paresis of an epiglottis and the soft palate the liquid food partially gets in a trachea, partially in a nose. The patient is choked over. At survey dryness of a mucous of a mouth, rich impose by a white or brown membrane on a tongue, restriction of mobility of the soft palate, absence of palatine and pharyngeal reflexes is marked. Speech is muffled with a nasal shade. It is phago-naso-glossoneurological syndrome connected to lesion of pharyngeal muscles.

Simultaneously with the phenomena of dysphagia there is a lesion of the voice apparatus. The voice becomes hoarse, weak and silent, that is explained by disturbance of closing of a voice fissure. It is phono-laryngoneurological syndrome connected to lesion of muscles of a throat that results in a combination to disorder of movement of a tongue and the soft palate in disturbance of articulate speech.

Diagnostics of botulism is based basically on the clinical and epidemiological data. From epidemiological factors it is necessary to take into account the use of tinned products at which manufacturing conditions for preservation and duplication of clostridias could be created: the anaerobic conditions, insufficient sterilization, the weak sour and weak salty environment, the big capacities. Should be estimated and circumstances of the usage of a product, group disease.

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Clinical criteria of the diagnosis include complaints of patients, development of semiology and an objective pathology. The differential diagnosis should be carried out with the diseases having semiology similar to botulism.Frequent presence of nausea and vomiting and sometimes diarrhea demand the differentiation from group of acute intestinal infections (dysentery, salmonellosis, food toxicoinfections). Revealing of the above-stated complaints at botulism does not exclude an opportunity of a combination of these infections. In diagnostics the estimation of additional semiology, characteristic for botulism (eye, bulbar), normal temperature has the big value.At a poisoning with methyl spirit the progressing blindness, hallucinations, fear, loss of consciousness, falling of cardiac activity is characteristic. In these cases the patients specify on the usage of substitute alcohol.In case of a poisoning with atropine or Belladonna the same as at botulism, dryness in a mouth, disturbance of vision, dysphagia are marked, but thus always there is an excitation, delirium, strong expansion of pupils. At a poisoning with poisonous mushrooms it is necessary to take into account the use in food of just prepared mushrooms. Delay of pulse, paleness of a face in heavy cases - delirium, hallucinations, convulsions strong salivation, hypoerhidrosis, profuse diarrhea, colicky pains in an abdomen are marked. At differential diagnostics with diphtheria changes in fauces – dyphtheric membranes matter. Neurologic disorder at diphtheria usually arises after disappearance of edema of a hypodermic cellular tissue. Paralyses come simultaneously with development myocarditis more often.Development of significant muscular weakness, paralyses, neurologic status results sometimes in an establishment of the diagnosis of two-wave tick-born encephalitis. For encephalitis presence in the beginning of disturbances of dynamics of dream, then development of drowsiness, loss of consciousness, a fever, development of paralyses is typical.Disturbance of vision at hemorrhagic fever with renal syndrome, that sometimes forms the basis for erroneous diagnostics of botulism, is combined with manifestations of hemorrhagic syndrome and acute renal insufficiency.

Laboratory diagnosticsLaboratory diagnostics is based on detection of botulinic toxin or the activator of

botulism in the materials taken from the patient (blood, emetic masses, washing waters of a stomach, feces), and also foodstuff which have caused a poisoning. Blood should be taken before introduction of medical serum in quantity of 10-20 ml from a vein in a sterile test tube. Washing waters of a stomach get in quantity of 50-100 ml, as well as emetic masses, feces 50-60 g into sterile banks which are closed by rubber or kapron fuses without preservation. On a researched material, the accompanying document with the instruction what material from whom it is taken, age of the patient, date of a capture, Surname, name, patronymic and a list of medical worker directing it in laboratory is

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filled.. The material goes to department of especially dangerous infections of organs of sanitary inspection.

For detection and identification of toxin biotest with reaction of neutralization to white mice is used. The principle of it consists that to the first control pair of mice intraperitoneally 0,5 ml of a researched material is introdused. If in 4-6 hours mice die, to the second pair mice (skilled) enter 0,5 ml of the material and polyvalent antibotulinic serum on 500 of U/d of types A, B and Е. If these animals are alive, pass to the following stage of experience. To the third pair of mice enter 0,5 ml of a material and 500 U/d of antibotulinic cerum of type A, the fourth - 0,5 ml of the material and 500 U/d of the serum of type B, the fifth - 0,5 ml of the material and 500 U/d of the serum such as Е. To control (sixth) pair of mice enter 0,5 ml of physiological solution.

