Management

Acute Renal Failure in ICUs

Serum creatinine estimation is not a reliable indicator of renal dysfunction

"Renal failure is reversible, if treated promptly and appropriately" - Dr Arpita Dwivedy Critical Care Specialist Dr LH Hiranandani Hospital Powai

Acute Renal Failure (ARF) is a common diagnosis in ICUs, which increases morbidity and mortality. Etiology varies but clinical finding, complications and treatment modalities usually remain same, in all cases.

Incidence

The incidence of ARF in ICU is almost 25-30 per cent. Mortality is considerable and if Renal Replacement Therapy (RRT) is required in these patients, mortalities of 50 to 75 per cent have been reported. Even in patients in whom RRT may not be required, the presence of ARF increases mortality. Even mild elevations of creatinine are associated with increase mortality.

Causes

The causes of renal failure may be classified as pre-renal, renal and post-renal.

Pre-renal renal failure is a state of renal hypo perfusion, which can be rapidly reversed with early intervention.

Causes of pre-renal failure are:

• Extra-cellular volume depletion.
• Dehydration.
• GI losses (vomiting), NG suction, diarrheoa.
• Renal losses (Diuretics, osmotic diuresis, nonliguric ATN, adrenal insufficiency).
• Peritoneal losses (surgical drains).
• Skin losses (burns).
• Hemorrhage (gastrointestinal, intra and retroperitoneal).
• Decreased cardiac output:
  - Myocardial infarction.
  - Pulmonary embolism.
  - Mechanical ventilation.
  - Trauma.
• Re-distribution of fluid:
  - Hypoalbuminemia (nephrosis, cirrhosis, malnutrition).
  - Vasodilatory shock (sepsis, hepatic failure).
  - Peritonitis.
  - Pancreatitis.
  - Crush injury.
  - Ascites.
  - Vasodilators.
• Auto-regulatory failure
  - NSAIDs (preglomerular vasoconstriction).
  - ACE Is (postglomerular vasodilatation).

Primary intra-renal vasoconstriction:

• NSAID.
  
• Hepatorenal syndrome.
• Pre-eclampsia.

Causes of Intrinsic Renal Failure

Glomerular and vascular disease:

• Acute glomerulonephritis.
• Renal arteries or vein thrombosis.
• Thrombotic thrombocytopenic purpura.
• Scleroderma and malignal hypertension.

Tubulo interstitial disease: Acute tubular necrosis

• Drugs: aminoglycosides, amphotericin B.
• Radiocontrast agents.
• Heavy metals.
• Rhabdomyolysis and haemolysis.
• Septic shock.

Acute interstitial nephritis

• Drugs: Penicillins, NSAIDs, ACEinhibitors
• Auto-immune disease.

Post Renal Failure:

• Caused by obstruction of urine flow from the kidney.

Ureteric obstruction:

• (Bilateral or unilateral single kidney)

Extrinsic:

• Tumour, retro-peritoneal fibrosis, accidental surgical ligation.

Intrinsic:

• Stones, blood clots, sloughed papillae, tumours.

Bladder or urethral obstruction:

• Prostatic hypertrophy.
• Neurogenic bladder.

Assessment of Renal Dysfunction

Noting the time of onset of renal problems helps to differentiate between ARF and natural progression of CRF. Patient's drug history should be sought to rule out renal dysfunction due to drugs like NSAIDs , aminoglycosides, ACE inhibitor or radio contrast agent.

Urine Output: Urine output of <400ml/day or <0.5ml/kg/hr is termed as oliguria. Anuria is defined as urine output of <50ml/day. Urine output in a critically ill patient should be measured hourly by placement of a foleys catheter.

Serum Chemistry

Creatinine is made in the muscle and released in the circulation at a rate of 15-25 mg/kg/day for middle aged male and 10-20 mg/kg/day for a middle aged female and increases many fold during rhabdomyolysis. Serum creatinine increases only when GFR is reduced by about half. As a result serum creatinine estimation is not a reliable indicator of renal dysfunction. In ARF, it increases by 1-2 mg/day. If rise is more than 2mg/day CPK level should be done to rule out rhabdomyolysis

Blood Urea Nitrogen (BUN): BUN is the breakdown product of protein. It varies with protein intake, increases in the presence of GI bleed and corticosteroid administration. BUN level decreases in starvation, malnutrition, muscle wasting and cirrhosis. Normal ratio of BUN to serum creatinine is 10:1. In pre renal azotemia it increases to > 20:1

Serum Electrolytes: Abnormalities of plasma sodium, potassium, bi-carbonate, calcium, magnesium and phosphate are common in ARF and their determination and monitoring are an integral part of the diagnosis and management of ARF.

