Hyperkalemia: A Clue to the Diagnosis of Adrenal Insufficiency Daniel El Fassi and Gert Nielsen Circulation. 2013;128:2620-2621 doi: 10.1161/CIRCULATIONAHA.113.005169 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2013 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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Images in Cardiovascular Medicine Hyperkalemia A Clue to the Diagnosis of Adrenal Insufficiency Daniel El Fassi MD, PhD; Gert Nielsen MD
A
54-year-old man with childhood-onset type I diabetes mellitus who had preserved renal function but blindness secondary to his diabetes mellitus presented with a 5-day history of malaise and diarrhea. On admission, he was dehydrated, hypotensive, and hypothermic (96.1ºF/35.6ºC). Initial laboratory values showed a potassium level of 9.2 (N, 3.6–5.0) mmol/L, and a sodium level of 122 (N, 137–145) mmol/L. The potassium level was confirmed on arterial samples. The initial ECG showed a regular idioventricular rhythm with bizarre, broad QRS complexes, and a frequency of 32 beats per minute (Figure A). Over a 5-hour period, on correction of the hyperkalemia, he converted to sinus rhythm (Figure B and C) initially with a first-degree atrioventricular block (Figure B). Furthermore, the characteristic peaking of the T waves related to the hyperkalemia normalized (Figure C). On follow-up, an increased level of adrenocorticotropic hormone, the absence of response to synthetic adrenocorticotropic hormone, and strongly positive adrenal antibodies revealed that the patient had developed autoimmune adrenal insufficiency (Addison disease). Thomas Addison recognized the potential effects of adrenal insufficiency on the heart, and he described one of the marked features of the condition as “a remarkable feebleness of the hearts action” in his original monograph from 1855.1 To this day, adrenal insufficiency is a condition that cardiologists should be aware of because of the common occurrence of hypoaldosteronism-mediated hyperkalemia, and because it is a differential diagnosis in patients with shock or circulatory collapse. Conditions predisposing to adrenal insufficiency are tumors, hemorrhage, or infections affecting the pituitary or the adrenal glands; iatrogenous adrenal insufficiency attributable to long-term glucocorticoid therapy; other autoimmune diseases; or, more rarely, hereditary diseases. In some developing countries, tuberculous adrenalitis is still common, whereas an autoimmune diathesis accounts for most cases in the Western world.2,3
Common clinical findings in patients with adrenal insufficiency include malaise, lethargy, abdominal discomfort, hypotension, hypothermia, and sometimes hyperpigmentation or signs of a predisposing state (eg, other autoimmune diseases, carcinomas, or glucocorticoid therapy). The occurrence of hypoglycemia, metabolic acidosis, affected kidney function, or the classic—but not invariably present—combination of hyponatremia and hyperkalemia may be other clues to the tentative diagnosis of adrenal insufficiency.2–4 Acute adrenal insufficiency or addisonian crisis is a lifethreatening condition, and, on suspicion, the administration of intravenous glucocorticoid, rehydration with saline, and treatment directed toward the triggering condition (eg, infections) should be initiated promptly. The glucocorticoid of choice has classically been hydrocortisone in an initial dose of 100 mg intravenously.2–4 If synthetic corticotropin is readily available and if the clinical condition allows for a delay in glucocorticoid administration, a short corticotropin test can easily be performed bedside in 30 minutes.3 The test results should not be awaited. Some authorities recommend intravenous dexamethasone (4 mg) as an alternative to hydrocortisone in patients without a previous diagnosis of adrenal insufficiency, because dexamethasone does not interfere with subsequent evaluation of cortisol levels.
Disclosures None.
References 1. Addison T. On the constitutional and local effects of diseases of the suprarenal capsules. London: Samuel Highley; 1855 (http://www.wehner.org/ addison/x4.htm) 2. Bornstein SR. Predisposing factors for adrenal insufficiency. N Engl J Med. 2009;360:2328–2339. 3. Neary N, Nieman L. Adrenal insufficiency: etiology, diagnosis and treatment. Curr Opin Endocrinol Diabetes Obes. 2010;17:217–223. 4. Leelarathna L, Powrie JK, Carroll PV. Thomas Addison’s disease after 154 years: modern diagnostic perspectives on an old condition. QJM. 2009;102:569–573.
From the Department of Hematology, Roskilde University Hospital, Roskilde, Denmark (D.E.F.); Institute for Inflammation Research, Department of Rheumatology, Rigshospitalet Copenhagen University Hospital, Copenhagen, Denmark (D.E.F.); and Department of Internal Medicine, Roskilde University Hospital, Roskilde, Denmark (G.N.). Correspondence to Daniel El Fassi, MD, PhD, Department of Hematology, Herlev University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark. E-mail [email protected] (Circulation. 2013;128:2620-2621.) © 2013 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org
DOI: 10.1161/CIRCULATIONAHA.113.005169
Downloaded from http://circ.ahajournals.org/ at 2620 Queen Mary, University of London on July 10, 2014
El Fassi and Nielsen Hyperkalemia in Adrenal Insufficiency 2621
Figure. Progressive normalization of ECGs on treatment of severe hyperkalemia.
