Robert Centor, MD

This issue of the Journal of Hospital Medicine features an important contribution concerning the current state of academic hospital medicine. The survey of 57 hospitalists revealed what many of us already suspected: the state of mentorship in academic hospitalist groups is unsatisfactory.1

While the conclusion is alarming, it is also not surprising. Over the past decade academic medical centers enthusiastically hired hospitalists to improve efficiency for inpatient services and to lessen the effect of Accreditation Council for Graduate Medical Education (ACGME) regulations on duty hours and patient caps. Few departments of internal medicine, however, hired academic hospitalists with the intent of creating academic divisions. Thus many institutions appear to view hospitalists primarily as hospital employees ignoring their potential academic contributions, and as a result it should not be a surprise that many hospitalist groups lack the mentorship infrastructure of other divisions within a typical Department of Medicine. Compounding the hospital employee problem, the new field of academic hospital medicine has emerged only in the last decade, a time frame that has resulted in very few hospitalists qualified to serve as senior mentors.

We cannot easily remove these limitations: the past is the past, and over time, hospital medicine will mature and develop more senior mentors. But what should we do until that maturation occurs? We believe that the academic work of hospitalists, both in education and research (Quality and Patient Safety) are important endeavors too valuable to be left to chance. With 30,000 hospitalists delivering care, it is critical that research in the optimal delivery of this care be performed, targeting systems improvements to enact anticipated outcomes in quality and patient safety. The physicians who are regularly and intimately involved in this system of inpatient care delivery, the hospitalists, are best suited for identifying the unique features of the inpatient care system needing improvement. Mentorship is essential in ensuring the advancement of both areas, and the sustainability of hospital medicine in medical academe. The article by Harrison et al.1 both establishes the depth of these issues and provides important insights into potential solutions for closing this mentorship gap while the field matures.

Utilizing Other Mentors

No measure of systems change will make young hospitalists immediately experienced, such that they have the sophistication to be senior mentors for younger hospitalists. But we can compensate for this temporary gap in mentorship experience. First, in the next 5 to 10 years, young academic hospitalists need explicit direction from those within Departments of Medicine who do have this mentorship experience, even if these mentors do not work in hospital medicine. Mentors within General Internal Medicine or the subspecialties can still provide the guidance and support to ensure that academic hospitalists are engaging in the appropriate endeavors toward promotion and intellectual growth. Second, academic hospitalists have to seek out mentorship from afar through their participation in the organizations primarily devoted to the academic welfare of hospitalists: The Society of Hospital Medicine (SHM) and the Society of General Internal Medicine (SGIM). Both organizations sponsor mentorship programs, and regular attendance at regional and/or national meetings (followed by email correspondence) can greatly improve an academic hospitalist's career trajectory. Finally, midlevel and senior‐level hospitalists have to learn mentorship skills; mere experience in the field does not ensure acquisition of the necessary mentorship skills, anymore than experience in medicine ensures teaching skills. Mentorship is its own skill set, and receiving appropriate training via the SHM or SGIM national meetings or the Academic Hospitalist Academy (referenced below) is critical.

