Emergency War Surgery NATO Handbook: Part II: Response of the Body to Wounding: Chapter X: Compensatory and Pathophysiological Responses to Trauma

Renal Subsystem

United States Department of Defense

Urinary output: The decrease in urinary output that occurs as a physiological response to wounding is the result of both metabolic and vascular changes. Normally, the urinary output is in excess of 500 ml per 24 hours when the blood pressure is within the normal range and the urinary flow is not mechanically obstructed. As the systolic blood pressure is lowered by hemorrhage to a level of 60-80 mm Hg or even lower, the urinary flow decreases and may progress to oliguria: that is, to a volume of urine less than 20 ml per hour, or less than 400 ml per 24 hours.

Obstruction of a urinary catheter is a particularly likely cause of absence of detectable urinary output. Most patients, even those with acute renal failure, excrete 50 ml or more of urine per day. When anuria develops, a mechanical reason for it should be suspected. Frequent causes are obstruction or actual destruction of the urethra or ureters by wounds in the pelvic region, spasm of the urethral sphincter, and atony of the bladder. Careful physical examination; catheterization of the urinary bladder; and intravenous pyelography, cystoscopy, or exploration, as indicated, will establish the presence or absence of adequate urinary flow from the kidneys. If a urethral catheter has been inserted, it may be obstructed by mucous plugs or blood clots. These are such obvious causes of oliguria and anuria that, paradoxically, they are sometimes overlooked.

Acute renal insufficiency: Acute renal insufficiency or acute renal failure indicates sudden and essentially complete failure of the excretory function of the kidneys. This complication, in which the pathological process is acute tubular necrosis (lower nephron nephrosis), must be suspected if less than 400 ml of urine is excreted in a 24 hour period. It is important to recognize, however, that some casualties who develop the syndrome of acute renal failure do not have oliguria but may become uremic nonetheless (high-output renal failure). Although urine volumes may be normal to high, a lack of concentration indicates failure to clear solutes. Failure to recognize this fact and to monitor the patient's fluid administration may result in overhydration and fatal circulatory embarrassment of the nonoliguric as well as the oliguric patient with acute renal failure. Failure to recognize high-output nonoliguric renal failure can result in worsening the hypovolemic state, further compounding the renal insult. Paradoxical polyuria should be replaced at 0.5 cc per cc of urine output, but care should be taken to avoid "chasing" the urine output and causing overhydration. Excessive urine output may be associated with significant urinary potassium losses, requiring frequent monitoring of the serum potassium level and replacement as indicated.

Factors which frequently cause acute renal insufficiency are long periods of hypotension, crushing injuries, burns, hemolytic reactions (most frequently from blood transfusions); drug nephrotoxicity, sepis and hypersensitivity phenomena.

At first, the urine is pale and dilute unless blood or hemoglobin is present. If hemolysis has occurred, it is characteristically dark brownish red. Proteinuria may be conspicuous for a day or two. Granular and heme-pigment casts soon appear. The specific gravity falls rapidly and by the third day it may be as low as 1.010 and fixed.

The BUN (blood urea nitrogen) level rises rapidly. The rate of increase is closely related to the extent of trauma or to factors which influence the catabolic rate. In a massively wounded and catabolic patient with renal failure, the BUN may rise as much as 120 mg percent per day. Hyponatremia is a frequent finding and is usually attributed to an excessive administration of water rather than to an actual sodium deficit. With the development of metabolic acidosis, the serum bicarbonate falls. Hypocalcemia is frequently present. Anemia and leukocytosis are usually present, even in the absence of infection. Because infection is a leading contributory cause of death in acute renal failure, search for foci of infection is mandatory. Diarrhea, sometimes with bloody stools, may develop if uremia persists. Abdominal distention may be marked. Drowsiness, disorientation, muscular twitchings, and even convulsions may occur. Diastolic hypertension of considerable degree is not unusual. Acute pulmonary edema and congestive heart failure are more likely to develop when hypertension is marked, especially if an excess of fluid has been given. Weight loss and hypoproteinemia, progressing to emaciation, reflect the catabolic state, and dependent edema may occur even when the fluid allowances are less than conventional. The clinical course may be complicated by extensive and progressive infection, impairment of wound healing, and a distinct tendency to bleed.