The account of results will carry out in 24 and 48 hours. At presence at an ill botulism the first control pair of mice always dies. The control (sixth) pair is always alive. And that pair of skilled mice which has remained alive, and will define type of toxin as the serum has neutralized toxin.

Bacteriological diagnostics of botulism is extremely inconvenient in connection with anaerobic conditions of duplication of clostridias.

Immunodiagnostics of botulism, based on revealing of antitoxins in blood of patients, can not be carried out because the quantity of toxin necessary for formation of antitoxic antibodies is lethal - about 0,3 mkg.

Changes of peripheral blood or do not happen or they are characterized by moderate leukocytosis, neutrophilosis and rodonuclear shift to the left.

TreatmentTreatment of botulism includes two basic directions. The first consists of the

actions directed on prevention of an opportunity of formation of toxin in an organism of the patient, on maximum fast deducing of toxin from an organism and on neutralization of toxin circulating in blood. The second are measures on elimination of pathological changes caused by botulinic toxin.

Therapy should begin already at a pre-hospital stage. The first obligatory action is a washing a stomach and an intestine that allows to remove from them the rests of some more the not resorpted toxin. It is made washing by probe of a stomach in the big volumes (up to 10 liters of total) 5 % of a solution of a hydrocarbonate of sodium. By the same volume of soda siphon enema is made. With the purpose of adsorption of toxic products in intestines the patient it is appointed inside 20-30 g of carbolen in a half-glass of warm water.

Neutralization of toxin circulating in blood is carried out by introduction of antibotulinic serum. Up to an establishment of type of toxin introduction of antitoxic polyvalent antibotulinic serum of type A, B, Е is recommended. One medical doze of serum makes 25 thousand: type A and Е on 10 thousand and type B - 5 thousand. Serum is introduced only intramuscularly warmed up to 37C. At the easy form of botulism enough unitary introduction of one medical doze.

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At the heavy form the doze of serum is increased, but the maximal daily doze should not exceed 30 thousand A and Е and 15 thousand of type B, and all course of serotherapy lasts no more than 3-4 days.

Technique of introduction of serum is on Bezredka. Skin test with the serum dissolved in 100 time (small role in a box of the serum) in a doze of 0,1 ml on palmar surfaces of the left forearm in the beginning is put. At negative test (in a place of introduction there are no changes or hyperemia no more than 10 mm) through 20 mines it is entered 0,1 ml of the not dissolvedserum hypodermically in a shoulder. At absence of reaction through 20-30 mines it is intramuscularly entered all doze of the serum.

At presence of local (hyperemia) or general (rise in temperature, a fever, tachycardia or another) reactions to introduction of the serum treatment by it will be carried out in a combination with glucocorticosteroids.

After an establishment of type of toxin and if necessary the further serotherapy type-specific monoserum is used.

Nonspecific desintoxicational therapy is carried out by a 5 % solution of glucose, crystalloid preparations of type Trisol, Disol and colloids of type Haemodesis, Reopolyglucin and others. Having properties to connect toxin, they simultaneously, strengthening renal blood flow, deduce toxin from an organism. Usually the patient with the heavy form of botulism requires 2,0-3,0 liters of crystalloids and up to 800 ml of colloids in days. Introduction of such volumes of a liquid is carried out on a background of forced diuresis with usage of Lazyx (40-80 mg). With the purpose of suppression of development of the activator of botulism it is appointed Laevomycetinum in average therapeutic dozes during 5-7 days. At disturbance of swallowing intramuscularly it is entered Laevomycetinsukcinate on 1,0 3 times in days.Symptomatic therapy of botulism includes:

- the substances strengthening an energetic maintenance of tissues in conditions of limited delivery of oxygen - ATP, Tyamine, Cocarboxylase, Riboflavine, an ascorbic acid;

- the substances stimulating synthesis of DNA and RNA and by that inhibiting development of hypoxic damage of nuclear apparatus of CNS (vitamin В12, a folic acid);

- inhibitors of cholinesterase (Proserin, Galantamin);- cardio-vascular means (caffeine, Cordiamine).