Defining Academic Expectations for Hospitalists

Harrison et al.1 note that academic hospitalists felt there was a lack of respect for the scholarly work that hospitalists do as part of their job, raising the proposition that the mentorship dearth for academic hospitalists might result from currently available mentors not knowing what to say. Even if mentors were plentiful today, we still must ask the question, What would the mentor advise the young hospitalist to do? The academic hospitalist offers extraordinary value to the Department, but in a way that is different from the standard R0RO‐1 Grant paradigm. Even if hospitalists acquire extramural funding, it will likely come from sources different from the National Institutes of Health (NIH): Agency for Healthcare Research and Quality (AHRQ), foundations (eg, The Robert Wood Johnson Foundation or The John A. Hartford Foundation), intramural hospital‐originating funding, etc. And while extramural funding may be a measure of a hospitalist's contribution to the Department, it should not be the only measure of the hospitalist's career development. There are 2 ways to get rich: acquire more money, or spend less money. Academic hospitalists, unlike other specialties in Medicine, are likely to fall into the latter category, by offering decreased hospital costs (ie, decreased length of stay, decreased never events, etc.). Further, hospitalists may save in opportunity costs: the hospitalist staffing a ward service is less costly than a subspecialist who could be performing procedures, or a basic science researcher who could be acquiring grants. The problem today is that there is no way to quantify this decreased loss, and having this sort of metric will greatly enable mentors to provide hospitalists with ways of showing value to the department outside of the standard NIH grant paradigm. The Quality Portfolio developed by the SGIM and the forthcoming Benchmarks for Academic Hospitalists Promotion white paper (as developed by the SHM's Academic Practice and Promotion Committee) will greatly improve the substance of mentorship for academic hospitalists.2 Leaders of academic hospital medicine must learn to educate chairs of medicine and medical school deans as to the value‐added services intrinsic in the integration of hospitalists into the academic environment.

Having an Academic Plan

Mentorship is a 2‐way relationship: the mentor has responsibilities, but so too, does the mentee. As we wait for the hospitalist field to further develop, new academic hospitalists must become proactive in seeking guidance in career development. The Academic Hospitalist Academy, cosponsored by SHM, SGIM, and ACLGIM, is an example of this type of training.3 As a part of this course, participants learn of the rules and the opportunities for success in academic hospital medicine. Success for academic hospitalist groups will likely follow from understanding what success looks like. The Academy provides an excellent program for distributing that knowledge.

Research Training in Hospital Medicine

Many traditionalists would insist that Hospital Medicine could evoke the same training paradigm as other subspecialties in medicine (ie, fellowships). Unfortunately there are not a sufficient number of GME‐funded positions to handle the number of hospitalists required to advance the mission of academic hospital medicine. Moreover, fellowship training for every academic hospitalist would be unlikely to produce the desired results of improving the delivery of inpatient care. The academic agenda for the hospitalist depends on understanding the hospital system, and then executing improvements that lead to safer, more efficient and effective care. In this way, the academic hospitalist academic training is much more akin to a Master of Business Administration (MBA) than it is to a Bachelor of Science (BS) degree: namely, via job immersion, the hospitalist develops a greater systems understanding that should inform his or her academic career. Thus, a fellowship right out of residency may not have the same urgency for the hospitalist as it does for the subspecialist. Nevertheless, those hospitalists seeking an academic scholarly career will experience major benefits from fellowship training. Academic hospitalists need not focus only on the few existing hospitalist fellowships; they can obtain the necessary training in research skills via a general medicine fellowship, of which there are many. For this cohort of hospitalists, we strongly encourage training in a general medicine, health services, or outcomes research fellowship, with an emphasis on research techniques as they apply to the measurement of quality, patient safety, and/or clinical education.

With respect to academic hospitalists, it is likely that nothing is as important as the question of mentorship. Even the hardest working hospitalist can lose their way without guidance and a roadmap; the mentor is central to both. But the lost opportunity is not borne by the individual physician alone; the academic department loses too. Because the hospitalist's value depends on sufficient familiarity with a specific system prior to leveraging improvements, the department accrues maximal benefits in efficiency and effectiveness only if it can maintain retention for at least 2 years.4 The turnover carries major costs; recruitment costs money, and every new hospitalist engenders major start‐up costs. Faculty members who become completely integrated into the department have higher retention rates than those who consider themselves outside the main stream. Mentorship will greatly increase the probability that hospitalists will progress and feel the importance to the department.

Academic hospital medicine must strive over the next 5 to 10 years to become totally integrated in the academic culture of every institution. This task will take great leadership both at the local level and at a national level. We agree with the authors that the SHM and the SGIM can both provide important assistance to young hospital medicine groups. We applaud the authors of this article for making explicit this next major challenge for the field.

