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A Paraneoplastic Potassium and Acid-Base Disturbance

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A Paraneoplastic Potassium and Acid-Base Disturbance SYMPTOMS TO DIAGNOSIS GREGORY W. RUTECKI, MD, Section Editor SAMUEL P. WILES, MD MATTHEW KICZEK, DO GREGORY W. RUTECKI, MD Department of Pulmonary and Critical Care, Department of Diagnostic Radiology, Department of Internal Medicine, Cleveland Clinic Cleveland Clinic; Clinical Assistant Professor, Cleveland Clinic Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH A paraneoplastic potassium and acid-base disturbance NOTE: The scenario presented here is partly ■ ASSESSING ACID-BASE DISORDERS based on cases reported elsewhere by Martínez- Valles et al1 and Fernández-Rodríguez et al.2 What type of acid-base disorder does this 1patient have? 55-year-old man is admitted to the hos- □ Metabolic acidosis A pital with generalized malaise, paresthe- □ Respiratory acidosis sias, and severe hypertension. He says he had □ Metabolic alkalosis experienced agitation along with weakness on □ Respiratory alkalosis exertion 24 hours before presentation to the emergency department, with subsequent on- The patient has metabolic alkalosis. set of paresthesias in his lower extremities and A 5-step approach perioral area. If a patient has an acid-base disorder, one He is already known to have mild chronic should use a 5-step process to characterize it obstructive pulmonary disease, with a ratio of (Table 2).3 forced expiratory volume in 1 second (FEV1) 1. Acidosis or alkalosis? The patient’s ar- A 55-year-old to forced vital capacity (FVC) of less than terial pH is 7.5, which is alkalemic because it smoker with COPD 70% and an FEV1 85% of predicted. In addi- is higher than 7.44. tion, he was recently diagnosed with diabetes, 2. Metabolic or respiratory? The primary presents resistant hypertension requiring maximum process in our patient is overwhelmingly met- with malaise, doses of 3 agents (a calcium channel blocker, abolic, as his partial pressure of carbon diox- paresthesias, an angiotensin-converting enzyme inhibitor, ide (Pco2) is slightly elevated, a direction that and a loop diuretic), and hyperlipidemia. would cause acidosis, not alkalosis. and severe He is a current smoker with a 30-pack-year 3. The anion gap (the serum sodium con- hypertension: smoking history. He does not use alcohol. His centration minus the sum of the chloride and family history is noncontributory. bicarbonate concentrations) is normal at 8 What is the cause? His blood pressure is 190/110 mm Hg de- mmol/L (DRG:HYBRiD-XL Immunoassay spite adherence to his 3-drug regimen. His oxy- and Clinical Chemistry Analyzer, reference gen saturation is 94% on room air, respiratory range 8–16). rate in the low 30s, and pulse 110 beats/minute. 4. Is the disturbance compensated? We He has normal breath sounds, normal S1 and have determined that this patient has a meta- S2 with an S4 gallop, bilateral lower-extremity bolic alkalemia; the question now is whether edema, truncal obesity, and abdominal striae. there is any compensation for the primary dis- Electrocardiography shows tachycardia with turbance. In metabolic alkalosis, the Pco may in- first-degree atrioventicular block. Chest radi- 2 ography shows an opacity in the right middle crease by approximately 0.6 mm Hg (range 0.5–0.8) above the nominal normal level of lung field. Initial laboratory results and those 40 mm Hg for each 1-mmol/L increase in bi- from 1 year ago are shown in Table 1. carbonate above the nominal normal level of doi:10.3949/ccjm.86a.18014 25 mmol/L.4 If the patient requires oxygen, CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 86 • NUMBER 3 MARCH 2019 187 Downloaded from www.ccjm.org on September 26, 2021. For personal use only. All other uses require permission. HYPOKALEMIA AND METABOLIC ALKALOSIS mm Hg, and in fact it is 51 mm Hg, which is TABLE 1 within the normal range of expected compen- Laboratory results on presentation sation (47.5–52 mm Hg). Therefore, yes, he is and 1 year earlier compensating for the primary disturbance. 5. In metabolic acidosis, is there a delta Current 1 year Reference Test levela earlier range gap? As our patient has metabolic alkalosis, not acidosis, this question does not apply in Sodium (mmol/L) 144 135 136–144 this case. Potassium (mmol/L) 2.8 4.0 3.7–5.1 Chloride (mmol/L) 96 100 97–105 ■ WHICH TEST TO FIND THE CAUSE? Bicarbonate (mmol/L) 40 28 22–30b Which is the best test to order next to Serum creatinine (mg/dL) 1.2 1.2 0.58–0.96 2determine the cause of this patient’s hypo- Blood urea nitrogen (mg/dL) 28 19 7–21 kalemic metabolic alkalosis? Glucose (mg/dL) 197 74–99 □ Serum magnesium level Calcium and magnesium Normal □ Spot urine chloride Arterial blood gases □ Renal ultrasonography □ 24-hour urine collection for sodium, pH 7.50 7.34 7.35–7.45 potassium, and chloride PCo (mm Hg) 51 