In last years in a complex of therapeutic actions at botulism it is included hyperbaric oxygenation.

The general actions in treatment:At any form of botulism long observance of a confinement to bed is necessary.

Early getting up can promote occurrence of collapses. At disorder of swallowing of a feed through a probe should be adjusted. It is necessary regular evacuation of an intestine (enema) and a bladder. Restrictions in a diet at botulism are not required.

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REALIZATION OF THE LESSON The purpose is to learn to diagnose botulism according to clinic, the

epidemiological anamnesis and also to make the plan of inspection and treatment of the patient.

Control questions to the beginning of the lesson1. What are the features of etiology and epidemiology at botulism?2. What pathogenetic mechanisms define clinic of botulism?3. Enumerate diagnostic clinical syndromes of botulism.4. Enumerate the diseases requiring for differential diagnostics of botulism.5. Rules of a fence of a material for laboratory researches at botulism.6. Problems of treatment and a sequence of medical actions at botulism.7. Dozes of antibotulinic serum and rules of its introduction.8. A technique of realization of bioprobe with reaction of neutralization for

diagnostics of botulism.9. Indications of transition of patients on a controlled (mechanical) ventilation of

lungs.10.Enumerate prophylactic actions at botulism.

The test1. Pathogenetic mechanisms of botulism are:

1. Best concentration of freely circulating toxin in blood in 1 day after infection2. Disturbance of synthesis of cholinacetyltransferase3. Decrease of a level of acetylcholine in nervous synapses4. Development of paresises and paralyses5. Influence of toxin on parasympathetic nervous system

2. Manifestations of the gastroenteritic variant of an initial stage of botulism are:1. Spastic pains in an epigastral area2. Unitary or double vomiting by the eaten food, an indulgence of stool3. Dryness of mucous membranes of a mouth4. Difficulty of passage of food on an esophagus (“clot in a throat”)5. High temperature with a fever

3. Manifestations of the eye variant of an initial stage of botulism are:1. “Sharp long-sightedness”2. Narrowing of pupils, short-sightedness3. Diplopia4. Midriasis, anisocoria5. Nystagmus, strabismus

4. Clinical symptoms of the period of heat of botulism are:1. Myasthenia2. Constipation, meteorism3. Disorder of sensitivity4. Tachycardia

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5. Meningeal symptoms5. Clinical manifestations of the period of heat of botulism are:

1. Ptosis of upper eyelids2. Midriasis3. Anisocoria4. Strabismus5. Diplopia

6. Clinical signs of botulism in the period of heat of the disease are:1. Dysphagia2. Dysartria3. Twang4. Absence of coughing reflex5. Aphonia

7. Laboratory diagnostics of botulism is:1. Bacteriological research of feces2. Separation of hemoculture3. Biological test (reaction of neutralization of toxin) on white mice4. RNHA5. Clinical analysis of blood

8. Botulism is differentiated with:1. Poisoning with a henbane

1. 2. Poisoning with poisonous mushrooms2. The bulbar form of poliomyelitis3. Steamic encephalitises4. Food toxicoinfections

9. Treatment of patients with botulism:1. Washing of a stomach2. Antibiotics of a wide spectrum of action inside3. Desintoxicational therapy4. Introduction of medical antibotylinic serum5. Controlled (mechanical) ventilation of lungs at respiratory disorders

10. Methods and means of specific antitoxic therapy at botulism:1. Polyvalent antibotulinic serum2. Human antibotulinic plasma3. Human antibotulinic immunoglobuline4. Intramuscular introduction of preparations5. Intravenous introduction of preparations

For discussion of a theme of the lesson students study a clinical problem. At the decision of problems students write in writing-books the clinical diagnosis in view of the form and severity of the disease, the plan of laboratory-instrumental inspection of the patient, the plan of treatment with reception in Latin language of preparations of antibacterial and pathogenetic action.

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PROBLEM Patient P., 25 years, has arrived in infectious branch for the 2nd day of the disease

in a heavy condition. She was ill acutely when sharp muscular weakness, dryness in a mouth, diplopia, “fog” before eyes has appeared. For the 2nd day of the disease symptoms accrued, disturbance of swallowing of firm, and then and liquid food, twang of a voice, dizziness has joined.