Serum Cystatin C: Measurement of serum cystatin C is useful in early detection of kidney disease as it is not affected by muscle mass, gender, age or race unlike creatinine. It is useful in those cases that have cirrhosis, morbid obesity, and malnourishment, and have a reduced muscle mass. It may identify ARF one to two days earlier than serum creatinine thereby preventing its progression.

Urine Chemistry

Urine sodium: In pre-renal failure due to hypo-perfusion sodium re-absorption increases leading to decreased excretion. Urinary sodium is typically <20, but if it is <10 hypatorenal syndrome is suspected. In ATN sodium re-absorption is hampered leading to increased urinary loss (>20meq/litre).

Urine analysis: The urine dipstick test provides information regarding the presence of haeme pigments and proteins. Microscopic analysis of urine may be diagnostic. The presences of blood suggest embolic phenomena and present of casts suggest acute tubular necrosis.

Ultrasonography

Abdominal ultrasonography is the diagnostic test of choice for post-renal failure. It is also useful in determination of kidney size to rule out underlying chronic kidney disease.

Treatment Of Pre-renal Azotemia

Fluid balance:

• Volume replacement if pre-renal azotemia is secondary to decreased extra-cellular fluid loss.
• Pre-renal failure associated with cardiac failure usually responds to fluid restriction, loop diuretics, vaso dilators, inotropic agents and oxygen. Low dose dopamine (<5µgm/kg/min.) is sometimes remarkably effective in diuretic resistant cases. If diuresis is associated with increased BUN, ACEI is useful in decreasing renal resistance.
• The hypoalbuminemic stats associated with cirrhosis can be corrected with intravenous albumin followed by diuretics. Salt and free water intake to be restricted.
• Vasodilatory shock requires both fluid and vasoconstrictor.
• Crush injury related renal failure is due to combination of volume depletion and myoglobuin induced ATN. Aggressive intravascular volume expansion and forced alkaline diuresis prevents myoglobin nephropathy.
• NSAID induced primary intra renal vasoconstriction is usually reversed spontaneously after cessation of drugs.
• Pre-eclamptic renal failure must be treated by delivery or termination of pregnancy.
• Contrast induced nephropathy is managed by hydration N-acetyl cystiene and bi-carbonate therapy

Acid base and electrolyte balance:

• Supplement bicarbonate if level is <15 meq/L.
• Hyperkalemia should be treated aggressively.

Drugs:

• Nephrotoxic drug should be avoided and drug doses to be adjusted as per creatinine clearance.

Nutrition:

• Restrict protein intake to <0.6 gm/kg/day, but careful attention to nitrogen balance is required.
• Adequate caloric intake is essential to minimise negative nitrogen balance.

Treatment of Post-Renal Failure

Rapid relief of obstruction is required either by aggressive hydration followed by diuresis or percutaneous nephrostomy.

Renal Replacement Therapy for ARF

Mandatory replacements for renal replacement therapy are:

• Uremia manifestating as encephalopathy, pericarditis and uremic bleeding.
• Refracting hyperkalemia.
• Intractable fluid overload.
• Acidosis leading to circulatory compromise.
• Increase of serum creatinine >2mg/day.

Elective dialysis is usually initiated in ICU, if general condition of the patient is poor.

There are five contemporary mode of dialysis:

• Peritoneal.
• Intermittent hemodialysis
• Sustained Low Efficiency Daily Dialysis (SLEDD).
• Continuous Arterio Venous Haemodialysis (CAVHD).
• Continuous Veno Veno Haemodialysis (CVVHD).

SLEDD Advantages

It is an increasingly popular renal replacement therapy for ICU patients.

• Duration of dialysis 8-12 hours

Compared to conventional intermittent haemodialysis:

• Lower blood flow.
• Fluid removal and solute clearance slower.
• Less haemodynamic instability.
• Excellent solute control.
• Not associated with significant urea dys-equilibrium when used over 12 hours.
• Commonest complication is clotting of circuit and so many patients require anti-coagulation.
• Less effective solute clearance than CVVH, particularly for middle and large molecules.
• Nocturnal scheduling of SLEDD allows free up machine for intermittent haemodialysis during the day.
• Less expensive than most CRRT.

Advantage of CRRT (CAVHD/CVVHD)

• Haemodynamically well tolerated.
• Minimal change in plasma osmolarity.
• Better control of azotemia and electrolytes and acid-base balance.
• Very effective in removing fluid.
• Technically simple.
• Membrane capable of removing cytokines in septic patients.

Conclusion

Renal failure definitely increases the mortality in critically ill patients. It ranges between 25-64 per cent depending on the co-morbid factors. It is reversible if treated promptly and appropriately.

arpita.dwivedy@hiranandanihospital.org