Anuria
Anuria is defined as the complete absence of
urine production. Oliguria is present when less than 300 ml of urine is excreted
in a day.
The
maintenance of renal function and urine production depends upon perfusion of the
kidneys with oxygenated blood. Reduced renal blood flow or hypoxia impairs renal
function. When both are present, the danger of acute renal failure is even
greater.
Renal
failure is traditionally divided into:
•
pre renal;
•
renal;
•
post renal (obstructive).
Pre
renal
Pre renal cause of acute renal failure include:
•
hypovolaemia;
•
blood loss;
•
sepsis;
•
cardiogenic shock;
•
anaesthesia;
•
hypoxia.
Hypovolaemia
This may result from inadequate fluid intake or from excessive
loss of body water. Dehydration, prolonged vomiting, diarrhoea and other
abnormal gastrointestinal fluid losses, burns and excessive sweating are all
common causes of hypovolaemia.
Blood
loss
This is usually caused by trauma or surgery,
but acute blood loss from the gastrointestinal tract or associated with
childbirth may be sufficient to cause hypovolaemic renal impairment.
Sepsis
Gram-negative septicaemia from a urinary tract
source is a particularly potent cause of bacteraemic shock. Sepsis from the biliary
tract and
overwhelming infection from other sites, especially in the immunocompromised
individual, are also associated with acute renal failure.
Cardiogenic
shock
Acute dysrhythmia secondary
to myocardial infarction, cardiac tamponade and pulmonary embolus may all result
in the reduced cardiac output of often poorly oxygenated blood.
Anaesthesia
Hypotension is a hazard of epidural and spinal
anaesthesia.
Hypoxia
Prolonged hypoxia from any cause may
occasionally be responsible.
Renal
• poisons;
•
contrast media;
•
eclampsia;
• myoglobinuria;
• incompatible
blood transfusion;
• disseminated intravascular coagulation.
It
is uncommon for patients with established glomerulonephritis to develop acute
oliguria; however, such patients are more prone to rapid deterioration of
remaining renal function should any renal insult occur.
Drugs
Aminoglycosides, cephalosporins and diuretics
can be nephrotoxic
particularly if used
in combination. They are quite
commonly used in
patients whose
renal function is already compromised by sepsis or circulatory abnormalities.
Prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs) can cause a
chronic interstitial nephritis and papillary necrosis; they also reduce renal
plasma flow and therefore have nephrotoxic properties. Angiotensin-converting
enzyme inhibitors used for the control of hypertension can cause a rapid
reduction in the glomerular
filtration rate;
this is particularly liable to occur in patients who have a reduced renal blood
flow.
Poisons
Some of these are nephrotoxic.
Contrast
media
Even modern contrast media may cause renal
failure when injected into a dehydrated patient with compromised renal function.
Eclampsia
The early recognition of pre-eclampsia is vital
to avoid the nephrotoxic consequences of toxaemia and uncontrolled hypertension.
Myoglobinuria
The presence of myoglobin in the urine is
associated with the ‘crush’ syndrome after major trauma. Less severe
injuries can also cause the syndrome, especially if a compartment syndrome is
unrecognised or pressure areas break down.
Incompatible
blood transfusion
This may lead to renal failure with
myoglobinuria.
Disseminated
intravascular coagulation
Disseminated intravascular coagulation usually
follows major sepsis or massive blood
transfusion and may occur postpartum.
Obstructive
Obstructive causes of acute renal failure
include:
•
calculi;
•
pelvic malignancy;
•
surgery;
•
retroperitoneal fibrosis;
•
bilharzia;
•
crystaluria.
Calculi
Renal calculus disease is probably the most
common cause of acute obstruction leading to anuria. The patient is likely to
have unilateral renal colic against a background of nonfunction of the
contralateral kidney, often due to previous surgery or pre-existing obstruction
by calculus.
Pelvic
malignancy
Carcinomas arising from the bladder, prostate,
cervix, ovary or rectum can all lead to obstruction of one or both ureters. A
history of haematuria and vaginal or rectal bleeding signpost the diagnosis. A
large pelvic mass is commonly palpable on bimanual examination.