Day prior to disease she ate tinned mushrooms of domestic preparation. At receipt a condition is heavy. She is languid, adynamic, pale. A tongue is dry, covered with a brown membrane, the pharyngeal reflex is absent. She can not swallow the firm food, the liquid food is poured out through a nose. Pupils are non-uniformly expanded, reaction to light is absent. A voice is nasal. She can not read. She has constraint in a chest at breath, feeling of a clot behind a chest. Pulse is 140 in one minute, weak filling. The arterial pressure is 90/50 m.Hg. She can’t urinate independently. Lips and nails are cyanotic.

1. Formulate the diagnosis.2. Define a degree of severity of the disease.3. Render the first aid to the patient, appoint specific treatment, having specified a

doze and a method of introduction of a preparation.

Tetanus

The Activator: Clostridium tetani; it is anaerobic spotogenous bacillus producing neurotropic exotoxin. In conditions of an environment clostridias form the spores which are not producing exotoxin. In an anaerobic conditions and, especially, at the presence of aerobic bacteria (staphylococci and other) spores sprout in mobile vegetative forms, and they develop specific toxin. Tetanic exotoxin consists of 2 fractions: tetanospasmin and tetanohemolysin. Tetanospasmin damages motor cells of the central nervous system and causes contraction of striated muscles. Tetanohemolysin dissolves erythroytes.

Epidemiology The tetanic bacillus is widely distributed in a nature. The vegetative form is the

constant inhabitant of an intestine of herbivores. Having got in ground, clostridias are long kept as spores. Together with a dust from ground spores of clostridias get on a skin, clothes of the person, and in case of damage of a skin and mucous membranes cause the disease. Disease by tetanus is connected to a traumatism.

Pathogenesis The entrance gate at tetanus is damage of integuments and mucous membranes.

The chipped and deep wounds promoting to anaerobic conditions with duplication of a tetanic bacillus and production of toxin are especially dangerous. Promotion of toxin occurs on motor fibers of peripheral nerves and also through blood in a back, an oblong brain and in a reticular formation of a trunk. Toxin is fixed by inserted neurons of

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polysinaptic reflex arches, carrying out correlation of the impulses arising in mononeurons. Owing to a paralysis of inserted neurons biocurrents from mononeurons act to any muscles is not coordinated, continuously. Effective impulsation is amplified; there is a convulsive syndrome - a constant tonic tension of any muscles. Amplification of afferent impulsation, connected with nonspecificirritators (painful, sound, light), is shown by occurrence of tetanic convulsions. All this is accompanied by occurrence of excitability of a cortex and reticular structures. The centers of a brain, especially respiratory and nucleus of n.vagus are damaged.

Convulsive syndrome results in development of metabolic acidosis that strengthens tonic and tetanic convulsions even more, develops hyperemia. Conducting factor at fatal outcome of the disease considers overexcitation of CNS and the general convulsions of a body that finally results in the phenomena of asphyxia, pneumonia, to an exhaustion and cardiovascular disorder. The paralysis of a heart or paralysis of central genesis, or as a result of lesion of modular centers by a toxin is possible.

Immunity after tetanus does not develop, as the doze of toxin causing tetanus, is insufficient for formation of antibodies. Only active immunization by tetanic anatoxin can cause tetanic immunity.

Clinic In clinical classification allocate tetanus general, or generalized, and local - more

often the disease proceeds as generalized process. The incubatory period makes 3-30 days. Duration of it depends on conditions for duplication of the activator in a wound and speed of toxicoformation. Manifestations of the disease begin gradually. The prodromal period as nagging pains in a wound, a tension and twitching of adjoining muscles, increase of irritability, a headache and hydrosis. One of the first symptoms of tetanus is intensity and difficulty at opening a mouth - trismus - owing to convulsive reduction of chewing muscles. In heavy cases a teeth are strong compressed and to open a mouth it is impossible. There are convulsive reductions in muscles of the person which give to it expression of a sardonic smile: the wrinkled forehead which has been stretched in width with lowered angles of a mouth. The head because of spasms of occipital muscles is thrown back back. There is a difficulty of swallowing owing to a convulsive spasm of muscles of a pharynx. Tonic spasms are distributed in the descending order to muscles of a neck, a back, an abdomen, extremities. Because of a sharp spasm of muscles of a back the patient is curved on bed, concerns it only a nape and heels. The hypertonus of intercostal muscles disturbs ventilation of lungs. Breath occurs only for the account of a diaphragm. Abdominal muscles become firm as a board. After all tonic spasms grasp muscles of extremities, except for hands and feet.

