Symptoms and complications of diphtheria

Diphtheria has an incubation period that lasts 2-12 (usually 5-7) days, after which symptoms of diphtheria appear.

Diphtheria is classified by the localization of the process and the severity of the disease. The most common forms are diphtheria of the oropharynx (pharynx) and respiratory tract. Diphtheria of the nose, eyes, ear, and genitals is also possible. These forms are usually combined with diphtheria of the oropharynx. Diphtheria of the skin and wounds occurs mainly in tropical countries.

Symptoms of oropharyngeal diphtheria are characterized by the presence of film-like plaque on the tonsils, which can spread beyond the tonsils to the soft palate, uvula, soft and hard palate. The plaque has a uniform white or gray color, is located on the surface of the tonsils ("plus tissue"), is removed with force with a spatula, and an eroded bleeding surface is exposed.

The plaques do not rub off, do not sink, and do not dissolve in water.

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Catarrhal form of diphtheria

Diphtheria of the oropharynx is diagnosed very rarely based on epidemiological, clinical and bacteriological data, when there are no plaques, there is only mild hyperemia and swelling of the tonsils. Symptoms of diphtheria of the oropharynx, as well as the nature of the plaques, allow us to divide it into the following forms:

• localized (island-like, membranous) - plaque does not extend beyond the tonsils;
• widespread - plaque spreads to the soft and hard palate, gums.

Formation of plaque on the mucous membrane of the cheeks after a chemical burn, on the wound after tooth extraction and tongue bite is possible. According to the severity of the course, these forms are classified as mild diphtheria. Mild diphtheria of the oropharynx is characterized by an acute onset with an increase in body temperature to 37.5-38.5 ° C, general malaise, sore throat (minor or moderate). Plaques appear after 24 hours, on the 2nd day they acquire a characteristic appearance. During examination, pallor of the face, moderate hyperemia of the tonsils with a bluish tint are noted. The submandibular lymph nodes, as a rule, are not enlarged, painless on palpation. Fever lasts up to 3 days. Without treatment, plaque persists for up to 6-7 days. In mild forms of diphtheria of the oropharynx (localized and widespread), swelling of the tonsils is possible.

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Toxic diphtheria

The presence of oropharyngeal edema provides grounds for diagnosing the toxic form of diphtheria, which occurs in moderate and severe forms. The severity of the course is determined by the degree of expression of the main syndromes, primarily the degree of functional changes in various organs and systems in all periods of the disease. The severity of the edema of the mucous membrane of the oropharynx and cervical tissue is only one of many signs characterizing the severity of diphtheria, often not the most important.

Subtoxic and toxic diphtheria of the oropharynx of the first degree often have a moderate course. These forms have more pronounced symptoms of diphtheria: general intoxication, higher (up to 39 ° C) and prolonged fever, pronounced asthenia, tachycardia, more severe pain in the throat. Plaques on the tonsils are widespread, sometimes only one tonsil is affected. The tonsils are edematous, brightly hyperemic. Edema of the cervical tissue is localized in the subtoxic variant in the submandibular region, and in toxic diphtheria of the first degree it extends to the middle of the neck.

Toxic diphtheria of grades II, III and hypertoxic diphtheria are characterized by the fact that the symptoms of diphtheria develop very quickly: general intoxication, chills, fever up to 40 °C and above, severe muscle weakness, headache, severe sore throat. Examination reveals pale skin, pronounced edema of the cervical tissue, which extends to the collarbones in toxic diphtheria of grade II, and below the collarbones to the chest in grade III. The edema is of a doughy consistency, painless. The submandibular lymph nodes are moderately painful, significantly enlarged, their contours are unclear due to edema and periadenitis. Examination of the mucous membrane of the oropharynx reveals diffuse hyperemia and severe swelling of the tonsils, which can close along the midline, making breathing and swallowing difficult, and giving the voice a nasal tint. On the first day, the plaque may look like a whitish web, on the 2nd-3rd day of the disease it acquires a characteristic appearance, and in this category of patients the films are dense, widespread, extend beyond the tonsils, and form folds.

In hypertoxic diphtheria, infectious toxic shock and multiple organ failure develop on the 2nd-3rd day of the disease. The hemorrhagic variant is characterized by the soaking of plaque with blood, which is why it acquires a crimson color.