40 34–46c 2 The first step in the algorithm for hypokale- PaO (mm Hg) 75 76 85–95 2 mic metabolic alkalosis (Figure 1) is to obtain Bicarbonate (mmol/L) 40 22–26 a spot urine chloride measurement. If this val- a Abnormal results are shown in bold. ue is low, the hypokalemic metabolic alkalosis b For acid-base problem-solving, a value of 25 mmol/L is considered normal. is volume-responsive; if it is high, the distur- c For acid-base problem-solving, a value of 40 mm Hg is considered normal. bance is volume-independent. The patient’s loop diuretic is withheld for An algorithmic the calculation may be unreliable, however, as 12 hours and a spot urine chloride is obtained, hypoxemia may have an overriding influence which is reported as 44 mmol/L. This high approach on respiratory drive. value suggests that a volume-independent can arrive Patients with chronically high Pco levels hypokalemic metabolic alkalosis is present 2 with potassium depletion. at the cause such as those with chronic obstructive pulmo- nary disease can become accustomed to high As for the other answer choices: of hypokalemic carbon dioxide levels and lose their hyper- Serum magnesium. Though hypomagne- metabolic capnic respiratory drive. Giving oxygen sup- semia can cause hypokalemia due to lack of plementation is thought to decrease respira- inhibition of renal outer medullary potassium alkalosis with tory drive in these patients, so that they will channels and subsequent increased excretion hypertension breathe slower and retain more carbon diox- of potassium in the apical tubular membrane, ide. There is some degree of respiratory com- it is not independently associated with acid- pensation for metabolic alkalosis that occurs base disturbances.5 by breathing less, though it is limited overall— Renal ultrasonography gives information even in very alkalotic patients, breathing less about structural kidney disease but is of lim- results in CO2 retention, which, by displacing ited utility in identifying the cause of hypoka- O2 molecules in the alveoli, will in turn result lemic metabolic alkalosis. in hypoxia. The brain then senses the hypoxia A 24-hour urine collection is unnec- and makes one breathe faster, thereby limiting essary in this setting and would ultimately this compensation. result in delay in diagnosis, as spot urine This patient’s serum bicarbonate level is chloride is a more efficient means of rap- 40 mmol/L, or 15 mmol/L higher than the idly distinguishing volume-responsive vs nominal normal level. If he is compensat- volume-independent causes of hypokalemic 6 ing, his Pco2 should be 40 + (15 × 0.6) = 49 metabolic alkalosis. 188 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 86 • NUMBER 3 MARCH 2019 Downloaded from www.ccjm.org on September 26, 2021. For personal use only. All other uses require permission. WILES AND COLLEAGUES TABLE 2 ‘Rules of 5’ for acid-base problem-solving 1 Determine the arterial pH pH < 7.38 is acidemic, pH > 7.42 is alkalemica Normal pH does not rule out an acid-base disorder 2 If the arterial pH is abnormal, determine pH PCO2 HCO3 whether the primary process is respiratory, a High — metabolic, or both Respiratory acidosis Low Metabolic acidosis Low — Low Mixed respiratory and metabolic acidosis Low High Low Respiratory alkalosis High Low — Metabolic alkalosis High Variesb High Mixed respiratory and metabolic alkalosis High Low High 3 Calculate the anion gap Anion gap = sodium – (chloride + bicarbonate) If serum albumin is low, add 2.5 mmol/L to the anion gap for every 1 g the serum albumin is below normal 4 Check the degree of compensation PCO2 and bicarbonate should increase or decrease together (respiratory or metabolic) Normal levels: bicarbonate 25 mmol/L, PCO2 40 mm Hg Acute respiratory acidosis: For every 10-mm Hg increase in PCO2, bicarbonate should increase by 1 mmol/L Chronic respiratory acidosis (> 48 hours): For every 10-mm Hg increase in PCO2, bicarbonate should increase by 4 mmol/L Metabolic acidosis: For every 1-mmol/L decrease in bicarbonate , PCO2 should decrease by 1.3 mm Hg Acute respiratory alkalosis: For every 10-mm Hg decrease in PCO2, bicarbonate should decrease by 2 mmol/L Chronic respiratory alkalosis (> 48 hours): For every 10-mm Hg decrease in PCO2, bicarbonate should decrease by 5 mmol/L Metabolic alkalosis: For every 1-mmol/L increase in bicarbonate , PCO2 may increase by 0.6 mm Hg 5 If the patient has metabolic acidosis with Delta gap = change in anion gap / change in bicarbonate an elevated anion gap, assess for ‘delta gap’ ([anion gap – 10] / [24 – bicarbonate]) (whether the decrease in bicarbonate = the increase > 1: Additional metabolic alkalosis in anion gap) 1: No additional disturbance present < 1: Additional non-anion gap metabolic acidosis present a Acidosis and alkalosis refer to acid-base disturbances with determined metabolic or respiratory etiologies.
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