High risk obstetrics acute kidney injury case file

High Risk Obstetrics Acute Kidney Injury Case File

Eugene C. Toy, MD, Edward Yeomans, MD, Linda Fonseca, MD, Joseph M. Ernest, MD

Case 22

A 36-year-old African American woman, G4P3003, presents to OB triage at 38 weeks’ gestation complaining of painful contractions, vaginal bleeding, and decreased fetal movement. Her prenatal course was complicated by chronic hypertension treated with labetalol 300 mg twice a day. Vital signs at presentation are: BP 116/60 mm Hg, temperature 98°F, pulse 116 bpm, RR 16 breaths/minute. The external monitor shows a baseline fetal heart rate of 120 beats per minute with minimal variability and no accelerations. Contractions are occurring every 1 to 2 minutes. Abdominal examination reveals a firm, tender fundus. The cervix is dilated to 5 cm and completely effaced, with the fetal head at −2 station. Fifty cubic centimeters of blood is removed from the vaginal vault. The patient is transferred from triage to labor and delivery where the nurse reports difficulty finding fetal heart tones. Ultrasound at the bedside confirms the absence of fetal heart activity. There is 100 cc of blood on the bed liner. A Foley catheter is inserted and the bladder is emptied of 50 cc of dark urine. Hemoglobin and hematocrit are not yet available. The patient is given a fluid bolus of 1 L of lactated Ringer and complains of pelvic pressure. Shortly thereafter a stillborn infant is delivered vaginally, the placenta follows immediately and estimated blood loss is 2 L. There has been no urine output since the bladder was catheterized.

➤ What is the most likely cause of anuria following placental abruption?

➤ What is your next step?

➤ What are the short-term and long-term consequences of this patient’s diagnosis?

ANSWER TO CASE 22:

Acute Kidney Injury

Summary: This is a 36-year-old G4P3003 at term with frequent contractions, vaginal bleeding, tachycardia, uterine tenderness, and fetal death. This presentation is attributable to abruption of the placenta. After delivery, the patient is hypovolemic and virtually anuric.

➤ Most likely cause of anuria following placental abruption: Sudden severe volume depletion from hemorrhage, leading to decreased renal blood flow (ischemia).

➤ Next step: Immediate volume replacement with typed and screened or O−(do not wait for cross match) blood and crystalloid. Check a CBC, complete metabolic profile, a coagulation panel, urinalysis, and toxicology screen. Tape a red-top tube containing 2 to 3 cc of blood to the wall.

➤ Potential complications: Acute tubular necrosis, acute cortical necrosis, possible hemodialysis to manage volume overload, acidosis, electrolyte imbalance, or worsening uremia, death.

ANALYSIS

Objectives

1. Recognize the most common causes of acute kidney injury (AKI) in the obstetric patient.
2. Learn how to prevent acute renal failure caused by hypovolemia, severe hypertension, and sepsis.
3. Be familiar with the evaluation and management of AKI.

Considerations

This is a multiparous 36-year-old African American woman with chronic hypertension requiring antihypertensive therapy. She initially presented with vaginal bleeding, frequent contractions, tachycardia, and was then discovered to have a fetal demise. The fetal monitor in the triage unit was actually amplifying and displaying the maternal pulse. Abruption severe enough to result in fetal death is associated with disseminated intravascular coagulation (DIC) in 30% of cases which, in turn, will exacerbate blood loss. Acute blood loss accounts for the postpartum anuria noted in this case.

APPROACH TO

Acute Kidney Injury

DEFINITIONS

ACUTE KIDNEY INJURY: An abrupt decline in renal function resulting in an inability to excrete metabolic waste products and maintain fluid, acid-base, and electrolyte balance. (See Table 22–1 for risk, injury, failure, loss, and end stage kidney disease [ESKD]. The acronym for these five stages is RIFLE, which highlights the spectrum of severity encompassed by the term “acute kidney injury.”)

