Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
62-1 METABOLIC ALKALOSIS Keep Me in the Loop . . . . . . . . . . . . . . . . . . . . . . . . . . . . Level I Jennifer Confer, PharmD, BCPS, BCCCP Generalized weakness and fatigue cause a 60-year-old woman to seek treatment in the emergency department (ED). She complains of weakness, fatigue, myalgias, and polyuria that have occurred over the past 2 days. She has also felt bloated and has taken extra doses of her “water pill.” She has thrown up three times since last night’s dinner and attributes this to eating bad food. Her past medical history is significant for HTN, heart failure (HF), type 2 diabetes mellitus, and dyslipidemia. Physical exam reveals signs of volume depletion (dry mucous membranes, hypotension, tachycardia, and dry/ wrinkled extremities). Laboratory values indicate the presence of metabolic alkalosis. Appropriate treatment measures include fluid administration with isotonic (0.9%) sodium chloride, intravenous potassium chloride supplementation, and temporary discontinuation of the loop diuretic. Identification of the patient’s baseline fluid status when not dehydrated will guide further modifications of the current drug regimen. The student must determine what parameters should be monitored after fluid administration to assess the effectiveness of treatment. Further, after the response to initial IV fluids is known, the student must determine whether alternative treatments are required based on physical exam and laboratory values. QUESTIONS Problem Identification 1.a. Identify the type of acid–base disturbance present in this patient. Interpret the patient’s arterial blood gas results and identify potential causes to support your response. • To assess arterial blood gas results, five steps should be taken: 1. What is the pH—normal, acidotic, or alkalotic? ✓The patient’s arterial blood pH of 7.54 signifies an alkalemia (pH 7.45 or greater). 2. What is the PaCO2—high, normal, or low? ✓ The patient’s PaCO2 of 46 is high (normal range 35–45 mm Hg. 3. What is the serum HCO3—high, normal, or low? ✓The patient’s serum HCO3 of 39 is high (normal range 22–30 mEq/L). 4. Is the primary problem respiratory or metabolic? ✓The patient has an elevated serum bicarbonate concentration, but the PaCO2 is not considerably increased. This information is evidence that the acid–base disturbance this patient is experiencing is metabolic. The fact that the PaCO2 is not considerably increased indicates that this disturbance does not yet contain a respiratory component. 5. Is the problem acute, partially compensated, or compensated? ✓For a compensation to occur, the arterial PaCO2 is estimated to increase 0.5–0.7 mm Hg for every 1 mEq/L ✓ Since this patient’s PaCO2 is 46 mm Hg, a partial compensatory response is beginning. • Evaluating the above results, it is determined that this patient’s disturbance is a partially compensated metabolic alkalosis. • When metabolic alkalosis occurs, the body attempts to compensate leading to alveolar hypoventilation, which causes a rise in the PaCO2, reducing the elevation in pH that is occurring.1 • The use of diuretics (typically thiazide or loop diuretics) causes an inhibition of ion reabsorption (sodium, chloride, potassium, and hydrogen) through either the loop of Henle or the distal tubules. This leads to increased excretion of sodium, chloride, potassium, hydrogen, and water. • Vomiting of gastric contents, which are abundant in hydrochloric acid (HCl), will cause an increase in serum bicarbonate. Although compensation can occur through the renal excretion of bicarbonate, the rapid loss of chloride anions with hydrogen causes an abrupt increase in serum bicarbonate producing a metabolic alkalosis.2 1.b. Create a list of this patient’s drug therapy problems. • Hypotension secondary to volume depletion. • Metabolic alkalosis secondary to excessive loop diuretic use and vomiting. • Constitutional symptoms (ie, generalized weakness, fatigue, and myalgias) likely the result of volume depletion. • Electrolyte abnormalities, including hyponatremia, hypokalemia, hypochloremia, hypocalcemia, hypomagnesemia, and elevated serum bicarbonate. • HF with poor medication adherence exhibited by excessive diuretic use. • Type 2 diabetes mellitus—diet controlled. • Dyslipidemia—obtain fasting lipid panel to assess the adequacy of current treatment. 