On a background of a constant hypertonus of muscles arise sharply painful tetanic spasms all over again limited, then with involving the big muscular groups. They can last some seconds or is continuous at a heavy tetanus. Thus a face of the patient becomes blue, the skin becomes covered by sweat, frequency of breath sharply accrues. The death from asphyxia is possible. There is a disorder of blood circulation with developments of

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stagnation and aspiration pneumonia. The hypertonus of muscles of perineum complicates urination and defecation. The general hypertonus, attacks of tetanic spasms result in hyperpyrexia. The consciousness usually remains clear. Characteristic changes by the side of the general analysis of blood are not present, neutrophilic leukucytosis is often observed.

The clinical cycle at tetanus lasts 2-4 weeks. The acute period of the disease is up to 10-14 days; it is especially dangerous. The death quite often comes in the first 4 days of the idsease. About 15 days begins reconvalescence. It proceeds very slowly. Hypertonus of muscles of a back, an abdomen and gastrocnemius muscles keeps about one month, tachycardia is long kept.

On severity of current the tetanus divides on:1. The easy form is observed seldom. The incubatory period of the disease is 20

days. Symptoms of the disease are developed during 5-6 days. Trismus, a sardonic smile, opistotonus are expressed moderately. The hypertonone of other muscles is shown poorly, tetanic spasms are insignificant. Temperature is subfebrile.

2. The average form - the incubatory period proceeds 15-20 days, clinical symptoms are developed during 3-4 days. At a constant hypertonus of muscles it is observed infrequent (some times per day) and moderately expressed spasms, moderate tachycardia and the raised temperature.

3. The heavy form - the incubatory period is 7-14 days, fast development of clinic - within 24-28 hours from the moment of occurrence of its first attributes. The high temperature and tachycardia, frequent tetanic spasms with a constant muscular hypertonus between attacks and hidrosis are characteristic. Development of pneumonia is frequent.

4. The very heavy form - the incubatory period does not exceed 7 days.5. The disease is developed instantly, accompanied by strong spasms on some times

within 1-5 minutes, tachycardia, cyanosis, menacing asphyxia. The rare form of tetanus is represented with the local tetanus described by a

muscular hypertonus and spasms only in the field of a wound.

Complications The most frequent complication at tetanus is bronchitis and bronchopneumonia.

In connection with spasms breaks of muscles are possible: dislocations, fractures of bones.

REALIZATION OF THE LESSON The purpose is to learn to diagnose tetanus according to clinic, the

epidemiological anamnesis and also to make the plan of inspection and treatment of the patient.

Control questions to the beginning of the lesson1. Characterize signs of the activator of infection.

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2. What forms a basis of diagnostics of tetanus?3. Name leading clinic-pathogenic syndrome of tetanus. 4. Than is the local tetanus characterized?5. What are the earliest manifestations of generalized tetanus?6. Define conditions of hospitalization of the patient with tetanus.7. What complications are possible at tetanus?8. What preparation and in what doze is it necessary to carry out specific treatment

at tetanus?9. In what therapy does the patient with tetanus require?10.What is the prognosis of the disease?11.How is the prophylaxis of tetanus made?

