Fluid, Electrolyte, and Acid-Base Disorders

1. Fluid, Electrolyte, and Acid-Base Disorders Darren Dreyfus, D.O. Associates In Nephrology, P.C. St. Vincent’s Health System

2. Question 1

3. Question 1 A 71-year-old man is evaluated because of intermittent cough and increasing dyspnea on exertion. He has smoked one pack of cigarettes per day for 49 years. He has no other symptoms. On physical examination, distant breath sounds are audible in both lungs and there are scattered rhonchi. Chest radiograph shows a perihilar mass. Abnormal laboratory results include hemoglobin of 10.5 g/dL and a serum sodium of 127 meq/L. Endobronchial biopsy reveals small-cell lung cancer.

4. Question 1 Which of the following is most appropriate treatment for this patient’s hyponatremia? • Chemotherapy • Hypertonic saline • Fluid restriction • Fluid restriction and demeclocycline

5. Answer

6. Question 1 - Answer Answer: A This patient with mild hyponatremia is newly diagnosed with small-cell lung cancer. He has no symptoms that are clearly attributed to the hyponatremia and there initiating non-specific therapy such as fluid restriction with or without demeclocycline therapy, or aggressively treating the hyponatremia with hypertonic saline is not warranted. The most important therapeutic intervention is to treat the underlying cancer with chemotherapy.

7. Question 2

8. Question 2 A 78-year-old woman with metastatic breast cancer involving the bones and soft tissues is evaluated in the emergency department because of lethargy and weakness, nausea, thirst, and dizziness. She has a history of congestive heart failure that has been controlled with medications. On physical examination she has orthostatic hypotension associated with dizziness and dry mucous membranes. Her lungs are clear and she has no dependent edema. • Blood urea nitrogen – 42 mg/dL • Total serum calcium – 11.4 mg /dL • Serum creatinine – 1.6 mg/dL • Serum albumin – 3.0 g/dL

9. Question 2 Administration of which of the following is the most appropriate treatment? • A biophosphonate, intravenously • Corticosteroids, intravenously • Half-normal saline • Normal saline • Furosemide

10. Answer

11. Question 2 - Answer Answer: D The patient has hypercalcemia, the most common metabolic complication of malignancy. She is volume depleted as evidenced by her orthostatic hypotension, dizziness and dry mucous membranes. Despite her history of congestive heart failure, the most appropriate initial therapy is to replace vascular volume as vigorously as possible with normal saline.

12. Question 2 - Answer Furosemide must not be given until the patient has first been adequately rehydrated. Administration of a bisphosphonate is not an appropriate initial therapeutic intervention in this patient because its delayed onset of effect and her more urgent need for volume repletion. Although corticosteroids can be considered as an adjunctive therapy in a patient with a potentially hormone-responsive tumor such as breast cancer, the top priority is volume repletion.

13. Question 3

14. Question 3 A 56-year-old man with a 25-pack-year smoking history, distant cerebrovascular accident, and a 10-year history of hypertension treated with hydrochlorothiazide is evaluated because of generalized fatigue. Blood pressure is 110/70 mm Hg. • Serum sodium – 128 meq/L • Serum potassium – 3.3 meq/L • Serum chloride – 79 meq/L • Serum biocarbonate – 38 meq/L • Arterial blood gases on room air: • pH – 7.50; PCO2 50 mm Hg, PO2 74 mm Hg

15. Question 3 Which of the following best explains the patient’s acid-base disturbance? • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis • Metabolic acidosis

16. Answer

17. Question 3 - Answer Answer: A The low blood pressure and hypochloremia suggest volume-sensitive metabolic alkalosis due to diuretic therapy. Metabolic alkalosis is indicated by the high serum bicarbonate level and pH greater than 7.4 Respiratory compensation for the metabolic alkalosis is appropriate. The PCO2 is 50 mm Hg, showing the expected 10-mm Hg increase that compensates for the 14-meq/L increase in serum bicarbonate level.

18. Question 3 - Answer Metabolic acidosis is not a possible diagnosis since the bicarbonate level and pH are elevated. The normal arterial-to-alveolar oxygen gradient makes underlying chronic obstructive pulmonary disease unlikely, and blood gas values do not indicate concurrent respiratory acidosis.

