Joshua Dilday, DO1, Catherine Cameron, MD2, and Christopher Bell, MD3 1 Department of Acute Care Surgery, University of Southern California, LAC + USC Medical Center, Los Angeles, CA, USA 2 Landstuhl Regional Medical Center, Germany 3 William Beaumont Army Medical Center, El Paso, TX, USA The above patient is presenting with another small bowel obstruction. If the vomiting from a small bowel obstruction is significant, it can lead to acid/base and electrolyte abnormalities. The main problem is the severe dehydration. Proximal GI losses can cause a contraction metabolic alkalosis. Sodium is the key element as it tries to maintain intravascular volume through retention of water. During volume contraction, bicarbonate and sodium are reabsorbed to maintain volume and electrical balance as there is insufficient chloride. The body does all it can to hold on to the sodium and the distal convoluted tubules will compensate sodium reabsorption by excreting potassium, leading to hypokalemia. This continues until the potassium concentration is below tolerable levels at which point it starts to excrete hydrogen. The reabsorption of bicarbonate causes a loss of chloride and thus the hypochloremia. In this setting, the person is alkalotic but because they are urinating hydrogen ions despite being alkalotic, the kidneys are causing a “paradoxical aciduria”. The chloride is also lost from GI losses. The first and foremost important treatment is the replenishment of water with any crystalloid solution. Answer A is incorrect as it is not metabolic acidosis nor hyperchloremia. B is incorrect because it is not hyperchloremic. Answer D is incorrect because it is not hyperchloremia as explained. Answers E and F are wrong due to previous explanations. Answer: C Khanna, A., & Kurtzman, N. A. (2001). Metabolic alkalosis. Respiratory Care , 46 (4), 354–365. Galla, J. H. (2000). Metabolic alkalosis. Journal of the American Society of Nephrology , 11 (2), 369–375. Luke, R. G., & Galla, J. H. (2012). It is chloride depletion alkalosis, not contraction alkalosis. Journal of the American Society of Nephrology , 23 (2), 204–207. When addressing the disorder of hyponatremia, it is important to first classify the disorder based on volume status of hypovolemia, euvolemia, and hypervolemia. In general, hyponatremia is treated with fluid restriction in the setting of euvolemia, isotonic saline in the setting of hypovolemia, and diuresis in the setting of hypervolemia. Sometimes, a combination of these therapies may be needed based on the presentation. If the patient is hypovolemic from bowel obstruction, the therapy usually consists of isotonic or hypertonic saline. Euvolemic hyponatremia such as an SIADH is usually treated with fluid restriction and loop diuretics. Hypervolemic hyponatremia such as in patients with heart failure are treated with diuretics, angiotensin converting enzyme (ACE) inhibitors, and beta‐blockers. With the addition of ACE inhibitors, congestive heart failure is treated and vasopressin secretion is reduced. One liter of normal saline will increase plasma sodium concentration by 1 mEq/L. Thus, treating hyponatremia in edematous patients with saline will only exacerbate the problem. The patient in this case is overloaded with fluids and thus choice A is incorrect. Decreasing IV fluids to 75 cc to restrict fluids may be helpful but restricting fluids is a better option and that is why choice B is incorrect. Choice C is incorrect because thiazide diuretics are contraindicated since it blocks reabsorption of sodium and chloride in the distal tubules and thus prevents the generation of maximally dilute urine. 3% hypertonic saline would in this case worsen the salt load and the hypervolemia. In a hypovolemic state, this may be a treatment option. If the patient is in a state of hypovolemia and hyponatremia and is symptomatic, a bolus of 100–150 mL of 3% hypertonic saline may be useful. Answer: E Adrogue, H. J., & Madias, N. E. (2000). Hyponatremia. New England Journal of Medicine , 342, 1581. Braun, M. M., Barstow, C. H., & Pyzocha, N. J. (2015). Diagnosis and management of sodium disorders: hyponatremia and hypernatremia. American Family Physician , 91 (5), 299–307. Konstam, M. A., Kiernan, M. S., Bernstein, D., et al. (2018). Evaluation and management of right‐sided heart failure: a scientific statement from the American Heart Association. Circulation , 137(20), e578–622. The patient has a metabolic acidosis likely from lactic acidosis in addition to hyperchloremic acidosis due to multiple saline boluses in an attempt to control his hypotension. Excessive saline infusion can cause a hyperchloremic non‐gap metabolic acidosis. The diagnosis of primary metabolic acidosis is made by the low pH and low plasma HCO3. Once the determination of metabolic acidosis is made, it should be determined if a gap acidosis is present. However, since no electrolytes were given to determine a gap, the next determination should be appropriate respiratory compensation. This can be done utilizing Winters’ formula [pCO2 = (1.5 × HCO3) + 8 ± 2]. The formula predicts the expected pCO2 in a primary metabolic acidosis. If the measured pCO2 is greater than expected, a superimposed respiratory acidosis is present. If the measured pCO2 is less