o Cover the eyes once the O2 hood is used, to prevent

excessive exposure of the eyes to O2 and cause drying

(retrolental fibroplasia or retinopathy of prematurity)
o Hardening of the cells behind the lens can lead to blindness
 IV fluids: LR

THALASSEMIA
 Abnormal hgb production (synthesis)
 Hgb has four parts, in thalassemia only has two or three parts (2
alpha and 2 betas)
 Lack of one beta: beta-thalassemia
 Lack of one alpha: alpha thalassemia
 Early hemolysis of the hgb → anemia and jaundice (from the heme of
the hgb)
 Autosomal recessive

Alpha Thalassemia
 Severe anemia

Beta Thalassemia
 Thalassemia minor: no s/sx
 Thalassemia major: severe anemia, bone deformities, and
splenomegaly
 Death of the hgb → release iron (heavy metal) → and further
kill RBCs
 Management is chelation therapy (binding of heavy metals within
the body)
 Chelator/ chelating agent is a drug that binds with iron:
deferoxamine (removal and decrease of FeSO4)
 Bart’s hydrops fetalis (a complication of Rh incompatibility:
intrauterine fetal death

Manifestations
 Pallor
 Jaundice
 Bronze skin color (may also be observed in phototherapy) d/t iron
deposits in the SQ and skin
 Hepatosplenomegaly (spleen is hyperreactive)
 Maxillary hyperplasia (jaw)
Diagnostics
 Electrophoresis
 CBC

Management
 Blood transfusion of PRBC every month
 Splenectomy d/t hyperactivity
 Avoid iron to prevent the proliferation of abnormal hgb