Downloaded from http://circ.ahajournals.org/ at Queen Mary, University of London on July 10, 2014
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/128/24/2620
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/
Downloaded from http://circ.ahajournals.org/ at Queen Mary, University of London on July 10, 2014
Images in Cardiovascular Medicine Hyperkalemia A Clue to the Diagnosis of Adrenal Insufficiency Daniel El Fassi MD, PhD; Gert Nielsen MD
A
54-year-old man with childhood-onset type I diabetes mellitus who had preserved renal function but blindness secondary to his diabetes mellitus presented with a 5-day history of malaise and diarrhea. On admission, he was dehydrated, hypotensive, and hypothermic (96.1ºF/35.6ºC). Initial laboratory values showed a potassium level of 9.2 (N, 3.6–5.0) mmol/L, and a sodium level of 122 (N, 137–145) mmol/L. The potassium level was confirmed on arterial samples. The initial ECG showed a regular idioventricular rhythm with bizarre, broad QRS complexes, and a frequency of 32 beats per minute (Figure A). Over a 5-hour period, on correction of the hyperkalemia, he converted to sinus rhythm (Figure B and C) initially with a first-degree atrioventricular block (Figure B). Furthermore, the characteristic peaking of the T waves related to the hyperkalemia normalized (Figure C). On follow-up, an increased level of adrenocorticotropic hormone, the absence of response to synthetic adrenocorticotropic hormone, and strongly positive adrenal antibodies revealed that the patient had developed autoimmune adrenal insufficiency (Addison disease). Thomas Addison recognized the potential effects of adrenal insufficiency on the heart, and he described one of the marked features of the condition as “a remarkable feebleness of the hearts action” in his original monograph from 1855.1 To this day, adrenal insufficiency is a condition that cardiologists should be aware of because of the common occurrence of hypoaldosteronism-mediated hyperkalemia, and because it is a differential diagnosis in patients with shock or circulatory collapse. Conditions predisposing to adrenal insufficiency are tumors, hemorrhage, or infections affecting the pituitary or the adrenal glands; iatrogenous adrenal insufficiency attributable to long-term glucocorticoid therapy; other autoimmune diseases; or, more rarely, hereditary diseases. In some developing countries, tuberculous adrenalitis is still common, whereas an autoimmune diathesis accounts for most cases in the Western world.2,3
Common clinical findings in patients with adrenal insufficiency include malaise, lethargy, abdominal discomfort, hypotension, hypothermia, and sometimes hyperpigmentation or signs of a predisposing state (eg, other autoimmune diseases, carcinomas, or glucocorticoid therapy). The occurrence of hypoglycemia, metabolic acidosis, affected kidney function, or the classic—but not invariably present—combination of hyponatremia and hyperkalemia may be other clues to the tentative diagnosis of adrenal insufficiency.2–4 Acute adrenal insufficiency or addisonian crisis is a lifethreatening condition, and, on suspicion, the administration of intravenous glucocorticoid, rehydration with saline, and treatment directed toward the triggering condition (eg, infections) should be initiated promptly. The glucocorticoid of choice has classically been hydrocortisone in an initial dose of 100 mg intravenously.2–4 If synthetic corticotropin is readily available and if the clinical condition allows for a delay in glucocorticoid administration, a short corticotropin test can easily be performed bedside in 30 minutes.3 The test results should not be awaited. Some authorities recommend intravenous dexamethasone (4 mg) as an alternative to hydrocortisone in patients without a previous diagnosis of adrenal insufficiency, because dexamethasone does not interfere with subsequent evaluation of cortisol levels.
Disclosures None.
References 1. Addison T. On the constitutional and local effects of diseases of the suprarenal capsules. London: Samuel Highley; 1855 (http://www.wehner.org/ addison/x4.htm) 2. Bornstein SR. Predisposing factors for adrenal insufficiency. N Engl J Med. 2009;360:2328–2339. 3. Neary N, Nieman L. Adrenal insufficiency: etiology, diagnosis and treatment. Curr Opin Endocrinol Diabetes Obes. 2010;17:217–223. 4. Leelarathna L, Powrie JK, Carroll PV. Thomas Addison’s disease after 154 years: modern diagnostic perspectives on an old condition. QJM. 2009;102:569–573.
From the Department of Hematology, Roskilde University Hospital, Roskilde, Denmark (D.E.F.); Institute for Inflammation Research, Department of Rheumatology, Rigshospitalet Copenhagen University Hospital, Copenhagen, Denmark (D.E.F.); and Department of Internal Medicine, Roskilde University Hospital, Roskilde, Denmark (G.N.). Correspondence to Daniel El Fassi, MD, PhD, Department of Hematology, Herlev University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark. E-mail [email protected] (Circulation. 2013;128:2620-2621.) © 2013 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org
DOI: 10.1161/CIRCULATIONAHA.113.005169
Downloaded from http://circ.ahajournals.org/ at 2620 Queen Mary, University of London on July 10, 2014
El Fassi and Nielsen Hyperkalemia in Adrenal Insufficiency 2621
Figure. Progressive normalization of ECGs on treatment of severe hyperkalemia.
Downloaded from http://circ.ahajournals.org/ at Queen Mary, University of London on July 10, 2014
![[Diagnosis and therapy of adrenal cortex insufficiency].](/assets/img/hold.png)
