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KMID : 0381219710030040277
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Journal of RIMSK
1971 Volume.3 No. 4 p.277 ~ p.294
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DIAGNOSIS AND TREATMENT OF RENAL FAILURE
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Abstract
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The vast majority of the cases of acute renal failure occur in a setting which hindsight would ;feed us to believe might have been staged differently, had its relation to the production of the renal lesion been foreseen. Among such iatrogenic causes for this syndrome must be listed the intravenous administration of distilled water, and its use as irrigating fluid during transurethral. resection of the prostate. Other causes include the transfusion of incompatible blood, wounding, crushing injuries, shock due to blood loss, and, most important, of cases of severe water and electrolyte depletion. An idea of the many and raried conditions reported to cause acute renal failure.
From the clinical standpoint it has seemed important to divide acute renal failure into three diagnostic categories; prerenal, renal, and postrenal. This division stresses the fact that only in the second category is there renal parenchymal damage adequate to cause in itself functional failure. By the same token, it stresses the fact that prerenal and postrenal factors may be immediately remediable by specific procedures, whereas acute lesions of renal parenchyma must heal spontaneously.
Prerenal Failure
Inadequate maintenance of the circulation is frequently attended by renal ischemia: When this ischemia is severe enough to cause necrosis, organic lesions of the renal parenchyma occur. Decreases in renal blood flow and filtration rate of lesser degree may result in minimal or no renal parenchymal changes. They may, however, be associated with profound changes in urine volume and the excretion of solute which precede and mimic the consequences of lesions of the renal parenchyma. For want of a better term, these nonparenchymal changes have been grouped under the heading prerenal failure.
Renal Failure
Damage to the kidney parenchyma in acute tubular necrosis is not curable in the sense that the physician may specifically treat the lesion. The parenchymal lesion must heal by itself, and in this
situation injudicious attempt:; to force the kidney to perform its urinary function may result i over hydration, pulmonary edema, and death.
The causes of acute renal failure are numerous. In general, two broad groups may be delineated. In the first are the many situations ischemia of renal tissue. The second is the group caused´
by the ingestion or inhalation of substance toxic to the renal parenchema.
The multiplicity of events included under the first heading, however, imply stresses our inability,´ to pinpoint the causes of all cases. It is the experience of these who have dealt most acute renal }y failure that 30 per cent or more of the cases cannot be attributed to any single causative agent. Two factors are provably responsible for this difficulty. The first is the fact that different patients, ´{ or even the same patient at a different times may respond differently to the same insult. Secondly, it is the response of the renal vasculature which determines the renal lasion, and renal blood flow or perfusion is not always faithfully reflected by the status of the peripheral circulation.
Postrenal failure
The category of postrenal failure comprises only a small group of disorders. Nevertheless, it is an important group because it is constituted largely of those cases in which urinary suppression is due to obstruction of the urinary tract, and in such cases it is imperative that the diagnosis be made at once so that relief of the specific obstruction may be effected. There are a number of diagnostic clues.
Total anuria is rare in acute renal failure due to parenchymal damage or to prerenal causes. , Daily urine volumes of 75 to 300ml. are the rule, although this may not be apparent when, in the absence of an inlying bladder catheter, complete emptying of the bladder is not obtained or when collection periods overlap. If, however, total anuria is truly present, the diagnosis is much more likely to be obstruction of the urinary tract, massive vascular accidents to the kidney, or acute glomerulonehritis.
Renal colic or flank pain preceding anuria may be a valuable clue when present, but it is frequently absent in total obstruction. Pain in the costovertebral angle may be present with other forms of acute renal involvement.
