Approach to a child with edema Prepared by : Madan Kumar Timalsena 1 st year resident Dept of Pediatrics(KISTMCTH) Moderator : Dr. Prabha Chhetri
Introduction  Edema is derived from the Greek words ‘etymon oidema ’ which mean to swell Results from an accumulation of fluid in the interstitial fluid compartment Severe generalized edema is known as anasarca Can be a manifestation of various underlying cause either local or systemic Can be pitting or non-pitting
Pathophysiology Increased capillary hydrostatic pressure more important in the production of localised oedema results from the release of chemical mediators, such as histamine, leukotrienes and cytokines Decreased plasma oncotic pressure Increased capillary leakage
Obstruction of lymph channels Renal salt and water retention Deposition of connective tissue components in subdermal region( myxedema )
Causes of generalized edema Nephrotic syndrome I ncreased hydrostatic pressure due to renal sodium retention D ecreased oncotic pressure due to hypoalbuminemia I ncreased capillary permeability mediated by a still unidentified factor marked proteinuria , hypoalbuminemia , and hyperlipidemia
Heart failure Left ventricular (LV): pulmonary, but not peripheral edema Pure right ventricular (RV) failure: may result in prominent edema in the lower extremities Cardiomyopathies : simultaneous onset of pulmonary and peripheral edema. Tachycardia, tachypnea, rales or wheezes, gallop rhythm, hepatomegaly
Acute glomerulonephritis primarily due to renal sodium and water retention Hypertension , hematuria and proteinuria , cola-colored urine, and/or azotemia Renal failure acute or chronic renal failure can present with edema due to renal retention of sodium and water
Cirrhosis Ireversible hepatic parenchymal injury with fibrosis Children with cirrhosis can develop portal hypertension I ncrease in venous pressure below the diseased liver, resulting in ascites and lower extremity edema R elatively uncommon in children can be caused by genetic disorders (alpha-1 antitrypsin deficiency, cystic fibrosis, Wilson disease), infectious etiologies (viral hepatitis), and structural problems of the biliary tree ( biliary atresia )
Lymphatic dysfunction/obstruction: Either a primary defect of the lymphatics or a secondary (acquired) defect Angioedema Swelling of the deep layers of the cutaneous or submucosal tissues Due to increased capillary permeability Usually affects the face, lips, tongue, or larynx
Venous obstruction Arises from extrinsic venous compression, thrombosis, or congestion Edema occurs distal to the site of obstruction Increased capillary permeability in patients with burns or sepsis
History (important points to consider) Edema location Time course (age at onset and duration of symptoms) Associated complaints : shortness of breath Additional concurrent illnesses or signs Past medical and family history Weight gain and tight-fitting clothes and shoes History of allergies and current medications.
Physical examination Child's growth parameters Full evaluation of cardiovascular system, including vital signs Tachycardia, tachypnea, gallop, rales , or hepatomegaly are seen in patients with heart failure Tachypnea and rales alone may be indicative of pulmonary edema Increased blood pressure (BP) levels may reflect hypervolemia from acute/chronic renal failure or glomerulonephritis
Examination for the presence of a pleural effusion pulmonary edema ascites scrotal/labial edema evidence of skin breakdown in regions of edema.
