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

  Renal causes of acute renal failure include:

  drugs;

 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 considered if ion exchange fails. The help of a renal physician is highly desirable.

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 into the one of the great veins (jugular, subclavian or femoral). Between sessions of dialysis, the lines are kept patent by filling them with heparin solution. Haemodialysis can result in a rapid correction of metabolic abnormalities but also tends to result in considerable fluctuations of the overall fluid balance. The other disadvantage is that heparinisation is necessary, and this may be undesirable after a recent surgical procedure.

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.

  Obstructive renal failure

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 encrustation if neglected. It is vital to keep careful records to account for all stents inserted.

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.