This issue of the Journal of Hospital Medicine features an important contribution concerning the current state of academic hospital medicine. The survey of 57 hospitalists revealed what many of us already suspected: the state of mentorship in academic hospitalist groups is unsatisfactory.1

While the conclusion is alarming, it is also not surprising. Over the past decade academic medical centers enthusiastically hired hospitalists to improve efficiency for inpatient services and to lessen the effect of Accreditation Council for Graduate Medical Education (ACGME) regulations on duty hours and patient caps. Few departments of internal medicine, however, hired academic hospitalists with the intent of creating academic divisions. Thus many institutions appear to view hospitalists primarily as hospital employees ignoring their potential academic contributions, and as a result it should not be a surprise that many hospitalist groups lack the mentorship infrastructure of other divisions within a typical Department of Medicine. Compounding the hospital employee problem, the new field of academic hospital medicine has emerged only in the last decade, a time frame that has resulted in very few hospitalists qualified to serve as senior mentors.

We cannot easily remove these limitations: the past is the past, and over time, hospital medicine will mature and develop more senior mentors. But what should we do until that maturation occurs? We believe that the academic work of hospitalists, both in education and research (Quality and Patient Safety) are important endeavors too valuable to be left to chance. With 30,000 hospitalists delivering care, it is critical that research in the optimal delivery of this care be performed, targeting systems improvements to enact anticipated outcomes in quality and patient safety. The physicians who are regularly and intimately involved in this system of inpatient care delivery, the hospitalists, are best suited for identifying the unique features of the inpatient care system needing improvement. Mentorship is essential in ensuring the advancement of both areas, and the sustainability of hospital medicine in medical academe. The article by Harrison et al.1 both establishes the depth of these issues and provides important insights into potential solutions for closing this mentorship gap while the field matures.

Utilizing Other Mentors

No measure of systems change will make young hospitalists immediately experienced, such that they have the sophistication to be senior mentors for younger hospitalists. But we can compensate for this temporary gap in mentorship experience. First, in the next 5 to 10 years, young academic hospitalists need explicit direction from those within Departments of Medicine who do have this mentorship experience, even if these mentors do not work in hospital medicine. Mentors within General Internal Medicine or the subspecialties can still provide the guidance and support to ensure that academic hospitalists are engaging in the appropriate endeavors toward promotion and intellectual growth. Second, academic hospitalists have to seek out mentorship from afar through their participation in the organizations primarily devoted to the academic welfare of hospitalists: The Society of Hospital Medicine (SHM) and the Society of General Internal Medicine (SGIM). Both organizations sponsor mentorship programs, and regular attendance at regional and/or national meetings (followed by email correspondence) can greatly improve an academic hospitalist's career trajectory. Finally, midlevel and senior‐level hospitalists have to learn mentorship skills; mere experience in the field does not ensure acquisition of the necessary mentorship skills, anymore than experience in medicine ensures teaching skills. Mentorship is its own skill set, and receiving appropriate training via the SHM or SGIM national meetings or the Academic Hospitalist Academy (referenced below) is critical.