Treatment of acute renal failure
The first approach to the management of acute renal failure of renal parenchymal function is a prophylactic one. It has been emphasized that the setting for these catastrophes is frequently one of trauma and, unfortunately, of occasional mismanagement. Adequate attention to the state of renal function antedating operation and to restoration of deficits of blood plasma and extra cellular fluid are essential. It has been stressed in a previous that acute renal failure occurs with much greater frequency under conditions of antidiuresis. In this regard, attention should be paid to the common practice of withholding food and, particularly, fluid for considerable periods of time prior to general anesthesia. Where any doubt exists, adequate urinary flow should be assured prior to operative intervention by the intravenous administration of fluids if necessary. In this connection, the use of mannito´, the reduced from of the 6-carbon sugar mannose, has been stressed a prophylactic measure in the prevention of acute functional renal failure particularly during resection of aneurysms of the abdominal aorta.
Circulatory Insufficiency
Circulatory insufficiency is a common cause of reversible acute renal failure. Included in this category are (1) hypotension from various and (2) dehydration. The two are not mutually exclusive, and dehydration may precipitate severe hypotension.
Hypotension may be due to inadequacies of the mechanisms by which normal blood pressure in supported. These mechanisms include, of course, abnormalities of the pumping action of the heart, the amount of blood in the intravascular compartment, and the capacity of the vasculature. The hypotension precipitating renal failure following hemorrhage or plasma loss due to burns is too well known to pursue further, and the immediate therapy is obvious. Occasionally in severe infections and other toxic states one may see hypotension result from failure of the arterial bed to constrict. This may be suggested clinically by warm extremities. Here, the use of vasoconstrictor drugs designed to decrease the arteriolar lumen and thus raise blood pressure may result in improved circulation in the kidney.
In hypotensive states where peripheral vasoconstriction is marked the renal circulation may already have been impaired, and the use pressor agents by producing further renal vasoconstriction may result in an actual decrease in blood perfusing the kidney. An excellent review by Greismann points out that although arteriolar constriction serves as an immediate lifesaving mechanism during rapid and severe blood loss, the resultant ischemia in certain tissues hastens the impairment of capillary vasomotor function and the progression to irreversible shock. Under these circumstances continued use of vasopressor agents may be analogous to whipping the tired horse and may result in a vicious circle of refractory hypotension.
Treatment of Nephrotixic Injury.
Among the nephrotoxins which produce acute renal failure, and whose action is potentially reversible, are bichloride of mercury, bismuth, lead, and certain of the sulfonamides. In the first two instances, unfortunately, specific treatment may be too late by the time acute renal failure is manifested, since nephrotoxic damage has already occurred. However, there can be no question but that administration of British antilewisite (BAL) in adequate amounts within 30 minutes to 1 hour after the ingestion of dichloride of mercury will greatly decrease the incidence of acute renal failure. An initial intramuscular dose of 5 to 6rng/kg of body weight should be given. This is followed within the first 12 hours by two, or even three, further injection of 3mg/kg. During the next 12 hours one or two additional injections of 3mg/kg are given, and depending upon the patient´s condition subsequent daily doses may be employed for the neat day or two. Since some 80% of the administered dose is excreted by the kidney within 24 hours, it is possible that a much smaller amount may be necessary in patients with acute renal failure. Fatal reactions to BAL may occur following administration of which doses in the presence of diminished kidney function. It has been suggested that, even in the presence acute renal failure following bichloide of mercury ingestion, severe gastroenteritis may necessitate continuance of small doses of BAL since the moiety of mercury that continues to be excreted by the colon is capable of causing colities in particularly sensitive persons.
Intravascular Heinolysis
The use of alkali to abort incipient renal failure has been suggested as a valuable adjunct
following intravascular hemolysis, whether spontaneous, due to mismatched blood, or to infusion of distilled water. Its advocates base their arguments upon the fact that the hemoglobin breakdown product (acid hematin) which enters the tubular fluid is more soluble in an alkaline than in an acid urines. However, it should be remembered that if one desires to alkalinize the urine in such an instance, the administration of intravenous sodium bicarbonate of lactate solutions presupposes the ability of the kidney to elaborate an alkaline urine in response to this alkali load.
