History
Liver disease
Determine the specific etiology of liver disease, because some etiologies are associated with worsened growth impairment. Consider the following:
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Patients with Alagille syndrome and familial cirrhosis do not demonstrate growth improvement after liver transplantation, suggesting the presence of congenital anomalies or other genetic defects as limiting factors. [29]
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Children with extrahepatic biliary atresia may have severe malnutrition. Although they can be particularly malnourished before transplantation, they are expected to have satisfactory catch-up growth in the postoperative period.
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Patients with Byler syndrome and other cholestatic conditions can also present with growth failure.
A comprehensive nutritional history is very important. Children with end-stage liver disease (ESLD) often develop behavioral feeding problems that should be recognized and corrected promptly. These problems may continue after transplantation and may lead to decreased oral intake. Anorexia, hospitalization-related depression, unpalatable diet, tense ascites, vomiting and diarrhea, cholestasis, and encephalopathy are some pretransplantation factors that lead to growth retardation.
Signs and symptoms of specific deficiencies include the following:
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Night blindness may be an indicator of vitamin A deficiency.
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Anemia may be caused by iron deficiency or vitamin B-12 and folate deficiencies.
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In the presence of cholestasis, a history of bleeding is suspicious for vitamin K deficiency.
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Failure to thrive (in infants), anorexia, hypogeusia, mood swings, and diarrhea may indicate zinc deficiency.
Among the factors that may cause growth retardation in the posttransplant period in liver recipients are the following:
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Preoperative stunting
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Prolonged hospitalization
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Medications, especially corticosteroids
Kidney disease
Specific etiologies of renal disease associated with worsened growth impairment include prenatal conditions and kidney disease that develops in infancy and childhood, such as the following:
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Congenital nephrotic syndrome is associated with massive urinary protein loss.
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Nephrotic syndrome in infancy and childhood presents as significant albuminuria and may result in growth retardation because of long-term steroid use.
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Nephrogenic diabetes insipidus is associated with fluid and electrolyte imbalance, polyuria, polydipsia, and growth retardation.
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Genetic defects include neonatal Bartter syndrome, polycystic kidney disease, and cystinosis.
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Developmental anomalies include obstructive uropathies such as prune-belly syndrome, posterior urethral valves, and renal dysplasia or hypoplasia, all of which are associated with polyuria and natriuresis that lead to growth impairment.
Anorexia, caloric deficits, hyposthenuria, salt wasting, anemia, metabolic acidosis, electrolyte depletion, renal osteodystrophy, and growth hormone resistance can lead to nutritional deprivation in chronic kidney disease (CKD). Management should be age specific and should be tailored to the underlying condition.
Renal dysplasia and obstructive uropathy are the 2 most common causes of renal failure in childhood. These children have a congenital polyuric, salt-wasting form of renal failure and have growth retardation because of chronic intravascular depletion and a negative sodium balance. These patients require nutritional support with water and salt supplementation.
Patients on maintenance dialysis may have deficiency of water-soluble vitamins and minerals due to insufficient intake, increased losses, and/or increased requirements.
Infant enteral formulas have low phosphorus; breast milk is encouraged. Formula is also low in protein for infants on peritoneal dialysis and needs to be supplemented with iron and vitamin D. Nasogastric or gastrostomy tube feedings may be necessary.
In older children, a high-calorie, low-phosphorus diet is important.
Patients with end-stage renal disease who have no residual renal function (anuric) need a low-sodium, low-potassium, and low-phosphorus diet with fluid restriction.
Determinants of posttransplantation growth in renal transplant patients include the following:
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Age at transplantation
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Corticosteroid use
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Growth hormone level
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Allograft function
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Posttransplantation sexual maturation
Physical
To assess nutritional status in patients after transplantation, perform anthropometric measurements, which include the following [30] :
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Height
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Weight
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Skinfold thickness (triceps and subscapular)
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Mid-arm circumference
Weight may not be an accurate indicator of nutritional status in patients with liver cirrhosis, because of the possibility of fluid retention and ascites, or in kidney recipients with nephrotic syndrome and peripheral edema. Height is a more accurate indicator of nutritional status in liver recipients and kidney recipients.
Peripheral edema may make assessing skinfold thickness and mid-arm circumference more difficult.
The clinical assessment for deficiencies/laboratory abnormalities includes the following:
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Vitamin E deficiency: Assess ophthalmoplegia, hemolysis, hyporeflexia, and ataxia
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Zinc deficiency: Assess acrodermatitis and alopecia
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Vitamin K deficiency: Assess ecchymosis and easy bruisability
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Vitamin A deficiency: Assess follicular hyperkeratosis, Bitot spots, and xerophthalmia
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Iron deficiency: Assess for signs and symptoms of anemia, including pallor, shortness of breath, fatigue, and tachycardia, especially in those with renal allograft dysfunction and CKD.