19. Question 4

20. Question 4 A 65-year-old man with chronic alcoholism is evaluated because of a seizure 1 hour ago. In the emergency department, he is lethargic but conversant and oriented. He reports a several-day history of diarrhea and has muscle cramps. He has no history of trauma or previous seizures. He is taking no medication but has smoked 1 pack of cigarettes daily for the past 30 years.

21. Question 4 On physical examination, blood pressure is 11/075 mm Hg, pulse rate is 100/min, and respiration rate is 18/min. The neck is supple. Carpopedal spasm and Chvostek’s signs are present. The remainder of the physical examination is normal.

22. Question 4 Serum creatinine – 1.4 mg/dL Serum sodium – 136 meq/L Serum potassium 2.7 meq/L Serum chloride – 98 meq/L Serum bicarbonate – 23 meq/L Serum calcium – 7.6 mg/dL Serum magnesium – 0.5 mg /dL Serum phosphorus – 3.0 mg/dL

23. Question 4 Which of the following will best correct the underlying deficiency responsible for this patient’s electrolyte disorders? • Calcium • Magnesium sulfate • Magnesium sulfate and potassium chloride • Potassium chloride

24. Answer

25. Question 4 - Answer Answer: C Hypomagnesemia is frequently seen in alcoholics and in persons with severe diarrhea. If the serum magnesium level is less than 1.0 mg/dL and carpopedal spasm, Chvostek’s or Trousseau’s sign, or seizures are present, intravenous treatment with magnesium is indicated.

26. Question 4 - Answer The hypokalemia is due to diarrhea and volume depletion (volume depletion triggers aldosterone release causing sodium conservation at the expense of potassium loss) and to the renal potassium wasting induced by hypomagnesemia. Attempts at correction of the hypokalemia will be ineffective unless hypomagnesemia and volume are also corrected.

27. Question 4 - Answer The hypocalcemia is due to reduced secretion and peripheral effects of parathyroid hormone, which are caused by the hypomagnesemia. When the hypomagnesemia is corrected, the parathyroid hormone levels will return to normal and the serum calcium level will normalize.

28. Question 5

29. Question 5 A 35-year-old man is evaluated because of recurrent nepholithiasis and is found to have a normal serum calcium concentration and hypercalciuria.

30. Question 5 Which of the following diets should this man avoid in order to reduce the risk of recurrent calcium stones? • Low-sodium diet • Low-calcium diet • Low-oxalate diet • Low-protein diet • Low-purine diet

31. Answer

32. Question 5 - Answer Answer: B Risk factors for calcium nephrolithiasis include low daily fluid intake, high dietary sodium and oxalate, hyperoxaluria, hypercalciuria, hypocitrauria, and hyperuricosuria. Several studies in men and women have shown that a high dietary calcium intake is associated with reduced risk for calcium stone disease. In a recent study, men with hypercalciuric nephrolithiasis placed on a low-calcium versus a high-calcium diet had greater risk of subsequent stone formation.

33. Question 5 - Answer Although not proven, it is believed that the risk for stone formation is lower with high dietary calcium because higher amounts of dietary calcium bind with dietary oxalate and lessen oxalate absorption and urinary excretion. For this same reason, oral magnesium therapy has also been used. A low sodium diet can reduce renal calcium excretion and may reduce calcium stone formation. A diet high in animal protein increases urinary excretion of calcium and uric acid while it decreases excretion of citrate, and is associated with increased risk of calcium stone formation. A diet low in animal protein may minimize this risk.

34. Question 5 - Answer A low-purine diet reduces uric acid excretion and, since uric acid crystals may act as a nidus for formation of calcium stones, may lessen calcium stone formation as well. A low oxalate diet may decrease absorption of oxalate and decrease urinary excretion of oxalate.

