Some standard content:
(GB17021-1997
Diagnostic Standard for Keshan Disease
This standard is revised and supplemented on the basis of the "Standard for the Prevention and Control of Keshan Disease (Trial)" (formulated in 1982), with reference to relevant data on the diagnosis and identification of cardiomyopathy at home and abroad. From the date of implementation of this standard, the original "Diagnostic Standards and Clinical Classifications of Various Keshan Diseases (Draft)" will be invalid. Appendices A, B and C of this standard are appendices to the standard. Appendices D and E of this standard are informative appendices. This standard was proposed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Keshan Disease Research Institute of the China Endemic Disease Prevention and Control Research Center, and the Yunnan Keshan Disease Prevention and Control Research Center and the Endemic Disease Research Institute of Bethune Medical University participated in the drafting. The main drafters of this standard: Xia Deyi, Yu Weihan, Ni Guozhi, Niu Cun Dragon. This standard is interpreted by the Chinese Academy of Preventive Medicine, the technical unit entrusted by the Ministry of Health. 1 Scope
This standard specifies the diagnostic points of Keshan disease and the technical indicators of clinical classification. This standard is applicable to the diagnosis of individual cases in Keshan disease areas and the differentiation from other myocardial diseases or heart diseases. 2 Diagnostic principles
Only when the following three conditions are met can Keshan disease be diagnosed: a) Keshan disease characteristics: It is often found in a certain area, time and population. Appendix A (Appendix to the standard) 1 Foreign population can only develop the disease when they live the same as local farmers in the disease area for more than three consecutive months; b) Have symptoms and signs of heart disease (enlarged heart or abnormal shape, pulsation, rhythm or electrocardiogram), or symptoms and signs of heart failure (shortness of breath, palpitations, gallop rhythm, enlarged liver and edema); c) And other diseases can be ruled out.
3 Diagnostic criteria
Having the characteristics of Keshan disease, and any one or one of the following manifestations can rule out other diseases: 3.1 Enlarged heart. See Appendix B (Standard Appendix) for the inspection methods and criteria. 3.2 Acute or chronic heart failure.
3.3 Arrhythmia:
a) Multiple premature ventricular beats (more than 6 times per minute, increased after exercise); b) Atrial fibrillation:
c) Paroxysmal ventricular or supraventricular tachycardia. 3.4 Gallop rhythm.
3.5 Embolism in the brain or other parts.
3.6 ECG changes:
a) Atrioventricular block;
b) Bundle branch block (except incomplete right bundle branch block); c) ST-T changes:
d) Significant prolongation of Q-T interval:
e) Multiple or multi-source ventricular premature beats;
f) Paroxysmal ventricular or supraventricular tachycardia; g) Atrial fibrillation or atrial flutter;
h) Abnormal P wave (enlargement of the left and right atria or increased load on both atria). For ECG examination methods and judgment criteria, see Appendix C (Standard Appendix). 3.7 X-ray findings: Cardiac enlargement (see B2 and B3 in Appendix B for examination and judgment). 3.8 Changes in echocardiography (including Doppler echocardiography (D-UCG): a) Enlargement of left atrial and left ventricular diameters; b) Ejection fraction (EF%) decreased to below 40%; c) Ventricular wall activity showed segmental dyskinesia; d) Peak A of mitral blood flow spectrum was greater than peak E. 3.9 Cardiac changes:
a) Pre-ejection period (PEP)/left ventricular ejection period (LVET) ≥ 0.40b) A wave ratio (A/EO ≥ 15%.
3.10 Laboratory examination:
a) Changes in myocardial enzyme spectrum;
b) Increased aspartate aminotransferase (GOT) and alanine aminotransferase (GPT), GOT/GPT>1; c) Increased lactate dehydrogenase (LDH) and its isoenzyme 1 (LDH), LDH>LDH2d) Increased creatine phosphokinase (CK or CPK) and its isoenzyme 2 (CPK2). 4 Clinical classification standards
According to the course of disease and cardiac function, it is divided into the following four types: 4.1 Acute type
Severe acute Keshan disease is defined as acute onset with acute myocardial ischemia and necrosis [see Appendix D (suggested Appendix)] or acute cardiac decompensation with any of the following manifestations: a) cardiogenic shock;
b) cardiocerebral syndrome caused by severe arrhythmia; c) acute pulmonary edema or acute left heart failure. 4.2 Chronic type
The heart is mostly moderately or significantly enlarged, manifested as chronic cardiac decompensation-congestive heart failure. 42,1 Natural chronic type: It is a group of chronic types without acute, subacute, chronic and latent medical history, and the disease develops slowly without knowing it. Currently, most cases are diagnosed with this type. www.bzxz.net
4.2.2 Chronic type classification: According to the classification of cardiac function, it is divided into chronic type II, IIII, and IV. 4.2.3 Slow-onset acute attack: Slow-onset patients with acute symptoms in the disease area and in the frequent season. 4.3 Subacute type
4,31 Definite subacute type: Keshan disease occurring in weaned and preschool children. The onset is relatively slow, and congestive heart failure and/or cardiogenic shock (in a minority) usually occur about a week after the onset of symptoms, with congestive heart failure as the main manifestation. There are often facial edema, hepatomegaly and gallop rhythm. Some cases may have myocardial necrosis. 4.3.2 Suspected subacute type: If there is mental depression, loss of appetite, cough and asthma, abdominal pain and vomiting, eyelid or lower limb edema, and there is also low blood pressure, low pulse pressure, significantly increased heart rate, weakened whole heart sounds or first heart sound, etc., timely treatment should be given as suspected subacute type, and the diagnosis can be confirmed once signs of heart failure appear. 4.3.3 Subacute to chronic: Subacute Keshan disease that has not been cured within three months of onset is called chronic.