1.c. Describe the physical exam and laboratory findings that are consistent with metabolic alkalosis and those that are inconsistent with this acid–base disorder. Consistent findings (physical): • Many of the signs of metabolic alkalosis are not specific and depend on the severity of the alkalosis. Findings that can be seen such as weakness, fatigue, and myalgias are due primarily to the volume depletion and electrolyte abnormalities that are associated with alkalosis; but not directly due to the alkalosis.3 Consistent findings (laboratory): • Elevated arterial blood pH • Elevated arterial bicarbonate • Elevated serum bicarbonate • Decreased serum chloride • Decreased serum sodium • Decreased serum potassium • Decreased serum calcium • Decreased serum magnesium Copyright © 2017 by McGraw-Hill Education. All rights reserved. Metabolic Alkalosis CASE SUMMARY ✓This patient’s serum bicarbonate concentration of 39 mEq/L is 13 mEq/L above the normal expected serum value; therefore, a compensatory PaCO2 response would be a PaCO2 of approximately 48 mm Hg (13 × 0.6, or 7.8 mm Hg above the expected value of 40 mm Hg). CHAPTER 62 62 increase in serum bicarbonate above a normal expected value.1 62-2 • Decreased urine chloride SECTION 5 • Elevated urine potassium • Elevated urine pH Inconsistent findings: Renal Disorders • An elevated white blood cell (WBC) count is generally not a sign of metabolic alkalosis. This finding in the case may be caused by physical stress the patient is experiencing because of hypotension and tachycardia secondary to volume depletion. Because of volume depletion, this elevated WBC count may also simply reflect hemoconcentration. While obtaining a WBC differential may assist in differentiating stress from infection, both can cause abnormalities (increases and decreases) in the percentage of each type of WBC. At this time, it is not necessary to obtain a WBC differential in this patient. If the WBC count did not decrease after fluid administration, then ordering a differential to rule out infection could be considered. • Constitutional symptoms (ie, generalized weakness, fatigue, and myalgias) do not result directly from metabolic alkalosis. This patient’s physical constitutional symptoms are suggestive of volume depletion. Secondary to the volume depletion are electrolyte disturbances (hypokalemia, hyponatremia, and hypocalcemia) that can be manifested as weakness, myalgia, or polyuria due to hypokalemia and/or muscle spasms or twitching due to hypocalcemia. • Polyuria alone is not a characteristic sign of metabolic alkalosis. In this patient, polyuria may be multifactorial caused by excessive diuretic use resulting in electrolyte abnormalities. Hypokalemia can cause polyuria, which would increase fluid excretion worsening the volume depletion. As fluids and/or potassium supplements (see question 4.a) are administered and the metabolic alkalosis is corrected, the potassium should normalize and the patient should not experience polyuria at that point. In addition, with a past medical history of diabetes mellitus that is currently diet controlled, the patient may benefit from a urinalysis and labs (ie, hemoglobin A1C) to assure that the diabetes mellitus is not progressing. • Extracellular fluid volume contraction can also intensify the increase in serum bicarbonate by limiting the volume in which bicarbonate can distribute. • Many of the causes of metabolic alkalosis are associated with hypokalemia, which in turn prolongs alkalosis. Hypokalemia will stimulate the shift of hydrogen ions intracellularly, enhancing bicarbonate reabsorption in the collecting duct, producing extracellular alkalosis. When potassium depletion occurs in conjunction with chloride depletion, metabolic alkalosis is four times as likely to occur.3 • Gastric secretions contain high concentrations of hydrochloric acid. Normally, gastric acid secretions stimulate the pancreas to secrete bicarbonate once the hydrochloric acid reaches the duodenum. These substances are then neutralized and there is equilibrium between hydrogen and bicarbonate. When gastric secretions are lost through vomiting, the pancreas is not stimulated to release bicarbonate and a net gain of bicarbonate in the serum occurs, leading to metabolic alkalosis.2 Volume depletion is also observed when gastric secretions are lost and metabolic alkalosis then occurs as described above. 