Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 797 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 


 
ARTICLE Table of Contents   
Year : 1998  |  Volume : 9  |  Issue : 3  |  Page : 267-272
Acute Renal Failure in the Intensive Care Unit


Division of Nephrology & Hypertension, King Fahd National Guard Hospital, Riyadh, Saudi Arabia

Click here for correspondence address and email
 

How to cite this article:
Mujtaba Quadri K H, Huraib SO. Acute Renal Failure in the Intensive Care Unit. Saudi J Kidney Dis Transpl 1998;9:267-72

How to cite this URL:
Mujtaba Quadri K H, Huraib SO. Acute Renal Failure in the Intensive Care Unit. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2019 May 21];9:267-72. Available from: http://www.sjkdt.org/text.asp?1998/9/3/267/39269

   Introduction Top


Acute renal failure (ARF) is a syndrome characterized by rapid decline in glomerular filtration rate and retention of nitrogenous waste products such as blood urea nitrogen and creatinine [1] . Pre-renal azotemia accounts for the majority of the cases (55 - 60%) of ARF. Intrinsic renal failure caused by acute diseases of the renal parenchyma is responsible for an additional 35 - 40% cases and post renal obstructive etiology contributes less than 5% to the overall list [2] . The last decade has .seen a revolution in the critical care nephrology area. The current article does not aim at giving an extensive account of already well­established causes of ARF but instead, seeks to deal with current debates in topical areas. These include: important prevailing etiologies in the intensive care unit (ICD) setting, non-oliguric versus oliguric renal failure, conservative and newer dialytic modalities in the treatment of ARF including the role of dopamine, atrial natriuretic peptide, biocompatibility of dialyzer membranes, hemodiafiltration as well as advances in nutrition.


   Important Prevailing Etiologies of ARF in the ICU Setting Top


Post-operative acute tubular necrosis (A TN) secondary to pre-existing volume depletion, intra-operative losses and/or third-spacing associated with anesthesia and surgery are frequently seen in ICUs especially after abdominal aortic aneury­smectomy, hepatobiliary surgery and cardiac surgery [3] . In addition, sepsis continues to play a leading role in the pathogenesis of ICD acquired ARF. Endotoxemia, perhaps by causing systemic hypotension, direct renal vasoconstriction or through cytokine release, may also play a role [4] . Nephro­toxins in the ICD setting may be either antibiotics like aminoglycosides, vasopressors such as norepinephrine and epinephrine or radiocontrasts employed in imaging. The main predisposing event in most cases appears to be preexisting volume depletion or renal failure.


   Oliguric Versus Non-oliguric ATN: Does it Matter? Top


This is an issue that has been debated for many years. However, experimental data from animal models appear to suggest a less severe structural and functional damage in non-oliguric renal failure [5] . Also, dialysis appears to be less frequently required in the non-oliguric variety. However, the issue of converting oliguric to non-oliguric form is still controversial and data appear to be emerging that early use of a loop diuretic or mannitol before established ATN may be beneficial [6] .


   Dopamine, 'The Renal Dose': What's the Evidence? Top


Dopamine is natriuretic through a variety of mechanisms and in intravenous doses of up to 3 µg/kg/min acts as a renal vasodilator with a predominant effect in increasing renal blood flow. Doses in excess of 5 µ/g/kg/min cause renal vasoconstriction. In a trial among post-operative patients after elective abdominal vascular surgery, saline infusion alone was compared with saline and renal dose dopamine; there was no difference in the renal outcome [7] . Another uncontrolled trial incorporated renal dose dopamine with furosemide given to oliguric patients within 48 hrs of ischemic insult. Those who responded with an increased urine output had a more rapid recovery of renal function (ID as opposed to 41 days). Further, these patients had a relatively reduced need for dialysis. However, since the clinical and lab data were suggestive of a less severe tubular injury in the group with better outcome, it is possible that they may have done as well without any therapy [8] . Dopamine may be considered at renal doses in oliguric patients at risk of developing ATN along with a loop diuretic but should be discontinued if no obvious benefit appears. There are clear-cut risks associated with dopamine infusion including cardiac arrhythmias, tachycardia and myocardial, and possibly intestinal, ischemia and in the absence of definite experimental or clinical data supporting its use, a more judicious approach is warranted [9] .