Defining Academic Expectations for Hospitalists

Harrison et al.1 note that academic hospitalists felt there was a lack of respect for the scholarly work that hospitalists do as part of their job, raising the proposition that the mentorship dearth for academic hospitalists might result from currently available mentors not knowing what to say. Even if mentors were plentiful today, we still must ask the question, What would the mentor advise the young hospitalist to do? The academic hospitalist offers extraordinary value to the Department, but in a way that is different from the standard R0RO‐1 Grant paradigm. Even if hospitalists acquire extramural funding, it will likely come from sources different from the National Institutes of Health (NIH): Agency for Healthcare Research and Quality (AHRQ), foundations (eg, The Robert Wood Johnson Foundation or The John A. Hartford Foundation), intramural hospital‐originating funding, etc. And while extramural funding may be a measure of a hospitalist's contribution to the Department, it should not be the only measure of the hospitalist's career development. There are 2 ways to get rich: acquire more money, or spend less money. Academic hospitalists, unlike other specialties in Medicine, are likely to fall into the latter category, by offering decreased hospital costs (ie, decreased length of stay, decreased never events, etc.). Further, hospitalists may save in opportunity costs: the hospitalist staffing a ward service is less costly than a subspecialist who could be performing procedures, or a basic science researcher who could be acquiring grants. The problem today is that there is no way to quantify this decreased loss, and having this sort of metric will greatly enable mentors to provide hospitalists with ways of showing value to the department outside of the standard NIH grant paradigm. The Quality Portfolio developed by the SGIM and the forthcoming Benchmarks for Academic Hospitalists Promotion white paper (as developed by the SHM's Academic Practice and Promotion Committee) will greatly improve the substance of mentorship for academic hospitalists.2 Leaders of academic hospital medicine must learn to educate chairs of medicine and medical school deans as to the value‐added services intrinsic in the integration of hospitalists into the academic environment.

Having an Academic Plan

Mentorship is a 2‐way relationship: the mentor has responsibilities, but so too, does the mentee. As we wait for the hospitalist field to further develop, new academic hospitalists must become proactive in seeking guidance in career development. The Academic Hospitalist Academy, cosponsored by SHM, SGIM, and ACLGIM, is an example of this type of training.3 As a part of this course, participants learn of the rules and the opportunities for success in academic hospital medicine. Success for academic hospitalist groups will likely follow from understanding what success looks like. The Academy provides an excellent program for distributing that knowledge.

Research Training in Hospital Medicine

Many traditionalists would insist that Hospital Medicine could evoke the same training paradigm as other subspecialties in medicine (ie, fellowships). Unfortunately there are not a sufficient number of GME‐funded positions to handle the number of hospitalists required to advance the mission of academic hospital medicine. Moreover, fellowship training for every academic hospitalist would be unlikely to produce the desired results of improving the delivery of inpatient care. The academic agenda for the hospitalist depends on understanding the hospital system, and then executing improvements that lead to safer, more efficient and effective care. In this way, the academic hospitalist academic training is much more akin to a Master of Business Administration (MBA) than it is to a Bachelor of Science (BS) degree: namely, via job immersion, the hospitalist develops a greater systems understanding that should inform his or her academic career. Thus, a fellowship right out of residency may not have the same urgency for the hospitalist as it does for the subspecialist. Nevertheless, those hospitalists seeking an academic scholarly career will experience major benefits from fellowship training. Academic hospitalists need not focus only on the few existing hospitalist fellowships; they can obtain the necessary training in research skills via a general medicine fellowship, of which there are many. For this cohort of hospitalists, we strongly encourage training in a general medicine, health services, or outcomes research fellowship, with an emphasis on research techniques as they apply to the measurement of quality, patient safety, and/or clinical education.

With respect to academic hospitalists, it is likely that nothing is as important as the question of mentorship. Even the hardest working hospitalist can lose their way without guidance and a roadmap; the mentor is central to both. But the lost opportunity is not borne by the individual physician alone; the academic department loses too. Because the hospitalist's value depends on sufficient familiarity with a specific system prior to leveraging improvements, the department accrues maximal benefits in efficiency and effectiveness only if it can maintain retention for at least 2 years.4 The turnover carries major costs; recruitment costs money, and every new hospitalist engenders major start‐up costs. Faculty members who become completely integrated into the department have higher retention rates than those who consider themselves outside the main stream. Mentorship will greatly increase the probability that hospitalists will progress and feel the importance to the department.

Academic hospital medicine must strive over the next 5 to 10 years to become totally integrated in the academic culture of every institution. This task will take great leadership both at the local level and at a national level. We agree with the authors that the SHM and the SGIM can both provide important assistance to young hospital medicine groups. We applaud the authors of this article for making explicit this next major challenge for the field.

