Congenital cardiac disease causes of finger clubbing Finger clubbing can also be caused by congenital cardiac diseases including: Tetralogy of Fallot (combination of four structural defects) Total anomalous pulmonary venous return (TAPVR; rare condition in which the pulmonary veins do not empty into the heart) Transposition of the great vessels (rare condition in which the major vessels entering or leaving the heart are misconnected
Respiratory disease causes of finger clubbing Finger clubbing may be caused by respiratory diseases including: Bronchiectasis (destruction and widening of the large airways) Chronic obstructive pulmonary disease (COPD), including emphysema and chronic bronchitisCOPD Cystic fibrosis (thick mucus in the lungs and respiratory tract) Lung abscess Lung cancer Pulmonary fibrosis (scarring of the lungs)
Gastrointestinal disease causes of finger clubbing Finger clubbing can also be caused by gastrointestinal diseases including: Celiac diseaseCeliac disease (severe sensitivity to gluten from wheat and other grains that causes intestinal damage) CirrhosisCirrhosis of the liver Inflammatory bowel diseaseInflammatory bowel disease (includes Crohn’s disease and ulcerative colitis)ulcerative colitis Liver cancer.
Other causes of finger clubbing Finger clubbing can also have other causes including: Dysentery (infectious inflammation of the colon, causing severe diarrhea)diarrhea Graves’ disease (type of hyperthyroidism resulting in excessive thyroid hormone production) Hodgkin’s lymphoma (cancer of the lymph tissues)
Septal defects: Inter atrial communication : Secundum ASD(the most common type) Primum ASD(is associated with MV cleft) Sinus venosous defect (SVC type ASD) Coronary sinus defect IVC type ASD Common atrium
According to Fossa Ovalis: PFO or ASD2 ASD1(Ant) Sinus venosous defect(Ant &Sup) Coronary sinus defect(Ant &Inf) IVC type ASD (Post & Inf ) Common atrium (near or total absence of inter atrial septum)
Anatomic closure of foramen oval in the first year of life. No closure: 25-30% PFO : < or = 3.5mm Small ASD2 : 3.5-5mm Mod : 5-8mm Large : > 8mm
Overally the clinical manifestations of ASDs depend on magnitude of intracardiac shunt.
Most infants with ASDs are asymptomatic, and the condition goes undetected. They may present at 6 to 8 weeks of age with a soft systolic ejection murmur and possibly a fixed and widely split S 2. Older children with a moderate left-to-right shunt often are asymptomatic.
Children with large left-to-right shunts are likely to complain of some fatigue and dyspnea. Growth failure is very uncommon. Rarely, ASDs in infants are associated with poor growth, recurrent lower respiratory tract infection, and heart failure.
Congestive heart failure rarely is found in the first decades of life, but it can become common once the patient is older than 40 years of age. The onset of atrial fibrillation or, less commonly, atrial flutter can be a hallmark in the course of patients with ASDs. The incidence of atrial arrhythmias increases with advancing age to as high as 13% in patients older than 40 years of age and 52% in those older than 60 years of age.
Pulmonary vascular disease can occur in 5% to 10% of patients with untreated ASDs, predominantly in females. Usually it occurs after 20 years of age, although rare cases in early childhood have been recorded.
Outcome: Secundum ASDs can close spontaneously, remain open, or enlarge. It appears that spontaneous closure, or a decrease in size, is most likely to occur in ASDs <7 to 8 mm and with younger age at diagnosis.
Spontaneous closure occures in all ASDs 8 mm. No follow-up is necessary if a defect is 80% of the defects will be closed.
In significant secundum ASDs at follow up 22% are closed spontaneously before 1year old, 33% between 1 and 2 years old and 3% between 2 and 4 years. Thus overally recommendation is to wait until after age 4 years for elective closure.
