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Indian J. Anaesth. 2003; 47 (5) : 367-372 ACUTE RENAL FAILURE
Dr. Rebecca Jacob
reliable indicator of underlying renal function than the Acute renal failure (ARF) is seen commonly in the BUN levels. (Values higher than 2 mgdl-1day-1 may be perioperative period and in the ICU.1 It is associated with a high morbidity and mortality (oliguric 50-80% and non Creatinine Clearance. Normal creatinine clearance oliguric 10-40%).2 It is therefore imperative to either is 120 mlmin-1. A crude estimation of the creatinine prevent its occurrence or recognize its presence and treat clearance may be obtained by the following formula.
it as soon and as efficiently as possible.
Definition of renal dysfunction and it’s diagnosis1,2
CrCl (ml/min) = ———————————— 72 x serum Cr (mg/dl) Urinary output
Traditionally oliguria is defined as a urine output of This equation is simply the ratio of the expected less than 0.5 mlkg-1hr-1 or 400 mlday-1. Anuria is defined amount of muscle breakdown (taking age and weight into as less than 50 ml per day (check that the Foley’s catheter account) to the breakdown product present in the serum is not blocked). However, a reduction in the urine output multiplied by a ‘fudge factor’ of 72. Women being smaller need not necessarily mean renal failure. It may just be an the resulting value is multiplied by 0.85 for females.
external sign of an underlying process such as hypotension However in acute renal failure with rapidly failing kidneys and hypovolemia which needs correction. Restoration of this formula may overestimate creatinine clearance and a blood pressure and blood volume may increase the urine more accurate estimation is required. This may be done output showing that the kidney is in perfect condition.
by collecting urine over a period of time, usually 24 hoursbut in the ICU situation even 2 hours has been shown to Urinalysis. The presence of blood may suggest the yield accurate results and may be more practical ads well presence of an embolic phenomenon and a large number of casts acute tubular necrosis. Also look for protein andmyoglobin. However, ‘dirty’ results on urinalysis are CrCl (ml/min) = —————————————————— Blood Urea Nitrogen (BUN) is the breakdown product of protein and in the presence of acute renal failure Urine sodium and osmolality. When perfusion of it typically rises by about 10 -15 mgdl-1day-1. However it the kidneys is reduced, sodium reabsorption increases must be remembered that the BUN level varies directly and excretion decreases and a urine sodium of less than with protein intake and increases in the presence of 20 meqL-1 results (urine osmolality >400 mosmolkg-1).
gastrointestinal bleeding, sepsis and corticosteroid This may occur in hypovolemia due to dehydration administration (and falls in starvation, malnutrition, muscle or haemorrhage, or from decreased forward flow as is wasting and liver disease). Thus interpretation of BUN seen in patients with cardiac failure. Urinary sodium values must rely more on the change over time rather than concentrations of less than 10 meqL-1 may be seen in on absolute values taking into account concomitant patients with hepatorenal syndrome or very severe hypo conditions such as those mentioned above as well as other When there is an acute injury to the kidney, as in acute tubular necrosis, sodium reabsorption is impaired and Creatinine is the breakdown product of muscle and there is an increase in sodium excretion resulting in urinary its level rises by 1 to 2 mgdl-1day-1 in acute renal failure.
sodium levels of greater than 20 meqL-1 or even greater Its absolute value and change over time is a much more than 40 meqL-1 (urine osmolality <400 mosmolkg-1).
Note that the above numbers are meaningless if diuretics have been given, Occasionally a combination of Correspond to :
factors like hypovolemia in addition to chronic renal failure INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003 may make the interpretation of urinary sodium levels Renal or intrarenal renal failure classically falls
difficult. In these cases fractional excretion of sodium into 3 categories: Tubular failure (including acute tubular may help determine whether the cause is renal or prerenal.
necrosis), interstitial nephritis and glomerulonephritis and vasculitis. However, it is probably more helpful to classifyintrarenal failure according to the causes of renal damage Fe Na = —————————————— x 100 Post renal
This occurs when there is an obstruction to renal A fractional excretion of sodium of less than 1% flow anywhere distal to the pelvis. Obstruction is always occurs in prerenal failure (hypovolemia and cardiac failure) the most likely diagnosis when there is anuria.
and that of more than 2% in renal failure (e.g. acutetubular necrosis) For this to occur both ureters, or the urethra should be obstructed. It is commonly seen in patients with Abdominal ultrasound can help differentiate chronic retroperitoneal or pelvic pathology and abdominal causes (small kidneys hypertension and chronic renal ultrasound is a good diagnostic tool. Do remember to failure, normal or large kidneys diabetes and amyloidosis) check the patency of the Foleys catheter.
and obstructive causes (large dilated pelvis and ureters). Itcan also estimate renal perfusion using Doppler ultrasound.
