Anuria pptx.pdf

ANURIA/ is defined as the complete absence of urine production. Oliguria is present when less than 300 ml of urine is excreted in aday. The maintenance of renal function and urine production depends upon perfusion of the kidneys with oxygenated blood. Reduced renal blood flow or hypoxia impairs rena...

ANURIA/ is defined as the complete absence of urine production. Oliguria is present when less than 300 ml of urine is excreted in aday. 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. Renal failure is traditionally divided into: Prerenal; Renal; Postrenal (obstructive).  Prerenal/ Prerenal causes of acute renal failure include:  Hypovolaemia/ This may result from inadequate fluid intake or from excessive loss of body water. Dehydration, prolonged vomiting, diarrhea, burns and excessive sweating.  Blood loss/ Any acute blood loss. usually caused by trauma or surgery  Sepsis/ Gram-negative septicaemia from a urinary tract source is a particularly potent cause of bacteraemic shock. Sepsis from other sites, especially in the immunocompromised individual.  Cardiogenic shock/ Acute dysarhythmia after myocardial infarction, cardiac tamponade and pulmonary embolus may reduce 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/ Aminoglycosides, cephalosporins and diuretics can be nephrotoxic, particularly if used in combination.. Prolonged use of non-steroidal anti- inflammatory drugs (NSAIDs) can cause a chronic interstitial nephritis and papillary necrosis;. 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/ 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/ is associated with the‘crush’ syndrome after major trauma.  Incompatible blood transfusion/ This may lead to renal failure with myoglobinuria.  Disseminated intravascular coagulation/ usually follows major sepsis or massive blood transfusion and may occur post-partum.  Obstructive(post renal)/ Obstructive causes of acute renal failure include:  Calculi/ is the most common cause of acute obstruction leading to anuria. The patient is likely to have unilateral renal colic against a background of non- function 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.  Surgery/ The ureters are vulnerable to damage during pelvic and retroperitoneal surgery.  Retroperitoneal fibrosis/ For details of retroperitoneal fibrosis will come later in lecture  Bilharzia / Schistosomiasis may lead to ureteric fibrosis and stenosis, and may be responsible for the development of squamous cell carcinoma of the bladder.  Crystalluria/ may be associated with sulphonamide medications but this is now rare.However, uric acid crystalluria 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 essential 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 a sample for culture and microscopy.  Is there an obvious prerenal 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 mark 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 aprevious history of renal failure is not available.  Management and treatment/ Renal failure caused by acute tubular necrosis may progress through three recognisable phases: oliguria; the diuretic phase; recovery.  The initial management is aimed at prompt restoration of the circulating volume deficit and correction of tissue hypoxia. Monitoring with a pulse oximeter and central venous pressure measurements.  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, lasix (furosemide) can be given but this is not always successful and the drug itself may be nephrotoxic. 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.  It may be that 100% oxygen is needed to maintain the oxygen tension (PO2).  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 abnormality of the oliguric phase.  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 because urgent dialysis may become necessary to save  The diuretic phase traditionally occurs between the eighth 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 need renal replacement therapy if they are to survive. There is a significant mortality rate.  Nutritional support/ If oral or 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 the successful management of these patients. Patients who are seriously ill or comatose need regular turning and care of 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 urgery, it 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 peritoneal 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. 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 haemodialysis may be life saving. A double lumen catheter is placed over a guide wire into 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.  Haemofiltration/ This, like haemodialysis, requires the use of an extracorporeal machine but causes much less haemodynamic upset. This may be of critical  Obstructive renal failure / When the patient is too ill for surgery to remove the cause of obstruction to the upper urinary tract, the treatment 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.This will drain urine and pus.  Insertion of a J-stent/ The ureter can be drained into the bladder by the insertion of a pigtail- or J-stent. The procedure begins with a retrograde ureterogram under fluoroscopic control to provide an image of the ureter. This will often give an indication of the cause of the obstruction. A guide wire is introduced through the ureteric orifice and guided up the ureter into the renal pelvis. The stent is rail-roaded over the guide wire 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. 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.