This issue of the Journal of Hospital Medicine features an important contribution concerning the current state of academic hospital medicine. The survey of 57 hospitalists revealed what many of us already suspected: the state of mentorship in academic hospitalist groups is unsatisfactory.1

While the conclusion is alarming, it is also not surprising. Over the past decade academic medical centers enthusiastically hired hospitalists to improve efficiency for inpatient services and to lessen the effect of Accreditation Council for Graduate Medical Education (ACGME) regulations on duty hours and patient caps. Few departments of internal medicine, however, hired academic hospitalists with the intent of creating academic divisions. Thus many institutions appear to view hospitalists primarily as hospital employees ignoring their potential academic contributions, and as a result it should not be a surprise that many hospitalist groups lack the mentorship infrastructure of other divisions within a typical Department of Medicine. Compounding the hospital employee problem, the new field of academic hospital medicine has emerged only in the last decade, a time frame that has resulted in very few hospitalists qualified to serve as senior mentors.

We cannot easily remove these limitations: the past is the past, and over time, hospital medicine will mature and develop more senior mentors. But what should we do until that maturation occurs? We believe that the academic work of hospitalists, both in education and research (Quality and Patient Safety) are important endeavors too valuable to be left to chance. With 30,000 hospitalists delivering care, it is critical that research in the optimal delivery of this care be performed, targeting systems improvements to enact anticipated outcomes in quality and patient safety. The physicians who are regularly and intimately involved in this system of inpatient care delivery, the hospitalists, are best suited for identifying the unique features of the inpatient care system needing improvement. Mentorship is essential in ensuring the advancement of both areas, and the sustainability of hospital medicine in medical academe. The article by Harrison et al.1 both establishes the depth of these issues and provides important insights into potential solutions for closing this mentorship gap while the field matures.

Utilizing Other Mentors

No measure of systems change will make young hospitalists immediately experienced, such that they have the sophistication to be senior mentors for younger hospitalists. But we can compensate for this temporary gap in mentorship experience. First, in the next 5 to 10 years, young academic hospitalists need explicit direction from those within Departments of Medicine who do have this mentorship experience, even if these mentors do not work in hospital medicine. Mentors within General Internal Medicine or the subspecialties can still provide the guidance and support to ensure that academic hospitalists are engaging in the appropriate endeavors toward promotion and intellectual growth. Second, academic hospitalists have to seek out mentorship from afar through their participation in the organizations primarily devoted to the academic welfare of hospitalists: The Society of Hospital Medicine (SHM) and the Society of General Internal Medicine (SGIM). Both organizations sponsor mentorship programs, and regular attendance at regional and/or national meetings (followed by email correspondence) can greatly improve an academic hospitalist's career trajectory. Finally, midlevel and senior‐level hospitalists have to learn mentorship skills; mere experience in the field does not ensure acquisition of the necessary mentorship skills, anymore than experience in medicine ensures teaching skills. Mentorship is its own skill set, and receiving appropriate training via the SHM or SGIM national meetings or the Academic Hospitalist Academy (referenced below) is critical.