Table - 24 : Causes of oliguria
Nuclear scans are useful in case of suspected Pre renal
Post Renal
Causes1 (Table 1)
Pre renal
Hypoperfusion due to any cause makes the kidney concentrate urine, decreases the urine output and causes the BUN and creatinine to rise. The BUN level usually, but not always, rises out of proportion to the creatinine level and a ratio of 20:1 is achieved. Therefore prerenal failure is most often not a failure at all but a normal response on the part of the kidney to an inadequate perfusion. Common causes include hypovolemia, congestive cardiac failure and extreme vasodilation. Treating the precipitating cause may rapidly and completely reverse the rise in BUN and creatinine levels. Genuine renal injury may only occur if there is a superimposed insult like GlomerulonephritisInterstitial nephritisPolyarteritis Table - 13 : Investigations to help differentiate pre renal
and renal causes of renal failure
Perioperative considerations
Pre renal
It is important to understand the pathogenesis of renal failure. Though the kidneys receive 25% of the cardiac output, they only get 10% of the total body oxygenuptake. Renal autoregulation does take care of the GFR over a wide range of blood pressures and glomerular ultra filtration is a balance between vasodilators andvasoconstrictors. However, of the blood that the kidneys receive the glomeruli receive 90-95% while the medullaonly receives 5-10%. Oxygen extraction on the other hand is much greater in the medulla due to active water and salt reabsorption. Thus the medulla is more prone to hypoxic Table - 3 : Risk Factors
Patient factors
Perioperative factors
The occurrence of perioperative renal failure depends upon the surgery, preoperative and intraoperative haemodynamics and renal conditions (diabetic patients have a 10 fold greater risk of renal deterioration in the presence of hypovolemia). All intravenous and volatile induction agents affect renal function by decreasing cardiac output and blood pressure. Extradural block (or high spinal) up to the level of T4 reduces sympathetic tone to the kidneys, resulting in a decrease in RBF and GFR. Mechanical ventilation with positive pressure also decreases renal blood flow. Major surgery with extensive third space losses can lead to hypovolemia and renal hypoperfusion.
Thus the progression of renal failure may take one of three paths as seen in Fig. 1. Exclusion of pre renal and post renal causes make intrinsic renal failure the most likely cause. This is often associated with an increased Physical examination and preparation for surgery
Fig - 14 : Pathogenesis of Acute Renal Failure
Check the adequacy of hydration, cardiac output and blood pressure. Also look at the daily intake and Pre renal Azotemia
Intrinsic Acute
Post renal
Renal Failure
Use a large bore cannula for intravenous fluid resuscitation and administer oxygen. Essential preliminary monitoring includes an electrocardiogram, noninvasive blood pressure monitoring and pulse oximetry. Invasivearterial monitoring and central venous pressure monitoring should be then considered. Echocardiography and pulmonary artery wedge pressure monitoring are helpful, Shift to the ICU for monitoring and preoperative Prevention of further deterioration of renal function and maintenance of adequate renal output (1-2 ml per kg– non oliguric renal failure) 2 Preoperative rehydration is essential especially in those patients who are significantly dehydrated e.g. thosewith large bowel obstruction or sepsis. Aim to measure and maintain the CVP at 10-15 cms. H O. The response to a fluid bolus (250-500 ml of normal saline) over 10–15 minutes may help to differentiate between hypovolemia per se and acute tubular necrosis, while more invasivemonitoring is got ready (CVP, Pulmonary artery Risk factors for developing renal failure
catheterization and echocardiography may be required.) successful prevention of perioperative ARF depends on Some authors suggest that we aim to maintain a mean the identification of patients who are at risk for developing arterial blood pressure of at least 50 mmHg, which is the lower limit for renal autoregulation.1 But most authorssuggest maintaining a higher blood pressure – a mean INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003 of >70 mmHg in normal patients and >85 mmHg in Reduce the administration of acid (commonly hypertensive patients2 using ionotropes if necessary.
administered in the form of 0.9% sodium chloridesolution which has a pH of 5), potassium, magnesium If intra abdominal pressure is raised more than and phosphates in maintenance IV and enteral feeds.
20 mmHg (normal 0-17 mmHg) anuria can resultfrom direct compression on the renal pelves.5 This isseen in 30% of emergency laparotomies and is verycommon after massive intra abdominal bleeding suchas leaking abdominal aortic aneurysms, intestinaldistension, paralytic ileus and ascitis. Improvementin renal function only occurs after decompression.
The probable mechanisms for a decrease in cardiacoutput and thus the GFR in these cases are as follows:reduced venous return, compression of the renal veinwith reflex renal artery vasoconstriction, elevationof renal tubular pressure with a decrease in thefiltration gradient and an increase in rennin,aldosterone and ADH production.