   Growth Factors and Atrial Natriuretic Peptide: What's the Hype About? Top


Current interest in growth factors like Insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF) and the well established atrial natriuretic peptide (ANP) stems from animal data suggesting an accelerated tubular regeneration and recovery of renal function in both post-ischemic and nephrotoxic renal failure following exogenous admini­stration of these factors [10] . Atrial natriuretic peptide in combination with dopamine appears to minimize the degree of renal failure in experimental animals if administered at the time of the ischemic insult [11] . The same effect has not been unequivocally demon­strated in humans as yet.


   Dialysis: Indications, Complications, Biocompatibility, Modalities: What's New? Top


In the ICD, some of the factors that influence the decision as to whom and when to dialyze include uremic symptoms such as otherwise unexplained encephalopathy, intractable volume overload, severe electrolyte and acid-base abnormalities, evidence of serositis (including pericarditis), uremic bleeding and toxicological emergencies. The level of azotemia per se is used by some practicing nephrologists as a marker despite absence of supporting data. Hemo-dynamic status, the presence of associated medical conditions as assessed by Apache scores, hypercatabolic status, pre and post­organ transplants and attitudes of families towards the critically ill have often come up as important issues faced by nephrologists when making dialysis-related decisions in the ICU.

Of practical importance are the issues pertaining to episodic hypotension, complement activation and' possible cessation of urine output associated with intermittent dialysis using bio-incompatible membranes. These effects are postulated, respectively, to occur as a result of impaired autoregulation of blood flow in ATN, neutrophil infiltration of kidneys and upregulation of intercellular adhesion molecules _e.g. ICAM-I) on granulocytes with complement activation, and due to excess removal of volume and urea during dialysis [12] . 'Theoretically, this latter effect should not delay recovery of renal function. A prospective study of patients randomized to biocompatible or incompatible membranes for ARF, demon­strated a high rate of recovery of renal function (62 vs. 37 percent) and improve­ment, albeit not statistically significant, in patient survival (57 vs. 37 percent) among patients in whom biocompatible membranes were used. This was particularly noted in Hon-oliguric patients [13] .


   Target Blood Urea Nitrogen (BUN): Is it Clinically Relevant? Top


Early initiation of dialysis or more frequent treatments to keep BUN below a certain target level, for instance 36 mmol/l (100 mg/dl) employed by some, does not appear to have strong scientific basis. A reasonable approach is to initiate dialysis in non-catabolic patients at glomerular filtration rates approximating 1.0-12 ml/min at which rate, solute retention may not be well tolerated.

Hypercatabolic patients need almost daily dialysis. One study randomized 72 patients with ARF to daily versus alternate day treatments and demonstrated a statistically significant reduction in mortality in the daily dialysis group (21 vs. 47%) [14] .


   Modalities of Dialysis in the ICU Top


Although, intermittent hemodialysis particularly with biocompatible membranes continues to have a role in the hemo­dynamically stable patient, the emergence of the continuous renal replacement therapies has been a major development in critical care nephrology. Here, the nephrologist is able to effectively regulate azotemia, fluid, acid base and electrolyte status and at the same time allow the intensivists to optimize nutrition and provide appropriate vaso­pressor support.

In institutions lacking these facilities, peritoneal dialysis, particularly automated cycler based regimens can be utilized in the appropriate setting. Continuous arteriovenous hemofiltration (CAVH) and CAVHD (with dialysis) require systemic anticoagulation and may be inappropriate in patients with bleeding diathesis or severe refractory hypotension.

More popular currently are pump­incorporated venovenous circuits such as continuous venovenous hemofiltration (CVVH) which provide minimal connective clearance equal to the ultrafiltration rate with some additional solute clearance by dilution with replacement fluids.

