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Acute Renal Failure in Pregnancy: Additional Professor Obstetrics and Gynaecology Aiims Bhubaneswar
Acute Renal Failure in Pregnancy: Additional Professor Obstetrics and Gynaecology Aiims Bhubaneswar
Acute Renal Failure in Pregnancy: Additional Professor Obstetrics and Gynaecology Aiims Bhubaneswar
IN PREGNANCY
DR SWETA SINGH
ADDITIONAL PROFESSOR
OBSTETRICS AND GYNAECOLOGY
AIIMS BHUBANESWAR
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SPECIFIC LEARNING OBJECTIVES
• Causes of AKI in pregnancy
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RENAL CHANGES IN NORMAL
PREGNANCY
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RENAL DISORDERS IN
PREGNANCY
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URINARY TRACT INFECTION IN
PREGNANCY
• Asymptomatic bacteriuria
• Acute cystitis
• Acute pyelonephritis
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CHRONIC RENAL DISEASE IN
PREGNANCY
Diseases: Factors determining pregnancy outcome:
• Chronic glomerulonephritis
• Hypertension predating pregnancy
• IgA nephropathy
• Chronic pyelonephritis
• Urolithiasis • Renal function:
• Polycystic kidneys • Mild impairment: S Cr < 1.5mg%
• Pheochromocytoma
• Moderate impairment: S Cr 1.5-3mg%
• Diabetic nephropathy
• Severe impairment: S Cr >3mg%
• Wegener’s granulomatosis
• Renal artery stenosis
• Takayasu arteritis • Type of disease
• Lupus nephropathy (SLE)
• Periarteritis nodosa
• Scleroderma
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ACUTE RENAL FAILURE IN
PREGNANCY
• Pregnancy-related acute kidney injury (AKI) is acute kidney injury
occurring during pregnancy, labor and delivery, and/or the
postpartum period
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CLINICAL FEATURES OF AKI IN
PREGNANCY
• AKI is a clinical diagnosis based on the abrupt deterioration in
kidney function
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CAUSES OF AKI IN PREGNANCY
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CAUSES OF AKI IN PREGNANCY
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AKI: POST DELIVERY DAY3
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CHALLENGES OF AKI IN
PREGNANCY
Management of AKI in pregnancy is challenging as:
a. Both maternal and fetal health must be considered
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KEY MANAGEMENT PRINCIPLES
1. Stabilize the patient
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MANAGEMENT OF AKI IN PREGNANCY:
2.IDENTIFY AND TREAT UNDERLYING CAUSE
• Commonest cause of AKI in pregnancy: Reduced renal perfusion
• Pregnancy specific causes of AKI :
1. Hypertensive disorders of pregnancy
• Preeclampsia
• Eclampsia
• HELLP syndrome
• Acute fatty liver of pregnancy
• Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome
(TTP/HUS)
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D/D AFLP/HELLP/TTP/HUS
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MANAGEMENT OF AKI IN PREGNANCY:
2.IDENTIFY AND TREAT UNDERLYING CAUSE
• 2.Volume depletion:
a) Obstetric hemorrhage – Uterine blood flow increases from 50 cc/min prior to
pregnancy to approximately 1000 cc/min at term. Causes include:
• Induced or spontaneous abortion
• Ectopic pregnancy
• Placenta previa
• Placental abruption
• Intra- or post-partum hemorrhage
• b)Hyperemesis gravidarum –Very severe, refractory, and untreated cases can lead to
severe dehydration, hypovolemia and prerenal AKI
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MANAGEMENT OF AKI IN PREGNANCY:
2.IDENTIFY AND TREAT UNDERLYING CAUSE
• 3. Infection:
• Pyelonephritis – This occurs in 1-2% of pregnancies and is associated with maternal and
fetal complications including sepsis, preterm labor and adult respiratory distress
syndrome.
• Chorioamnionitis – Intrauterine infection involving the chorion and amniotic
membranes. This most commonly results from ascending infection of organisms
colonizing the lower genital tract.