Intra abdominal pressure may be measured via the bladder. Instill 50 ml saline into the bladder via a Foley’scatheter, clamp it off and measure the manometric pressureof the fluid within the bladder via a needle inserted intothe catheter lumen Raised intra abdominal pressure may also give rise to a false high CVP leading to under filling of the patient.
- On first recognition of deteriorating renal function immediately eliminate or appropriately reduce the dose ofnephrotoxic drugs like gentamicin and vancomycin (measurelevels where possible) and change amphotericin tofluconazole if possible.
Fig. 2 : Treatment algorithm for management of acute oliguria during the Table - 45 : Nephrotoxins and nephrotoxic drugs, which
could precipitate renal failure .
Start enteral feeds as early as possible and maximize Nephrotoxic drugs
enteral nutrition, as there is now evidence thatoutcomes are better in patients on enteral rather than Other management issues
Use of diuretics
Assoc. with crystal production
The rationale for their use rests on the assumption that they decrease oxygen consumption in the tubular cells by inhibiting trans cellular sodium transport and thus prevents ischemic cell injury. In addition, loop diuretics may vasodilate cortical vessels and improve oxygenation.
If the blood pressure is normal and hypovolemia is Finally augmentation of tubular blood flow may reduce not an issue drastically cut down on the IV fluid intratubular obstruction and back leak of filtrate thus rapidly therapy, thereby preventing a fluid overload.
accelerating resolution of ARF.6 However, in patients withestablished ARF several studies have shown no benefit of The use of dopamine and diuretics remains It is believed that the outcome of non-oliguric renal failure is better than oliguric renal failure. However, in a recent retrospective survey of critically ill patients with stroke volume. However, adrenaline has detrimental effects ARF diuretic use was associated with an increased risk of on splanchnic blood flow and causes transient decreases in death and non recovery of renal function.9 The authors suggested that the adverse outcome was due to either direct Dobutamine may be used to improve cardiac output.
deleterious effects of diuretics or indirect effects owing to However, it causes peripheral vasodilatation and is usually a delay in the recognition of the severity of ARF and institution of dialysis support.9,10 Other authors believe that The use of Fenoldopam is also controversial diuretics may also prove harmful as frusemide can causeinterstitial nephritis and hearing loss.1 Calcium channel blockers.5 During ischaemia,
calcium channels open resulting in vasospasm. It is believed Therefore, diuretics should be used cautiously in that calcium channel blockers exert direct vascular effect critically ill patients and no patient should be given with preservation of renal autoregulation and enhanced furosemide unless they are adequately filled and the recovery of RBF, GFR and natriuresis among other effects.
systemic arterial pressure is adequate as an already damaged However it must be remembered that calcium channel kidney may be profoundly injured by a relatively mild blockers in high doses may compromise the haemodynamic decrease in perfusion pressure.6 Frusemide has been given in a bolus of 20 – 40mg. In patients with established renal Specific pharmacological treatments6 have been
insufficiency (raised serum creatinine) and sustained oliguria used in cases of acute renal failure associated with sepsis.
this treatment should be withdrawn.6 However, in Examples of these include Anti-TNF-± therapy, inhibition responders 250 mg may be given as an infusion over an of platelet-activating factor, inhibition of nitric oxide hour2 as infusions are more effective and less toxic than synthase, endothelin antagonism, inhibition of arachidonic bolus doses.10 Mannitol 0.5 to 1gkg-1 may also be given2 acid metabolism, natriuretic peptides, inhibition of leukocyte Use of Dopamine
adhesion, inhibition of coagulation and growth factors – Low dose dopamine (1 to 3 ¼gkg-1 per min) the details of whose use is beyond the scope of this article increases diuresis and natriuresis in healthy experimental Emergency management of raised serum potassium2
animals and humans. These effects are not seen uniformly Treatment should be initiated if the serum potassium in the critically ill.11,12,13 However after extensively is > 6.5 mmol.L or ECG changes are present. Intervention reviewing the data available the same authors came to the is important as cardiac compromise may occur.
conclusion that the use of dopamine in renoprotectivedoses should be abandoned as there was no evidence Table - 5 : Treatment of hyperkalemia.
supporting its effectiveness in preventing ARF and it shouldnot be used as a panacea for oliguria. In addition, dopamine Treatment
can precipitate serious cardiovascular and metabolic of action
of effect of action
complications such as depression of the respiratory drive, triggering of tachyarrhythmias, causing myocardial ischemia, accelerating intestinal ischemia, depression of anterior pituitary hormones and decreased T-cell Noradrenaline
It markedly improves mean arterial pressure and glomerular filtration. This is especially seen in high output- low resistance septic shock. Urine flow reappears with restoration of systemic haemodynamics and renal function improves without the use of low dose dopamine or frusemide. This fact supports the hypothesis that renal ischaemia observed during hyperdynamic septic shock isnot worsened by nor adrenaline infusion and even suggests that this drug may effectively optimize renal blood flow Adrenaline In patients who fail to respond to fluid
administration and other vasopressor adrenaline can increase arterial pressure primarily by increasing cardiac index and INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003 Other complications of renal failure include severe metabolized by the liver the excretion of their active metabolic acidosis which is dealt with by dialysis metabolites are by the kidney and thus a reduction in doseis often necessary.