The counter-current flow of dialysate across the filter provides the dialysis component of continuous venovenous hemodialysis (CVVHD) by incorporating diffusive solute clearance. Upward adjustment of blood flow or dialysate flow provides improved clearance. Slow continuous ultrafiltration (SCUF) may be employed without using dialysate or replacement fluids when modest volume removal alone is the end-point.

Although some circuits can be operated by flushing the filter with saline based solution periodically, obviating the need for heparinization, usage of heparin is required in most currently available venovenous circuits with its attendant side-effects. Over a 48-hr period more urea is removed with continuous renal replacement therapy (CRRT) than with conventional hemodialysis although urea clearance is slower per unit time (17 ml/min with CA VB versus 160 ml/min with hemodialysis) [15] .

Data is also accumulating with CRR T, particularly with very porous membranes such as AN69, pointing towards the removal of inflammatory mediators of sepsis, which have cardiodepressant, vasodilatory or immunomodulatory properties [16] . The overall clinical impact is not fully clear yet. In one series of critically ill patients with sepsis and ARF, CRRT was associated with a lower mortality (62% versus 100%) from preliminary reports [17] .

In general, CVVH with a venovenous access assures a more reliable blood flow rate as opposed to that generated by the arteriovenous pressure difference during CA VH. In a study that looked at ultra­filtration in these two modalities, 16 litres/ day ultrafiltration was noted in CVVH versus 7 litres/day with CAVH and a survival rate of 29% was noted in CVVH group as opposed to 12% in the CAVH group [18] .

For performing CVVH, some of the commonly available blood pumps include Gambro AK10, Hospal BSM-22, Redy 2000 and the Baxter BM-11. We use the Hospal BSM - 22 circuit in our institution.

We utilize double lumen temporary hemodialysis catheters inserted either in the femoral, internal jugular or subclavian sites. We initiate the procedure with a blood flow rate at 75-100 ml/min and move up to 125­150 ml/min if tolerated hemodynamically. Some other workers utilize blood flows of nearly 175-200 ml/min [19] .

When incorporating the dialysis modality, we use either PD 1 (1.5% glucose dianeal with no K +) or hemofiltrate (PD 2) with 2.0 mEq/l K +. Occasionally, lactate-free dianeals could be considered for patients with liver cirrhosis or those with increased lactate generation. A roller pump attached to the ultrafiltration drainage line can regulate the ultrafiltration rate. We use a net negative volume to specify the desired net fluid removal (all measurable output i.e. urine + nasogastric + drains + ultrafiltrate minus all measurable input i.e. replacement solutions + parenteral/nasogastric feeding + pressors + medications + blood products). Some authorities tend to exclude plasma expanders if given for hypotension from the input limb. Replacement fluid consists of balanced compatible electrolyte solutions incorporating saline + calcium chloride or bicarbonate with Y2 normal saline and KC!. We monitor ionized calcium, magnesium and phosphorous daily and replace deficits accordingly. Of the newer machines, the "PRISMA" circuit appears to be promising. Anticoagulation is unfortunately the weakest spot in our armamentarium and thrombo­cytopenia or bleeding continues to plague us every few treatments. A reasonable approach is to give a bolus heparin (e.g. 1000-2000 units) and a subsequent infusion (300-400 units/hr) aiming to keep venous limb post filter PTT at 1.5-2.0 times the control value. Regional anticoagulation with protamine or citrate based reversal can be employed but is more cumbersome.

Although in most places nephrologists handle CRRT, in some country e.g. Australia, a substantial number of institutions have CRR T performed by intensivists. At our institution an extensive in-service program has been initiated by the nephrology service incorporating dialysis and critical care nurses liasing with nephrologists and the intensivists. We work closely with our ICD colleagues and provide this service readily, when indicated.