than expected, a combined respiratory alkalosis is present. In the case above, the expected pCO2 = (1.5 × 18) + 8 ± 2 = 35 ± 2. The measured pCO2 in the above patient (34) is an expected respiratory compensation for primary metabolic acidosis. As a general rule of thumb, a change in the PCO2 by 10 results in a change in the pH by 0.08. For example, if the PCO2 was 30, the pH would be expected to be at 7.48. If the PCO2 was to be 50, then the pH would be 7.32. Thus, in the patient above, the respiratory compensation was not enough to normalized pH. Although many are biased against hyperchloremic metabolic acidosis caused by saline infusions, the numerous randomized clinical studies using hypertonic saline has not shown any clinically relevant complications from the iatrogenically caused hyperchloremic metabolic acidosis. Answers A and E are wrong because the patient is not alkalotic. Answer D is incorrect because the patient does not have respiratory acidosis. Answer B is incorrect as the patient is not alkalotic. Answer: C Bulger, E. M., May, S., Kerby, J. D., et al. (2011). Out‐of‐hospital hypertonic resuscitation after traumatic hypovolemic shock: a randomized, placebo controlled trial. Annals of Surgery , 253(3), 431–441. Kellum, J. A. (2007). Disorders of acid‐base balance. Critical Care Medicine , 35 (11), 2630–2636 Winter, S. D., Pearson, J. R., Gabow, P. A., et al. (1990). The fall of the serum anion gap. Archives of Internal Medicine , 150 (2), 311–313. Which of the following is true regarding the acid‐base status? The above patient has a respiratory acidosis as evidenced by his decrease in pH and increase in PaCO2. Given the information that he has suboptimal COPD control, it can be assumed that he likely has a chronic respiratory acidosis. The adequate metabolic compensation in a chronic respiratory acidosis can be determined by the following equation: HCO3 = 24+ [0.4 x (PaCO2 – 40)] HCO3 = 24+ [0.4 x (55 – 40)] HCO3 = 24+ [0.4 x (15)] HCO3 = 24+ [6] HCO3 = 30 Thus, the expected bicarbonate level is within the correct range for compensation. If the patient were to have a combined metabolic acidosis, the bicarbonate would be lower than expected. As a general rule, a change in the PCO2 by 10 results a change in the pH by 0.08. For example, if the PCO2 was 30, the pH would be expected to be at 7.48. If the PCO2 was to be 50, then the pH would be 7.32. The patient above has a PCO2 of 55 and a pure respiratory acidosis would result in pH of lower than 7.27. Since the pH is higher than expected, there is some metabolic compensation. Answers A, C, and E are incorrect as the patient does not have metabolic acidosis. Answer D in incorrect as the patient does have metabolic compensation with a higher than normal bicarbonate level. Answer: B Kellum, J. A. (2007). Disorders of acid‐base balance. Critical Care Medicine , 35 (11), 2630–2636. Plant, P. K., Owen, J. L., & Elliott, M. W. (2000). One year period prevalence study of respiratory acidosis in acute exacerbations of COPD: implications for the provision of non‐invasive ventilation and oxygen administration. Thorax , 55 (7), 550–554. Winter, S. D., Pearson, J. R., Gabow, P. A., et al. (1990). The fall of the serum anion gap. Archives of Internal Medicine , 150 (2), 311–313. Which of the following is true regarding the acid‐base status? The above patient has an anion gap metabolic acidosis. The first step in management of acidemia is determining whether it is respiratory or metabolic in nature. Since the bicarbonate level is low and in the same direction as the pH, a metabolic acidosis is present. The next step is to determine if an anion gap (AG) is present. The AG can provide information as to whether the acidosis is due to increased acid accumulation or bicarbonate loss. This can be determined by the equation AG = Na – (Cl + HCO3). Normal AG ranges are 3–12 mEq/L. The above patient has an AG of 23 mEq/L (143‐(99+21), thus causing a high anion gap metabolic acidosis. Common causes of this can be remembered by the mnemonic – MUDPILES: (Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Isoniazid. Iron, Lactic acidosis, Ethylene glycol, and Salicylates). This patient most likely ingested ethylene glycol which is antifreeze and found in the garage. Hyperchloremic metabolic acidosis is usually normal AG acidosis. Low AG is typically associated with hypoalbuminemia. Albumin constitutes 80% of the unmeasured anions. Answers A and E are incorrect because the patient has AG acidosis. Answers C and D are incorrect as the patient does not have respiratory acidosis as the PaCO2 is 39 mm Hg. The utilization of Winter’s formula, [expected pCO2 = (1.5 × HCO3) + 8 ± 2], determined that there is an appropriate respiratory response. Expected pCO2 = 31.5 +8 = 39.5. Thus, the respiratory response is appropriate. Answer: B Kellum, J. A. (2007). Disorders of acid‐base balance. Critical Care Medicine , 35(11), 2630–2636 Kraut, J. A., & Xing, S. X. (2011) Approach to the evaluation of a patient with an increased serum osmolal gap and high‐anion‐gap metabolic acidosis. American Journal of Kidney Diseases , 58 (3), 480–484.
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Acid‐Base, Fluids, and Electrolytes
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