Dialysis may be emergent or elective. The indications for dialysis are volume overload, hyperkalemia, Acute renal failure is a common and in many cases severe acidosis, and uremia (with a change in mentation, it is a preventable and/or eminently treatable problem seen pericarditis, pleuritis or bleeding). Emergency dialysis is in the operation theaters and intensive care units and the rarely required in hospitalized patients .In the ICU set up physician treating the critically ill patient should be well BUN and creatinine clearance is assessed daily and dialysis versed in the diagnosis and management of renal failure.
is usually started when the BUN level exceeds 100 mgdl-1or the creatinine clearance is less than15 mlmin-1. (these References
figures are arbitrary and vary from center to center).
1. Leibowitz AB, Approach to renal failure.In Apostolakos MJ and Papadakos PJ(eds.)The Intensive Care ManualTata There are four contemporary modes of dialysis: Peritoneal Dialysis (PD, not usually considered in 2. Purday J, Acute renal failure in Allman KG and Wilson IH the post operative general surgical patient with Eds. Oxford Handbook of Anaesthesia. Oxford UniversityPress: 2001; 116-118.
abdominal pathology or respiratory compromise).
3. Stoelting RK, Dierdorf SF Eds, Renal diseases IN Anaesthesia Hemodialysis (HD, difficult to do especially in the and Co-Existing Diseases, Stoelting & Dierdorf Eds. ,Churchill hypotensive post operative or septic patient, requiring Livinstone Elsevier IndiaPubl.4th Ed 2002; 356-360.
4. Nightingale P & Edward DJ Critical Care In Wylie and Continuous Arterio Venous Hemofiltration (CAVH, Churchill Davidsons A Practice of Anaesthesia6th Ed. CohenPJ, Healy TEJ Eds. Edward Arnold Publ. London 1995; relies on an adequate pressure head, has no external apparatus to control flow or provide warning andrequires the insertion of a wide bore catheter into an 5. Reddy VG. Prevention of Postoperative Acute Renal Failure – A Review. Journal of Post graduate Medicine, 2002; 48; artery which may result in bleeding, an aneurysm, 6. De Vries. AS, Prevention and treatment of acute renal failure It has been largely replaced by Continuous Veno in sepsis. J Am Soc Nephrol 2003; 14: 792-805.
Venous Hemofiltration CVVH, is a slow method of 7. Brown CB, Ogg CS, Cameron JS: High dose frusemide in solute and fluid removal, results in a largely acute renal failure: a controlled trial Clin. Nephrol 1981; 15: haemodynamically stable milieu and can remove a large quantity of cytokines which may reduce the 8. Shilliday IR, Quinn KJ, Allison ME: Loop diuretics in the incidence or progression of multi-organ failure. The management of acute renal failure: a prospective double blind, newer machines have improved safety features such placebo-controlled randomized study. Nephrol Dial Transplant as an air detector and a pressure monitor. They do however require one on one nursing and frequent, 9. Mehta RL, Pascual MT, Soroko S, Chertow GM: PICARD 4-6 hourly, potassium assessment. They are capable Study group: Diuretics, mortality and nonrecovery of renal of removing upto 10 litres of fluid at one sitting and function in acute renal failure JAMA 2002; 288: 2547-2553.
is often helpful in weaning from mechanical 10. Martin SJ, Danziger LH: Continuous infusion of loop diuretics in the critically ill: A review of literature: Critical CareMedicine 1994; 22: 1323-1329.
Prescribing common drugs in renal failure1
11. Denton MD, Chertow GM, Brady HR : “Renal dose’’ All medications prescribed for these patients should dopamine for the treatment of acute renal failure: Scientific be reviewed and dose adjusted to accommodate the rationale, experimental studies and clinical trials. Kidney Int decreasing renal function and the effects of dialysis. Failure to do this may result in drug toxicity or further damage to 12. Burton CJ, Tomson CR; Can the use of low-dose dopamine for the treatment of acute renal failure be justified? PostgradMed J 1999; 75: 269-274.
Drugs most commonly used in the ICU, which will require adjustment, include penicillins, carbipenems, 13. Marik PE Low dose dopamine: a systematic review Int. Care cephalosporins, vancomycin, aminoglycosides, amphotericin,digoxin, and some muscle relaxants. Anaesthetists should 14. Vincent JL Haemodynamic support in septic shock Int Care remember that though opioids and benzodiazepines are


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