   Nutrition Top


Patients with ARF are markedly catabolic. This is due to a combination of increased catabolism of proteins arid diminished utilization of available nutrient [20] . Additional factors may be nutrient losses with dialysis, membrane incompatibility or inadequate dialysis dose. It appears that malnutrition in ARF patients approaches 30-60% [21] . The markers that can be utilized for this purpose are serum albumin, creatinine, BUN, transferrin, prealbumin and possibly insulin-like growth factor-I. More sophisticated anthropometric analysis or creatinine kinetics may be used in research settings.

Continuous renal replacement therapies allow maximum margin in administration of enteral or parenteral nutrition. Despite multiple studies evaluating the effects of intensive nutritional support in ARF patients, no specific recommendations can be made at this time because of the complexity created by associated disease processes involved. Nevertheless, the main objective is to provide sufficient calories to avoid catabolism and ketoacidosis from starvation, while limiting excess nitrogenous waste production.


   Adjunctive Therapy Top


Restriction needs to be implemented for the intake of water, dietary salt, potassium and phosphate, as well as ingestion of magnesium containing antacids. On the other hand, provision of sodium bicarbonate to maintain serum HCO3 - > 15 mEq/L, supplemental calcium, phosphate binders and adjustment of drug dosing for the level of renal function or dialysis/ CRRT are all vitally important in the management of ARF in the ICD. A detailed discussion of these is beyond the scope of the present article.


   Prognosis Top


Acute tubular necrosis usually lasts 7-21 days and frequently recovers. Irreversible loss of renal function is known to occur more frequently in the setting of pre­existing renal disease, repeated ischemic and/or nephrotoxic insults and repeated hypotensive episodes. Bioincompatibility of dialyzer membranes as described earlier appears to be an additional factor. The often-quoted mortality rate of 4060% for ARF in the ICD setting seems to be finally improving. A recent paper reviewed two time periods between 1977 to 1979 and 1991 to 1992 and despite having similar AP ACHE scores, demonstrated an improved in-hospital survival (52 versus 32 percent) and one year survival (30 versus 21 percent) in the latter group [22] . Renal failure itself was shown in a recent study to independently affect the in-hospital mortality in a group of patients with radio contrast induced A TN. The relative risk in this group was 5.5 [23] .


   Conclusion Top


As our understanding of pathophysiology improves and technological advances in therapeutics of renal failure occur, the challenges facing the nephrology community include appropriate application of biotech­nology to the relevant clinical setting and bridging the gap between theory and practice. This is particularly essential in the ICD set-up.