The test

1. The basic mechanism determining development of convulsive syndrome at tetanus is:

1. Direct action of exotoxin on striated muscles2. Amplification of afferent impulsation owing to irritation toxin of peripheral

receptors3. Influence of toxin on the centers of sensitive sphere of a cortex of a brain4. Development of metabolic acidosis5. Paralysis of inserted neurons of polysynaptic reflex arches of a back and an

oblong brain2. Symptoms of an initial stage of tetanus are:

1. Blunt nagging pains in the field of an entrance gate of an infection2. Dysphagia3. Trismus of chewing muscles4. Sardonic smile5. Dyspnea

3. Clinical symptoms of tetanus in heat of the disease are:1. Constant muscular hypertonus

1. 2. Trismus2. Tetanic spasms3. Disorder of consciousness4. Arterial hypertension

4. Categories of heavy current of tetanus are:1. High fever, expressed hyperhidrosis2. Difficulty of urination and defecation3. Opistotonus4. Frequent and intensive spasms5. Expressed respiratory disorder

5. Variants of current of tetanus are:

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1. Head tetanus of Brunner2. Obverse paralytic tetanus of Rose3. Gynecologic tetanus4. Tetanus of newborn5. Traumatic tetanus

6. Clinical features of head tetanus of Brunner:1. Heavy current2. Primary lesion of muscles of a face, a neck and a pharynx3. Spasm of ingestional and intercostal muscles4. Spasm of a voice fissure and a diaphragm5. Lesion of respiratory and vasomotor centers

7. Complications of tetanus are:1. Spasm of coronary vessels2. Asphyxia3. Pneumonia4. Breaks of muscles and ligaments, fractures of bones5. Gastrointestinal bleeding

8. The researches necessary for diagnostics of tetanus are:1. Bacteriological method2. Biological test on white mice3. Intradermal allergic test4. Serological reactions5. Clinical inspection of the patient

9. Tetanus is differentiated with:1. Hysteria2. Epilepsy3. Poisoning with strychnine4. Tetania5. Encephalitises

10. Medical actions at tetanus are:1. Neutralization of toxin2. Anticonvulsive therapy3. Guarding regimen4. Struggle with acidosis5. Surgical processing of a wound

Discussion of a theme is preceded with studying archival case histories of thematic patients. Students prepare for the brief report in the investigated case. The following data are necessary:

- surname, name, patronymic, the patient, age, a residence and works, date of disease and hospitalization;

- complaints at the moment of hospitalization;

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- the first symptoms of the disease: paresthesias in a wound, difficulty at opening a mouth, constraint in a face, a neck, a back, spasms;

- development of these symptoms during the disease (increase, stability, reduction);

- epidemiological data: circumstances of a trauma, duration of the incubatory period, initial processing of a wound, usage of antitetanic serum, presence of vaccins against tetanus.

- The objective data of survey of the patient:- the general condition (satisfactory, average, heavy);- appearance, color of external covers;- position of the patient: compelled, cyanosis, hypertonus of muscles, the

sardonic smile, the thrown back head, opistotonus, presence of spasms and their frequency;

- condition of system of breath: breath is free, productive or complicated and superficial, Frequency of breath movements, pneumonia;

- condition of cardiovascular system: dullness of tones, tachycardia, hypertension;

- condition of system of digestion: an opportunity or disturbance of defecations;

- condition of urine-excreting system: an opportunity or disturbance of diuresis.

For discussion of a theme of the lesson students study a clinical problem. At the decision of problems students write in writing-books the clinical diagnosis in view of the form and severity of the disease, the plan of laboratory-instrumental inspection of the patient, the plan of treatment with reception in Latin language of preparations of antibacterial and pathogenetic action.

PROBLEM. Patient B., 25 years, has addressed to the stomatologist polyclinic in connection

with difficulty at opening a mouth. The stomatologist has not revealed pathology, but has noted, that the patient opens a mouth no more than on 3 sm and has directed him to the neurologist. The neurologist has noted revival of tendinous reflexes and recommended calming mixture with Valeriane. Next day the patient again has addressed in a polyclinic to the therapist in connection with full impossibility to open a mouth and occurrence of difficulty at breath. Temperature is 37,5ºС. By the side of internal organs pathology is not revealed. Pulse is 88 in one minute, the arterial pressure is 130/85 m.Hg. In an out-patient card the therapist has noted inadequacy of behaviour of the patient, shown in an “unmotivated smile”. Not having received the help, the patientl has addressed to the surgeon who has found out, that for 10 days prior to the beginning of the disease of the patient has received a graze of the left shin during game in football,

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and after survey, conversations were established with the diagnosis.

1. What diagnosis was established by the surgeon? Prove it.2. Therapeutic tactics.3. What occurrences of symptoms are possible for expecting at absence of medical aid?4. What is pathogenesis of the given disease?

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