ACUTE TUBULAR NECROSIS (ATN): Renal tubule cell damage and death. This is seen at the severe end of the spectrum of acute kidney injury. Muddy brown granular or tubular epithelial cell casts may be found on urinalysis.

ACUTE CORTICAL NECROSIS (ACN): This requires a renal biopsy for diagnosis, but biopsy can miss the diagnosis due to the patchy nature of the disease process. This severe kidney injury can follow a prolonged period of acute tubular necrosis. In the developing world, obstetric emergencies like the placental abruption presented still contribute many cases of cortical necrosis.

TILT TEST: A decrease in systolic pressure of 20 mm Hg or an increase in pulse of 20 beats per minute associated with a change in posture, for example, lying to sitting, sitting to standing, lying to standing (allowing at least 2 min for equilibrium after position change).

CLINICAL APPROACH

For decades the lack of clear, concise, and widely accepted definitions for acute renal failure has made it difficult to compare incidence and outcomes between studies. In 2005, the term acute renal failure was changed to acute kidney injury. At around the same time, the RIFLE criteria (Table 22–1) were proposed to clarify the spectrum of acute kidney injury.1 The literature search conducted for this review included the terms pregnancy, acute renal failure, acute kidney injury, hemodialysis, and renal replacement therapy. Because the term AKI and the RIFLE criteria have been in use for only a relatively short time, the authors have referenced some of the earlier work on acute renal failure in pregnancy.

The incidence of AKI related to pregnancy varies widely, from just under 1/1000 to 1/20,000.2,3 It is plausible that the higher figure includes women with serum creatinine levels greater than 0.8 mg/dL while the lower figure is confined to women requiring dialysis. Allowing for this degree of disparity in definition, other factors affecting incidence include study methodology and country of origin (developed or developing). Separate RIFLE criteria have not been applied to pregnant women and, given the 50% increase in glomerular

GFR = glomerular filtration rate

AKI = acute kidney injury

filtration rate (GFR) during pregnancy, this may be problematic. Over 80% of cases of AKI related to pregnancy are confined to the postpartum period, and thus do not affect the fetus. There may be a distinction between postpartum AKI encountered in the first 48 hours compared to those that are diagnosed 3 or more days postpartum.

Most cases of AKI in pregnancy result from hypertensive disease (preeclampsia, eclampsia, and HELLP syndrome) and hemorrhage (especially placental abruption severe enough to cause the death of the fetus, as in the case presented).4 Other causes include microangiopathic diseases (HUS and TTP), sepsis, and obstruction. No matter what the cause, it is axiomatic that drugs such as magnesium and gentamicin used commonly by obstetricians require dosage adjustment or discontinuation if severe renal dysfunction is present.

One factor which may contribute to the recent decline in AKI secondary to hypertensive disorders is the early detection and subsequent prompt delivery of women with these disorders. There is no evidence that loop diuretics like furosemide favorably affect the prognosis in AKI and their use is not recommended, particularly when they are used in an attempt to convert oliguric to nonoliguric renal failure.

Before considering general management principles in pregnant or postpartum women, it is important to emphasize that prevention of AKI in the case presented at the start of this chapter is both possible and desirable. More than 40 years ago, obstetricians at Parkland Hospital developed transfusion guidelines for the management of hypovolemia secondary to hemorrhage.5 These guidelines, referred to as the “30-30 rule,” called for transfusion to maintain the woman’s hematocrit at or close to 30% and her urine output at ≥ 30 mL/h. If available, whole blood was given, but it is recognized that whole blood is not readily available at many centers, so packed red blood cells +/− fresh frozen plasma may be substituted. A recent publication from Parkland Hospital reported an incidence of ATN of 0.3% (2/659) among women who were transfused with whole blood, compared to 2% (12/593) who received only packed red blood cells (PRBCs).6 This difference was statistically significant. Finally, whole blood contains considerably more clotting factors than PRBCs. This is important because DIC complicates 30% of cases of placental abruption severe enough to result in fetal death. Using either crystalloid or colloid alone is not recommended for volume replacement. Criteria for hypovolemia include hypotension (systolic blood pressure < 100 mm Hg) unrelated to regional anesthesia, resting tachycardia (pulse > 100 bpm), a positive tilt test (see Definitions), and low urine output (< 30 mL/h). Even if evidence of hypovolemia is lacking, transfusion is indicated if the hematocrit is less than 20% in the setting of hemorrhage.

