Case Study – Acute Renal Failure She was found behind anoverturned table after the bomb blast destroyed the sidewalk coffeeshop. She had several large wounds and had lost quite a bit ofblood. She was also burned over about 10% of her body surface. Atthe scene, rescuers stopped the major blood loss and evacuated her,but they were not able to rouse her and it was several hours untilshe could be delivered to the hospital. Her heart rate was 120 bpmand her blood pressure was 60/42. She was immediately givenintravenous fluids while her wounds were being tended to. After shewas treated in the emergency room she was kept in the hospital forfurther evaluation. By this time her pulse was 90 bpm and her bloodpressure was 75/60. She was only producing 20 ml of urine per hourand her blood work revealed high BUN (blood urea nitrogen),creatinine and potassium concentrations. A creatinine clearancetest indicated that her GFR was 26 ml/minute. They decided that shewas suffering from prerenal acute renal failure, caused by theextreme hypovolemia from her hemorrhage and burns. The treatmentwas intravenous administration of isotonic solutions containingglucose and bicarbonate, the fluid to replace lost blood volume andthe bicarbonate to lower serum potassium concentrations. Because ofconcerns about the hyperkalemia, her electrocardiogram was closelymonitored for any increases in the size and shape of the T-wave.After her fluids had been adequately managed, her renal functiondid not fully return to normal right away. She was showing someindications of acute tubular necrosis. After a few weeks of carefulmonitoring of her hydration and electrolyte concentrations herrenal function returned to normal.
1. Why was her heart rate so high and blood pressure so low whenshe was first discovered?
2. What was the cause of the decreased GFR and urine volume?
3. What was the cause of the elevated BUN, creatinine and serumpotassium?
4. Why would hyperkalemia be expected to cause dangerous changesin her ECG?
5. Why would bicarbonate administration help thehyperkalemia?
6. Why did prerenal acute renal failure progress to acutetubular necrosis?