With regional edema localization of the area of swelling to help deduce where a region of venous or lymphatic obstruction is likely to be present cellulitis also can manifest with regional edema, assessment of the patient for fever and local signs of inflammation is important If the edema is localized to the face, the child also should be evaluated for concurrent airway involvement
Symptoms constellation Diaphoresis, dyspnea on exertion, and/or a history of heart disease heart failure Acute onset,food allergies,airway involvement,pruritis Urticaria and angioedema Jaundice, failure to thrive, steatorrhea , or abdominal pain Liver failure/disease or protein-losing enteropathy Progressive anasarca , significant periorbital component, minimal systemic complaints Nephrotic syndrome Cola-colored urine, generalized or facial edema, hypertension Acute glomerulonephritis Edema, anorexia, and growth impairment Chronic kidney disease Family history of angioedema Hereditary angioedema Newborn girl,edema of the hands and feet, webbed neck, nail dysplasia, high palate, and short fourth metacarpal Turner syndrome
Initial laboratory evaluation Complete blood count (CBC) Serum chemistry tests (serum creatinine , blood urea nitrogen [BUN]) Albumin Liver function studies Urinalysis The results of these initial tests, the clinical history and physical examination should provide information on the underlying general cause and help to select subsequent tests
Urinalysis including a dipstick for proteinuria markedly positive dipstick for protein with hypoalbuminemia and clinical edema is virtually diagnostic of the nephrotic syndrome Hematuria with red cell casts and dysmorphic red cells, with or without heavy proteinuria , is virtually diagnostic of glomerulonephritis , such as poststreptococcal glomerulonephritis
Heavy proteinuria , few cells or casts : consistent with a noninflammatory cause of nephrotic syndrome such as minimal change disease (MCD) or focal segmental glomerulosclerosis (FSGS ). A dditional testing based on a suspected etiology and results of the initial evaluation.
Kidney disease : suspected based on abnormal kidney function tests (elevated serum creatinine and BUN) or abnormal urinalysis Suspected glomerulonephritis Complement testing can classify glomerulonephritis as either hypocomplementemic or normocomplementemic Serologic testing may identify specific disorders and includes antistreptococcal antibodies ( poststreptococcal glomerulonephritis ) antinuclear antibodies (ANA), anti-double-stranded DNA antibodies (lupus nephritis )
antiglomerular basement membrane (GBM) antibodies (anti-GBM [ Goodpasture ]) disease antineutrophil cytoplasmic autoantibodies (ANCA vasculitides ) R enal biopsy may be considered in children with suspected glomerulonephritis S ignificant renal dysfunction Normocomplementemia H eavy proteinuria without an underlying diagnosis T o stage the histologic severity to guide approach to treatment for suspected lupus nephritis
Suspected nephrotic syndrome: C3, C4, ANA, and anti-double stranded DNA Renal imaging is used to determine if there is an underlying congenital or acquired structural abnormality of the kidney. The most commonly used modality is renal ultrasonography .
Chronic liver disease or protein-losing enteropathy : suspected in the child with hypoalbuminemia , but no proteinuria liver function tests total serum protein levels prothrombin times stool level of alpha-1 antitrypsin is the best screening test for protein-losing enteropathy
Congestive cardiac failure : suspected based on the pattern of general edema with findings(tachycardia , tachypnea, gallop, rales , or hepatomegaly ) chest radiography Electrocardiogram Echocardiography B rain natriuretic peptide
Venous thrombosis : Suspected based on the pattern of edema localized swelling with associated discoloration of the extremity D uplex ultrasonography establishes the diagnosis
Supportive care (specific treatment based on cause) Sodium and fluid restriction: Sodium restriction is usually appropriate in the setting of generalized edema, which includes patients with renal failure, acute glomerulonephritis , heart failure, hepatic ascites , and nephrotic syndrome 2 to 3 mEq of sodium/kg per da Fluid restriction can be considered M ust be done cautiously in patients with reduced effective circulating blood volume
Diuretics U sed in case of edema and an associated expanded intravascular volume ( eg . Heart failure and kidney failure) R isk of both precipitating acute kidney injury and decreasing perfusion to peripheral tissues C reatinine and BUN levels should be monitered Should be avoided or used cautiously in children with intravascular depletion
Intravenous albumin infusion N ephrotic syndrome P rotein-losing enteropathy P rotein malnutrition C irrhosis and severe ascites 25 percent albumin at a dose of 0.5 g/kg infused over four hours with intravenous furosemide at a dose of 1 mg/kg Respiratory status should be monitored
Thank you!
References https://www.uptodate.com/contents/evaluation-and-management-of-edema-in-children https://www.uptodate.com/contents/pathophysiology-and-etiology-of-edema-in-children https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707228/ https://www.sciencedirect.com/science/article/abs/pii/S0889852918304869 https://epomedicine.com/clinical-medicine/approach-to-a-child-with-edema/ C Leung AK, M Robson Alexander K C Leung WL, M Robson WL, of Paediatricts P, C Leung AK. Article Oedema in childhood