Surgery
The ureters are vulnerable to damage during
pelvic and retroperitoneal surgery but injury should be avoided if proper care is taken. It is unusual, but not
impossible, to damage both ureters.
Retroperitoneal
fibrosis
For details of retroperitoneal fibrosis see
Chapter 64 on ‘The kidneys and the ureters’.
Bilharzia
Schistosomiasis may lead to ureteric fibrosis
and stenosis, and may be responsible for the development of squamous cell
carcinoma of the bladder.
Crystaluria
Crystalunia causing urinary tract obstruction
used to be associated with sulphonamide medications. This is now rare.
However, uric acid crystaluria can develop in patients receiving chemotherapy
for leukaemia or lymphoma unless they are given prophylactic treatment with allopurinol.
Clinical
aspects
Answers to the following questions should
indicate the probable cause of reduced urine output.
Is
urine being produced? Catheterisation of the bladder is mandatory if a voided
sample cannot be obtained. If urine is available check the specific gravity,
look for the presence of
casts (implying a renal cause), test for
myoglobinuria and send some for culture and microscopy.
Is
there an obvious pre renal cause? This can usually be answered by clinical
examination, assessment of the patient’s vital signs, examination of the fluid
balance chart and measurement of the arterial oxygen concentration.
Is
there ureteric obstruction? Hydronephrosis may not be marked in acute
obstruction, but ultrasonography will usually show some degree of ureteric
dilatation. A plain abdominal radiograph should be checked for calculi.
What
drugs have been given recently? If a drug is thought to be responsible for renal
impairment it should obviously be withdrawn unless its use is vital.
Is
this a progression to chronic renal failure? The presence of shrunken kidneys on
ultrasound, normochromic anaemia and hypertension suggest progression to a
chronic state even if a previous history of renal failure is not available.
Management
and treatment
Renal failure caused by acute tubular necrosis
may progress through three recognisable phases:
•
oligunia;
•
the diuretic phase;
•
recovery.
The
initial management is aimed at prompt restoration of circulating volume deficit
and correction of tissue hypoxia. Most patients will require a level of care
available only in a specialised unit. As a minimum, monitoring with a pulse
oximeter
and central venous pressure measurement will supplement basic observations.
For patients with hypovolaemia or sepsis, inotropic support with dopamine may
improve cardiac efficiency and increase renal blood flow. If urine production is
not promptly restored, frusemide can be given but this is not always successful
and the drug is itself associated with nephrotoxicity. Mannitol may be used as
a plasma expander and osmotic diuretic, but care must be taken not to overload
the circulation. The aim is to achieve the best possible blood pressure with a
central venous pressure of 7—9 cmH2O. One-hundred per cent oxygen
may be needed to maintain the oxygen tension (P02).
If
these measures fail, acute tubular necrosis has supervened. Excess fluid loads
must be avoided and fluid input restricted to match the reduced output plus
insensible losses (500—800 ml per 24 hours depending on ambient conditions).
Abnormal losses due to vomiting, nasogastric aspiration, diarrhoea or fistulae
will be monitored and replaced.
A
hyperkalaemic acidosis is the characteristic metabolic abmormality of the
oliguric phase of renal failure. Correction of the metabolic acidosis with
intravenous bicarbonate is tempting but not always advisable. Rising serum
potassium is life threatening and requires effective intervention. A calcium
resonium enema is the simplest remedy. The ion-exchange resin can also be
administered orally but is unpalatable. Cautious use of intravenous dextrose and
insulin should be
The
diuretic phase traditionally occurs between the 8th and 10th day but may be delayed
as long as 6
weeks. Glomerular filtration recommences but tubular function takes longer to
recover. A heavy loss of sodium and potassium can be expected, and fluid and
electrolyte requirements must be carefully judged. In most patients, the
diuretic phase is followed by the recovery phase but some never recover and will
need renal replacement therapy if they are to survive.
