Complications Associated With Sickle Cell Anemia

March 29, 2024

Sickle cell anemia is a severe hereditary disease of the red blood cells. Red blood cells in healthy individuals are round in shape, while the red blood cells in individuals with sickle cell anemia are irregularly shaped. This happens due to the hemoglobin in the red blood cells that becomes defective. The defective hemoglobin, called hemoglobin S, ends up taking the place of healthy hemoglobin, called hemoglobin A. As a result, over time the red blood cells become shaped like crescent moons instead of round. Sickle cells are notorious for clogging blood vessels and cutting off the supply of oxygen to organs and other tissues. Sickle cell anemia is a hereditary disease, which means it is passed through genes from parent to child when both parents have the sickle cell trait.

This type of anemia is very serious and can lead to numerous life-threatening complications. Reveal some of these now.

Acute Chest Syndrome

The leading cause of death in sickle cell anemia patients is a complication called acute chest syndrome, which can be best described as a combination of symptoms that happen when the defective red sickle cells become clustered together in the lungs. This can occur due to a possible underlying infection or excessive oxidative stress in individuals with sickle cell anemia. Acute chest syndrome results in a decrease in oxygen saturation and excessive inflammation in the lungs that can be life-threatening. Common symptoms include shortness of breath, fever, excessive sputum production, tightness in the chest, low oxygen levels, cough, and excruciating pain. It can be difficult to distinguish acute chest syndrome from pneumonia, as they both present the same way on an x-ray. To treat this condition, antibiotics and intravenous fluids will be given. Oxygen will also be given if oxygen levels appear to be too low. In some cases, a blood transfusion may also be needed to replenish the patient's supply of healthy and fully functional red blood cells.

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Leg Ulcers

Individuals with sickle cell anemia are prone to developing leg ulcers, the most common cutaneous manifestation of sickle cell anemia. An ulcer, in general, is defined as a break in the skin that allows for the exposure of bacteria and air to the underlying tissues. Sickle cell anemia can cause a simple skin laceration on the leg to develop into a full-blown infected ulcer. This happens because the irregularly shaped sickle cells cause blockages in blood vessels and inhibit proper blood circulation to the skin tear. This effectively allows any bacteria to invade, replicate, and grow in the tear until it is fully infected. Leg ulcers in individuals with sickle cell anemia can take up to sixteen times longer to heal than leg ulcers that occur from other causes. The lack of proper circulation prevents the body's natural healing factors from having sufficient access to the site of the ulcer. When components of the body's defense and natural healing mechanisms cannot access the site of the infection, they are not able to work together and do their job to heal the infected wound. The best way for an individual with sickle cell anemia to prevent these ulcers is to stimulate circulation with compression stockings and leg elevation, limit salt intake, wear protective clothing on the legs, and use insect repellant.

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Another complication associated with sickle cell anemia is the development of gallstones, which occur when certain substances harden in the gallbladder. A healthy gallbladder is responsible for storing and releasing a compound that aids in digestion, called bile. Bile is produced in the liver and travels via the bile duct to the gallbladder. In individuals who have sickle cell anemia, most gallstones are formed from an excess of bilirubin. Bilirubin is a compound in bile that is a byproduct of the process the liver uses to breakdown old red blood cells. The body has no use for it after the process is complete, and it is excreted by the body through the stool. In individuals with sickle cell anemia, there is an excess of red blood cell breakdown, which creates excessive amounts of bilirubin, which is then stored in the gallbladder and attempts to follow the normal process of excretion. However, it ends up sitting in the gallbladder longer than normal. This happens because the body cannot keep up with the liver's bilirubin production. Gallstones then form in the gallbladder from the bilirubin.

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Pulmonary Hypertension

Pulmonary hypertension is a common complication seen in patients who have sickle cell anemia. It can be described as high blood pressure inside of the arteries that supply the lungs with blood. This results in the hardening and narrowing of the pulmonary arteries or the blood vessels that carry blood to the lungs from the heart. As a result, the heart has to work harder at pumping to send the correct amount of blood to the lungs. This happens more often in sickle cell anemia patients because of the impairment caused to their blood circulation. When red blood cells are broken down in the blood vessels excessively, levels of nitric oxide decrease and inflammation is increased. Nitric oxide is a substance that relaxes the blood vessels in order for the blood to flow easier. Low nitric oxide levels and excessive inflammation stimulate the small arteries of the lungs to constrict, and this mechanism causes pulmonary hypertension to occur. It is important for pulmonary hypertension to be caught early because if it goes untreated, it can easily result in heart failure for sickle cell anemia patients.

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When the flow of blood in an individual's brain stops, a stroke occurs. It takes just minutes for the cells in the brain to die from a lack of oxygen due to an insufficient blood supply. A stroke is a serious medical emergency, and often the damage that occurs to the brain is permanent. A combination of factors can cause this kind of blood flow blockage in sickle cell anemia patients. Because the red blood cells are irregularly shaped, they can easily form a clot anywhere in the body. In addition, the blood vessels of individuals with sickle cell anemia are already constricted due to a low level of nitric oxide and widespread inflammation due to the excessive breakdown of red blood cells. Furthermore, the membranes of these irregular sickle cells are abnormal, and they have a tendency to stick on the endothelium or the blood vessel wall. A combination of one or more of these occurrences will easily result in a blood clot that travels to the brain and causes an obstruction in blood supply.

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