Many of the abnormalities observed in acute renal insufficiency are the result of potassium intoxication. Because of catabolism, the potassium ion shifts from its normal intracellular location to the extracellular fluid compartments. The process may be more rapid in the presence of necrotic tissue or hematoma formation and should be suspected whenever major injury to muscles is present. In the presence of acidosis and uremia, the plasma potassium levels are abnormally high, and potassium intoxication can occur on the first day after wounding in casualties who are oliguric. Frequently, physical signs or symptoms do not reflect the gravity of the situation until death is imminent. Neuromuscular and cardiac changes are manifestations of potassium intoxication. Tendon reflexes are diminished to absent, and complete paralysis may follow. Potassium intoxication causes certain electrocardiographic changes, such as high-peaked T waves in the precordial leads, a widening of the QRS complex, a depression of the P waves, and a sloping ST segment in the limb leads. Conduction disturbances can lead to ventricular arrhythmia and death. Fatalities from cardiac arrest secondary to potassium intoxication have been observed as early as the fourth day after wounding.

The earliest sign of acute renal failure is usually the appearance of oliguria with no other obvious cause for a decreased urinary output. Volume expansion, monitored by the CVP, will help in identifying and treating cases of prerenal oliguria. This is accomplished by rapidly administering a test load (500-1,000 ml) of intravenous fluid, rapidly followed by a single dose of diuretic agent. The urine specific gravity is usually 1.010 in the syndrome of acute tubular necrosis, and the urine sodium concentration is relatively high (60 to 100 meq/l). The UUN/BUN (urine to serum urea ratio) is usually less than 10:1. Electrocardiographic and chemical determinations may confirm the presence of hyperkalemia.

The clinical manifestations of sepsis, shock, and necrosis of undebrided tissue are quite similar to those of uremia, but the differential diagnosis is seldom difficult because these manifestations appear considerably earlier than those of uremia. Even though both oliguria and azotemia may be present in the first few days after wounding, the nausea, vomiting, disorientation, and convulsions which occur at this time are not likely to be of uremic origin.

Since renal insufficiency usually is not diagnosed in its incipiency, treatment during this phase, when the only manifestation is oliguria, is vascular volume expansion using blood and other suitable electrolyte solutions, with monitoring of the central venous pressure. adequate debridement of any wounds, a trial of mannitol intravenously injected in a 12.5-25 gm bolus, and the administration of antibiotics as indicated. The concern of the medical officer in a forward unit should be the collection of potentially reversible renal failure by prompt restoration and preservation of adequate blood volume and urinary flow.

In a temperate climate, the total fluid intake for 24 hours, exclusive of blood. plasma, or plasma expanders, should be 500 ml to cover insensible loss, plus the measured output. The measured output is the total of urinary excretion, vomitus, diarrhea, fluid removed by gastric suction, and fluid lost from burned surfaces. Allowance must also be made for increased insensible fluid losses. These vary accordingly to climatic conditions and body temperature. In humid tropical regions and febrile states, these losses may be 2,000 ml per day or more.

Maintenance of the proper relationship of fluid intake to fluid output is important, for increasing the fluid intake will not increase the urinary output in acute renal insufficiency. An excessive intake, in fact, will endanger the patient's life. The responsible medical officer must give his personal attention to the calculations. A careful record must be kept, and nurses and aidmen must be instructed specifically about how to keep it. A warning notice to keep the fluid intake output chart must be displayed prominently on the patient's bed.

The patient's thirst must not be allowed to influence the volume of intake, and close supervision is necessary to insure that he does not overhydrate himself. A daily weight record should be maintained if practical. An increase in weight implies water retention and, therefore, overhydration. A useful general rule is the maintenance of 0.5 pound daily weight loss under usual catabolic conditions.

