of other acute complications (e.g., head (stroke), flank (papillary necrosis), and abdomen (hepatic or splenic sequestration, constipation from opioid toxicity, or another Hepatobiliary complication). Patients 8 with more than three hospitalizations for a VOC in a year are considered to be at an increased risk of early death (Ballas et al., 2005) 1.2.3.3. Hand‐Foot Syndrome When sickle cells block the small blood vessels at hands or feet, pain and swelling along with fever may occur. The first VOC may appear as early as at 6 months of age, often presenting as dactylitis, but there after VOCs occur with variable frequency. This may be the first sign of sickle cell anemia in infants (Pham, 2005) 1.2.3.4. Fever- Infections Patients with SCD have an increased risk for severe bacterial infection, resulting primarily from reduced or absent splenic function (Booth et al., 2010). The result is an extremely high risk of septicemia and meningitis, primarily due to Streptococcus pneumonia. The risk of such infections continues throughout childhood and to a lesser extent in adults. Fever, as a presenting symptom, heralds many acute and sometimes life-threatening conditions, such as ACS and osteomyelitis. It is critical that fever alone is taken seriously in these patients and considered a potential emergency situation. Fever associated with pain should not be considered a VOC until infection is ruled out. Acute osteomyelitis, another complication associated with fever, may be unifocal or multifocal and may be caused by Staphylococcus aurous, salmonella, or other enteric pathogens (Booth et al., 2010). Pneumonia is the most common cause of death in young children with sickle cell disease. Meningitis, influenza, and hepatitis are other infections that are common in people with sickle cell disease (Olujohungbe et al., 2011). 9 1.2.3.5. Acute Renal Failure Acute renal failure is defined as a rapid reduction in renal function manifested by a rise in serum creatinine and reduction in glomerular filtration rate (GFR), with or without a decline in urine output. Acute renal failure may be due to pre-renal (e.g., dehydration) or post-renal (e.g., obstruction) insults, or result from intrinsic renal disease (e.g., glomerular injury). It may occur during an acute VOC, most often in association with ACS or acute multisystem organ failure. Renal papillary necrosis due to medullary infarction from obstruction of the blood supply in the vasa recta affects up to 15–30 percent of individuals with SCD (Pham et al., 2005) Signs and symptoms include pain and hematuria. When present, fever suggests possible infection. The serum creatinine levels are generally low or low-normal in patients With SCD and the values in acute renal function may still be within normal limits even if serum creatinine level increase two times from baseline (Pham et al., 2005). Identification of early renal disease in people with SCD is important as these patients hyper secrete creatinine through the proximal tubules, thus making significant renal impairment before the serum creatinine rises (Ataga and Orringer , 2000). Micro albuminuria is most often the first manifestation of chronic kidney disease in SCD. Proteinuria due to glomerular injury is also common, but both micro albuminuria and macro albuminuria are typically asymptomatic. The most common renal complication in people with SCD is hyposthenuria, or the Inability to concentrate the urine, which is progressive with age (Francis and Worthen, 1968). 1.2.3.6. Hepatobiliary complications Biliary tract abnormalities are common in SCD patients. These abnormalities include cholelithiasis, acute cholecystitis, and biliary sludge. Hemolysis of any etiology results in increased secreted unconjugated bilirubin that tends to precipitate 10 and leads to gallstones and sludge. Acute hepatic sequestration of red blood cells in the liver often develops over a few hours to a few days, and the resultant stretching of the hepatic capsule is usually painful. Acute intrahepatic cholestasis (also called sickle cell hepatopathy or “drepanocyte” liver) is also associated with SCD. It is characterized by the sudden onset of pain, increasing jaundice, a progressively enlarging and extremely tender liver, light-colored stools, and extreme hyperbilirubinemia (both conjugated and Unconjugated). This complication may prove fatal if not recognized and treated promptly (Shao and Orringer, 1995). 1.2.3.7. Splenic sequestration Splenic sequestration is defined as sudden enlargement of the spleen and reduction in hemoglobin concentration by at least 2 g/dL below the baseline value. Splenic sequestration (pooling) - crises are a result of sickle cells pooling in the spleen. This can cause a sudden drop in hemoglobin and can be life threatening if not treated promptly. The spleen can also become enlarged and painful from the increase in blood volume. After repeated episodes of splenic sequestration, the spleen becomes scarred, and permanently damaged. Most children, by the age of 8 years old, do not have a functioning spleen from repeated episodes of splenic sequestration. The risk of infection is a major concern of children without a functioning spleen. Infection is the major cause of death in children under the age of 5 years in this population. It is a major cause of acute anemia and it may present acutely accompanied by severe anemia and hypovolemic shock. The