4.4 Latent
Heart function class I (normal), the heart is slightly enlarged or not enlarged during the compensatory stage of heart function, and the electrocardiogram often shows ventricular premature beats or complete right bundle branch block or ST-T changes. 5 Differential diagnosis
5.1 Acute type needs to be differentiated from acute myocarditis, acute myocardial infarction, acute gastritis, and biliary ascariasis. 5.2 Chronic type needs to be differentiated from dilated cardiomyopathy (DCM), peripartum cardiomyopathy, coronary heart disease, pericarditis (chronic) and rheumatic heart disease.
5.3 Subacute type needs to be differentiated from acute and chronic glomerulonephritis or nephropathy, bronchopneumonia (combined with heart failure), endocardial fibroelastosis, and pericarditis.
5.4 Latent type needs to be differentiated from focal myocarditis, hypertrophic non-obstructive cardiomyopathy, and cardiac neurosis. 5.5 For the differential diagnosis criteria, please refer to Appendix E (Suggested Appendix). Appendix A
(Standard Appendix)
Criteria for the region, time, and population of Keshan disease A1 Regionality
The disease area in my country is between 21° and 53° north latitude and 89° and 135° east longitude. The disease areas in 15 provinces, municipalities, and autonomous regions, including Heilongjiang, Jilin, Liaoning, Inner Mongolia, Hebei, Henan, Shandong, Shanxi, Shaanxi, Gansu, Sichuan, Yunnan, Tibet, Guizhou, and Hubei, have been confirmed. The agricultural population in the disease areas is about 100 million. Most of them occur in remote areas of the above-mentioned areas, inconvenient transportation, and difficult living in rural areas.
A2 Population selectivity
The agricultural population in the disease area and the local farmers who live in the disease area from non-disease areas to the disease area live the same as women in the childbearing period (20-40 years old) and preschool children (2-7 years old) after weaning (regardless of gender). In the year of high incidence, 1/2-1/3 of the patients often have more than 2 cases in the family, showing family high incidence. A3 Time
It is high annually (i.e., the outbreak year) and seasonally. The acute and subacute types are high in the hot summer in the southwest (Yunnan and Sichuan), but the latter is more common in May to July, and it is high in the cold winter (November to March of the following year) in the north: the chronic and latent types can occur all year round.
Appendix B
(Standard Appendix)
Methods and criteria for examination of enlarged heartB1 Methods and judgment of cardiac examination
B1.1 Examination method
The patient lies in the supine position, and the relative dullness boundary of the heart is determined by the light diagnosis method. B1.2 Judgment
B1.2.1 Mild enlargement (mild enlargement): The dullness boundary of the left border of the heart is 0.5-1.0 cm beyond the left clavicle midline in the fifth intercostal space. B1.2.2 Moderate enlargement (moderate enlargement): The left border of the heart exceeds the left clavicle midline, but does not exceed the left anterior axillary line. B1.2.3 Significant enlargement (significant enlargement): The left border of the heart exceeds the anterior axillary line. B2 X-ray examination method
B2.1 X-ray film requirements
In the state of natural deep inspiration and no breath holding, take the heart image in the posteroanterior standing position and left lateral position (abbreviated as frontal and lateral position) respectively (must include the chest and ribs). According to the need, the left anterior oblique position (55°～60°) and the right anterior oblique position (45°50°) can be simultaneously irradiated, and sulfuric acid lock can be taken orally to make the esophagus visible. The distance from the focus to the film clamp in the anteroposterior position is 200cm, and that in the lateral and oblique positions is 150cm. It is advisable to irradiate with high voltage and short time, preferably less than 0.1s (Fuwai Hospital uses more than 100kV, exposure time 0.02～0.06s, and no filter is added to the large focus).
