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Treatment of the condition is specific to the cause of hemolysis, but intense phototherapy and exchange transfusion can be used to help the patient excrete accumulated bilirubin. [11] Complications related to hemolytic jaundice include hyperbilirubinemia and chronic bilirubin encephalopathy , which may be deadly without proper treatment.
Hyperbilirubinemia is a clinical condition describing an elevation of blood bilirubin level due to the inability to properly metabolise or excrete bilirubin, a product of erythrocytes breakdown. In severe cases, it is manifested as jaundice, the yellowing of tissues like skin and the sclera when excess bilirubin deposits in them. [1]
Normal levels of bilirubin in blood are below 1.0 mg/dl (17 μmol/L), while levels over 2–3 mg/dl (34–51 μmol/L) typically result in jaundice. [4] [9] High blood bilirubin is divided into two types: unconjugated and conjugated bilirubin. [10] Causes of jaundice vary from relatively benign to potentially fatal. [10]
Conventionally, a leukocytosis exceeding 50,000 WBC/mm 3 with a significant increase in early neutrophil precursors is referred to as a leukemoid reaction. [2] The peripheral blood smear may show myelocytes, metamyelocytes, promyelocytes, and rarely myeloblasts; however, there is a mixture of early mature neutrophil precursors, in contrast to the immature forms typically seen in acute leukemia.
Bilirubin is not normally detectable in the urine of healthy people. If the blood level of conjugated bilirubin becomes elevated, e.g. due to liver disease, excess conjugated bilirubin is excreted in the urine, indicating a pathological process. [56] Unconjugated bilirubin is not water-soluble and so is not excreted in the urine.
High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) [normal 3.5–5.0 mmol/L] and they include [8] palpitations, cardiac conduction abnormalities, and arrhythmias (can be fatal) muscle weakness or paralysis; Hyperphosphatemia.
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