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Lecture notes, cheat sheets
Infectious diseases. Diphtheria. Etiology, clinical picture, diagnosis, complications. Features of the course of diphtheria (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 2. Diphtheria. Etiology, clinic, diagnostics, complications. Features of the course of diphtheria Diphtheria is an acute infectious disease with an airborne transmission mechanism caused by diphtheria toxigenic corynebacteria, characterized by croupous or fibrinous inflammation of the mucous membrane at the gates of infection (in the pharynx, nose, larynx, trachea, less often) in other organs and general intoxication. Etiology. The causative agent is a toxigenic diphtheria bacillus, thin, slightly curved with thickenings at the ends, does not form spores and capsules, gram-positive, stable in the external environment, tolerates drying well, is sensitive to high temperature and disinfectants. Diphtheria exotoxin is the main factor in the pathogenicity of diphtheria bacilli. It belongs to potent bacterial toxins, has a tropism for the tissues of the nervous and cardiovascular systems, adrenal glands. Epidemiology. Sources of infection - a sick person or a carrier of toxigenic strains of diphtheria bacteria. A patient with diphtheria can be contagious on the last day of the incubation period and during the height of the disease. The route of transmission is airborne. Due to the long-term preservation of the viability of microorganisms on household items, transmission of infection through these items is possible, ml. el. household contact. Immunity after diphtheria infection is unstable. Pathogenesis. Having entered the body, the pathogen stops in the area of the entrance gate (in the pharynx, nose, larynx, on the mucous membranes of the eyes, genitals, etc.). There it multiplies and produces exotoxin, under the influence of which coagulative necrosis of the epithelium, vasodilation and increase in their permeability, sweating of exudate with fibrinogen and the development of fibrinous inflammation occur. The toxin produced by the pathogen is absorbed into the blood and causes general intoxication with damage to the myocardium, peripheral and autonomic nervous system, kidneys, and adrenal glands. Diphtheria bacillus vegetates on the mucous membranes of the pharynx and other organs, where croupous or diphtheria inflammation develops with the formation of films. Classification. Depending on the localization of the inflammatory process, diphtheria of the oropharynx, nose, larynx, eyes, ear, external genital organs, and skin are distinguished. According to the prevalence of raids, localized and widespread forms are distinguished. According to the severity of the toxic syndrome - subtoxic, toxic, hemorrhagic, hypertoxic forms. Clinic. The following periods of the disease are distinguished: incubation period (from 2 to 10 days), peak period, recovery period. With a localized form of diphtheria, the onset of the disease is acute, with an increase in body temperature to 37-38 ° C. General intoxication is not expressed: headache, malaise, loss of appetite, pallor of the skin. The pharynx is moderately hyperemic, there is moderate or mild pain when swallowing, swelling of the tonsils and palatine arches, fibrinous membranous plaques are formed on the tonsils, regional lymph nodes are slightly enlarged. Plaques on the tonsils look like small plaques, often located in lacunae. The membranous form is characterized by the presence of raids in the form of a translucent film. They are gradually impregnated with fibrin and become dense. At first, the film is removed easily and without bleeding, later accompanied by bleeding. The island form of diphtheria is characterized by the presence of single or multiple plaques of irregular shape in the form of islands. Sizes from 3 to 4 mm. The process is often bilateral. The catarrhal form of diphtheria is characterized by minimal general and local symptoms. Intoxication is not expressed. Subfebrile temperature, there are unpleasant sensations in the throat when swallowing. Hyperemia and swelling of the tonsils are noted, raids are absent. With a common form of pharyngeal diphtheria, the onset is acute, intoxication is pronounced, body temperature is high, regional lymph nodes are enlarged. Complaints of sore throat, malaise, loss of appetite, headache, weakness, lack of appetite, pale skin. Examination of the oropharynx reveals hyperemia and swelling of the mucous membranes of the palatine tonsils, arches, and soft palate. Toxic diphtheria of the pharynx: acute onset (with an increase in temperature to 39-40 ° C), severe intoxication. When examining the oropharynx, hyperemia and