B2.2 Cardiac X-ray measurement method
B2.21 Measurement of heart area: When the measured heart area in the anteroposterior film is 11% to 35% larger than the expected area, it is mildly enlarged; 36% to 60% is moderately enlarged; and more than 61% is significantly enlarged. B2.2.2 Measurement of cardiothoracic ratio: This method is simple and easy to perform, but it is greatly affected by body type and transverse position. Therefore, it is generally required to be measured with an inspiratory X-ray film (the surface of the diaphragm is at the level of the sixth anterior rib or the tenth posterior rib of the hand), and this method is not suitable for transverse and vertical heart. In adults, a cardiothoracic ratio greater than 0.5 indicates an enlarged heart, 0.51 to 0.55 indicates a mild enlargement, 0.56 to 0.60 indicates a moderate enlargement, and more than 0.61 indicates a significant enlargement. The cardiothoracic ratio of children over 2 years old is basically the same as that of adults, and the upper limit of the normal value of the cardiothoracic ratio under 2 years old can reach 0.60.
B3 Criteria for judging X-ray abnormalities of various types of Keshan disease
Based on the clinical diagnosis of various types of Keshan disease, their respective line performances are as follows. B3.1 Acute Keshan disease
a) Both lungs have varying degrees of congestion, interstitial edema or combined alveolar edema; b) The heart is flask-shaped, aortic-shaped, and a few are mitral-shaped, with varying degrees of low myocardial tension; c) About 1/3 to 2/3 of the hearts are slightly enlarged, and moderate enlargement is rare. 1/3 of the patients have small hearts. The left and right ventricles are mainly enlarged, followed by the left and right atria;
d) The pulmonary artery segment is not protruding, and the aorta and superior vena cava are normal; e) Most of the heart beats are weakened.
B3.2 Subacute Keshan disease
a) Both lungs have varying degrees of congestion and interstitial edema, and a few are combined with alveolar edema (about 1%) or pulmonary hypertension (2%);
b) The heart is mostly ordinary in shape, followed by intermediate and spherical (60%, 25%, and 15% respectively), with varying degrees of low cardiac tension:
c) In most cases, the heart is moderately to significantly enlarged (73%), followed by mild enlargement (20%), and a few early or mild cases have a small heart (7%). The left and right ventricles are enlarged most, followed by the left and right atria, and the left side of the atrial and ventricular enlargement is more serious than the right side: d) The pulmonary artery segment is slightly concave (40%), straight and slightly convex (60%), the aortic knot is normal (62%) or reduced (38%), and the superior vena cava is normal (68%) or slightly dilated (32%); e) Most heart beats are weakened (80%), followed by normal beats (16%), a few have irregular beats (3%) and are combined with localized pulse disappearance and abnormal beats (2%). B3.3 Chronic Keshan disease
a) Most cases have varying degrees of pulmonary congestion and interstitial edema (90%), a few are combined with alveolar edema (4%) and pulmonary hypertension (5%), and in addition, the pulmonary blood of patients with heart function grade II is close to normal (9%): b) The heart morphology is mostly normal (74%), and the others are normal aorta, normal mitral valve and intermediate type. Myocardial tension decreased to varying degrees, and the septal surface of the heart widened: c) Most hearts were moderately to significantly enlarged (96%), and a few hearts were slightly enlarged (4%). Each room and chamber enlarged to varying degrees, and the ventricle was generally heavier than the atrium, and the left side was heavier than the right side. In very few cases, the right atrium and chamber were significantly enlarged; the pulmonary artery segment was slightly concave (20%), straight and slightly convex (77%), and moderate protrusion was less common (3%), the aortic knot was normal or shrunken (18% and 82% respectively), the superior vena cava and azygos vein were dilated to varying degrees (63%), and the number of non-dilated cases was less (37%); the heart beat was weakened (79%), the beat was irregular (9%), and a few patients had local abnormal beats, mainly absent and abnormal beats at the apex (6%), and the number of cases with normal beats was also less (6%). B3.4 Latent Keshan disease
a) All cases have normal pulmonary blood;
b) Heart shape is mostly close to normal, myocardial tension is good (88%), and a few have poor myocardial tension (12%); c) The heart is not large or slightly enlarged, and the left ventricle is slightly enlarged in most cases (95%), and the right ventricle is slightly enlarged in a few cases (3%):
d) The pulmonary artery segment, aortic node, and superior vena cava are all within the normal range; e) Most cases have normal heart beats, and a few cases have weakened or disappeared left ventricular apex beats. Appendix C
(Standard Appendix)
Electrocardiogram examination method and judgment criteria
C1 Electrocardiogram examination method
Requirements for instruments and inspection precautions:
C1.1 A single-lead electrocardiogram is sufficient, but damping verification must be performed. The damping of the electrocardiogram should be moderate, that is, normal. Excessive or insufficient damping can lead to non-pathological ST-T changes. Therefore, before checking the patient, it is necessary to set the standard voltage (1.OmV) and check the instrument damping at the same time (see Figure C1). Only when there is no error can the inspection be carried out to reduce the error. Damping positive band
With fat too large
Damping fat too small
Figure C1 only Instrument damping
C1,2 When the skin is rough or unclean, use alcohol to scrub it vigorously to make the skin close to the electrode and conduct electricity well to prevent (skin or alternating current) interference.