Other measures used to prevent progression of AKI to ATN include early recognition and treatment of sepsis and avoidance of vasoconstrictors if sepsis is not suspected.

The definition of AKI in Williams Obstetrics5 is a rapid decrease in the glomerular filtration rate (GFR) over minutes to days. Clinically, creatinine clearance is used to approximate GFR and is calculated as:

where urine and plasma creatinine are measured in milligrams per deciliter and V̇ = urine flow, in units of milliliters per minute. Classically, the period of urine collection is 24 hours (1440 min). Thus, the

V̇ term represents the volume of urine excreted (in 24 h) divided by 1440 minutes.

Another important formula in managing women with AKI is the fractional excretion of sodium (FEN). This formula makes use of the general formula for clearance of a substance (see preceding equation) and compares the clearance of sodium to the clearance of creatinine:

Manipulating the right side of the equation and multiplying by 100 yields FENa as a percent:

A FENa of less than 1% suggests that AKI is due to prerenal causes, often hypovolemia, whereas a FENa greater than 1% implies that intrinsic renal injury is present. Prior use of diuretics invalidates the FENa result. The values used in the formula require the determination of both plasma and urine electrolytes.

Diagnostic Evaluation

Evaluation of women suspected of having acute kidney injury is relatively simple and straightforward. Frequent assessment of vital signs (including testing for orthostatic changes), monitoring of urine output hourly if indicated, daily weight determination, and heart and lung examination should be supplemented by hemoglobin and hematocrit, serum and urine electrolytes, urinalysis and, if abruption is suspected, a coagulation panel. Taping a red top tube to the wall, mentioned at the beginning of this chapter, has practical utility. Also called the clot observation test, the important feature is the size of the clot that evolves and persists, not measuring the time it takes to clot. A small, soft, “mushy” clot which later dissolves indicates a high probability of overt hypofibrinogenemia long before a fibrinogen result is returned from the lab. The absolute level of serum creatinine, rate of rise, and weight-based urine output are each incorporated into the RIFLE criteria (Table 22–1).

Management Considerations

Management by the obstetrician of acute kidney injury obviously depends on the severity of the injury. Prompt restoration of circulating volume and appropriate management of preeclampsia, eclampsia, and HELLP syndrome including expeditious delivery are critically important steps. Close observation and supportive care usually suffice for mild to moderate azotemia. Cases complicated by persistent oliguria despite volume resuscitation and resulting in steady increase in serum creatinine to levels beyond 3 to 4 mg/dL (F level in the RIFLE criteria) should prompt nephrology consultation and, in turn, a high likelihood of the need for some type of renal replacement therapy (hemofiltration or hemodialysis). Dialysis for acute kidney injury is most often indicated for worsening uremia. Other indications include volume overload, acidosis, and hyperkalemia.

Finally, there remains a debate about whether postpartum renal failure is a unique clinical entity in some cases. First reported more than 40 years ago and regarded as idiopathic, postpartum renal failure (PPRF) was differentiated from renal failure secondary to obstetric complications like the one outlined in this chapter. The time of onset, 3 or more days postpartum for the idiopathic type, was felt to be one of the key distinguishing features. A case report from 2008 that would have fulfilled the criteria for idiopathic PPRF instead concluded that renal failure occurred as a result of catastrophic antiphospholipid antibody syndrome.7 The woman who was the subject of that report was admitted 2 weeks postpartum with a creatinine of 2.4 mg/dL (stage I or F of the RIFLE criteria). Within just a few days she became persistently oliguric, the serum creatinine increased to 5.4 mg/dL, and she was treated with hemodialysis for 24 days in the hospital. Because her kidneys did not recover by the time of discharge, hemodialysis was continued as an outpatient. This suggests that a proportion of PPRF cases may no longer be properly classified as idiopathic.