Hemorrhages in the area of edema, nosebleeds and other manifestations of hemorrhagic syndrome are also observed.

In severe cases of the disease, symptoms of diphtheria, fever and intoxication persist for up to 7-10 days, the plaque is rejected at an even later date, leaving behind an eroded surface.

Diphtheria of the respiratory tract

Diphtheria of the respiratory tract (diphtheritic croup) is a common form of the disease. Diphtheritic croup can be localized (diphtheria of the larynx), widespread (diphtheria of the larynx and trachea) and descending, when the process spreads to the bronchi and bronchioles. The severity of this form of the disease is determined by the degree of stenosis (i.e. the severity of respiratory failure).

Diphtheritic croup begins with a slight increase in body temperature, the appearance of a dry, "barking" cough, hoarseness of the voice, turning into aphonia. Within 1-3 days, the process progresses, typical symptoms of diphtheria and signs of laryngeal stenosis appear: noisy breathing, accompanied by retraction of the epigastric region, intercostal spaces, supra- and subclavian fossae, jugular fossa. After a few hours - 2-3 days, signs of respiratory failure join: motor restlessness, insomnia, cyanosis, pale skin, tachycardia, increased blood pressure, followed by lethargy, convulsions, arterial hypotension. Blood tests reveal increasing hypoxemia, hypercapnia, respiratory acidosis. In adults, due to the wide lumen of the larynx, symptoms such as aphonia and stenotic breathing may be absent, the process develops slowly. Signs of respiratory failure appear on the 5th-6th day of the disease with the development of descending croup: a feeling of shortness of breath, tachycardia, pale skin, cyanosis, and auscultation reveals weakened breathing. Localized and widespread croup is often detected only by laryngoscopy - diphtheria films are found on the vocal cords. The films are easily removed and can be removed with an electric suction device.

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Diphtheria of the nose

Nasal diphtheria is the third most common form of the disease. Symptoms of nasal diphtheria begin gradually. Body temperature is normal or subfebrile. Serous or mucopurulent discharge is noted, often one-sided, maceration of the skin at the entrance to the nose appears, rhinoscopy reveals erosions, crusts, fibrinous films in the nasal passages, which can spread to the skin, mucous membrane of the maxillary sinuses. In rare cases, facial edema occurs.

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Diphtheria of the eye

The process is usually one-sided. Characteristic are swelling of the eyelids, narrowing of the palpebral fissure, and purulent-serous discharge. A fibrinous film appears on the transitional fold of the conjunctiva, which can spread to the eyeball. Swelling of the soft tissues in the orbital area is possible.

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Diphtheria of the genitals

Diphtheria of the genitals occurs in girls. Symptoms of diphtheria of the genitals are characterized by swelling of the vulva, discharge. Fibrinous films are localized in the area of the labia minora and the entrance to the vagina.

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Diphtheria of skin and wounds

Diphtheria of the skin and wounds occurs mainly in the tropics; symptoms of diphtheria of the skin and wounds are characterized by the presence of a superficial, slightly painful ulcer covered with a fibrinous film. The general condition is slightly disturbed; the course is sluggish, up to 1 month.

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Combined diphtheria

Most often, there is a combination of diphtheria of the oropharynx with diphtheria of the respiratory tract and nose, less often the eyes and genitals.

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Clinical syndromes of diphtheria

Severe toxic forms of diphtheria are characterized by damage to various organs and systems. In clinical practice, it is advisable to distinguish several clinical syndromes.

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Local manifestation syndrome

Syndrome of local manifestations (edema of the subcutaneous tissue of the neck, oropharynx, widespread fibrinous deposits, etc.). In the vast majority of cases, it is on the basis of this syndrome that a doctor can diagnose diphtheria.

Intoxication syndrome

Intoxication syndrome is observed in all patients with toxic forms of diphtheria. Characteristic are severe weakness, fever, arterial hypotension, thirst, tachycardia, decreased diuresis, anorexia and insomnia.

The severity of the intoxication syndrome in the acute period of the disease is one of the criteria for the severity of the course.