C1.3 When checking the patient, 12 leads are made: I, II, II, aVR, aVL, aVF, Vi-6, and V, R are added when necessary; 9 leads can be made during the general survey (chest leads are Vl, V3, Vs, and the others are the same). Paper speed 25mm/s. C2 Judgment criteria
Judgment criteria are based on the electrocardiogram examination part of the "Keshan Disease Prevention and Control Manual" (published by the China Endemic Disease Prevention and Control Research Center in 1989). Combined with the special situation of Keshan disease, the following points are emphasized: C2.1 Low voltage:
refers to the R+S wave of the three standard leads I, II, II and the pressurized unipolar limb leads aVR, aVL, and aVF being less than 0.5mV or the R+S wave of the Vi~6 precordial leads being less than 1.OmV. C2.2 Atrial load:
a) Left atrial load - P wave width increases, more than 0.12s for adults and more than 0.09s for children: P wave width and notch are called mitral valve type P wave: V, P wave terminal potential (PTF) increases, that is, V, negative P wave width (s) × depth (mm) ≤ -0.03mms, children ≤ -0.015mms.
b) Right atrial load - P waves of IⅡ, IIII, and aVF are high and sharp (more than 0.25mV). c) Bi-atrial load-
-It is characterized by a "mixed type" with left and right atrial load. The front part of the P wave represents the right atrium, so when the right atrial load is indicated, the II and IIP waves are upward (higher than 0.25mV), and the rear part of the P wave indicates the left atrial load, and the P wave of III is flat or negative (downward): or the amplitude of the P wave in each lead (all) is widened by >0.11s; or the biphasic amplitude of the P wave of Vi and Vz is >0.5mV. Appendix D
(Suggested Appendix)
Diagnosis of myocardial necrosis and the criteria for determining cardiac insufficiencyD1 Electrocardiographic manifestations of myocardial necrosis
D1.1 Findings of acute myocardial injury: ST segment elevation >4mm (subepicardial) or ST segment depression ≥3mm (subendocardial) in any lead, with or in combination with abnormal Q waves or clinical manifestations of myocardial necrosis. D1.2 Findings of old myocardial necrosis: The Q wave in the R wave-dominant lead is larger than 1/4 of the R wave, with a duration of ≥0.04s, or is QS-shaped, especially in the precordial leads. No clinical findings of myocardial necrosis. D2 Clinical and laboratory findings of myocardial necrosis
D2.1 General findings: elevated body temperature (37.5-38°C), increased leukocytosis (15,000-20,000/mm2), and left shift of nuclei. ESR (tube length 300mm, scale 200mm) Male >15mm/1 hour (>20mm/1 hour for those over 50 years old); Female >20mm/1 hour (>30mm/1 hour for those over 50 years old). D2.2 Enzymatic changes: See Table D1.
Table D1 Enzyme changes
Normal value
8~40 units
50~400 units
0~20 units
55~140 units
Time when alcohol begins to rise
Time to reach high peak
24~48h
Time when enzyme drops to normal
10~15d
Both myocardial enzyme spectra listed above increase by more than two times and change with time. Note that the normal values vary due to different methods. D3 Criteria for judging cardiac insufficiency
D3.1 Based on the patient's subjective symptoms (same as the judgment of cardiac function of general heart disease, omitted). D3.2 Instrumental examination criteria for cardiac insufficiency: D3.2.1 Impaired systolic function: Ejection fraction less than 40% (echocardiographic examination): pre-ejection period/left ventricular ejection period ≥
0.40 (echocardiographic or electrocardiographic examination); mVCF≤0.8C/s; SV≤40mL or CI<2.3L/(m2min). If any of the above occurs, it can be considered that there is impaired systolic function. D3:2.2 Impaired diastolic function: A wave rate ≥ 15% (seen on the echocardiogram); reduced left ventricular compliance: low EF slope < 65 mm/s (M-mode echocardiogram); slow left ventricular descent rate ≤ 70 mm/s (M-mode echocardiogram); mitral valve anterior leaflet B point platform (M-mode echocardiogram); mitral valve blood flow A peak greater than E peak (Doppler echocardiogram). Those who present any of the above items can be considered to have impaired diastolic function.