1.e. What medications, dietary supplements, and medical procedures could contribute to metabolic alkalosis? Include those that may not apply to this patient. • Medications that can contribute to metabolic alkalosis include:1,4 ✓Thiazide diuretics ✓Loop diuretics ✓Nonabsorbable antacids (ie, magnesium, calcium, or aluminum with a hydroxide or carbonate base) ✓Excessive use of laxatives causing sufficient losses through diarrhea ✓ Mineralocorticoids glucocorticoids) (ie, fludrocortisone, some ✓ Excessive administration or retention (in renal insufficiency) of sodium bicarbonate ✓Intravenous penicillins (eg, ampicillin, penicillin) 1.d. What is the pathophysiology underlying this patient’s metabolic alkalosis? • This patient is taking the loop diuretic furosemide in an unprescribed manner • As described above (see question 1.a.), this patient’s metabolic alkalosis is due to excessive loop diuretic use, combined with three episodes of recent vomiting. • Glycyrrhizinic acid-containing compounds (eg, licorice, chewing tobacco) • Loop and thiazide diuretics cause metabolic alkalosis (also referred to as “contraction alkalosis” or “chloride depletion alkalosis”) through the enhanced excretion of sodium, chloride, potassium, and water in the ascending limb of the Loop of Henle and distal convoluted tubule, respectively. Evaluation of urine electrolytes demonstrates increased urine concentrations secondary to the enhanced excretion. This results in increased osmolality in the renal tubules and a subsequent reduction of extracellular fluid volume.3 • Hemodialysis utilizing citrate-containing dialysate solutions • Extracellular fluid volume contraction promotes the secretion of renin and aldosterone that leads to an increase in the reabsorption of sodium in the distal tubule and accelerated secretion of potassium and hydrogen ions, leading to alkalosis and hypokalemia. The increased secretion of hydrogen ions leads to increased luminal bicarbonate. The kidneys are normally able to secrete excess bicarbonate through an apical chloride–bicarbonate exchanger. With an excessive renal loss of chloride, the kidneys are unable to appropriately secrete bicarbonate, thus elevating the concentration in the serum.1 Copyright © 2017 by McGraw-Hill Education. All rights reserved. • Hemodialysis utilizing bicarbonate-rich dialysate solutions • Blood transfusions that contain citrate as a preservative agent Desired Outcome 2.What are the desired therapeutic outcomes for this patient? Hypotension: • Normalize blood pressure (goal <140/90 mm Hg). • Maintain mean arterial pressure (MAP) ≥65 mm Hg.5 • Achieve urine output 0.5 mL/kg/hour or more.5 • Maintain adequate organ perfusion [based on MAP ≥65 and either superior vena cava oxygenation saturation (Scvo2) or mixed venous oxygen saturation (Svo2) of ≥70% or 65%, respectively].5 Metabolic alkalosis/electrolyte abnormalities: • Cessation of vomiting • Correction of pH to 7.35–7.45 62-3 • Correction of serum bicarbonate to 22–30 mEq/L • Correction of serum potassium to 3.5–5.0 mEq/L • Correction of serum sodium to 135–145 mEq/L • Correction of serum calcium (corrected) to 8.5–10.5 mg/dL • Correction of serum magnesium to 1.6–2.4 mEq/L • Correction of urine pH to <6.0 • Correction of volume depletion Constitutional symptoms: • Cessation of vomiting • Correction of volume depletion • Normalization of body temperature • Resolution of weakness, fatigue, and myalgias Congestive HF: • Improve patient’s quality of life. • Minimize fluid overload. • Avoid exacerbations of HF requiring hospitalization. • Maintain vital signs within normal limits. • Maintain adequate urine output. Therapeutic Alternatives 3.What pharmacologic and nonpharmacologic alternatives should be considered for the treatment of metabolic alkalosis in this patient? • The first step in determining a pharmacologic plan is to determine the cause of the metabolic alkalosis and to predict if the alkalosis is chloride responsive or chloride resistant. The most likely cause(s) of the alkalosis in this patient are excessive use of furosemide and recent vomiting, which are considered chloride-responsive states (see answer to questions 1.d and 1.e). • IV fluid resuscitation with isotonic sodium chloride is firstline therapy in chloride-responsive cases (urine chloride <10 mEq/L). Isotonic sodium chloride will restore extracellular fluid volume and in patients with normal renal function, bicarbonate excretion will be enhanced as sodium, potassium, and chloride stores are repleted. Fluid therapy should be administered to patients who can tolerate the volume load. Fluid therapy should be cautiously administered or not given in patients who are volume overloaded or who may have difficulty with excess volume (ie, patients with HF or renal insufficiency).1,4 Although this patient has a history of HF, it is obvious based on presentation that she is severely volume depleted; therefore, cautious administration of isotonic sodium chloride should be initiated. • Ringer’s lactate IV solution contains less chloride than sodium and should not be used to treat metabolic alkalosis. In addition, the