Toxic-metabolic shock syndrome

In particularly severe cases of diphtheria (fulminant form) and severe intoxication, toxic-metabolic shock develops in 3-7% of patients. It is characterized by severe DIC syndrome (manifested not only by laboratory changes, but also by clinical symptoms), severe hypovolemia, acute respiratory failure and renal failure, myocardial dysfunction (impaired contractility and conduction) and damage to the cranial nerves. In toxic-metabolic shock syndrome, there is rapid and severe damage to target cells, and subsequently, dysfunctions of many organs and systems are decompensated. With the development of toxic-metabolic shock syndrome, a fatal outcome is observed in almost 100% of cases.

Respiratory distress syndrome

Respiratory failure syndrome in severe diphtheria may be caused by the following main reasons: infectious toxic shock, laryngeal stenosis, partial obstruction of the upper respiratory tract (edema of the epiglottis, severe edema of the oropharynx with dysfunction of the soft palate, retraction of the root of the tongue, mainly in alcoholics, aspiration of the film into the trachea), descending croup, rapid intravenous, administration of large doses of diphtheria antiserum with the development of respiratory distress syndrome, obstructive bronchitis and severe pneumonia, polyneuropathy with damage to the diaphragm and accessory respiratory muscles.

Respiratory failure syndrome during its manifestation almost always determines the severity of the disease; in severe cases of diphtheria it is observed in 20% of cases.

The most common signs of respiratory failure are shortness of breath, cyanosis (acrocyanosis), depression of consciousness of varying degrees, unstable hemodynamics (arterial hypertension, tachy- and bradyarrhythmia), decreased diuresis, hypoxemia, hyper- or hypocapnia.

Laryngeal stenosis and descending croup are the most common causes of death in diphtheria (especially in the first 10 days of illness). In the later stages of the disease (after the 40th day), respiratory failure syndrome also often leads to the death of patients: it develops primarily due to a disruption of the innervation of the respiratory muscles and the addition of pneumonia.

Disseminated intravascular coagulation syndrome

Disseminated intravascular coagulation syndrome (DIC syndrome) is observed in all forms of toxic diphtheria. Clinical signs of DIC syndrome in severe forms are recorded in 15% of cases. The development of serum sickness aggravates the course of DIC syndrome.

Myocardial infarction syndrome

The heart suffers as a result of the direct action of the exotoxin. In severe forms of diphtheria, additional damaging factors are at work: hypoxic conditions of various genesis (DIC syndrome, respiratory failure, anemia), volume overloads in acute renal failure, electrolyte disturbances. Heart damage in most cases determines the severity of the patient's condition, especially from the 10th to the 40th day of the disease.

Symptoms of diphtheria in this syndrome consist of cardiac complaints, heart failure syndrome and physical data. Cardiac complaints in diphtheria are inconstant and do not reflect the severity of heart damage. During examination, the most important thing is to detect arrhythmia and pulse deficit. pallor or cyanosis. For a more accurate and early assessment of the myocardium, ECG data, echocardiography studies, as well as the results of a study of the activity of cardiac-specific enzymes are necessary.

Criteria defining severe myocardial damage with an unfavorable prognosis:

• progressive heart failure, predominantly of the right ventricular type (according to clinical data);
• severe conduction disturbances, such as atrioventricular dissociation with idioventricular rhythm, type 2 Mobitz type 2 AV block, combined with di- and trifascicular bundle branch blocks (according to ECG data);
• decreased contractility, i.e. a decrease in the left ventricular ejection fraction by less than 40% (according to echocardiography);
• a marked increase or, conversely, relatively low levels of activity of cardiac-specific enzymes in combination with the signs listed above;
• development in the late stages of the disease of electrical instability of the myocardium in the form of frequent tachyarrhythmias and ventricular fibrillation.

Myocardial damage syndrome in severe diphtheria is constantly detected; in combination with other syndromes, this is the most common cause of death in severe forms of oropharyngeal diphtheria.

Peripheral nervous system syndrome

Peripheral nervous system damage syndrome is associated with the direct effect of exotoxin on nerve fibers and autoimmune processes, and manifests itself in the form of bulbar paresis (paralysis) and polyneuropathy.

Bulbar paresis (paralysis) in toxic forms of diphtheria is detected in 50% of cases. Nasal voice and choking when taking liquid food occur. These changes are recorded both in the initial period (3-16 days) and at later stages (after 30 days) of the disease. Damage to other pairs of cranial nerves (III, VII, X, XII) is less common, paresis (paralysis) of the muscles of the pharynx, tongue, facial muscles occurs, skin sensitivity is impaired.