Defining Academic Expectations for Hospitalists

Harrison et al.1 note that academic hospitalists felt there was a lack of respect for the scholarly work that hospitalists do as part of their job, raising the proposition that the mentorship dearth for academic hospitalists might result from currently available mentors not knowing what to say. Even if mentors were plentiful today, we still must ask the question, What would the mentor advise the young hospitalist to do? The academic hospitalist offers extraordinary value to the Department, but in a way that is different from the standard R0RO‐1 Grant paradigm. Even if hospitalists acquire extramural funding, it will likely come from sources different from the National Institutes of Health (NIH): Agency for Healthcare Research and Quality (AHRQ), foundations (eg, The Robert Wood Johnson Foundation or The John A. Hartford Foundation), intramural hospital‐originating funding, etc. And while extramural funding may be a measure of a hospitalist's contribution to the Department, it should not be the only measure of the hospitalist's career development. There are 2 ways to get rich: acquire more money, or spend less money. Academic hospitalists, unlike other specialties in Medicine, are likely to fall into the latter category, by offering decreased hospital costs (ie, decreased length of stay, decreased never events, etc.). Further, hospitalists may save in opportunity costs: the hospitalist staffing a ward service is less costly than a subspecialist who could be performing procedures, or a basic science researcher who could be acquiring grants. The problem today is that there is no way to quantify this decreased loss, and having this sort of metric will greatly enable mentors to provide hospitalists with ways of showing value to the department outside of the standard NIH grant paradigm. The Quality Portfolio developed by the SGIM and the forthcoming Benchmarks for Academic Hospitalists Promotion white paper (as developed by the SHM's Academic Practice and Promotion Committee) will greatly improve the substance of mentorship for academic hospitalists.2 Leaders of academic hospital medicine must learn to educate chairs of medicine and medical school deans as to the value‐added services intrinsic in the integration of hospitalists into the academic environment.

Having an Academic Plan

Mentorship is a 2‐way relationship: the mentor has responsibilities, but so too, does the mentee. As we wait for the hospitalist field to further develop, new academic hospitalists must become proactive in seeking guidance in career development. The Academic Hospitalist Academy, cosponsored by SHM, SGIM, and ACLGIM, is an example of this type of training.3 As a part of this course, participants learn of the rules and the opportunities for success in academic hospital medicine. Success for academic hospitalist groups will likely follow from understanding what success looks like. The Academy provides an excellent program for distributing that knowledge.

Research Training in Hospital Medicine

Many traditionalists would insist that Hospital Medicine could evoke the same training paradigm as other subspecialties in medicine (ie, fellowships). Unfortunately there are not a sufficient number of GME‐funded positions to handle the number of hospitalists required to advance the mission of academic hospital medicine. Moreover, fellowship training for every academic hospitalist would be unlikely to produce the desired results of improving the delivery of inpatient care. The academic agenda for the hospitalist depends on understanding the hospital system, and then executing improvements that lead to safer, more efficient and effective care. In this way, the academic hospitalist academic training is much more akin to a Master of Business Administration (MBA) than it is to a Bachelor of Science (BS) degree: namely, via job immersion, the hospitalist develops a greater systems understanding that should inform his or her academic career. Thus, a fellowship right out of residency may not have the same urgency for the hospitalist as it does for the subspecialist. Nevertheless, those hospitalists seeking an academic scholarly career will experience major benefits from fellowship training. Academic hospitalists need not focus only on the few existing hospitalist fellowships; they can obtain the necessary training in research skills via a general medicine fellowship, of which there are many. For this cohort of hospitalists, we strongly encourage training in a general medicine, health services, or outcomes research fellowship, with an emphasis on research techniques as they apply to the measurement of quality, patient safety, and/or clinical education.

With respect to academic hospitalists, it is likely that nothing is as important as the question of mentorship. Even the hardest working hospitalist can lose their way without guidance and a roadmap; the mentor is central to both. But the lost opportunity is not borne by the individual physician alone; the academic department loses too. Because the hospitalist's value depends on sufficient familiarity with a specific system prior to leveraging improvements, the department accrues maximal benefits in efficiency and effectiveness only if it can maintain retention for at least 2 years.4 The turnover carries major costs; recruitment costs money, and every new hospitalist engenders major start‐up costs. Faculty members who become completely integrated into the department have higher retention rates than those who consider themselves outside the main stream. Mentorship will greatly increase the probability that hospitalists will progress and feel the importance to the department.

Academic hospital medicine must strive over the next 5 to 10 years to become totally integrated in the academic culture of every institution. This task will take great leadership both at the local level and at a national level. We agree with the authors that the SHM and the SGIM can both provide important assistance to young hospital medicine groups. We applaud the authors of this article for making explicit this next major challenge for the field.