lactate in the solution is a precursor to bicarbonate, which could further exacerbate the existing alkalosis. • Potassium supplementation (either orally or intravenously depending on severity) is usually needed because metabolic alkalosis resulting from diuretic therapy and/or vomiting causes potassium depletion. Given that this patient is experiencing chloride-responsive alkalosis with volume depletion, potassium supplementation should be initiated with appropriate electrolyte monitoring. Caution should be given when potassium supplementation is initiated in patients with renal insufficiency, as hyperkalemia could develop. • Acidifying agents (ie, ammonium chloride, arginine monohydrochloride, and hydrochloric acid) may be considered in patients with severe (pH >7.55) symptomatic metabolic alkalosis, as well as patients who are not responsive to sodium chloride hydration therapy and those who are not able to endure excessive volume replacements due to edematous states.1,3 ✓Ammonium chloride, metabolized by the liver to urea and hydrochloric acid, is an alternative treatment for metabolic alkalosis. Caution must be used for patients with hepatic and/or kidney impairment. Patients with hepatic dysfunction are unable to properly convert ammonia to urea, leading to increased serum ammonia levels, which can cause or worsen encephalopathy. In patients with renal insufficiency, the generation of increased urea may worsen uremic symptoms. If prescribed, ammonium chloride can be administered through a peripheral vein. ✓Arginine hydrochloride, similar to ammonium chloride, undergoes metabolism by the liver that results in the production of hydrogen ions. Additionally, because arginine binds to circulating ammonia that leads to the production of urea, it may be used safely in patients with hepatic insufficiency. Patients with renal insufficiency should not be given arginine hydrochloride. Arginine may cause intracellular to extracellular shifts in potassium, which in renal insufficiency may lead to severe hyperkalemia. ✓Hydrochloric acid is indicated when sodium or potassium chloride cannot be administered because of volume overload or advanced renal failure, or in states where prompt correction is needed and other acidifying agents are contraindicated (eg, cardiac arrhythmias, hepatic encephalopathy). Due to the potential for severe adverse effects such as metabolic acidosis, hemolysis, and extravasation, hydrochloric acid should be administered slowly through a central vein and the infusion rate should not exceed 0.2 mEq/kg/hour.7 • Hemodialysis may be considered in patients with advanced renal failure, who are volume overloaded and resistant to acetazolamide.3 With hemodialysis, the use of either a lowbicarbonate or acetate-free solution is recommended in patients with metabolic alkalosis. Based on the laboratory data (ie, SCr and BUN), it does not appear that this patient is in advanced renal failure; therefore, hemodialysis is not recommended. Optimal Plan 4.a. What drug, dosage form, dose, schedule, and duration of therapy are best for this patient? • IV hydration with 0.9% sodium chloride solution is the firstline therapy for this patient. • Based on the patient’s vital signs and laboratory values, this patient is volume depleted. Intravenous boluses of 1000 mL of 0.9% sodium chloride can be given repeatedly, each one Copyright © 2017 by McGraw-Hill Education. All rights reserved. Metabolic Alkalosis • Prevent/minimize complications CHAPTER 62 • Correction of serum chloride to 95–105 mEq/L • Acetazolamide is an alternative for patients who are unable to tolerate increased fluid volume. The drug inhibits carbonic anhydrase, thereby reducing the reabsorption of sodium and bicarbonate in the proximal tubule and leading to their enhanced excretion. In addition, acetazolamide stimulates the excretion of potassium and phosphate. It is not recommended if the patient is experiencing hypokalemia, but if it used in the setting of hypokalemia then potassium supplementation should be initiated. A single 500-mg IV dose has been shown to correct metabolic alkalosis and return serum bicarbonate levels to normal.6 This patient should be reassessed after an initial fluid challenge before administering acetazolamide. 