18 Flashcards
FTT
Criteria 3
2 categories of causes
Failure to Thrive
Failure to gain weight adequately in childhood is referred to as “failure to thrive.” Failure to thrive can be considered when:
an infant is < 5th percentile for weight
an infant is < 5th percentile in weight for length, or
the rate of growth results in the infant crossing more than 2 major lines on the standard infant growth curve.
Failure to thrive can be divided into two categories: organic and non-organic. Most sources report that organic problems account for < 10% of cases of failure to thrive.
Organic causes of failure to thrive include:
Congenital heart defects
Cystic fibrosis
Gastroesophageal reflux
Neurologic disorders
Metabolic disease
Psychosocial problems account for the majority of cases of non-organic failure to thrive. Poverty and neglect are important issues to consider in the evaluation of a child with failure to thrive.
In many cases of failure to thrive, no specific etiology is found.
Feeding patterns of infants
Young infants who are breastfeeding usually nurse for 10-30 minutes a time, as often as every 1-2 hours. Bottle-fed infants will often take more per feed and thus feed a little less often.
Dx consideration of reps distress and difficulty feeding in infant
Congestive heart failure (CHF)
Infants with CHF often present with a history of respiratory distress, difficulty feeding and poor weight gain (also called failure to thrive).
There are many potential causes of CHF in infancy.
Respiratory infection
Respiratory infections, such as bronchiolitis or pneumonia, present with respiratory distress, typically also with fever.
Anything causing respiratory difficulty in an infant can also cause difficulty with feedings.
Sepsis
Sepsis is always an important consideration in a young infant.
The early signs of sepsis can be subtle and non-specific, including lack of fever.
Metabolic disorder
There are many metabolic disorders that could potentially cause poor feeding.
Most are tested for on newborn screening.
For Tyler, you are concerned about:
CHF (A): His presentation is consistent with a diagnosis of heart failure.
Respiratory infection (B): A respiratory infection certainly may cause difficulty with feedings. More typically this would be accompanied by a history of fever.
Sepsis (D): This is an important consideration for Tyler. In infants signs of sepsis can be very non-specific, poor feeding being one.
Metabolic disorder (G): The negative newborn screen makes this less likely, but it is still an important possibility.
The remaining choices are much less likely:
Hyperbilirubinemia (C) is unlikely to cause poor feeding unless there is kernicterus, and there is no history of jaundice.
Poor feeding may be sign of any GI disease, including GE reflux (E), but the absence of spitting up or emesis makes this less likely.
Hypotonia (F) may cause poor feeding, but is not expected to cause respiratory difficulty, and would more likely have been present from birth.
Grading murmur
1 barely audible 2 faint 3 audible and loud 4 3 + thrill 5 4 + stethoscope barely off chest 6 audible without stethoscope
Cardiac exam
Cyanotic congenital heart defects
Heart sounds
Murmurs
Color of skin and mucus membranes
The patient’s color is important because cyanosis is associated with cyanotic congenital heart defects, most commonly tetralogy of Fallot. Much less common cyanotic heart defects include:
Truncus arteriosus Transposition of the great arteries Tricuspid atresia Total anomalous pulmonary venous return. Keep in mind that oxygen desaturation is difficult to detect, and is even more difficult to appreciate in darkly pigmented individuals. This is why it is important to inspect the mucous membranes and nail beds for cyanosis.
Precordial activity
The value and importance of assessing precordial activity in a newborn in this setting cannot be overstated. The hyperactive precordium is a strong indicator that Tyler’s heart is functioning at an increased workload.
Heart sounds
After palpating the precordium, the first step in auscultation includes carefully listening for S1 and S2, including listening for the physiologic split of the second heart sound. A gallop rhythm (S3 or S4) and clicks can also be heard when listening to the heart sounds.
Murmur
Although the term holosystolic implies that the murmur encompasses all of systole, that is not necessarily the case. A “holosystolic” murmur is S1 coincident (beginning during isovolumic contraction), meaning that the murmur starts with S1, not after it.
A ventricular septal defect (VSD), mitral insufficiency, and tricuspid insufficiency all cause holosystolic murmurs. A VSD causes a holosystolic murmur because flow through the VSD starts with the onset of ventricular contraction.
An ejection murmur is also systolic but does not start until after S1 because there is a delay from S1 to the onset of ejection–the isovolumic contraction time. Ejection murmurs occur with aortic and pulmonic valve stenosis.
Chf in infants
Heart defects that cause murmur and CHF 4
The classic findings of CHF in an infant a few weeks after birth are:
An infant with congestive heart failure presents primarily with feeding difficulties and respiratory symptoms.
Rapid and labored respirations are common, and often lead to difficulty feeding.
The history will often reveal that the infant is feeding for longer periods of time than normal, and that the feedings are terminated due to respiratory distress.
Infants frequently become diaphoretic with feedings.
Ultimately, due to poor feeding and increased caloric expenditure, poor weight gain ensues.
Tachycardia is common.
Hepatomegaly is a reliable finding in infants with heart failure.
an active precordium
An inefficient circulation—whether due to poor cardiac function, increased myocardial demand, or shunt lesions—leads to adrenergic activation. This in turn leads to increased metabolic demands that contribute to poor weight gain, as well as diaphoresis with any type of activity, including feeding.
CHF itself does not typically cause a murmur
Heart defects that present with a murmur and signs of CHF in infancy:
VSD Severe aortic stenosis Coarctation of the aorta Large patent ductus arteriosus Many other congenital heart defects, such as atrial septal defects (ASDs), do not cause CHF.
Most cyanotic heart defects, such as tetralogy of Fallot, present wtih cyanosis rather than progressive CHF findings.