Factors
that influence the outcome of acute renal failure include the need for
artificial ventilation, the need for inotropic support and the presence of
jaundice. There is a significant mortality.
Nutritional
support
Many of these patients are unable to eat. If
enteral feeding is impossible, parenteral nutrition must be administered with
extreme care to avoid circulatory overload.
Infection
These patients are at increased risk of
generalised infection. Swabs taken from the nose and throat, sputum specimens and urine, if available,
should be sent for culture. If antibiotics are required, they should be non
nephrotoxic.
General
nursing care
Meticulous recording of fluid balance is obviously central to
successful management of these patients. Patients who are seriously ill or
comatose need regular turning and
care to pressure areas if they are to avoid pressure sores. Physiotherapy to
the chest and extremities will aid recovery.
Renal
support
Renal replacement is needed for those patients
in whom the oliguric or anuric phase is associated with significant uraemic
symptoms (vomiting, muscular twitching, itching and altered states of
consciousness) or uncontrollable hyperkalaemia.
Peritoneal
dialysis. Provided that the patient has not had recent abdominal surgery,
penitoneal dialysis can be performed by insertion of a fenestrated catheter
under local anaesthesic. This is placed just inferior to the umbilicus in the
midline. Sterile dialysis fluid is then run into the penitoneal cavity where it
equilibrates with the extracellular fluid using the peritoneum as a dialysis
membrane. After a variable time, the fluid is drained into a closed drainage
system. The process is repeated in
cycles.
Occasionally, when anuria is prolonged, a Tenckhoff cuffed catheter needs to be
inserted, as used in chronic ambulatory penitoneal dialysis. The disadvantages
of acute peritoneal dialysis are the potential for introducing infection into
the peritoneum and the rather slow rate of correcting metabolic imbalance,
particularly hyperkalaemia.
Haemodialysis.
A few sessions of haemo dialysis may be life saving. A double-lumen catheter is
placed over a guidewire
Haemofiltration.
This, like haemodialysis, requires the use of an extracorporeal machine but
causes much less haemodynamic upset. This may be of critical importance for the
acutely ill
patient.
When the patient is too ill for surgery to
remove the cause of obstruction to the upper urinary tract, the treatment of
obstructive renal impairment is drainage either externally using a nephrostomy
or internally using an indwelling stent.
Percutaneous
nephrostomy. Under ultrasonographic guidance and local anaesthetic, a fine-bore
hollow needle is introduced via the flank through the parenchyma and into the
expanded collecting system of the obstructed kidney. Once it penetrates the
system, contrast medium can be injected through the needle to define its
exact position. A wire passed through the lumen of the needle is used to guide
the insertion of a series of dilators which enlarge the track until it will
accept a suitably sized nephrostomy tube (Fig. 63.10). This will drain urine and
pus, provided that the latter is not too viscous. The tube is anchored firmly in
place to allow continued drainage as renal function recovers.
Insertion
of a J-stent. The ureter can be drained into the bladder by the insertion of a
pigtail- or J-stent (see Fig. 63.10). The procedure begins with a retrograde
ureterogram under fluoroscopic control to provide an image of ureter. This will
often give an indication of the cause of the obstruction. A guidewire is
introduced through the ureteric orifice and guided up the ureter into the renal
pelvis. The stent is rail-roaded over the guidewire until its distal end also
lies within the renal pelvis above the obstruction. When the guidewire is
removed, the ends of the stent curl to form a J-shape or a pigtail to secure the
device against migration. Stents can be placed under topical urethral
anaesthesia using the flexible cystoscope and may be safely left in position for several months. They are a
foreign body in the urinary tract and are prone to infection and
If
the J-stent cannot be inserted cystoscopically, it may be
placed from above through a nephrostomy.
Open
surgery. This is a rarity when the minimally invasive methods described above
are available. Retrograde insertion of a nephrostomy through an incision in the
renal pelvis is the preferred method because it can be surprisingly difficult to locate even dilated
calyces by blind puncture of the renal parenchyma.