D3.3 The objective criteria for determining the degree of cardiac insufficiency are shown in Table D2. Table D2 Instrumental examination findings of different degrees of heart failure
Mild 1 grade
Chinese grade
Severe W grade
"A wave rate" (A/EO)
1) mainly represents diastolic function, left ventricular hyperresponsiveness, and myocardial stiffness, and the remaining periods represent systolic function. Note: One of the five items and the exclusion of other causes indicates heart failure. Appendix E
PEP/LVET
0.44~0.65
E1 Differentiation of acute Keshan disease
(Appendix of suggestions)
Differential diagnosis criteria of Keshan disease
E1.1 Acute myocarditis: Myocarditis is divided into acute and chronic. Acute Keshan disease often needs to be differentiated from acute myocarditis . Pay attention to whether there is a history of infection. The pathogens include bacteria, fungi, parasites, rickettsia and viruses. Diphtheria myocarditis is the most common bacterial infection and has a high mortality rate. In recent years, viral myocarditis has gradually increased. The key points of differentiation are: those caused by infection have an increase in white blood cells, especially the increase in neutrophils is more obvious than the acute type, while those caused by viruses may have a decrease in white blood cells, an increase in fractional lymphocytes, and an increase in serum myocardial enzyme activity that is not as obvious as the acute type, especially GOT, LDH and CPK and their isoenzymes. Specific antibodies caused by viral infections often appear within one week after onset, and the titer is generally highest in the third week. Therefore, serum samples can be taken once in the acute phase and once in the recovery phase of 2 to 3 weeks. This is called a double (paired) serum test. The titers of the two times are compared: if the latter is higher than the former 4 times or more has diagnostic value E1.2 Acute myocardial infarction (AMI): It develops suddenly, accompanied by cardiogenic shock, severe arrhythmia or heart failure and ST-T changes on the electrocardiogram, especially the single-phase curve (upward or downward), which is very similar to the acute type, but the difference is that AMI often occurs in older people (over 45 years old), while young people are mostly male. They often have angina pectoris or discomfort in the precordial area. The electrocardiogram often shows obvious ST-T changes, and there is a systematic evolution process, combined with abnormal Q waves. Keshan disease rarely presents with the latter, and most of the risk factors for coronary heart disease are not present, such as hypertension, hyperlipidemia, obesity, etc. E1.3 Acute gastritis: upper abdominal discomfort, nausea, vomiting, sometimes vomiting bile (vomiting yellow water), fatigue, cold limbs, etc. are similar to the acute type. Similar, but without cardiac signs: such as small heart, no arrhythmia, and more importantly, no abnormal electrocardiogram. This disease often has a history of overeating or eating unclean food, often with abdominal pain, diarrhea, etc. E1.4 Biliary tract worm disease: abdominal pain, nausea, vomiting, vomiting yellow water (bile) are easily confused with acute Keshan disease in children, but biliary worm disease presents paroxysmal upper abdominal pain, colic, abdominal worm mass (visible on X-ray), muscle tension and tenderness in the upper abdomen, and no cardiac symptoms and signs. E2 Differentiation of chronic Keshan disease
E2.1 Dilated cardiomyopathy (DCM): The clinical manifestations of this disease are extremely difficult to distinguish from chronic Keshan disease, but the latter has a more obvious degree of cardiac enlargement than DCM, and the electrocardiogram is more RBBB (30% to 50%), while DCM is more LBBB or LVH. Pay attention to the onset characteristics of Keshan disease patients and the coexistence of the two in areas with Kaschin-Beck disease, which can also be distinguished. E2.2 Peripartum cardiomyopathy: Its clinical manifestations are the same as DCM, but it only occurs in women, and from the end of pregnancy to 2 to 20 weeks after delivery, it manifests as heart failure, dyspnea, bloody sputum, hepatomegaly, and edema. Because the heart was previously healthy, it does not have the characteristics of Keshan disease, so it is easy to identify.
