Transcript RENAL FAILURE IN PREGNANCY

ACUTE RENAL FAILURE IN
PREGNANCY
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BASIC OUTLINE
Investigations
MANAGEMENT PRINCIPLES
Prerenal Vs ATN Vs ACN
ROLE OF
Nutrition
Volume & metabolic control
Diuretics : helpful or harmful ??
Dopamine : helpful or harmful ??
Dialysis : when & which ??
Renal biopsy ??
Delivery
Conditions specific to pregnancy
DEFINITIONS OF ARF
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The syndrome is characterised by a
sudden
in parenchymal function
(UOP<400ml/d;30ml/hr) which is
usually but not always reversible
This produces disturbance of water,
electrolyte, acid base balance and
nitrogenous waste products & blood
pressure.
Normal Physiologic
Alterations of Pregnancy
Physiological changes in
normal gestation
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Kidney weight and size
increase
Dilation of renal calyces,
pelves, and ureters
Urinary stasis
Glomerular filtration,
effective renal plasma
flow, fractional clearance
of urate increase
Bicarbonate reabsorption
threshold decreases
Clinical relevance
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Concentrations of serum creatinine, urea N,
and uric acid of 0.9, 14, and 5.6 mg/dl,
normal in nonpregnant subjects, are already
suspiciously high in gravid women.
Asymptomatic bacteriuria - frank
pyelonephritis.
PP reduction in size should not be mistaken
for parenchymal loss
Post renal failure difficult to diagnose
S.bicarb lower,PCO2 10 mmHg lower
Causes
Early in Pregnancy
Most common cause is pre-renal failure
due to hyperemesis gravidarum
 ATN due to septic abortion
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Causes - ARF Late in
Pregnancy/Postpartum
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Thrombotic microangiopathy
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Renal Cortical Necrosis
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TTP-HUS
Severe preeclampsia usually with HELLP syndrome
Placenta previa
Prolonged intrauterine fetal death
Amniotic fluid embolism
Intrinsic renal disease/autoimmune diseaes
ARF Late in
Pregnancy/Postpartum
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Acute pyelonephritis
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Acute fatty liver of pregnancy
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ATN from septicemia or hypotension
ARF from microabscesses
ARF in up to 60% of cases
Preeclampsia + hypoglycemia, hypofibrinogenemia,
LFT abnormalities, prolonged PTT
Obstructive uropathy
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Mild-moderate hydronephrosis is normal
Occasionally, degree of obstruction sufficient to
cause ARF.
Nephrolithiasis if solitary functioning kidney
Causes - Severe
Preeclampsia/HELLP
Typically develops late in 3rd trimester; a
few percent of cases can happen up to
48 hours post-partum.
 Preceded by hypertension, proteinuria,
and severe edema
 ARF not typical unless marked DIC
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Severe
Preeclampsia/HELLP
But, there are cases reported in which
renal abnormalities begin post-partum
WITHOUT prior proteinuria
 Typically, spontaneous recovery 2-3 days
post-partum; complete recovery typical by
8 weeks post-partum.
 Corticosteroids have been utilized but no
large randomized clinical trials
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Causes - TTP-HUS
Thrombocytopenia + microangiopathic
hemolytic anemia + ARF
 Traditionally, TTP if neurologic
symptoms are abundant; HUS if ARF is
dominant. BUT, distinctions are often
unclear and may not be important for
management decisions
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TTP-HUS
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Timing variable:
25% before mid-pregnancy
 65% peri-partum
 20% postpartum: may follow normal
pregnancy or be preceded by findings
indistinguishable from preeclampsia
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Can relapse if TTP-HUS occurred once
prior to pregnancy; can occasionally
relapse in subsequent pregnancy
TTP-HUS
Plasma infusion +/- plasma exchange
(plasmapheresis)
 In one series of 11 women:
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2 died
 4 with residual CKD
 5 recovered completely
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Prior to use of plasmapheresis, 90%
mortality rate reported
Causes - Renal Cortical
Necrosis
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Bilateral cortical necrosis
Severe renal ischemia or DIC with resultant
endothelial damage
Abruptio placenta, placenta previa, prolonged
intrauterine death, amniotic fluid embolism
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THEN, patient develops acute onset of oliguria or
anuria, gross hematuria, flank pain, and hypotension
ANURIA, GROSS HEMATURIA, FLANK PAIN – triad
that is unusual in other causes of renal failure
Renal Cortical Necrosis
US or CT can be suggestive
 Biopsy can demonstrate necrosis
 No specific therapy – many patients
require dialysis but 20-40% have partial
recovery with CrCl between 15 and 50
mL/min.
