Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (136 page)

   Structural (e.g., diaphragmatic hernia, jejunal atresia, volvulus, intestinal malrotation) Peritonitis caused by GI tract perforation, congenital infection (e.g., syphilis, TORCH [
t
oxoplasmosis,
o
ther agents,
r
ubella,
C
MV, and
h
erpes simplex], hepatitis), meconium peritonitis

   Lymphatic duct obstruction

   Biliary atresia

   Nonstructural (e.g., congenital nephrotic syndrome, cirrhosis, cholestasis, hepatic necrosis, GI tract obstruction)

   Lower GU tract obstruction (e.g., posterior urethral valves, urethral atresia, and ureterocele) is most common cause

   Inherited skeletal dysplasias (enlarged liver causing extramedullary hematopoiesis)

   Fetal tumors, most often teratomas and neuroblastomas

   Vascular placental abnormalities

   Genetic metabolic disorders (e.g., Hurler syndrome, Gaucher disease, Niemann-Pick disease, G
_M1
gangliosidosis type I, I-cell disease, β-glucuronidase deficiency)

   Immune (maternal antibodies reacting to fetal antigens [e.g., Rh, C, E, Kell])

PERITONITIS, ACUTE

   See Figures 5-3 and 5-4.

Figure 5–3
Algorithm for differentiating secondary from spontaneous bacterial peritonitis. AF, ascitic fluid; PMN, polymorphonuclear leukocytes; LD, lactate dehydrogenase; ULN, upper limit of normal; WBC, white blood cell; SBP, spontaneous bacterial peritonitis.