| ID | 383 |
|---|---|
| Name | VENTRICULAR SEPTAL DEFECT (VSD) |
| Cause | |
| Signs Symptoms | |
| Diagnosis | Diagnosis: 1. X-ray fmdings- a Gross cardiomegaly with left or biventricular hypertrophy, b. Pulmonary vasculature engrogement 2. ECGfmdings- a. Biventricular hypertrophy. b. P-wave may be notched or picked & tall due to enlargement of both atria. 3. Echocardiogram. 4. Cardiac catheterization & Angiocardiography. |
| Investigations | |
| Management | Management: A. Small VSD- 1. Small VSD should be left alone, no surgical repair is recommended as asymptomatic & chance of spontaneous closer. 2. Protection against infective endocarditis-Prophylaxis during dental & oropharyngial sur-gery & during instrumentation of genitourinary & lower intestinal tracts. 3. Full physical activity is encouraged in all respect. B. Large VSD - 1. Medical management- medical management of large VSD is primarily aimed at the control of CCF. Those pts may show signs of repeated or ch. pulmonary disease & often fail to thrive. If early treatment is successful; the shunt may diminish in size i.e spontaneous improvement, specially during the 1st yr. of life. 2. Young symptomatic infants with high pulm. blood flow a pressure after an unsuccessful medical trial must go for closure of the defect even efectively early in the 2nd yr of life to prevent irriversible pulm. vascular disease. Normally pulm. vascular disease is prevented when surgery is performed in the first 2 years of life. Surgical complications in long-term problems e.g. heart block is extremely rare. After obliteration of VSD, the heart almost become quiet & all the s/s disappear. The long term prognosis after surgery is excellent. |
| Introduction | VSD is the most common acyanotic cardiac malformation accounting for about 25% of CHD. Clinically, the defects are usually of three varities: 1. small left to right shunt without pulmonary hypertension, 2. moderate left to right shunt without or mild pulmonary hypertension, 3. very large left to right shunt with pulmonary hypertension. When pulmonary hypertension is severe cyanosis usually present. Anatomy of VSD: According to site - two types 1. Membranous type (majority)- situated in a postero-inferior position anterior to the septal leaflet of the tricuspid valve. 2. Muscular type (minority)- situated in the midportion or apical region of the ventricular septum & may be single or multiple. The defects may be small in size & relatively benign (Maladie-de-Roger), or large & associated with a reduction in life expectency. |
| History | |
| Etiology | |
| Clinical Features | Clinical presentations: A. Small VSD - the child may be symptomless & develop normally cardiac lesion is usually found during routine physical exam. This is the most common form of VSD. Auscultatory findings - a loud, harsh or blowing left parasternal pancystolic murmur, may be accompanied by a palpable systolic thrill in the left parasternal area. Radiological findings- usually normal; although minimal cardiomegaly & a mild increase in pulm. vasculature may be observed. ECG- usually normal; but may suggest left ventricular hypertrophy. B. Large VSD- Menifestations- 1. Dyspnoea. 2. Feeding difficulty (i.e becomes dyspnoic & tired). 3. Poor growth. 4. Profuse perspiration (sweating). 5. Recurrent pulmonary infections. 6. Cardiac failure in early infancy. * Cyanosis is usually absent. On palpation- 1. Pulses are normal, in absence of heart failure. 2. Prominence of left precordium & sternum is common. 3. Palpable parasternal heave- as is cardiome-galy. 4. Shifted apex beat (commonly) with an apical forceful thrust. 5. A systolic thrill at left parasternal border. On auscultation- 1. A loud pansystolic murmur (Similar to that of smaller defects) best heard at the left sternal border at the level of 4th intercostal space. 2. The second sound is louder at pulm. area, may be single or very closely split 3. Presence of a short apical mid-diastolic murmur caused by the increased blood flow accross the mitral valve. |
| Preventions | |
| Treatment | |
| Complications | |
| Prognosis | Prognosis & Complications: The natural course of VSD includes the following 1. Spontaneous closure: A. Significant number (30-50%) of small VSD close spontaneously, most frequently during the first year of life. 2. Shunts too small to justify repair: Asymptomatic patients with hearts normal in size and without pulmonary hypertension are generally not subjected to surgical repair. 3. Infective endocarditis occurs in fewer than 1%. 4. A significant mumber infants with large VSD have repeated eipsodes of infection & C.C.F. 5. Pulm. hypertension occurs as a result of high pulm. blood flow. A few pts will develop elevated pulm. vascular resistance with time if the defect is not repaired. 6. Development of infundibular pulmonary stenosis: A small number (about 5%) acquire pulm. stenosis, which protects the pulm. circulation from the long-term effects of pulm. hypertension. In these pts. the clinical picture changes from VSD with large left to rt. shunt to VSD with pulm. stenosis, & a diminished left to rt. shunt, a balanced shunt, or a rt. to left shunt. |
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