35. Question 6

36. Question 6 A 26-year-old woman with type 1 diabetes mellitus is evaluated in the emergency department because of a serum glucose concentration of 450 mg/DL and abdominal pain for the past 24 hours. Her temperature is 38 oC (101 oF). • Serum sodium – 133 meq/L • Serum potassium – 3.9 meq/L • Serum chloride – 97 meq/L • Serum bicarbonate – 10 meq/L • Arterial blood gases – pH 7.2; PCO2, 23 mm Hg • Whole blood lactacte - 0.6 mmol/L

37. Question 6 Which of the following best explains the patient’s acid-base status? • Diabetic ketoacidosis • Diabetic ketoacidosis and proximal renal tubular acidosis • Diabetic ketoacidosis and respiratory acidosis • Diabetic ketoacidosis and metabolic alkalosis

38. Answer

39. Question 6 - Answer Answer: A The patient has an anion gap metabolic acidosis with appropriate respiratory compensation consistent with a diabetic ketoacidosis. Metabolic acidosis is indicated by a low serum bicarbonate level and an arterial blood pH less than 7.4. The respiratory compensation is appropriate; thus, there is not a concomitant respiratory disorder accompanying this metabolic acidosis. The patient has an anion gap of 26. The change in the anion gap is 14. The change in the bicarbonate level is 14, calculated as the normal bicarbonate concentration minus the measured bicarbonate concentration.

40. Question 6 - Answer Thus, the ration between the change in the anion gap and the change in the serum bicarbonate is 1, suggesting that a concurrent non-anion gap metabolic acidosis or a concurrent metabolic alkalosis is not present. Proximal renal tubular acidosis causes a non-anion gap metabolic acidosis, and if it were present with ketoacidosis, we would expect both a non-anion gap and an anion gap metabolic acidosis. That is, the ration between the change in the anion gap to the change in the serum bicarbonate level would be less than 1.

41. Question 7

42. Question 7 A 23-year-old woman with type 1 diabetes mellitus is evaluated in the emergency department because of a 2-day history of dysuria and urinary frequency. Three years ago she had “cystitis” twice in 6 months; in both occasions, she was treated with antibiotics. She uses insulin to control her diabetes and takes 1 or 2 ibuprofen tablets daily for headaches.

43. Question 7 On physical examination, the blood pressure is 115/80 mm Hg, pulse rate is 80/min, and temp is 37.4 oC (99.3 oF). Optic fundoscopy reveals microaneurysms and the neurological examination demonstrates diminished sensitivity to pinprick and light touch in the lower extremities. The remainder of the examination is unremarkable.

44. Question 7 Serum creatinine – 1.8 mg/dL (1.6 a month ago) Serum sodium – 138 meq/L Serum chloride – 106 meq/L Serum potassium – 6.2 meq/L Serum bicarbonate – 21 meq/L Urinalysis – Specific gravity 1.020; 3+ proteinuria; 25 leukocytes/hpf

45. Question 7 On renal ultrasonography, the right kidney is 11.0 cm and the left kidney is 10.9 cm. No hydronephrosis or stones are present. Which of the following is the most likely cause of her hyperkalemia? • Acute renal failure • Diabetic ketoacidosis • High sodium diet • Hyporeninemic hypoaldosteronism

46. Answer

47. Question 7 - Answer Answer: D The most likely cause of hyperkalemia is hyporeninemic hypoaldosteronism, a condition that occurs in 20% to 30% of diabetic persons. Hyperkalemia occurs most often in diabetic patients who have mild to moderate renal failure (as in this case) superimposed on the hyporenin hypoaldosterone state. The later condition seems to be due to unresponsiveness of the adrenal zona glomerulosa to stimulation by angiotensin II, renin, and hyperkalemia itself. Many diabetic patients with hyperkalemia have low renin levels, caused by impaired conversion of prorenin to renin.

48. Question 7 - Answer Since prostaglandins stimulate renin, use of ibuprofen may contribute to the hypoaldosterone state, but by itself rarely causes hyperkalemia. Diabetic ketoacidosis is not present. A change in serum creatinine concentration from 1.6 to 1.8 would not cause hyperkalemia in a patient who had normal renin-aldosterone function. A high-sodium diet does not cause hyperkalemia.

49. Question 8

50. Question 8 A 63-year-old man is evaluated because of upper and lower extremity cramps and diffuse muscle weakness of 2 weeks’ duration. He has been taking aspirin for 6 weeks because of low back pain. The physical examination is normal. • Serum sodium – 135 meq/L • Serum potassium – 2.6 meq/L • Serum chloride – 117 meq/L • Serum bicarbonate – 15 meq/L • Arterial blood gases – pH, 7.30; PCO2, 31 mm Hg • Urine pH – 5.0