Polyneuropathy occurs in 18% of cases and is manifested by dysfunction (paresis or paralysis) of the limbs, diaphragm, and intercostal nerves. Polyneuropathy usually occurs after the 30th day of illness. Peripheral paresis (or paralysis) is detected with inhibition or absence of tendon reflexes, decreased muscle strength, sensory disturbances, and limited mobility of the diaphragm (determined radiographically or by excursion of the lower edge of the lungs). Patients complain of muscle weakness, sensory disturbances, numbness of the fingers, gait disturbance or inability to walk, a feeling of shortness of breath, and dyspnea. Limb damage always occurs before respiratory disorders, and the function of the respiratory muscles is restored earlier.

The severity of polyneuropathy is assessed based on the patient's complaints and the results of conventional clinical examination methods (determination of reflexes, skin sensitivity, respiratory rate, etc.). Electroneuromyography can reveal a significant dissociation between the rate of development and severity of clinical signs and the degree of electrophysiological disorders. ENMG studies reveal a reduced speed of impulse conduction along the nerves and a decrease in the amplitude of the M-response not only with obvious clinical signs, but also in their absence. Electroneuromyography changes occur 2-3 weeks before clinical manifestations. Polyneuropathy most often and severely occurs in people who abuse alcohol.

Kidney failure syndrome

Kidney damage in diphtheria is usually characterized by the term "toxic nephrosis". In severe cases of the disease, kidney damage is manifested by macrohematuria, leukocyturia, cylindruria, and proteinuria.

The direct damaging effect of exotoxin on the renal parenchyma is minimal, does not lead to clinical manifestations of renal failure and does not affect the severity of the course. The development of acute renal failure in diphtheria is determined only by secondary factors of influence:

• development of severe DIC syndrome and hypovolemia on the 5th-20th day of illness;
• development of multiple organ (septic) failure after 40 days;
• iatrogenic causes (overdose of antidiphtheria serum, administration of aminoglycosides).

With the development of acute renal failure, patients experience oligoanuria, increased urea levels, and to a lesser extent, creatinine and potassium in the blood plasma. A greater increase in urea levels compared to creatinine levels is associated with high activity of catabolic processes. With an increase in the concentration of potassium in the plasma, asystole and death are possible.

Syndrome of non-specific infectious complications

The severity of this syndrome depends on the severity of diphtheria and the damage to the immune system. The syndrome of non-specific infectious complications can occur both in the first week of the disease and at a later date (after the 30th day of illness). Most often, pneumonia, bronchitis, urinary tract infection are recorded; the development of tonsil abscess, peritonsillar abscess is possible.

These complications are much more often observed in people who abuse alcohol. They are caused by inadequate sanitation of the tracheobronchial tree during prolonged artificial ventilation, catheterization of the bladder and central veins. Sepsis may develop even in the late stages of the disease.

Complications of diphtheria

All the above syndromes and symptoms of diphtheria are associated with the action of the toxin, a local process. They determine the severity, course and outcome of the disease, so they are considered as characteristic manifestations, not complications. In severe diphtheria, complications of a non-specific nature are possible, which can prevail in the clinical picture and even be the direct cause of a fatal outcome.

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Iatrogenic complications of diphtheria

The following types of iatrogenic complications are possible.

• Complications associated with the development of serum sickness due to the administration of diphtheria antiserum: exanthema, myocarditis, polyarthritis, "exacerbation" of DIC syndrome, kidney damage, respiratory failure; anaphylactic shock is possible.
• Complications caused by long-term administration of glucocorticosteroids, which leads to suppression of the immune system, hypokalemia (with the development of muscle weakness, extrasystole, sluggish intestinal peristalsis, with bloating), erosive gastritis, trophic disorders.
• Kidney damage due to aminoglycoside use.

Mortality and causes of death in diphtheria

Severe symptoms of diphtheria lead to a fairly high mortality rate, which is 10-70%. The main causes of death are heart damage, paralysis of the respiratory muscles, asphyxia in diphtheria of the respiratory tract, infectious toxic shock, and secondary bacterial complications.