diphtheria myocarditis
Introduction
Introduction to diphtheria myocarditis Diphtheria myocarditis is an acute respiratory infection caused by Corynebacterium diphtheriae. It is clinically characterized by pharyngeal tonsillitis and/or laryngitis, typical grayish white pseudomembrane formation in the throat and symptoms of poisoning caused by exotoxin. It can be combined with myocarditis, called diphtheria myocarditis, the most serious complication of diphtheria and a major cause of death health search. In pathological morphology, diphtheria myocarditis manifests as myocardial hyaline degeneration or myocardial necrosis with only a small amount of cellular infiltration. Diphtheria myocarditis is caused by exotoxin of diphtheria bacilli. Due to the prevention of infectious diseases after liberation, diphtheria is very rare. 10% to 25% of patients with this disease have myocarditis. Strictly speaking, it should be called myocardial damage instead of myocarditis. disease. Diphtheria myocarditis is one of the most important complications of diphtheria, accounting for about 50% of deaths. basic knowledge The proportion of illness: 0.002% Susceptible people: more common in children Mode of infection: non-infectious Complications: arrhythmia, diphtheria myocarditis, cardiogenic shock
Cause
Causes of diphtheria myocarditis
(1) Causes of the disease
The acute infectious disease caused by diphtheria bacilli is infected with the patient or the carrier, often limited to the upper respiratory tract, forming a tough pseudomembrane, attached to the tissue underneath, tearing open, ie bleeding, the pseudomembrane begins to appear In the pharyngeal area of one side of the tonsil, severe cases can be extended to the other side of the tonsils and uvula, soft palate, pharyngeal wall and can extend to the larynx, trachea, bronchus and cause bronchial obstruction, and finally die of hypoxia, diphtheria can also be expressed as skin Type, occasionally invading the eyes, middle ear, buccal mucosa, genitalia, often secondary, systemic effects are mainly myocarditis, peripheral neuritis, caused by diphtheria exotoxin.
(two) pathogenesis
The mechanism of myocardial damage in diphtheria myocarditis is due to the release of toxins by diphtheria bacilli, which interfere with the conversion of amino acids from soluble ribonucleic acid to polypeptide structures, thereby inhibiting protein synthesis.
Diphtheria bacillus has weak invasiveness and only locally grows and reproduces in the skin and mucous membranes at the site of injury. However, the exotoxin produced is extremely toxic, and the body can produce toxic symptoms after absorption, and cause systemic pathological changes to the myocardium, adrenal gland and For peripheral nerves, diphtheria myocarditis mainly involves myocardial cells and cardiac conduction system. The pathological changes show that the heart is obviously enlarged at the early stage, the myocardial cells are turbid and swollen and steatosis, followed by multiple focal hyalinosis, granular degeneration and myocardial Cell necrosis, accompanied by polymorphonuclear leukocyte infiltration; late connective tissue hyperplasia, cardiac conduction system can be degeneration, necrosis and scar formation, leading to abnormal function of the conduction system.
The exotoxin of diphtheria can cause degeneration, necrosis and scar formation in the myocardium and heart conduction system, which is common in the first weekend of the diphtheria and the beginning of the second week. At the end of the second week, there may be restorative changes, including granulation tissue formation, myocardial lesion recovery. Collagen tissue and fibroblasts proliferate, and the scar tissue can form in the myocardium at the 3rd and 4th week of the disease.
Prevention
Diphtheria myocarditis prevention
1. Protect the susceptible population, control the infection source to isolate the patients until the symptoms disappeared, and the nasopharyngeal culture was negative.
2. Cut off the route of transmission.
3. Improve the body's immunity. It can be injected with white, hundred, broken mixed vaccine or adsorbed and purified diphtheria toxoid.
Complication
Complications of diphtheria myocarditis Complications arrhythmia diphtheria myocarditis cardiogenic shock
1. Arrhythmia Diphtheria myocarditis is prone to arrhythmia, including sinus tachycardia, sinus bradycardia, ventricular premature contraction, paroxysmal tachycardia, atrial flutter or tremor, atrioventricular and Bundle branch block, etc., in severe cases, high atrioventricular block can occur.
2. Heart failure Severe diphtheria myocarditis is extensive and severe due to myocardial damage, and the clinical manifestations of heart enlargement and congestive heart failure may occur.
3. Cardiogenic shock When diphtheria myocarditis has severe myocardial damage and a wide range, the performance of peripheral circulatory failure may occur due to the decrease of cardiac blood flow, and there may be a decrease in blood pressure and insufficient perfusion of surrounding tissues, and severe cardiac shock may occur. .
