*2.3.1 Treatment*

They are challenging to treat, given distinct treatments. The basic treatment for TTP and complement-mediated HUS is the exchange of plasma. Delivery is the basic treatment for other pregnancy-related thrombotic microangiopathies (HELLP and preeclampsia) that occur during the third trimester [20].

## **2.4 Aplastic anemia**

Aplastic anemia (AA) is a non-cancerous disorder in which the stem cells in the bone marrow (the cells responsible for making all mature blood cells) are attacked and destroyed by the patient's immune system. Aplastic Anemia can be mild or severe; it can develop suddenly at very early stages of life or slowly at later stages of life [21].

If the parents have defective genes which are constructing antibodies against their stem cells, then this disorder can be inherited into the offspring through parents. The other causes of this disorder can be the usage of some medicines and certain toxins in the environment. An individual who has a record of certain infectious diseases, such as AIDS, HIV, hepatitis, viral diseases, Epstein–Barr, or having a record of consuming several medicines, such as antibiotics and anticonvulsants can also develop aplastic anemia. Subjection to certain toxins and heavy metals such as cadmium, mercury, lead, and thallium can cause aplastic anemia. Exposure to radiation and a history of having an autoimmune disorder, such as lupus are some other major causes of aplastic anemia [22].

Aplastic anemia is a rare disease that occurs due to the destruction of pluripotent stem cells in the bone marrow. Significant factors including extremely low platelet counts, low bone marrow cellularity, and late disease presentation result in severe Aplastic anemia during pregnancy [23]. In pregnancies with Aplastic anemia, Low

hemoglobin concentration and platelet counts may be the primary risk factors for obstetric complications. Premature labor, gestational diabetes, pre-eclampsia, acute heart failure, postpartum hemorrhage, and severe postpartum infection are the major maternal complications [24].

#### *2.4.1 Treatment*

The principle of aplastic anemia treatment is to know about the cause and treatment of cytopenias and minimize the side effects of therapy for mother and fetus. Abortion is also preferred in case of severe pancytopenia. It is also treated by the transplantation of hemopoietic stem cells and by using immunosuppressive regimens. Hemopoietic stem cell transplantation (HSCT) is done after the delivery and it may lead to reduced fertility so the patient is asked before the treatment [25].

Antithymocyte globulin (ATG) is also used for the treatment. ATG is a safe medication but it may cause allergic reactions, vein irritation, nausea, vomiting, and diarrhea. It does not cause any drug toxicity but in pregnant women, it may cause low birth weight. Corticosteroids are also used for aplastic anemia treatment. As they cannot cross the placenta so it reduces fetal brain exposure but it also may lead to glucose intolerance, gestational diabetes, and premature rupture of membranes.

Transfusion of blood products is the basic treatment for aplastic anemia. It also causes some complications such as hemochromatosis and HLA alloimmunization. Alloantibodies may cause platelet-transfusion refractoriness (PTR). They are challenging to treat, given distinct treatments. The basic treatment for TTP and complement-mediated HUS is the exchange of plasma. Delivery is the basic treatment for other pregnancy-related thrombotic microangiopathies (HELLP and preeclampsia) that occur during the third trimester.

#### **2.5 Sickle-cell anemia**

In normal conditions, the body produces red blood cells which are round and flexible and can flow easily through the blood vessels. But in the case of sickle cell anemia, the body forms sickle-shaped or C-shaped red blood cells which become rigid, sticky and these irregularly sickle-shaped cells become stuck in small blood vessels, which can slow down or inhibit the flow of blood and supply of oxygen to all parts of the body (**Figure 4**). The average life of every red blood cell is 120 days which means that after 120 days red blood cells are replaced with new ones in the circulation. But in the case of sickle cell anemia red blood cells usually die within 10 to 20 days, causing a red blood cell deficiency that leads to Anemia and cannot supply oxygen properly throughout the body [26].

Pregnancy and sickle cell disease have reciprocal impacts on each other and it's a risky situation. The risk of infection becomes significantly higher during pregnancy in sickle cell anemia. The risk of low birth weight increases by 4 times than in the general population in homozygous sickle cell disease. The presence or conjunction of several risk factors including chronic fetal distress, vasculorenal syndrome, acute vaso occlusive crisis, or pelvic dystocia due to bone lesions of the pelvis explains the high cesarean rate in sickle cell women [27].

In the postpartum period, nearly half of women with sickle cell disease experienced a vasoocclusive crisis. Actually, it's a period at high risk of decompensation of sickle cell disease that combines maternal fatigue, intense pain in the absence of epidural analgesia, fasting with dehydration, a state of metabolic acidosis linked to uterine muscle work, and respiratory alkalosis. All of these factors result in a vaso occlusive accident [28].

**Figure 4.** *Formation of sickle-shaped RBC'S blocking the blood vessels.*