E2.3 Coronary heart disease (myocardial sclerosis or congestive heart failure as the main manifestation): Pay attention to age, history of angina pectoris and risk factors for coronary heart disease (see E1.2), and the fact that the enlargement of the heart is not as significant as the chronic type, so it is not difficult to identify. E2.4 Pericarditis: Exudative or constrictive, with pericardial tamponade, and the signs of ventricular incomplete dilatation due to venous return obstruction are very similar to those of chronic Keshan disease. The difference is that the heart beats very weakly in pericarditis, and the ST-T changes of the electrocardiogram are changes in all leads, without a cardiomyopathy-like mirror relationship. Echocardiography can show ultrasound fluid dark areas (ultrasound free cavities). E2.5 Rheumatic heart disease: Rheumatic heart valve disease with mitral insufficiency as the main cause of heart failure is similar to chronic Keshan disease. However, the systolic murmur of the apex of this disease is strong and transmitted to the axilla, and is often accompanied by the diastolic murmur of mitral stenosis. Echocardiography shows strong mitral valve reflection, thickened valve leaflets, "wall-like" changes in the anterior leaflet of the mitral valve, and a history of rheumatic fever. E3 Differentiation of subacute type
E3.1 Acute and chronic glomerulonephritis or chronic kidney disease: Children's kidney disease or acute and chronic nephritis is often misdiagnosed as subacute type due to edema, especially facial edema or heart failure. If you pay attention to high blood pressure, urine protein (+++) or hematuria and casts, it can be distinguished from subacute Keshan disease. E3.2 Bronchopneumonia: When complicated with heart failure, it is also often mistaken for subacute type. This disease has a history of fever, obvious cough, significant dry and wet rales in the lungs, and the heart is not large, which can often be distinguished. E3.3 Endocardial fibroelastosis: It is an endocardial cardiomyopathy in the field of pediatrics. Most children die before the age of two. Those who develop the disease at an older age and respond well to digitalis treatment have a better prognosis. The main manifestation is global enlargement, especially left heart enlargement. As long as endocardial hypertrophy (strong reflection) is found in echocardiography, the diagnosis of this disease is clear. E3.4 Pericarditis: See the differential diagnosis of chronic type. E4 Differentiation of latent Keshan disease
E4.1 Focal myocarditis: Ectopic excitement caused by local myocardial necrosis, scarring, and fibrosis presents as "ventricular premature beats" or \RBBB\, which is often confused with the latent type. The difference is that there is a history of myocarditis, double serum reactions are mostly positive, the heart is not large, and the prognosis is good.
E4.2 Hypertrophic non-obstructive cardiomyopathy (HCM): Latent patients may sometimes have mild ventricular septum or left ventricular thickening or both, but unlike HCM, the thickness does not exceed 15mm, and left ventricular hypertrophy or abnormal Q waves are rarely seen on the electrocardiogram.
Cardiac neurosis is also called neurocirculatory asthenia or increased excitability of β receptors: patients with this disease often have palpitations or fast heart rate, discomfort in the precordial area, easy fatigue or excessive breathing. There may also be "ventricular premature beats", that is, many subjective symptoms, but no cardiac signs: such as no abnormal electrocardiogram (or ST-T changes but positive propranolol test), and no cardiac enlargement.2 Acute myocardial infarction (AMI): It occurs suddenly, with cardiogenic shock, severe arrhythmia or heart failure and ST-T changes on the electrocardiogram, especially the single-phase curve (upward or downward), which is very similar to the acute type. However, the difference is that AMI often occurs in older people (over 45 years old), while young people are mostly men. They often have angina pectoris or discomfort in the precordial area. The electrocardiogram often shows obvious ST-T changes, and there is a systematic evolution process, combined with abnormal Q waves. Keshan disease rarely presents with the latter, and most of them do not have risk factors for coronary heart disease, such as hypertension, hyperlipidemia, and obesity. E1.3 Acute gastritis: upper abdominal discomfort, nausea, vomiting, sometimes vomiting bile (vomiting yellow water), fatigue, cold limbs, etc. are similar to the acute type, but there are no cardiac signs: such as the heart is not large, there is no arrhythmia, and more importantly, there is no abnormality in the electrocardiogram. This disease often has a history of binge eating or eating unclean food, often with abdominal pain, diarrhea, etc. E1.4 Biliary tract insufficiency: abdominal pain, nausea, vomiting, vomiting yellow water (bile) are easily confused with acute Keshan disease in children, but biliary tract insufficiency presents with paroxysmal severe upper abdominal pain, colic, worm masses in the abdomen (visible by X-ray), muscle tension and tenderness in the upper abdomen, and no cardiac symptoms and signs. E2 Differentiation of chronic Keshan disease
E2.1 Dilated cardiomyopathy (DCM): The clinical manifestations of this disease are extremely difficult to differentiate from chronic Keshan disease, but the latter has a more obvious degree of cardiac enlargement than DCM, and the electrocardiogram has more RBBB (30% to 50%), while DCM is more likely to have LBBB or LVH. Pay attention to the characteristics of Keshan disease patients and the coexistence of the two in areas with Kaschin-Beck disease, which can also be distinguished. E2.2 Peripartum cardiomyopathy: Its clinical manifestations are the same as DCM, but it only occurs in women, and manifests as heart failure, dyspnea, bloody sputum, hepatomegaly, and edema from the end of pregnancy to 2 to 20 weeks after delivery. Because the heart was previously healthy and does not have the characteristics of Keshan disease, it is easy to distinguish.