Symptom
Diphtheria myocarditis symptoms common symptoms nausea skin diphtheria dyspnea cyanosis abdominal pain respiratory tract obstruction
The disease is more common in children. Winter and spring are multiple seasons. They are mainly caused by droplets. They can also be transmitted indirectly through toys, clothes and utensils. The following clinical manifestations are available:
1. Signs of diphtheria include fever, nausea, vomiting, pharyngeal, larynx, nasal, occasional larynx formation in the skin and other areas, local lymphadenopathy, "cow neck", etc., diphtheria can still appear respiratory tract Blocking symptoms, there is a buzzing sound when inhaling or a "three concave sign".
2. Circulatory system involvement includes fatigue, pale complexion, cyanosis, difficulty breathing, etc. Physical examination has a mild to moderate enlargement of the heart, low heart sounds, fetal heart sounds, tachycardia or bradycardia (mostly atrioventricular conduction) Blocking phenomenon), apical area may appear systolic hairy murmur and diastolic galloping, extensive myocardial lesions can cause cardiogenic shock, mostly in the second week after onset, often pale skin, nausea, vomiting Symptoms such as abdominal pain, followed by cold limbs, weak pulse, decreased blood pressure, etc. In addition, the toxic effects of exotoxin of diphtheria on peripheral small blood vessels and vasomotor center may also be the cause of shock in this disease. May have signs of congestive heart failure, including symptoms of pulmonary congestion and systemic congestion, signs.
Examine
Examination of diphtheria myocarditis
1. Blood routine can have white blood cell count and increased proportion of neutrophils. In severe cases, poisonous particles can be seen in white blood cells and neutrophils.
2. Bacteriological examination at the junction of the pseudomembrane and mucosa, smear examination and culture, often can find Gram-positive bacilli or diphtheria bacilli, bacterial culture can also be positive, if necessary, can do bacterial toxin test and virulence test .
3. Other pseudomembrane collected by applying 2% potassium ferrite solution, the pseudomembrane turned black.
4. Early ECG can see ST segment depression, T wave low or inverted, sinus tachycardia is common, followed by different degrees of atrioventricular block, the prognosis of complete conduction block is dangerous, mostly in the acute phase Others may have bundle branch block, sinus bradycardia, ventricular premature contraction, paroxysmal tachycardia, atrial flutter or tremor and other abnormal ECG.
5. X-ray and echocardiography showed a mild to moderate increase in heart, and the heartbeat was generally weakened. Cardiac function tests often had changes in cardiac output and decreased ejection fraction.
Diagnosis
Diagnosis and diagnosis of diphtheria myocarditis
Clinically, patients with symptoms of infection and pseudomembrane formation in the throat may have diphtheria myocarditis if there are various manifestations of myocardial involvement, including abnormal electrocardiogram, circulatory failure or congestive heart failure. For diagnosis.
Differential diagnosis
The disease should be differentiated from rheumatic myocarditis, suppurative tonsillitis and beta-receptor hyperfunction syndrome.
1. Rheumatic myocarditis Rheumatic myocarditis often has a history of streptococcal infection such as tonsillitis or angina, anti-"O" increased, blood sedimentation increased significantly, C-reactive protein (CRP)-positive, ECG changes extended by PR interval More common, throat swab culture often has streptococcus growth, and more arthritis, in view of rheumatoid myocarditis often endocarditis, so mitral regurgitation systolic murmur is more obvious, and may be due to valve edema, Inflammation has a diastolic murmur (Carey Coombs murmur). If the heart is not enlarged, and the murmur is louder, the possibility of rheumatism is greater. Although diphtheria myocarditis has myocarditis, there are many typical diphtheria manifestations. Diastolic murmur, ECG can have ST-T changes, PR interval prolongation and T wave changes, etc., the smear staining of the cells at the junction of the pseudomembrane and mucosa, often seen diphtheria, pay attention to identify from the above points.
2. Suppurative tonsillitis The disease is acute, fever, sore throat, redness and swelling of the pharynx, a little or small piece of yellow-white exudate on the tonsil, but looser and easier to erase, no bleeding after wiping off, This feature is differentiated from diphtheria.
3. -receptor hyperactivity syndrome is more common in young women, often with certain mental factors as incentives, complaints are more variable, and objective signs are less, no fever, increased erythrocyte sedimentation rate and other evidence of inflammation, mainly as ECG ST segment , T wave changes and sinus tachycardia, oral propranolol 20 ~ 30mg after half an hour can make ST segment, T wave changes back to normal, diphtheria myocarditis on the electrocardiogram ST-T changes caused by myocardial damage, After oral propranolol, it can not return to normal in a short period of time. In addition, there is no evidence of structural heart disease such as cardiac enlargement and cardiac insufficiency in -receptor hyperactivity syndrome.