62-4 SECTION 5 infused over 1 hour, keeping the following goals of fluid resuscitation in mind: MAP ≥65 mm Hg, urine output ≥0.5 mL/ kg/hour and Scvo2 ≥70% or a Svo2 ≥65%.5 Typically, goals are achieved after 3–4 L of fluid. • Because this patient’s metabolic alkalosis is chloride responsive, the estimated volume of isotonic fluid needed can be calculated based on the chloride (Cl) deficit using the following equation:1,4 Renal Disorders Cl deficit (mEq) = 0.2 × wt (kg) × (normal Cl – actual Cl) The factor 0.2 signifies the extracellular volume as a fraction of body weight. Once the chloride deficit is calculated, the volume can be determined as a ratio of Cl deficit/154, where 154 represents the amount of chloride in mEq in 1 L of isotonic sodium chloride. For this patient, who weights 80 kg and has a serum chloride level of 85 mEq/L, the chloride deficit can be calculated as follows: Step 1: Calculate the Cl deficit (mEq) = 0.2 × 80 × (100 – 85) = 240 mEq Step 2: Determine the minimum volume (L) of NaCl to infuse = 240 mEq/154 mEq/L = 1.6 L • Fluid resuscitation should be completed gradually and cautiously to avoid fluid overload in this patient with a history of HF. The patient should be reassessed for signs and symptoms of fluid overload after each liter of isotonic saline infused. • Furosemide therapy should be discontinued until the metabolic alkalosis has been resolved and the hypotension/volume depletion has been corrected. • Potassium chloride supplementation should be initiated at a dose of 20–40 mEq per day, with the understanding that the patient’s requirements may need to be modified as volume depletion resolves and furosemide is reinitiated. Potassium supplementation may be given either orally in divided doses or added to the sodium chloride solution (ie, 20–40 mEq/L) and given as a continuous infusion. Further monitoring of serum potassium should continue to ensure that overcorrection has not occurred. 4.b. What other modifications in the patient’s current drug regimen are warranted? Include your rationale. • The patient should first be asked, or medical records reviewed, for any changes that the patient may have experienced or may be experiencing that are different from baseline due to HF (eg, difficulty breathing, noticeable weight gain or loss, increase edema, etc.). Currently, it is not appropriate to change therapy based on the presentation of the patient because she is volume depleted. • If the patient is not fluid overloaded at baseline, it would be suitable to decrease the dose of the furosemide to 20 mg daily after the metabolic alkalosis resolves and the hypotension/ volume depletion have been corrected. Dietary restriction of sodium should be reiterated to the patient to avoid fluid overload. • If the patient is fluid overloaded at baseline, adding a potassium-sparing diuretic, such as spironolactone 25 mg PO once daily, would assure proper diuresis and may prevent hypokalemia. • Currently, the doses of carvedilol, lisinopril, and atorvastatin are within appropriate dosing recommendations for the disease states of the patient. The lisinopril dose may need to be Copyright © 2017 by McGraw-Hill Education. All rights reserved. adjusted or discontinued if the patient is receiving potassium as a treatment option for metabolic alkalosis in the acute treatment phase. Once the metabolic alkalosis is corrected and the underlying cause treated, dose adjustments for the lisinopril may need to be modified back to the original dose. In addition, routine monitoring of potassium levels should occur to avoid hyperkalemia while the patient is receiving potassium. The patient does not appear to be having adverse effects from atorvastatin, but it would be beneficial to obtain a baseline fasting lipid panel to assess the efficacy of therapy and adherence. In addition, the patient presented with complaints of myalgias (likely secondary to electrolyte abnormalities), but it would be beneficial to obtain a myoglobin and creatine kinase level to assure the statin does not need to be discontinued. • Patient education on adherence to the prescribed regimen (as described in question 6) is necessary to avoid potential adverse effects. Outcome Evaluation 5.a. What clinical and laboratory parameters are necessary to evaluate the therapy for achievement of the desired outcome and to detect or prevent adverse effects? Efficacy: • Obtain repeat arterial blood gas in 24 hours and reassess treatment response. • Obtain serum electrolytes (ie, sodium, potassium, chloride, and bicarbonate), calcium, BUN, and serum creatinine every 12 hours for the first 24 hours and then reassess. • Obtain vital signs every 4 hours. • Obtain repeat set of urine electrolytes (ie, sodium, potassium, and chloride). ✓Urine sodium when a patient is euvolemic is generally >40 mEq/L. ✓Urine potassium concentration should be between 20 and 30 mEq/L. ✓Urine chloride concentration should be between 25 and 40 mEq/L. • Measure fluid intake and urine output every 2 hours for 24 hours, then once every shift. Toxicity: • Assess the patient for signs and symptoms of fluid overload (shortness of breath, crackles on chest auscultation, and peripheral edema). 