53.3 Renal failure after an injury

If you don’t transfuse a patient in severe hypovolaemic shock rapidly and adequately, he either dies immediately, or the cortices of his kidneys necrose so that his kidneys fail. Post–traumatic renal failure is thus the major complication of hypovolaemic shock. Although a period of acute hypovolaemia can injure his lungs, his heart or his liver, it is its effect on his kidneys that is so marked and so preventable. The more severe his hypovolaemia and the longer it lasts, the more likely are his kidneys to stop working and shed their tubular cells. If they do, days or weeks may elapse before they start working again. During this time he can die from uraemia, potassium intoxication, or infection. Prevent these disasters by treating hypovolaemic shock quickly. In good units post traumatic renal failure has almost disappeared, but preventing it may require 50 units of blood. It can also complicate extensive burns, crush injuries, severe muscle wounds (especially if they are heavily infected), or transfusion reactions.

If a patient passes no urine, suspect that his catheter is kinked or blocked, or that his urinary tract is obstructed. If he passes less than 20 ml an hour (for a child, see Fig. 58-6), suspect that he has post traumatic renal failure. Before diagnosing it, consider these other possibilities:

(1) He may still be hypotensioe due to hypovolaemia. If his blood pressure is still below 80mm, or his peripheral circulation is still severely constricted, his glomerular filtration rate will be low. If you correct his hypovolaemia and restore his blood pressure, his urine output may increase, but only provided that hypotension has not lasted long enough to damage his kidneys.

(2) He is showing the metabolic response to injury. If his urine output is low, look for signs of hypovolaemia and renal failure. If you have excluded these, his urine output may be low because of the ’metabolic response to trauma’ due to increased antidiuretic hormone secretion. This may reduce his urine output for 8–36 hours. Don’t rely on this diagnosis unless his condition is stable in other respects, his urine is chemically normal and its specific gravity is high. The practical consequence of this is that you should not infuse more fluid to increase his urine output if all other signs are satisfactory.

If you have excluded these two conditions, and a patient has passed less than 20 ml/hour of urine for 12 hours, he probably has acute post traumatic renal failure. Diagnose it early, before his blood urea starts to rise, by monitoring his urine output. His kidneys are probably failing if: (1) The specific gravity of his urine is less than 1016 in the absence of glycosuria or albuminuria, or (2) there is pigment or protein in his urine, whatever its specific gravity.

If he recovers, he will go through two phases:

(1) An oliguric phase during which his kidneys cannot correct for his water and electrolyte intake, so you will have to restrict these for him. While he is oliguric, one of his dangers is that too much potassium will enter his plasma from dead or dying tissues, so try to minimize this. Unfortunately, you cannot diagnose the earlier phases of hyperkalaemia clinically. Don’t give him potassium containing solutions such as Darrow’s solution or Ringer’s lactate in this phase. It may be followed gradually or suddenly by the next one.

(2) A phase of diuresis, during which he may pass 6 to 9 litres of urine a day, regardless of his fluid intake. While this phase lasts, he is in danger of losing electrolytes. So replace them, and the water he loses. One difficulty is knowing when to stop giving him large volumes of fluid. If you go on giving them, he has to go on excreting them, so you won’t know if he needs them or not!