Historically, the milk‐alkali syndrome developed as an adverse reaction to the Sippy regimen of frequent feedings of milk, cream, and alkaline powders as treatment for peptic ulcer disease.1 The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. This syndrome seemingly disappeared when modern acid suppression therapies such as histamine‐2 blockers and proton pump inhibitors improved dyspepsia treatment. Over the past 20 years, milk‐alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased.2 Calcium carbonate supplements are a popular over‐the‐counter treatment for osteoporosis, dyspepsia, hypocalcemia, and hyperphosphatemia; these supplements provide both the calcium and alkali required for the development of milk‐alkali syndrome.

A 46‐year‐old man presented to the emergency department after his physician ordered outpatient laboratory tests to evaluate his fatigue. The patient was found to have acute renal failure and hypercalcemia. His serum creatinine was 3.6 mg/dL, increased from his baseline of 1.1 mg/dL several months prior, and his serum calcium was 14.9 mg/dL. Ten days prior to admission he developed increasing fatigue, decreased appetite, and decreased urine output, which he attributed to recent manual labor during summer. He reported taking an occasional calcium carbonate (Tums) for dyspepsia. He did not report pain or other complaints.

His medical history included hypertension and hyperlipidemia. He had a colonoscopy 1 year prior to presentation that was significant for a high‐grade dysplastic polyp and was currently due for repeat colonoscopy. His medications included clonidine, lisinopril, and aspirin. He had no recent medication changes. He had a 30 pack/year history of cigarette smoking and drank occasionally.

On physical exam, his temperature was 99.8F, blood pressure 97/48 mmHg, heart rate 89 beats per minute, respirations 20 breaths per minute, with a room air saturation of 97%. He had dry mucus membranes and the remainder of the physical exam was unremarkable.

In the emergency department laboratory testing revealed a creatinine of 4.6 mg/dL, serum total calcium of 15.9 mg/dL, serum bicarbonate level of 26 mmol/L, phosphate of 3.9 mg/dL, albumin of 4.4 gm/dL, and alkaline phosphatase of 92 IU/L. The urine specific gravity was 1.019 gm/mL (see Table 1 for the patient's complete admission laboratory values).

His intact parathyroid (PTH) hormone was 18.8 pg/mL (normal, 15‐65). PTH hormone‐related peptide (PTHrP) was <2.5 pmol/L. After reviewing these laboratory test results, we proceeded with further questioning, during which he admitted to taking approximately 15 to 20 Tums (>7.5 gm of calcium carbonate) daily for dyspepsia rather than the occasional Tums he had originally reported. Over the next 3 days, his calcium decreased to 8.4 mg/dL and his creatinine decreased to 1.6 mg/dL with intravenous hydration. His fatigue improved. His 25‐hydroxy vitamin D (25‐OH‐Vitamin D) level was 23 ng/mL (normal, 16‐74 ng/mL).

At his 1 week follow‐up, his calcium was 8.1 mg/dL, and his creatinine had returned to normal at 0.9 mg/dL. His intact PTH level was elevated at 240 pg/mL.

Discussion

Milk‐alkali syndrome is now believed to be the third most common reason for hypercalcemia hospital admission.2, 3 Malignancy and primary hyperparathyroidism are the only 2 causes of hypercalcemia more common than milk‐alkali syndrome in hospitalized patients; these must be excluded before making a definitive diagnosis of milk‐alkali syndrome. The differential diagnosis for hypercalcemia also includes other less common etiologies such as medications (hydrochlorothiazide and lithium), as well as familial hypocalciuric hypercalcemia, hyperthyroidism, Addison's disease, acromegaly, tertiary hyperparathyroidism, and vitamin D intoxication. Physicians often discover hypercalcemia incidentally on routine laboratory tests, and diagnostic workup should include a thorough history and physical examination, as well as further laboratory evaluation.