swelling of the mucous membranes of the palatine tonsils are noted with a sharp increase in the tonsils, significant swelling of the mucous membrane of the pharynx and the formation of plaque 12-15 hours from the onset of the disease in the form of an easily removable film. On the 2-3rd day, the plaque becomes thick, dirty gray in color (sometimes lumpy in shape), moving from the tonsils to the soft and hard palate. Breathing through the mouth may be difficult, and the voice becomes choked. Regional lymph nodes are enlarged, painful, and the surrounding subcutaneous tissue is edematous. An important sign of toxic diphtheria is swelling of the tissue in the neck. With toxic diphtheria of the 39st degree, the swelling spreads to the middle of the neck, with the 40nd degree - to the collarbone, with the XNUMXrd degree - below the collarbone. The general condition of the patient is serious, high temperature (XNUMX-XNUMX °C), weakness. Disorders of the cardiovascular system are observed. Diphtheria of the larynx (or true croup) is rare and is characterized by croupous inflammation of the mucous membrane of the larynx and trachea. The course of the disease progresses rapidly. The first stage is catarrhal, its duration is 2-3 days. At this time, body temperature rises and hoarseness increases. The cough is rough and barking at first, but then loses its sonority. The next stage is stenotic. It is accompanied by an increase in stenosis of the upper respiratory tract. Noisy breathing is observed, accompanied by increased work of the auxiliary respiratory muscles during inhalation. During the third (asphyxtic) stage, severe gas exchange disorders are observed (increased sweating, cyanosis of the nasolabial triangle, loss of pulse at the height of inspiration), the patient experiences anxiety and restlessness. The hemorrhagic form is characterized by the same clinical symptoms as toxic diphtheria of the oropharynx of II-III degree, but on the 2-3rd day the syndrome of disseminated intravascular coagulation develops. Filmy deposits become saturated with blood and turn black. Nosebleeds, bloody vomiting, and bloody stools occur. Diphtheria of the nose, conjunctiva of the eyes, and external genitalia has almost never been encountered lately. Complications that arise from toxic diphtheria of II and III degrees and from late treatment: in the early period of the disease, symptoms of vascular and heart failure increase. Detection of myocarditis occurs more often in the second week of illness and is manifested by a violation of the contractility of the myocardium and its conduction system. Reversal of myocarditis occurs slowly. Mono- and polyradiculoneuritis are characterized by flaccid peripheral paresis and paralysis of the soft palate, muscles of the limbs, neck, and trunk. A dangerous complication for life is paresis and paralysis of the laryngeal, respiratory intercostal muscles, and diaphragm. The hypertoxic form of diphtheria is characterized by severe intoxication, body temperature rises to 40-41 ° C, consciousness is darkened, indomitable vomiting may appear. The pulse is frequent, weak, blood pressure is lowered, the skin is pale. Swelling of the oropharyngeal mucosa is pronounced, rapidly spreading from the cervical tissue below the collarbones. The general condition of the patient is severe, the skin is pale, cyanotic, the pulse is filiform, the heart sounds are deaf, the blood pressure decreases, death may occur on the first day. Diphtheria of the larynx (diphtheria true croup). The clinical syndrome is accompanied by a voice change up to aphonia, a rough "barking" cough and difficult stenotic breathing. The disease begins with a moderate increase in temperature, mild intoxication, the appearance of a "barking" cough and a hoarse voice. Stenosis of the XNUMXst degree: difficult breathing, noisy breathing, hoarseness of voice, rapid breathing, slight retraction of the compliant parts of the chest. The cough is rough, barking. Stenosis II degree: more pronounced noisy breathing with retraction of compliant chest areas, aphonic voice, silent cough. Attacks of stenotic breathing become more frequent. Stenosis III degree: constant stenotic breathing, inhalation is lengthened, difficult, breathing is noisy, audible at a distance, aphonia, silent cough, deep retraction of the chest, respiratory failure. Cyanosis of the nasolabial triangle, cold sticky sweat, frequent pulse. The child is restless, rushing about. Breathing in the lungs is bad. This period of stenosis III degree is called transitional from the stage of stenosis to the stage of asphyxia. Stenosis IV degree: the child is lethargic, adynamic, breathing is frequent, superficial, general cyanosis. The pupils are