Most common murmur in a child
Innocent murmurs are by far the most common cause of a murmur in children, occurring in 70% to 80% of otherwise healthy patients at some point during their childhood, particularly between 3 and 7 years of age. An innocent murmur is by definition normal, and is not due to any heart abnormality.
The most commonly heard innocent murmur is the Still’s murmur. This is often described as musical or vibratory, and is heard best at the left lower sternal border in the supine position.
A murmur heard in a young infant, or in a child who is not otherwise healthy is less likely to be innocent. In deciding if a murmur is innocent, it is important to make sure there are no other signs of significant heart disease.
Questions to ask yourself:
Is the child otherwise well?
Is the precordial activity normal?
Is the second heart sound normally split?
Is the murmur less than or equal to grade II/VI?
Is the oxygen saturation normal?
If the answer to any of these questions is “no,” the murmur should not be considered innocent.
Structural defects age presentation
Atrial septal defect (ASD)
Often first detected at 3-5 years of age.
The pathognomonic physical finding of an ASD is a widely split, fixed S2, which is a subtle physical finding and difficult to detect on a potentially uncooperative infant with a higher resting heart rate.
Listening for wide splitting of the second heart sound is the most helpful way to distinguish an ASD from an innocent murmur.
Coarctation of the aorta
Can present in infancy or at any age beyond because it tends to be a progressive problem, gradually getting more severe over a period of years.
Coarctation presents with a murmur, hypertension in the upper extremities, and a discrepancy between the upper and lower extremity blood pressures.
Ventricular septal defect (VSD) - most common type of congenital heart dis Most commonly presents in infancy
Aortic stenosis
Most commonly presents in infancy
Pulmonic stenosis
Most commonly presents in infancy
Patent ductus arteriosus
Most commonly presents in infancy
Tetralogy of Fallot
Most common cyanotic congenital heart disease in children
Most commonly presents in infancy
Bicuspid aortic valve
This is a common heart abnormality.
If the bicuspid valve is not stenotic or regurgitant, then there will be no murmur.
The physical examination finding of a bicuspid aortic valve is an early systolic click made by the abnormal valve when it opens (occurring shortly after the first heart sound, signifying the end of isovolumic contraction when the aortic valve opens to allow left ventricular outflow). This is a subtle exam finding that is often not heard in infants with higher heart rates, and is commonly not detected until later in childhood (if not adolescence or even adulthood).
Most common cyanotic congenital heart defect in newborns
Transposition of the great arteries
Transposition of the great arteries is the most common heart defect presenting with cyanosis in the newborn period, although the overall incidence is less than tetralogy of Fallot. This defect often requires urgent intervention to support mixing of oxygenated and de-oxygenated blood.
Evaluation of congenital heart defects 3 tools
ECG
An ECG is appropriate in this situation, although the findings would not be specific to a given defect.
The ECG is expected to be abnormal, demonstrating chamber enlargement.
Chest x-ray
A chest x-ray will provide information about heart size and prominence of pulmonary vasculature markings.
Cardiomegaly
Increased pulmonary vascular markings = pulm blood flow
Pulmonary edema
Echocardiography
An echocardiogram is more informative when combined with the cardiology consultation.
Use of echocardiography in the primary pediatric care setting is controversial, and most pediatric cardiologists still agree that it is not appropriate as first-line testing.
high voltage QRS complexes in leads V1 and V2), suggesting both LV volume overload and RV pressure overload.
Admission criteria for congenital heart disease 2
In general, children with significant congenital heart defects presenting with cyanosis or congestive heart failure need to be admitted to the hospital for management
All children in shock need to be admitted urgently to an intensive care unit.
How vsd cause CHF
Why vsd is not heard in the nursery
The infant with a VSD is supplying enough blood to the tissues to meet the body’s metabolic needs, but is doing so from an elevated filling pressure (due to the left ventricular volume overload). The adequate cardiac output is achieved by creating a high adrenergic state and by activating the renin-angiotensin system. Many of the symptoms of CHF in the infant are caused by these neurohormonal changes.
Contractility is increased
Newborns have elevated pulmonary vascular resistance.
When the systemic and pulmonary vascular resistances (PVR) are nearly equal, there is no reason for blood to shunt through the VSD.
The murmur of a VSD will not appear until the PVR drops, usually at a few days to weeks of age. This is why, typically, VSD murmurs are not heard in the nursery.
Tx of CHF
Meds 3
1 other add on thing to do
Surgery?
Medications
Furosemide (Lasix)
Diuretics are particularly effective at relieving the symptoms of CHF.
Diuretics work to counteract the fluid retention that occurs as a result of activation of the renin-angiotensin system.
Furosemide is the diuretic used most commonly for CHF in infants.
Digoxin
Has been shown in some studies to improve symptoms in infants with CHF due to a VSD.
The mechanism responsible for the clinical improvement is not altogether clear, as infants with a VSD do not have impaired contractility.
Enalapril
Afterload reduction with ACE inhibitors will decrease systemic vascular resistance and promote forward flow of blood from the left ventricle rather than flow through the VSD to the pulmonary vasculature.
Enalapril (twice daily dosing) and captopril (three times daily dosing) are both ACE inhibitors that are frequently used in infants with a VSD.
It should be noted that the aim of these medications are to control symptoms and help the child grow; there are no medications to encourage closure of a VSD.
Increasing Caloric Intake
Another consideration is to optimize feeding by fortifying expressed breast milk or formula to provide greater caloric density.
Patients with a large unrepaired VSD universally develop Eisenmenger’s syndrome - pulm vascular system gets high and cause right to left shunt (cyanosis, polycythemia, die in their 20s without a quality life before then) but typically not before 6 months of age. Therefore, to prevent its development, it is now recommended that VSD closure be performed in an infant with a large defect and pulmonary hypertension before 6 months of age. (Most vsd get smaller on there own)