Since most ASDs are well tolerated in infancy and may spontaneously close, elective repair frequently has been deferred until the child is at least 4 years of age. Is some patients with very large ASDs, closure is done at younger ages. There is no advantage in delaying repair much beyond this age, and there may be harm in delaying repair to the teenage years and beyond.
Spontanious closure of other types of ASDs is not possible and must be closed surgically if indicated. Commen atrium usually must be repaired in infancy because the most of them present with symptoms of excess pulmonary blood flow,fatigue,tachypnea and failure to thrive.
Perimembranous: most common defect, 80% of surgical and autopsy series; usually extends into muscular, inlet, or outlet areas (synonyms: infracristal, membranous) Outlet: 5%-7% of autopsy and surgical series (29% in the Far East), situated just beneath the pulmonary value (synonyms: supracristal, conal, infundibular, subpulmonary, doubly committed subarterial) Inlet: 5%-8%, posterior and inferior to perimembranous defect Muscular: 5%-20% – Central: mid-muscular, may have multiple apparent channels on RV side and coalesce to single defect on LV side – Apical: multiple apparent channels on RV side may be single defect on LV side as with central defect – Marginal: along RV septal junction – Swiss cheese septum: large number of muscular defects
In infants with small VSDs, a murmur usually is detected at 1 to 6 weeks of age. However, the murmur can be heard during the first days of life associated with a rapid decrease in pulmonary vascular resistance. With small defects, the clinical course is benign throughout infancy and childhood. There are normal patterns of feeding, growth, and development. The only risk is that of endocarditis, which is rare before the age of 2 years.
In some patients, the murmur can extend cephalad along the left parasternal region, owing to ejection across the outflow tract of the right ventricle. The murmur also can radiate to the right of the sternum. In children with an outlet defect, the murmur and thrill can be maximal at the second left intercostal space or suprasternal notch.
Infants with moderate or large VSDs may develop symptoms as early as 2 weeks of age. The initial symptoms consist of tachypnea with increased respiratory effort, excessive sweating owing to increased sympathetic tone, and fatigue when feeding. The infant progressively tires with feeding; this symptom begins during the first month and increases in severity as pulmonary vascular resistance decreases. Symptoms occur earlier in the premature than in the full-term infant.
It is not unusual for symptoms to be preceded by respiratory infection. This complication makes it difficult to clarify the degree to which the respiratory distress is due to heart failure from a large left-to-right shunt versus infection. In the absence of infection, the cardiovascular basis for the respiratory symptoms probably is pulmonary edema.
In infants with a large left-to-right shunt secondary to a VSD, dyspnea can occur with mean left atrial pressures slightly lower than 15 mm Hg. In the presence of large shunts across the VSD, infants often have normal length and decreased weight.
In children with large shunts for â‰¥4 to 6 months, the left anterior thorax bulges outward. Persistent cyanosis from birth indicates a more complicated lesion than isolated VSD. However, the occurrence of cyanosis after infancy suggests reversal of the shunt to right to left because of progressive pulmonary vascular disease or the development of significant infundibular pulmonary stenosis.
Those with moderate to large right-to-left shunts will be cyanotic at rest. This is rare in infants, is occasionally seen by the age of 2 to 3 years, and is frequently seen in the adolescent and young adult. The eponym Eisenmenger's complex is now applied to the condition characterized by a VSD with marked elevation of pulmonary vascular resistance and a predominant right-to-left shunt.
Indications for VSD closure: 1-Uncontrolled CHF including growth failure or reccurent respiratory infections. 2-Elevated PAP even in the absence of symptoms.Repair must be done before 2 years of age and often before 1 year of age. 3-QP/QS >2 4-Significant dilation of LV 5-Aortic insufficiency
Pulmonary vascular obstructive changes can occur as early as 2 years of age. Generally, infants with VSD and increased pulmonary artery pressure should undergo repair between 3 and 12 months of age.
Development of pulmonary hypertension is rare (4%) as is sinus node dysfunction (4%) but progressive aortic valve insufficiency is fairly common (16%).