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To summarise
Causes
 Bimodal
distribution -peaks in the
first trimester (related to
unregulated and/or septic
abortion,hyperemesis) and the
late third trimester (related to
obstetric complications
APH,PPH,Preeclampsia,
Chorioamnionitis,AFE etc).
ETIOLOGY OF
ACUTE RENAL FAILURE
PRERENAL
CAUSES
INTRARENAL
CAUSES
POSTRENAL
CAUSES
ATN
CORTICAL NECROSIS
THOMBOTIC MICROANGIOPATHIES
The RIFLE classification (ADQI group) of ARF:
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Risk (R) - Increase in serum creatinine level X
1.5 or decrease in GFR by 25%, or UO <0.5
mL/kg/h for 6 hours
Injury (I) - Increase in serum creatinine level
X 2.0 or decrease in GFR by 50%, or UO <0.5
mL/kg/h for 12 hours
Failure (F) - Increase in serum creatinine level
X 3.0, decrease in GFR by 75%, or serum
creatinine level > 4 mg/dL; UO <0.3 mL/kg/h
for 24 hours, or anuria for 12 hours
Loss (L) - Persistent ARF, complete loss of
kidney function >4 wk
End-stage kidney disease (E) - Loss of kidney
function >3 months
PHASES
OLIGURIA
POLYURIA
RECOVERY
Investigations
BLOOD
CBC
Urea,creatinine,uric
acid
Electrolytes
LFT
S.proteins
Coagulation profile
ABG
RBS
Osmolality
URINE
sp.gravity
osmolality
electrolytes
proteins
pigment casts
c/s
ECG
Management
Restore or maintain fluid balance
 The maintenance of electrolytes and
acid base balance
 The maintenance of nutritional
support
 Prevention of infection
 Avoid renal toxins (including NSAIDS)
 Instigate renal replacement therapies
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Prerenal failure
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Adequately replace blood & fluid losses,maintain BP.
Control continuing blood loss
Mannitol (100ml, 25%) trial to d/d b/w reversible
prerenal failure & established ATN (provided oliguria <48
hrs & U:P osmolality > 1.05)
If diuresis (>50ml/hr or doubling) established within 3
hrs,maintain NS infusion acc to UOP & replace
electrolytes acc to urinary loss estimations.
If unsuccessful –objective is to support the functionally
anephric pt till kidneys recover.
Volume control
IP/OP charting daily
 State of hydration-wt,hct,protein
 Input = Output/24hrs + 500ml(nonfebrile)
+ 200 ml/ deg C of inc. in Tem
Balance : 0.3-0.5kg wt loss/d
 Avoid overhydration : Rx diuretics,dialysis
 CVP monitoring (b/w 10-15cm H2O)
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Diuretics
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Diuretics commonly have been
given in an
attempt to convert the oliguric state to a nonoliguric
state. However, diuretics have not been shown to be
beneficial, and they may worsen outcomes.
In the absence of compelling contradictory data from
a randomized, blinded clinical trial, the widespread
use of diuretics in critically ill patients with acute
renal failure should be discouraged.
Useful only in management of fluid-overloaded
patients
Cantarovich F, Rangoonwala B, Lorenz H, Verho M, Esnault VL. High-dose furosemide for
established ARF: a prospective, randomized, double-blind, placebo-controlled, multicenter trial.
Am J Kidney Dis 2004;44:402-9.
Kellum JA. Systematic review: The use of diuretics and dopamine in acute renal failure: a
systematic review of the evidence. Critical Care1997;1(2):53–9.
DOPAMINE
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Dopamine traditionally has been used to promote
renal perfusion(1-5 mcg/kg/min )
However, systematic reviews of dopamine
treatment in critically ill patients and in patients
with sepsis do not support the use of dopamine to
prevent renal insufficiency, morbidity, or
mortality. In the majority of ARF studies,
dopamine was associated only with an increase in
urine output.
Kellum JA, Decker MJ. Use of dopamine in acute renal failure: a meta-analysis. Crit Care Med
2001;29:1526-31.
Denton MD, Chertow GM, Brady HR. "Renal-dose" dopamine for the treatment of acute renal
failure: scientific rationale, experimental studies and clinical trials. Kidney Int 1996;50:4-14.
