Question

Case Study – Acute Renal Failure She was found behind an overturned table after the bomb blast destroyed the sidewalk coffee shop. She had several large wounds and had lost quite a bit of blood. She was also burned over about 10% of her body surface. At the scene, rescuers stopped the major blood loss and evacuated her, but they were not able to rouse her and it was several hours until she could be delivered to the hospital. Her heart rate was 120 bpm and her blood pressure was 60/42. She was immediately given intravenous fluids while her wounds were being tended to. After she was treated in the emergency room she was kept in the hospital for further evaluation. By this time her pulse was 90 bpm and her blood pressure was 75/60. She was only producing 20 ml of urine per hour and her blood work revealed high BUN (blood urea nitrogen), creatinine and potassium concentrations. A creatinine clearance test indicated that her GFR was 26 ml/minute. They decided that she was suffering from prerenal acute renal failure, caused by the extreme hypovolemia from her hemorrhage and burns. The treatment was intravenous administration of isotonic solutions containing glucose and bicarbonate, the fluid to replace lost blood volume and the bicarbonate to lower serum potassium concentrations. Because of concerns about the hyperkalemia, her electrocardiogram was closely monitored for any increases in the size and shape of the T-wave. After her fluids had been adequately managed, her renal function did not fully return to normal right away. She was showing some indications of acute tubular necrosis. After a few weeks of careful monitoring of her hydration and electrolyte concentrations her renal function returned to normal.

1. Why was her heart rate so high and blood pressure so low when she 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 serum potassium?

4. Why would hyperkalemia be expected to cause dangerous changes in her ECG?

5. Why would bicarbonate administration help the hyperkalemia?

6. Why did prerenal acute renal failure progress to acute tubular necrosis?

Answer 1

1. Because of hypovolemia ,sympathetic nervous system is activated so there will be increased heart rate.

Because of hypovolemia, there will be decreased cardiac output. So which further leads to decreased blood pressure.

2. Blood loss and body fluids loss through burns causes decreased blood volume and blood pressure. Sympathetic nervous system will be activated which leads to afferent arteriole contraction. So there will be decreased filtration across glomerulus.

There decreased gfr and urine formation.

Decreased urine formation is due to increased adh secretion.

3. Due to decreased gfr there will be decreased clearance of creatinine and urea.

So there will be increased serum concentrations of creatinine and blood urea nitrogen.

4. Increased potassium increases the resting membrane potential. The difference between resting membrane potential and threshold will be decreased. So the neuron gets excited easily and produces arrhythmia.

5. Bicarbonate decreases potassium levels by various mechanisms

A. Alkalosis increases potassium secretion

B. Bicarbonate shifts potassium into the cells.

6. Decreased perfusion in acute renal failure produces acute tubular necrosis.