• Septic abortion – This has become less common, but it is still a significant cause of
maternal mortality and morbidity, including AKI
• Pneumonia
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MANAGEMENT OF AKI IN PREGNANCY:
2.IDENTIFY AND TREAT UNDERLYING CAUSE
•4. Obstruction – Although uncommon in pregnancy, the overdistended, gravid uterus is a risk
factor. Additional contributors are:
•Polyhydramnios (increased amniotic fluid)
•Multi-fetal gestation (twins and higher)
•Large uterine fibroids
•5. Cardiovascular collapse – While any cardiovascular collapse can lead to AKI during
pregnancy, amniotic fluid embolism or “anaphylactoid syndrome of pregnancy” occurs only
in pregnancy
• It presents suddenly with fulminant respiratory failure, hypoxemia, cardiogenic shock, and
hypotension, and is often accompanied by disseminated intravascular coagulation and multi-
organ failure
•Maternal mortality is estimated to be as high as 60%
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MANAGEMENT OF AKI IN PREGNANCY
3. PREVENT PROGRESSION OF KIDNEY DAMAGE
• Maintain adequate renal perfusion to • All nephrotoxic medications should be
limit ongoing damage and reverse any stopped or the dose adjusted to prevent
pre-ischemic changes further renal damage
• Volume resuscitation should be • Pharmacologic therapies to prevent
accomplished with intravenous progression of renal decline are largely
crystalloid or colloid solutions as well secondary
as blood and blood products as • Vasoactive and diuretic medications may
indicated affect fetal well-being by reducing uterine
blood flow and placental perfusion
• Volume status should be monitored
clinically, with close attention to urine • Post-renal causes of progressive renal
injury such as obstruction of the urinary
output and pulmonary function
tract by the pregnant uterus can be
• Invasive hemodynamic monitoring in relieved by ureteral stents, percutaneous
an ICU setting is often warranted nephrostomy, or delivery, if indicated.
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MANAGEMENT OF AKI IN PREGNANCY
4. MAINTAIN SUPPORTIVE CARE
• Hyperkalemia – should be promptly corrected using glucose/insulin
or potassium-binding resins such as polystyrene sulfonate
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MANAGEMENT OF AKI IN
PREGNANCY
4. MAINTAIN SUPPORTIVE CARE
• Renal replacement • Hemodialysis is generally used in the
therapy/dialysis – Indications for acute setting.
renal replacement therapy in • Recommendations in pregnancy:
pregnancy are similar to those in a. Increase in dialysis time and
the nonpregnant patient: frequency
b. Keeping serum urea <45-60 mg/dL
a. Volume overload
c. Minimizing fluid shifts and
b. Hyperkalemia refractive to hypotension, which can affect fetal
medical management well-being.
c. Metabolic acidosis • Renal replacement therapy is often
short term in AKI in pregnancy until
d. Symptomatic uremia there is recovery of renal function
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MANAGEMENT OF AKI IN PREGNANCY
5.OPTIMIZE FETAL HEALTH
• In general, maternal health takes priority; however, the fetal condition should be optimized
whenever possible
• Fetal well-being and neonatal outcomes are closely linked to maternal status. Adequate blood
flow to the uterus and feto-placental unit are key factors in preventing fetal compromise; as such,
intravascular volume depletion should be avoided and hypotension treated promptly
• Fetal monitoring –
• For viable pregnancies (greater than 23-24 weeks of pregnancy), fetal well-being should be
assessed at least daily
• Fetal heart rate monitoring (continuous or intermittent) and/or biophysical profile evaluation by
ultrasound may be used depending on the clinical situation
• If preterm delivery is indicated after 24 weeks but prior to 34 weeks, then antenatal
glucocorticoids should be administered
• Maternal-fetal medicine specialists and neonatologists should be closely involved if preterm
delivery is a consideration
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CONCLUSION
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Thank You
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