Nutrition
INTAKE
1500 cal (protein free)
Oral/parenteral
If vol limitation-50%D
via central vein
Essential L-aminoacids:
K,Mg,P:Improve wound
healing, hasten
recovery
Protein intake of 0.6 g
per kg per day
Electrolyte & acid-base
correction
Hyperkalemia, which can be life-threatening,
should be treated by
 decreasing the intake of potassium,
 delaying the absorption of potassium,
 exchanging potassium across the gut lumen
using potassium-binding resins,
 controlling intracellular shifts
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dialysis.
Acidosis- sodabicarb ,dialysis
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Treat coagulopathy with FFP for a
prolonged aPTT, cryoprecipitate for
a fibrinogen level less than 100
mg/dL, and transfuse platelets for
platelet counts less than
20,000/mm3
Timely identification of UTI, proper
treatment & prevention using
prophylactic antibiotics
Should we Initiate Dialysis
in Pts w/Low Cr Clearance?
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Hou, S., Pregnancy in Women on Hemodialysis,
1994, revealed better outcomes of pregnancy in
women w/ significant residual renal function or
who initiate pregnancy before they need dialysis.
May reduce incidence of polyhydramnios, lower
urea and lowers water load, also reducing risk of
dialysis-induced hypotension
Hou, et al, 1998
Hou, et al, 1998
Hou, et al, 1998
Indications for Kidney
Replacement Therapy
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Acidosis unresponsive to medical therapy
Acute, severe, refractory electrolyte
changes (e.g., hyperkalemia)
Encephalopathy
Significant azotemia (blood urea nitrogen
level >100 mg per dL [36 mmol per L])
Significant bleeding
Uremic pericarditis
Volume overload
Early “Prophylactic” Dialysis
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Allows more liberal
fluid, protein & salt
intake.
Prevent hyperkalemic
emergencies.
infectious Cx.
Improves comfort &
survival
Hemodialysis
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Limited usefulness
if hypotension
C/I in actively
bleeding pt.
Controlled
anticoagulation reqd
Volume shiftscareful
Faster correction
Vs
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Peritoneal
dialysis
Can be used in
preg/PP pt.
Easily available
Simple,inexpensive
Lower Cx rate
Minimises rapid
metabolic
pertubations & fluid
shifts
Insert cath high
direct vision
Delivery
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Development of ARF in obs pt is indication
of delivery in majority cases.
Deliver if UOP<20 ml/>2hrs despite
adequate vol expansion & immediate delivery
not expected
Redistribution of CO – better renal
perfusion.
Remove fetus from hostile environment.
Neonate urea –osmotis diuresis dehydration
Renal biopsy
 Potentially
v.risky in pregnancy
 Defer until postpartum even if
ACN( for prognostication).
 Rare indication sudden renal
failure before 32 wks with no
obvious cause.
Preeclampsia
A decrease in the GFR occurs
secondary to intrarenal
vasospasm. This may manifest as
a "prerenal" picture. Acute renal
failure (ARF) may develop, and
acute tubular necrosis (ATN) may
ensue if this hypoperfusion
persists.
Pre-eclampsia: Management
Renal problems
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Hyperuricaemia and proteinuria are
NOT indications for delivery per se
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Consider delivery for progressive renal
impairment (creatinine >0.09 mmol/L)
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Care with fluids (pulmonary oedema can
kill!)
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Kidney Function is Critical
for Drug Elimination
Pre-eclampsia
Invasive monitoring
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CVP monitoring may NOT be helpful!
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poor correlation between CVP and PCWP
PA catheters have risks!
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rare indications:
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pulmonary oedema resistant to diuretics
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oliguric renal failure despite volume
expansion
Idiopathic postpartum renal
failure
Associated primarily with
microangiopathic processes
 Postpartum hemolytic-uremic syndrome.
 These were often irreversible and were
associated with substantial mortality.
 Now improved outcome with plasma
exchange,dialysis,prostacyclin infusion,
correcting coagulopathy
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ACUTE FATTY LIVER OF
PREGNANCY
Associated with acute renal failure
in up to 60 percent of cases.
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The diagnosis should be suspected
in a woman with preeclampsia who has
jaundice,hypoglycemia,
hypofibrinogenemia, and a prolonged
PTT in the absence of abruptio
placentae.
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KEY RECOMMENDATIONS
FOR PRACTICE
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Identify & prevent at prerenal phase as
early as possible
Dopamine should not be used to prevent
acute renal failure. (Evidence level A)
Diuretics should not be used to treat
oliguria in patients with acute renal failure
unless volume overload (Evidence level B)
Early prophylactic dialysis should be strongly
considered.
The maintenance of electrolytes,acid base
balance & nutritional support plays vital role.
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