lthough obstetrical cases of AKI that require dialysis have become less prevalent, acute renal ischemia is still often associated with severe preeclampsia and hemorrhage (Gurrieri, 2012; Jim, 2017). Particularly contributory are HELLP (hemolysis, devated liver enzymes, low .latelet levels) syndrome and placental abruption (Audibert, 1996; Drakely, 2002). Septicemia is another frequent comorbidity, especially in resource-poor countries (Acharya, 2013; Srinil, 2011; Zeeman, 2003). AKI is also common in women with acute fatty liver of pregnancy (Sibai, 2007). Some degree of renal insuiciency was found in virtually all of 52 such women cared for at Parkland Hospital (Nelson, 2013). Another woman from Parkland Hospital developed AKI from dehydration caused by severe hyperemesis gravidarum at 15 weeks (Hill, 2002). Other causes include thrombotic micro angiopathies (Balofsky, 2016; Ganesan, 201a1) (Chap. 56, p. 1088).
In most women, AKI develops postpartum, thus management is usually not complicated by fetal considerations. An abrupt rise in serum creatinine level is most often due to renal ischemia. Oliguria is an important sign. In obstetrical cases, both prerenal and intrarenal factors are often contributory. For example, with total placental abruption, severe hypovolemia from massive hemorrhage is common, and preexistent renal ischemia from preeclampsia is often comorbid. In addition, disseminated intravascular coagulopathy may be contributory.
When azotemia is evident and severe oliguria persists, some form of renal replacement treatment is indicated. Hemofiltration or dialysis is initiated before marked deterioration occurs. Hemodynamic measurements are normalized. Importantly, medication doses are adjusted, and magnesium sulfate, iodinated contrast agents, aminoglycosides, and nonsteroidal antiinlammatory drugs (NSAIDs) are prominent examples (Waikar, 2015). Early dialysis appears to reduce the maternal mortality rate appreciably and may enhance the extent of renal function recovery. With time, renal function usually returns to normal or near normal.
AKI in obstetrics is most often due to acute blood loss, especially that associated with preeclampsia. hus, it may often be prevented by the following means: 1.
Prompt and vigorous volume replacement with crystalloid solutions and blood in instances of massive hemorrhage, such as in placental abruption, placenta previa, uterine rupture, and postpartum uterine atony (Chap. 41, p. 788).
2.
Delivery or termination of pregnancies complicated by severe preeclampsia or eclampsia, and careful blood transfusion ifloss is more than average (Chap. 40, p. 718).
3.
Close observation for early signs of sepsis syndrome and shock in women with pyelonephritis, septic abortion, chorioamnionitis, or sepsis from other pelvic infections (Chap. 47, p. 921).
4.
Avoidance of loop diuretics to treat oliguria before ensuring that blood volume and cardiac output are adequate for renal perfusion.
5.
Judicious use of vasoconstrictor drugs to treat hypotension, and only after it has been determined that pathological vasodilatation is the cause.