E2.3 Coronary heart disease (myocardial sclerosis or congestive heart failure as the main manifestation): Pay attention to age, history of angina pectoris and risk factors for coronary heart disease (see E1.2), and the fact that the heart is not as enlarged as the chronic type, so it is not difficult to distinguish. E2.4 Pericarditis: exudative or constrictive with pericardial tamponade, ventricular insufficiency due to venous return obstruction, and the signs of ventricular insufficiency are very similar to those of chronic Keshan disease. The difference is that the heart beats are extremely weak in pericarditis, and the ST-T changes of the electrocardiogram are changes in all leads, without a cardiomyopathy-like mirror relationship. Echocardiography may show ultrasound liquid dark areas (ultrasound free cavities). E2.5 Rheumatic heart disease: Rheumatic heart valve disease with mitral regurgitation as the main cause of heart failure is similar to chronic Keshan disease. However, the systolic murmur of the apex of this disease is strong and transmitted to the axilla, and is often combined with the diastolic murmur of mitral stenosis. Echocardiography shows strong mitral valve reflection, thickened valve leaflets, "wall-like" changes of the anterior leaflet of the mitral valve, and a history of rheumatic fever. E3 Differentiation of subacute type
E3.1 Acute and chronic glomerulonephritis or chronic kidney disease: Kidney disease or acute and chronic nephritis in children is often misdiagnosed as subacute type due to edema, especially facial edema or heart failure. If you pay attention to high blood pressure, urine protein (+++) or hematuria and casts, it can be distinguished from subacute Keshan disease. E3.2 Bronchopneumonia: When complicated with heart failure, it is also often mistaken for subacute type. This disease has a history of fever, obvious cough, obvious dry and wet rales in the lungs, and the heart is not large, which can often be distinguished. E3.3 Endocardial fibroelastosis: It is an endomyocardial cardiomyopathy in the field of pediatrics. Most children die before the age of two. Those who are older in age and respond well to digitalis treatment have a better prognosis. The main manifestation is global enlargement, especially left heart enlargement. As long as endocardial hypertrophy (strong reflection) is found in cardiac ultrasound examination, the diagnosis of this disease is clear. E3.4 Pericarditis: See the differential diagnosis of chronic type. E4 Differentiation of latent Keshan disease
E4.1 Focal myocarditis: Ectopic excitation due to local myocardial necrosis, scarring, and fibrosis presents as "ventricular premature beats" or \RBBB\, which is often confused with the latent type. The difference is that there is a history of myocarditis, double serum reactions are mostly positive, the heart is not large, and the prognosis is good.
E4.2 Hypertrophic non-obstructive cardiomyopathy (HCM): Latent patients sometimes also have mild ventricular septum or left ventricular thickening or both, but the difference from HCM is that its hypertrophy does not exceed 15mm, and left ventricular hypertrophy or abnormal Q waves are rarely seen on the electrocardiogram.
Cardiac neurosis is also called neurocirculatory asthenia or increased excitability of β receptors: Patients with this disease often have palpitations or rapid heart rate, discomfort in the precordial area, easy fatigue or hyperventilation. There may also be "ventricular premature beats", that is, there are many subjective symptoms, but no cardiac signs: such as no electrocardiogram abnormalities (or ST-T changes but positive propranolol test), and no heart enlargement.2 Acute myocardial infarction (AMI): It occurs suddenly, with cardiogenic shock, severe arrhythmia or heart failure and ST-T changes on the electrocardiogram, especially the single-phase curve (upward or downward), which is very similar to the acute type. However, the difference is that AMI often occurs in older people (over 45 years old), while young people are mostly men. They often have angina pectoris or discomfort in the precordial area. The electrocardiogram often shows obvious ST-T changes, and there is a systematic evolution process, combined with abnormal Q waves. Keshan disease rarely presents with the latter, and most of them do not have risk factors for coronary heart disease, such as hypertension, hyperlipidemia, and obesity. E1.3 Acute gastritis: upper abdominal discomfort, nausea, vomiting, sometimes vomiting bile (vomiting yellow water), fatigue, cold limbs, etc. are similar to the acute type, but there are no cardiac signs: such as the heart is not large, there is no arrhythmia, and more importantly, there is no abnormality in the electrocardiogram. This disease often has a history of binge eating or eating unclean food, often with abdominal pain, diarrhea, etc. E1.4 Biliary tract insufficiency: abdominal pain, nausea, vomiting, vomiting yellow water (bile) are easily confused with acute Keshan disease in children, but biliary tract insufficiency presents with paroxysmal severe upper abdominal pain, colic, worm masses in the abdomen (visible by X-ray), muscle tension and tenderness in the upper abdomen, and no cardiac symptoms and signs. E2 Differentiation of chronic Keshan disease
E2.1 Dilated cardiomyopathy (DCM): The clinical manifestations of this disease are extremely difficult to differentiate from chronic Keshan disease, but the latter has a more obvious degree of cardiac enlargement than DCM, and the electrocardiogram has more RBBB (30% to 50%), while DCM is more likely to have LBBB or LVH. Pay attention to the characteristics of Keshan disease patients and the coexistence of the two in areas with Kaschin-Beck disease, which can also be distinguished. E2.2 Peripartum cardiomyopathy: Its clinical manifestations are the same as DCM, but it only occurs in women, and manifests as heart failure, dyspnea, bloody sputum, hepatomegaly, and edema from the end of pregnancy to 2 to 20 weeks after delivery. Because the heart was previously healthy and does not have the characteristics of Keshan disease, it is easy to distinguish.