Comprehension Questions

22.1 With placental abruption severe enough to cause fetal death, what is the incidence of DIC?

A. 10%

B. 30%

C. 50%

D. 70%

22.2 Most cases of acute kidney injury in pregnancy and the postpartum period are caused by which of the following?

A. Hypertension and hemorrhage

B. Sepsis and DIC

C. HUS and TTP

D. Acute fatty liver

22.3 The fractional excretion of sodium (FENa) is expressed in which of the following units?

A. mg/dL

B. mL/min

C. %

D. mg/min

22.4 An increase in GFR by 50% in normal pregnancy accounts for which of the following facts?

A. Decreased FENa in pregnancy

B. Increase in blood volume by 50%

C. A slight decrease in pH to 7.37

D. An upper limit of normal for plasma creatinine of 0.8 mg/dL

ANSWERS

22.1 B. DIC complicates 30% of abruptions severe enough to cause fetal death. DIC is most often manifested by overt hypofibrinogenemia.

22.2 A. The combination of hypertension and hemorrhage accounts for more than 80% of cases of AKI in pregnancy.

22.3 C. FENa is expressed in %. The urine flow cancels out in numerator and denominator, and so do the units of urine and plasma sodium and creatinine.

22.4 D. The upper limit of normal for plasma creatinine is 0.8 mg/dL. The meaning of an increased clearance from blood of a substance like creatinine is that there is a lower than normal amount left in the blood. This fact is very important to the diagnosis of AKI in pregnancy.

Clinical Pearls

See US Preventive Services Task Force Study Quality levels of evidence in Case 1

➤ Normal pregnancy is associated with an increase in GFR and a decline in serum creatinine.Therefore,in pregnancy,a creatinine greater than 0.8 mg/dL is abnormal (Level II-3).

➤ All obstetricians should be able to calculate, interpret, and use clinically the fractional excretion of sodium and the creatinine clearance (Level III).

➤ Magnesium sulfate is excreted primarily (> 95%) by the kidneys. Both oliguria (< 100 cc in 4 h) or elevated creatinine (> 1 mg/dL) necessitate at least careful monitoring of serum magnesium level and possibly dose reduction or discontinuation of the intravenous administration of magnesium sulfate (Level II-3).

➤ Appropriate indications for nephrology consultation have not been codified. However, severe oliguria less than 0.3 mL/kg/h or anuria for 6 to 12 hours, accompanied by rapid rise in serum creatinine suggests the need for consultation. Early initiation of dialysis may hasten recovery (Level II-3).

REFERENCES

1. Ricci Z, Cruz D, Ronco C. The RIFLE criteria and mortality in acute kidney injury: a systematic review. Kidney Int. 2008;73:538-546. 

2. Gammill HS, Jeyabalan A. Acute renal failure in pregnancy. Crit Care Med. 2005;33:372S-384S. 

3 Drakeley AJ, Le Roux PA, Anthony J, Penny J. Acute renal failure complicating severe preeclampsia requiring admission to an obstetric intensive care unit. Am J Obstet Gynecol. 2002;186:253-256. 

4. Silva GB Jr., Monteiro FA, Mota RM, et al. Acute kidney injury requiring dialysis in obstetric patients: a series of 55 cases in Brazil. Arch Gynecol Obstet. 2009;279:131-137. 

5. Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rouse DJ. Williams Obstetrics. 23rd ed. New York, NY: McGraw Hill; 2010:1045-1046. 

6. Alexander JM, Sarode R, McIntire DD, Burner JD, Leveno KJ. Whole blood in the management of hypovolemia due to obstetric hemorrhage. Obstet Gynecol. 2009;113:1320-1326. 

7. Magee CC, Coggins MP, Foster CS, Muse VV, Colvin RB. Case 2-2008: A 38-yearold woman with postpartum visual loss, shortness of breath and renal failure. N Engl J Med. 2008;358:275-289.

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