dilated. The pulse is frequent, thready, arterial pressure is reduced. Consciousness is obscured or absent. Breath sounds in the lungs are barely audible. Nasal diphtheria: the inflammatory process is localized on the nasal mucosa. The disease begins gradually, without disturbing the general condition. Discharge from the nose appears, which at first have a serous color, then a serous-purulent or sanious character. When examining the nasal cavity, there is a narrowing of the nasal passages due to swelling of the mucous membrane, erosions, ulcers, crusts, spotting are found on the nasal membrane. The occurrence of edema in the region of the bridge of the nose and paranasal sinuses indicates a toxic form of diphtheria. The course of the disease is long. Diphtheria of the eyes is divided into croupous, diphtheria, catarrhal. The croupous form begins acutely, the temperature is subfebrile. First, one eye is involved in the inflammatory process, then the other. The skin of the eyelids is edematous, hyperemic. The cornea is not affected. Fibrinous films are located on the mucous membranes, when plaque is removed, the mucous membrane bleeds. The diphtheria form begins acutely, with febrile temperature, intoxication. The raids are dense and are located not only on the mucous membrane of the eyelids, but also pass to the eyeball. The eyelids are closed, the skin of the eyelids is edematous, the color of a ripe plum. Eyelids turn out with great difficulty. There is a moderate serous-bloody discharge from the eyes. The cornea may be affected and vision may be impaired. The catarrhal form of diphtheria of the eyes is characterized by swelling and hyperemia of the mucous membranes, there are no fibrinous films. Diphtheria of the external genital organs is characterized by tissue edema, hyperemia with a cyanotic tint, the appearance of fibrinous films on the labia majora or foreskin, and an increase in inguinal lymph nodes. Fibrinous plaques are dense, extensive and pass to the mucous membranes of the labia minora, vagina, and surrounding skin. The appearance of edema of the subcutaneous tissue in the inguinal region and on the thighs indicates a toxic form of diphtheria. Complications: myocarditis, nephrosis, peripheral paralysis. Diagnostics. Based on clinical and laboratory data, the presence of toxigenic diphtheria bacilli is determined, in peripheral blood - leukocytosis with a shift to the left, a decrease in the number of platelets, an increase in blood clotting and retraction of a blood clot. Differential diagnosis is carried out with tonsillitis, infectious mononucleosis, false croup, membranous adenoviral conjunctivitis (with diphtheria of the eye). Treatment. Patients with diphtheria are subject to mandatory hospitalization, they are prescribed bed rest, etiotropic treatment, the earliest, intramuscular administration of antitoxic antidiphtheria serum in appropriate doses. Detoxification therapy is carried out (including fresh frozen plasma, rheopolyglucin, hemodez), as well as non-specific pathogenetic therapy, intravenous drip infusions of protein preparations, such as albumin, glucose solution. Administer prednisolone. Antibacterial therapy, cocarboxylase, vitamin therapy. Diphtheria croup requires rest, fresh air. Sedatives are recommended. The weakening of laryngeal stenosis contributes to the appointment of glucocorticoids. Steam-oxygen inhalations are used in chamber tents. Suction of mucus and films from the respiratory tract with the help of an electric suction can have a good effect. Given the frequency of pneumonia in croup, antibiotic therapy is prescribed. In the case of severe stenosis and during the transition of stage II of stenosis to stage III, nasotracheal intubation or lower tracheostomy is used. Prevention. Active immunization is the backbone of successful diphtheria control. Immunization with adsorbed pertussis-diphtheria-tetanus vaccine (DTP) and adsorbed diphtheria-tetanus toxoid (DT) applies to all children, subject to contraindications. Primary vaccination is carried out starting from the age of 3 months three times, 0,5 ml of the vaccine with an interval of 1,5 months; revaccination - with the same dose of vaccine 1,5-2 years after the end of the vaccination course. At the age of 6 and 11 years, children are revaccinated only against diphtheria and tetanus with ADS-M toxoid. Author: Gavrilova N.V. << Back: Modern understanding of infectious diseases. Vaccination. Vaccination calendar, complications after vaccination (Infectious diseases. Vaccination. Vaccination calendar, complications after vaccination) >> Forward: Whooping cough. Etiology, pathogenesis, clinic, diagnosis, treatment
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