5.b. What is your assessment of the patient’s response to the IV fluids? What modifications in therapy are warranted, if any? • The infusion of 0.9% sodium chloride, along with potassium chloride supplementation, appears to have facilitated the normalization of sodium, potassium, and chloride. • There has also been improvement of the volume depletion as noted by a normalization of serum creatinine and BUN. • While there has been an improvement in several parameters of the arterial blood gas (ie, pH, PaCO2, HCO3) and serum bicarbonate, the values are still slightly elevated. • Although the patient is experiencing 1+ pitting edema in the lower extremities, evaluation of the full appearance of the patient is necessary to assess fluid status before continuing treatment. This includes (but is not limited to) lung auscultation, repeat chest X-ray, and assessment for the presence of JVD. 62-5 ✓ A single dose of acetazolamide 500 mg IV (if utilized) should result in correction of the metabolic alkalosis.6 Patient Education 6.What information should be provided to the patient to help enhance adherence, ensure successful outcomes, and prevent future complications? • The extra doses of the diuretic furosemide that you were taking for treatment of congestive HF have caused you to lose too much fluid and essential electrolytes such as potassium, sodium, and chloride. This caused you to become dehydrated and feel weak and tired. To avoid this in the future, do not take your furosemide more than as prescribed. If you consistently feel bloated or if you develop difficulty breathing, dizziness, weakness, fatigue, or muscle aches, let your doctor know as soon as possible. • It is beneficial to weigh yourself on a daily basis to assess if you are experiencing any fluid retention due to your congestive HF. In addition, if you find your weight is decreasing, this can be due to a depletion of fluid that can result in electrolyte imbalances and possible injury to your kidneys. Some of the medications that you are taking (eg, furosemide and lisinopril) may also worsen electrolyte imbalances and kidney injury. For • It is highly recommended to limit the amount of salt you use when you eat. Extra salt will cause your body to hang on to fluid, which will cause your heart to work harder. This can also cause symptoms such as shortness of breath and swelling of your feet. • Furosemide removes fluid from your body, but it also causes loss of potassium in the urine. Potassium is very important for normal heart function. For this reason, please keep all followup appointments with your doctor so your lab work can be monitored. • Store these and all other medications in the original container in a cool, dry place out of the reach of children. REFERENCES 1. Shah N, Shaw C, Forni LG. Metabolic alkalosis in the intensive care unit. Neth J Crit Care 2008;12(3):113–119. 2. Gennari FJ, Weise WJ. Acid–base disturbances in gastrointestinal disease. Clin J Am Soc Nephrol 2008;3:1861–1868. 3. Soifer JT, Kim HT. Approach to metabolic alkalosis. Emerg Med Clin N Am 2014;32:453–463. 4. Seifter JL. Integration of acid–base and electrolyte disorders. N Engl J Med 2014;371(19):1821–1831. 5. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013;41:580–637. 6. Moviat M, Pickkers P, van der Hoeven PHJ, et al. Acetazolamidemediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients. Crit Care 2006;10:R14. doi: 10.1186/cc3970. 7. Oh YK. Acid–base disorders in ICU patients. Electrolyte Blood Press 2010;8:66–71. Copyright © 2017 by McGraw-Hill Education. All rights reserved. Metabolic Alkalosis • If it appears that the patient cannot tolerate any further treatment with IV fluids due to fluid overload, acetazolamide should be considered as an option to assist with further excretion of bicarbonate.1,3 As described above (see question 3), acetazolamide will also cause potassium excretion, and therefore it is important to follow electrolytes carefully while administering this medication. Supplementation of potassium may be considered to avoid hypokalemia. this reason, it is important that you let your doctor know if you are unable to maintain your normal fluid intake or if you are not going to the bathroom as often as you normally do. CHAPTER 62 • Continued treatment with 0.9% sodium chloride is warranted if no further symptoms of fluid overload are apparent. Full normalization of the serum bicarbonate and pH should occur within 24 hours.