Administration of fluids should be oral if tolerated and feasible. When parenteral administration is required, as it often is, it should be a continuous intravenous infusion at a constant rate. It is technically simple to pass a polyethylene catheter into the superior vena cava via a peripheral vein, and little trouble need be expected if the tube is allowed to remain in situ for no longer than five days. This technique minimizes the risk of thrombosis, which would be associated with infusion by a needle or cannula in a peripheral vein for this period of time. It also makes movement of the patient simpler and allows CVP monitoring through the same catheter. Although wound management is essentially the same as in patients without renal failure, early debridemerlt is even mole critical in that damaged tissue aggravates the effects of renal failure. Hypoxia and respiratory acidosis during anesthesia should be particularly avoided, since they may promote the release of intracellular potassium into the plasma.

Caloric intake should be maintained by the use of carbohydrates and fats, with the complete elimination of protein-containing foods. Hypertonic glucose can be given effectively through a central venous catheter. Potassium should not be administered to the oliguric patient unless the concentration of the ion is deficient.

The early use of mannitol as an osmotic diuretic has been mentioned. If diuresis results from a 12.5-25 g bolus, a sustained infusion of 20% mannitol may be used to titrate an adequate urine volume. Furosemide and ethacrynic acid should be used as an initial diuretic. Caution is required in their use, however; serious adverse reactions have been reported, including deafness and death. The treatment of hyperkalemia with cation exchange resins, such as Kayexalate, has decreased the requirement of dialysis for the sole purpose of treating hyperkalemia. Usual doses are 10-50 gm by mouth or enema every two to six hours. Sorbitol, as an osmotic cathartic (5-10 ml) by mouth or by enema, also promotes diarrhea and intestinal potassium losses. Since many drugs are excreted through the kidneys, decreased renal function requires decreased doses of most antibiotics and other drugs such as digitalis. Magnesium-containing compounds, such as antacids, should be used sparingly in the oliguric patient because of the possibility of magnesium toxicity.

An oliguric patient should not be kept in the forward area any longer than necessary. Instead, he should be evacuated as expeditiously as possible to a center that possesses an artificial kidney and that is otherwise specially equipped to treat acute renal insufficiency. If he cannot be evacuated, a patient who remains oliguric for 72 hours should be treated by the following emergency measures, designed to reduce or counterbalance an excess of serum potassium:

1. Intravenous glucose is given in 10% concentration through the superior vena cave. This measure will cause potassium to be reincorporated into intracellular glycogen and will lower the serum concentration. The concomitant use of insulin may facilitate this process.

2. Since calcium is a specific antagonist of potassium, a continuous infusion of 10% calcium gluconate will counterbalance excess potassium, large amounts of this ion should not be an antagonist of potassium, large amounts of this ion should not be used during the first days of acute renal insufficiency. Sodium, in this setting is used sparingly and only to replace that lost by urinary excretion, gastric suction, or diarrhea. Generally, one-third normal saline is used to replace urine output , and normal saline to replace gastric fluid loss.

3. Fluid balance is maintained by the use of carefully calculated amounts of the required fluids. consider, for example, a patient who has excreted 50 ml of urine and who has lost 150 ml of fluid in vomitus or by gastric suction within 24 hours. His measured output is thus 200 ml. This amount should be added to the basic allowance of 500 ml to give a total intake for 24 hours of 700 ml. Of this, 100 ml may be 10% glucose in water with 10 units of regular insulin, and 200 ml should be isotonic saline. Sodium bicarbonate in 7.5% solution may replace saline if the pH determination reveals metabolic acidosis. Since some wounded patients develop respiratory alkalosis, monitoring of serum pH is necessary to determine appropriate fluid replacement. Peritoneal and extracorporeal dialyses are effective techniques of treatment but are not usually feasible outside a special center staffed by personnel trained in these techniques.

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Operational Medicine 2001

Health Care in Military Settings

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