 
   References Top

1.Anderson RJ, Schrier RW. Clinical spectrum of oIiguric and non-oliguric renal failure. In: Brenner BM, SteinJH(eds). Acute renal failure. Contemporary issues in Nephrology, Churchill, Livingstane, New Yark 1980;6.  Back to cited text no. 1    
2.Acute renal failure, p1200, Brenner & Rector's.The Kidney, 5th edition, 1996.  Back to cited text no. 2    
3.Bhat JG, Gluck MC, Lowerstein J, Baldwin DS.Renal failure after open heart surgery. Ann Intern Med 1976;84:677-82.  Back to cited text no. 3    
4.Badr KF, Kelley YE, Rennke HG, Brenner BM. Roles for thromboxane A2 and leukotrienes in endotoxin-induced acute renal failure. Kidney Int 1986;30;474-80.  Back to cited text no. 4    
5.Honda N, Hishida A. Pathophysiology of experimental nonoliguric acute renal failure. Kidney Int 1993;43:513-21.  Back to cited text no. 5  [PUBMED]  
6.Brown CB, Ogg CS, Cameron JS. High dose fmsemide in acute renal failure: a controlled trial. Clin NephroI1981;15:90-6.  Back to cited text no. 6    
7.Baldwin L, Henderson A, Hickman P.Effect of post-operative low-dose dopamine on renal function after elective major vascular surgery. Ann Intern Med 1994;120:744-7.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Graziani G, Cantaluppi A, Casati S, et al. Dopamine and frusemide in oliguric acute renal failure. Nephron 1984;37:39-42.  Back to cited text no. 8  [PUBMED]  
9.Denton MD, Chertow GM, Brady HR. "Renal-dose" dopamine for the treatment of acute renal failure: Scientific rationale, experimental studies and clinical trials. Kidney Int 1996;50:4-14.  Back to cited text no. 9  [PUBMED]  
10.Miller SB, Martin DR, Kissane J, Hammerman MR. Insulin-like growth factor I accelerates recovery from ischemic acute tubular necrosis in the rat. Proc Natl Acad Sci USA 1992;89:11876-80.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Conger JD, Falk SA, Hammond WS. Atrial natriuretic peptide and dopamine in established acute renal failure in the rat. Kidney Int 1991;40:21-8.  Back to cited text no. 11  [PUBMED]  
12.Schulman G, Fogo A, Gung A, Badr K, Hakim R. Complement activation retards resolution of acute ischemic renal failure in the rat. Kidney Int 1991;40:1069-74.  Back to cited text no. 12  [PUBMED]  
13.Hakim RM, Wingard RL, Parker RA. Effect of the dialysis membrane in the treatment of patients with acute renal failure. N Eng1 J Med 1994;331:1338-42.  Back to cited text no. 13    
14.Schiff H, Lang SM, Konig A, Held E. Dose of intermittent hemodialysis and outcome of acute renal fuilure: A prospective randomized. Study (abstract). J Am Sac Nephrol 1997;8:290A.  Back to cited text no. 14    
15.Golper TA. Continuous renal replacement therapy in acute renal failure. Up to date on CD ROM 6.1 June 17, 1997;p1.  Back to cited text no. 15    
16.Hoffinann IN, Hartl WH, Deppisch R, et al. Hemofi1tration in human sepsis: evidence for elimination of imrnunomodulatory substances. Kidney Int 1995;48:1563-70.  Back to cited text no. 16    
17.Wendon J, Smithies M, Sheppard M, et al. continuous high volume veno-venous hemofiltration in acute renal failure. Inten Care Med 1989;15:358.  Back to cited text no. 17    
18.Storck M, Hartl WH, Zimmerer E, Inthron D. Comparison of pump driven ana spontaneous continuous haemofiltration in postoperative acute renal failure. Lancet 1991;337:452-5.  Back to cited text no. 18    
19.Golper TA. Continuous hemodiafi1tration: technical consideration. Up to date on CD ROM 6.1 Aug. 21, 1997;p.1.  Back to cited text no. 19    
20.Shuler CL, Wolfson M. Nutrition in acute renal failure in Rombeau JL, Ca1dwell MD (eds) Clinical Nutrition: Parenteral Nutrition (2nd ed) 1993;667-675.  Back to cited text no. 20    
21.T. Alp Ikizer. Nutrition and catabolic stress in acute renal failure. 6th NKF Annual Spring Clinical Meeting. Proc 1997;p.134.  Back to cited text no. 21    
22.McCarthy JT. Prognosis of patients with acute renal failure in the intensive-care unit: a tale of two eras. Mayo C1in Proc 1996; 71:117-26.  Back to cited text no. 22    
23.Levy EM, Vis coli CM, Horwitz RI. The effect of acute renal failure on mortality. A cohort analysis. JAMA 1996;275;1489-94.  Back to cited text no. 23    

Top
Correspondence Address:
Sameer O Huraib
Division of Nephrology & Hypertension, King Fahd National Guard Hospital, Riyadh
Saudi Arabia
Login to access the Email id


PMID: 18408299

Rights and Permissions




 

Top
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Introduction
    Important Prevai...
    Oliguric Versus ...
    Growth Factors a...
    Dialysis: Indica...
    Target Blood Ure...
    Modalities of Di...
    Nutrition
    Adjunctive Therapy
    Prognosis
    Conclusion
    Dopamine, 'The R...
    References
 

 Article Access Statistics
    Viewed1967    
    Printed49    
    Emailed0    
    PDF Downloaded374    
    Comments [Add]    

Recommend this journal