Bowman Milk Alkali

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  WILLIS S. BOWMAN, MD Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA Heartburn or heart attack?A mimic of MI A 󰀷󰀱-󰁹󰁥󰁡󰁲-󰁯󰁬󰁤 󰁭󰁡󰁮 with a history of hypertension, 4 prior myocardial infarctions (MIs), and well-compensated ischemic cardiomyopathy presented to the emergency department after 2 episodes of sharp pain in the left upper abdomen and chest. The epi-sodes lasted 1 to 2 minutes and were not relieved by rest. Their location was similar to that of the pain he experienced with his MIs. He could not identify any exacerbating or ameliorating factors. The pain had re-solved without speci󿬁c therapy before he arrived. He reported polydipsia and constipation over the past 2 weeks and generalized muscle weakness and acute exacerbations of chronic back pain in the past 2 days. Neither he nor a friend who accompanied him noticed any confusion. He had been taking as many as 15 calcium carbonate tablets a day for 6 weeks to self-treat dyspepsia refractory to once-daily ranitidine, and hydrochlorothiazide for his hypertension for 3 weeks.   ■ FURTHER EVALUATION, CARDIOLOGY CONSULT On physical examination, he had diffuse weakness, dry mucous membranes, and an irregular heart rhythm. Electrocardiography (ECG) (  Figure 1 ) showed ST-segment elevation in leads V 1 , V 2 , V 3 , II, III, and aVF and ST-segment depression in leads I and aVL. The corrected QT interval was 360 ms, compared with 426 ms 4 months earlier (  Figure 2 ). Laboratory testing showed the following:ã Troponin I 0.11 ng/mL (reference range ≤ 0.04); re-peated, it was 0.12 ng/mLã Serum creatinine 3.4 mg/dL (0.44–1.27) (9 months earlier it had been 0.99 mg/dL)ã Serum calcium 17.3 mg/dL (8.6–10.5) THE CLINICAL PICTURE doi:10.3949/ccjm.84a.16093 AMIR FARID, MD Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA PAUL ARONOWITZ, MD Health Sciences Clinical Professor of Medicine, Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA FIGURE 1.  Electrocardiography at presentation showed a corrected QT interval of 360 msec. In addition to ST-segment elevations (blue arrows) and ST-segment depressions (blue diamonds), varying ectopic beats (red arrows) were present that were absent on previous studies. 664 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 84 ã NUMBER 9 SEPTEMBER 2017  CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 84 ã NUMBER 9 SEPTEMBER 2017  665 BOWMAN AND COLLEAGUES FIGURE 2.  An electrocardiogram 4 months earlier showed no ST-segment elevations (blue arrows) or ST-segment depressions (blue diamonds). ã Parathyroid hormone 9 pg/mL (12–88) ã Serum bicarbonate 33 mmol/L (24–32); 2 weeks earlier, it had been 27 mmol/L. A cardiology consult was ordered out of concern for ST-elevation MI (STEMI). The cardiology con-sult team did not recommend coronary angiography because the patient’s chest pain had resolved sponta-neously, its presentation was atypical, and the results of laboratory studies indicated acute kidney injury, a relative contraindication to angiography. ■ DIAGNOSIS: MILK-ALKALI SYNDROME The diagnosis, based on the presentation and the results of the workup, was milk-alkali syndrome complicated by recent hydrochlorothiazide use. This syndrome con-sists of the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, all due to excessive ingestion of calcium and alkali, usually calcium carbonate. His hydrochlorothiazide and calcium carbonate were discontinued. He was given intravenous normal saline and subcutaneous calcitonin, and his serum cal-cium level came down to 11.5 mg/dL within the next 24 hours. His dyspepsia was treated with pantoprazole. The patient had no further episodes of chest pain, and the cardiology consult team again recommended against coronary angiography. Repeat ECG after the hypercalcemia resolved showed results identical to those 4 months before his admission. Two months later, his serum calcium level was 9.4 mg/dL and his creatinine level was 1.24 mg/dL.   ■ A MIMIC OF STEMI In numerous reported cases, these electrocardiographic 󿬁ndings coupled with chest pain led to misdiagnosis of STEMI. 1–3  While STEMI and occasionally hypercal-cemia can cause ST elevation, hypercalcemia causes a signi󿬁cant shortening of the corrected QT interval that is not associated with STEMI. 4,5  Ultimately, the diagnosis of MI involves clinical, laboratory, and ECG 󿬁ndings, and if a strong clinical suspicion for myocardial ischemia exists, STEMI can-not reliably be distinguished from hypercalcemia by ECG alone. It is nonetheless important to be aware of this complication of hypercalcemia to avoid unneces-sary cardiac interventions. ■   ■ REFERENCES  1.  Ashizawa N, Arakawa S, Koide Y, Toda G, Seto S, Yano K . Hypercal-cemia due to vitamin D intoxication with clinical features mimick-ing acute myocardial infarction. Intern Med 2003; 42:340–344. 2.  Nishi SP, Barbagelata NA, Atar S, Birnbaum Y, Tuero E . Hypercalce-mia-induced ST-segment elevation mimicking acute myocardial infarction. J Electrocardiol 2006; 39:298–300. 3.  Turnham S, Kilickap M, Kilinc S . ST segment elevation mimicking acute myocardial infarction in hypercalcemia. Heart 2005; 91:999. 4.  Nierenberg DW, Ransil BJ . Q-aTc interval as a clinical indicator of hypercalcemia. Am J Cardiol 1979; 44:243–248. 5.  Ahmed R, Hashiba K . Reliability of QT intervals as indicators of clinical hypercalcemia. Clin Cardiol 1988; 11:395–400.  ADDRESS : Willis S. Bowman, MD, Department of Internal Medicine, University of California Davis Medical Center, 4150 V Street, Suite 3100, Sacramento, CA 95817; wbowman@ucdavis.edu
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