E2.3 Coronary heart disease (myocardial sclerosis or congestive heart failure as the main manifestation): Pay attention to age, history of angina pectoris and risk factors for coronary heart disease (see E1.2), and the fact that the heart is not as enlarged as the chronic type, so it is not difficult to distinguish. E2.4 Pericarditis: exudative or constrictive with pericardial tamponade, ventricular insufficiency due to venous return obstruction, and the signs of ventricular insufficiency are very similar to those of chronic Keshan disease. The difference is that the heart beats are extremely weak in pericarditis, and the ST-T changes of the electrocardiogram are changes in all leads, without a cardiomyopathy-like mirror relationship. Echocardiography may show ultrasound liquid dark areas (ultrasound free cavities). E2.5 Rheumatic heart disease: Rheumatic heart valve disease with mitral regurgitation as the main cause of heart failure is similar to chronic Keshan disease. However, the systolic murmur of the apex of this disease is strong and transmitted to the axilla, and is often combined with the diastolic murmur of mitral stenosis. Echocardiography shows strong mitral valve reflection, thickened valve leaflets, "wall-like" changes of the anterior leaflet of the mitral valve, and a history of rheumatic fever. E3 Differentiation of subacute type
E3.1 Acute and chronic glomerulonephritis or chronic kidney disease: Kidney disease or acute and chronic nephritis in children is often misdiagnosed as subacute type due to edema, especially facial edema or heart failure. If you pay attention to high blood pressure, urine protein (+++) or hematuria and casts, it can be distinguished from subacute Keshan disease. E3.2 Bronchopneumonia: When complicated with heart failure, it is also often mistaken for subacute type. This disease has a history of fever, obvious cough, obvious dry and wet rales in the lungs, and the heart is not large, which can often be distinguished. E3.3 Endocardial fibroelastosis: It is an endomyocardial cardiomyopathy in the field of pediatrics. Most children die before the age of two. Those who are older in age and respond well to digitalis treatment have a better prognosis. The main manifestation is global enlargement, especially left heart enlargement. As long as endocardial hypertrophy (strong reflection) is found in cardiac ultrasound examination, the diagnosis of this disease is clear. E3.4 Pericarditis: See the differential diagnosis of chronic type. E4 Differentiation of latent Keshan disease
E4.1 Focal myocarditis: Ectopic excitation due to local myocardial necrosis, scarring, and fibrosis presents as "ventricular premature beats" or \RBBB\, which is often confused with the latent type. The difference is that there is a history of myocarditis, double serum reactions are mostly positive, the heart is not large, and the prognosis is good.
E4.2 Hypertrophic non-obstructive cardiomyopathy (HCM): Latent patients sometimes also have mild ventricular septum or left ventricular thickening or both, but the difference from HCM is that its hypertrophy does not exceed 15mm, and left ventricular hypertrophy or abnormal Q waves are rarely seen on the electrocardiogram.
Cardiac neurosis is also called neurocirculatory asthenia or increased excitability of β receptors: Patients with this disease often have palpitations or rapid heart rate, discomfort in the precordial area, easy fatigue or hyperventilation. There may also be "ventricular premature beats", that is, there are many subjective symptoms, but no cardiac signs: such as no electrocardiogram abnormalities (or ST-T changes but positive propranolol test), and no heart enlargement.
Tip: This standard content only shows part of the intercepted content of the complete standard. If you need the complete standard, please go to the top to download the complete standard document for free.