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Acute renal failure in the obstetric patient
1. ACUTE RENAL FAILURE IN THE OBSTETRIC PATIENT – CLINICAL
MANAGEMENT: PART 1
In general, medical staff should be cautioned against excessive concern regarding
oliguria, as this may result in fluid overload causing serious iatrogenic problems. The
diagnosis is usually apparent from clinical circumstances, a careful history and physical
examination. Patients at risk of renal failure should have the bladder catheterised with
an indwelling catheter. Normal urine output is approximately 0.5 ml/kg body weight/hour
with oliguria defined as urine output of less than 400 ml in 24 hours. However, due to
the fact that it is important to identify high-risk cases early, urine output consistently less
than 30 ml/hour over a four-hour period should prompt careful assessment.
Management approach
Therapy consists of symptomatic and supportive care of the mother until renal function returns. This
consists of close observation of fluid balance aided by invasive central monitoring when necessary and
serial evaluation of serum electrolytes, particularly urea, creatinine and potassium. In most cases it is
difficult to decide which of the three types of acute renal failure (pre-renal failure, acute tubular necrosis,
acute cortical necrosis) is present. When anuria is present obstruction must be excluded.
Key point: Patients not responding to the simple conservative measures outlined here must be referred
earlier rather than later to a specialist centre.
Fluid management
The central principle is to adequately replace blood and fluid losses and maintain blood pressure levels to
ensure adequate renal perfusion, i.e. maintain euvolaemia. Blood loss must be taken into account as it is
frequently concealed (as in placental abruption) or underestimated. Volume correction must always precede
the use of diuretics. Differentiation between renal insufficiency due to dehydration or hypotension and acute
tubular or cortical necrosis is important, as the therapy for these conditions is very different. Administration
of large amounts of fluid in acute tubular necrosis is more dangerous than beneficial. The initial approach to
a patient who develops oliguria is shown below.
After the diagnosis of acute tubular necrosis (persisting oliguria with rising serum urea and creatinine) fluid
restriction and careful biochemical monitoring should be instituted. Volume balance is achieved by giving an
adult, non-febrile woman an intake of 500 ml of fluid plus the total output of the preceding 24 hours. Specific
attention must be given to serum potassium levels (danger of potentially fatal hyperkalaemia) and the acid-
base balance (danger of metabolic acidosis).
2. Key point: Useful formulae are given in “Clinical Management: Part 2”.
Overhydration must be avoided. By contrast careful supervision and replacement of electrolytes is important
in the polyuric phase. After commencement of a sustained diuresis, the CVP monitoring can be
discontinued and the bladder catheter removed. Renal function tests and electrolytes must be monitored
until they have returned to normal.
Diuretics and dialysis follow in “Clinical Management: Part 2”.
Initial management of oliguria
3. * Macroscopic haematuria is an ominous sign that may be associated with HELLP syndrome. These cases
should be referred early to a specialist centre.
Management will be continued in “Clinical Management: Part 2”.
Prof DR Hall
Department of Obstetrics and Gynaecology, University of Stellenbosch
E-mail: dhr@sun.ac.za
5. ACUTE RENAL FAILURE IN THE OBSTETRIC PATIENT –
CLINICAL MANAGEMENT: PART 2
Oliguria is not uncommon during pregnancy and the postpartum period. Most of the problems
that are linked to acute renal failure, including those with pre-eclampsia will resolve
completely following delivery in correctly managed cases. Approximately one case in 13 500
pregnancies will require dialysis. In cases of “patchy” cortical necrosis the acute phase is
followed by a variable return of function, manifesting as a stable period of renal insufficiency.
Management
Diuretics
Although often given, there is no evidence of any beneficial effect of furosemide on the period of oliguria or
renal prognosis. Nonetheless the early use (within the first 48 hours) of diuretics in a patient with acute
renal failure is rarely harmful and may make fluid management easier if some simple precautions are taken.
Care must be taken to establish that the patient is volume replete before using diuretics. Their use should
also be avoided in patients with pre-eclampsia unless pulmonary oedema is present or central monitoring
indicates intravascular volume expansion (CVP 10 cm H20). Repeated high doses of furosemide cause
ototoxicity. Avoiding rapid infusion (rate not to exceed 15 mg/minute) can also lessen this danger.
Useful formulae when hyperkalaemia or metabolic acidosis are present
Hyperkalaemia:
+
K 5.6-6.8 mmol/l Kayexelate 20-30 g every 2-4 hours orally or 50-100 g rectally.
+
K 6.9-7.9 mmol/l 10 units short-acting insulin and 50 ml of 50% glucose.
Sodium bicarbonate 100 ml of 4.2% solution.
Kayexelate as above.
+
K 8 mmol/l Insulin and glucose as above.
Sodium bicarbonate as above.
Calcium gluconate 10 ml of 10% solution.
Dialysis.
Metabolic acidosis: Maintain plasma bicarbonate above 12 mmol/l. When it falls below this:
Sodium bicarbonate 100 ml of 4.2% solution.
Calcium gluconate 10 ml of 10% solution and check
biochemistry again.
Acute renal failure in pre-eclampsia
6. Pre-eclampsia is a major cause of renal dysfunction during pregnancy. It is accompanied
by a specific renal lesion known as glomerular endotheliosis, in which the glomeruli
enlarge and become ischaemic. Pre-eclampsia is characterised by general
vasoconstriction and haemoconcentration with a reduced intravascular volume.
Key point: When pre-eclampsia is complicated by placental abruption or HELLP syndrome it may progress
to acute renal failure and even cortical necrosis.
Left ventricular dysfunction and capillary leak complicate fluid management in severe pre-eclampsia. These
patients should receive 80 ml crystalloid solution intravenously/hour. Central venous pressure monitoring is
misleading, as it does not correlate well with the pulmonary capillary wedge pressure in these women. Due
to the fact that the pulmonary wedge pressure may be high in the absence of an elevated CVP, assessment
of whether the myocardium is handling therapeutic volume expansion can only be assessed after placement
of a pulmonary artery catheter. This will only be necessary in selected cases.
Key point: Patients with severe pre-eclampsia, who have developed oliguria and have not responded to two
blind fluid challenges should be referred to a specialist centre as they are candidates for invasive
haemodynamic monitoring.
The great danger of plasma volume expansion by intravenous fluid therapy in patients with pre-eclampsia is
fluid overload and pulmonary oedema. For this reason it is better to intensively restrict fluid in these patients
(“dry management” as noted above), thus avoiding more dangerous iatrogenic pulmonary problems. Even
with this approach, acute renal shut down is extremely unlikely unless complicated by hypotension,
coagulopathy or the use of anti-inflammatory agents such as diclofenac.
Key point: Anti-inflammatory agents such as diclofenac should be avoided in severe pre-eclampsia.
Dialysis
Most of the problems linked to acute renal failure will respond to conservative
management, but if this approach is unsuccessful, dialysis will be necessary. Both
haemodialysis and peritoneal dialysis can be used in pregnant or recently delivered
women. The main indications for dialysis are:
Volume overload with congestive heart failure (pulmonary oedema)
Severehyperkalaemia
Severe acidosis
Uraemic symptoms not manageable by conventional methods.