If the kidney can respond to the infusion of alkali by alkalinizing the urine, it is probable also that it will respond to the administration of the carbonic anhydrase inhibitor actazolamice (Diamox), Intravenous infusion of Diamox under such circumstances should result in a prompt,
although brief, alkalinization of the urine which may achieve the desired result without the administration of excess sodium
Immediate,
Treatment of the Renal Lesion and Acute Renal Failure.
Once it has been determined that oliguria is not immediately reversible by removal of the obstruction or correction of the circulatory inadequacy, the question arises of measures designed to modify the renal lesions itself. This lesion and the possible role of interstitial edema have been discussed. If, as has been suggested, differential vasoconstriction mediated by nervous influences causes shunting of blood from the cortex of the kidney through juxtamedullary glomeruli, the possibility exists that interruption of nervous pathways might release of prevent such vasospasm, interrupt the shunt, and effect resumption of perfusion and reestablish the function of cortical nephrons. In theory again, such a block might be achieved by the infusion of intravenous procaine, by spinal anesthesia, or a lumbar block. If interstitial edema does play a role, the relief or pressure by the removal of the constraining renal capsule (decapsulation) might have a beneficial effect upon renal function by decreasing intrarenal pressure. However, it has been pointed out that experimentally produced elevation of renal interstitial pressure only
slightly modified by decapsulation.
Since the role of ACTH and cortisone in the treatment of the inflammatory edema of other clinical situations is well known, it was natural that this therapy should be attempted in acute renal failure.
The expectation was that amelioration of the inflammatory response and edema would imply decreased intrarenal pressure and more rapid resumption of function. Again, although there have been sporadic claims for this, its efficacy has not been documented. Furthermore, the catabolic response to steroid administration and, particularly, potassium release is a real contraindication on Principles of Management of the Oliguric Phase.
Once the possibilities for immediate therapy of the functional defect have been dealt with; the therapeutic regimen during the period of continuous oliguriamust be considered. In so far as the renal defect involves failure to regulate water and electrolyte balance, as well as to excrete the products of protein breakdown, primary concern must be for the regulation of these functions without the help of the kidney. We are aware. too, that the kidney has certain metabolic functions which must be disturbed during acute renal failure. These are certainly concerned with the production of ammonia, probably that of creatinine, and possibly with glucose and fat metabolism
The production of pressor substances by the damaged kidney is a function which may we contributing role in the hypertension occasionally seen during acute renal failure. Since, however, the therapeutic implications of disorders of renal metabolic function in acute renal unclear at the present time, they will not be stressed further. Water Balance, omission of calories, and electrolyte replacement are must considered Infection.
It is generally agreed that the most common cause of death in patients with acute renal failure
It is not a direct consequence of the chemical abnormalities, but of bacterial infection. Acute renal failure frequently occurs in the setting of trauma of major surgery.
Flesh wounds offer a convenient portal for infection, and prolonged immogility appears to enhance this. Impairment of wound healing as result of severe uremia and malnutrition further add to the problem. Infection also markedly increases the catabolism of prote in with its undesirable sequelae, and it has been pointed out by many observers that infection impairs the beneficial effects of high caloric diets in decreasing protein catabolism in patients and in experimental animal.
Infection, when present, should be vigorously treated. Appropriate antibiotics should be determine by culture and by determination of the sensitivity of the cultured organism if possible. In urgent situations clinical judgment should determine the appropriate agent before results of the culture and drug sensitivity are returned from the laboratory. Prophylactic antibiotics,. however, should never be administered in the absence of definite evidence of infection. The occurrence of Staphylococcus aureus, enteritis, and septicemia, as well as local and even blood stream invasion by monilia, cryptococcus, and other fungi, have occurred following the use of many of the so-called broad spectrum antibiotics.
It has been our policy in the past routinely to employ testosterone propionate in the treatment of acute renal failure. The rationale for its use is based upon the demonstration that the administration of androgens to experimental animals markedly decreases protein catabolism. A more pertinent criticism is that these results have been most striking in demonstrating the incorporation of dietary nitrogen as body protein and the protein-free intake in anuria may minimize this effect.
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