The diagnosis of milk‐alkali syndrome requires a history of increased calcium and alkali intake, but is otherwise a diagnosis of exclusion. Given the increasing consumption of nonprescribed calcium supplements, one should have a high index of suspicion for the diagnosis of milk‐alkali syndrome, as patients may not consider calcium carbonate to be hazardous or even a medication and thus may not report calcium carbonate consumption. Patients often view calcium carbonate as a benign treatment for dyspepsia. Its over‐the‐counter availability and economical price make it a common self‐treatment for minor dyspepsia or as prevention of osteoporosis. Calcium supplementation is increasingly added to many products, making it easy for patients to consume large quantities of calcium unknowingly. Of note, without the absorbable alkali supplied by the carbonate in calcium carbonate (Tums), milk‐alkali syndrome does not occur. The amount of calcium carbonate necessary to cause milk‐alkali syndrome is not well known, though it is speculated to be as little as 5 to 10 g of calcium in the form of calcium carbonate, especially in those with other risk factors for hypercalcemia such as chronic renal insufficiency or vomiting.2 Workup of hypercalcemia should entail careful questioning about medications, as well as over‐the‐counter supplements, vitamins, and foods.

Manifestations of the milk‐alkali syndrome include renal failure, metabolic alkalosis, and volume contraction. Normally, the kidneys prevent hypercalcemia by excretion of excess calcium. Hypercalcemia can cause tubular damage and vasoconstriction of the renal afferent arteriole leading to acute renal failure.2, 4 Hypercalcemia can also cause nephrogenic diabetes insipidus, causing impaired renal concentrating ability, leading to increased sodium excretion and volume contraction.2 In addition, alkalosis further impairs calciuresis.2 Laboratory values usually reveal suppressed PTH and vitamin D levels due to hypercalcemia caused by exogenous intake of calcium.5 Hypercalcemia causes suppression of PTH, which can lead to hyperphosphatemia, as well as decreased conversion of vitamin D to the active 1,25‐dihyroxyvitamin‐D form.

The management of hypercalcemia due to milk‐alkali syndrome is supportive and includes saline hydration as well as withholding calcium carbonate. Management of hypercalcemia due to malignancy and hyperparathyroidism includes bisphosphonates with the addition of calcitonin if symptoms are severe.6, 7 There is no evidence that supports the use of bisphosphonates in the treatment of milk‐alkali syndrome. Loop diuretics are sometimes used to promote calciuresis, though evidence is lacking to support this, and it may worsen renal failure.6

In this case, a middle‐aged man took greater than the recommended dose of calcium carbonate for dyspepsia, which led to the development of acute renal failure and hypercalcemia. At first, the patient did not provide an accurate history of the extent of his calcium carbonate ingestion, leading us to focus on hyperparathyroidism or malignancy. With aggressive hydration and cessation of calcium carbonate, his renal function and serum calcium returned to baseline. Because we initially assumed occult malignancy as the most likely diagnosis, we gave the patient pamidronate. The patient did not have a significant alkalemia (serum bicarbonate level was normal). This was thought to be due to the patient's degree of renal failure causing a concomitant metabolic acidosis. The patient's follow‐up elevated PTH level may be explained by bisphosphonate administration or underlying primary hyperparathyroidism. Of note, decreasing calcium levels have also been speculated to be a cause of high PTH levels.8

In conclusion, physicians should have a high index of suspicion for milk‐alkali syndrome in patients with hypercalcemia. Calcium carbonate is responsible for most cases of milk‐alkali syndrome, and clinicians should inquire about the use of this supplement in all patients with hypercalcemia. Milk‐alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hospital admissions for hypercalcemia.

Historically, the milk‐alkali syndrome developed as an adverse reaction to the Sippy regimen of frequent feedings of milk, cream, and alkaline powders as treatment for peptic ulcer disease.1 The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. This syndrome seemingly disappeared when modern acid suppression therapies such as histamine‐2 blockers and proton pump inhibitors improved dyspepsia treatment. Over the past 20 years, milk‐alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased.2 Calcium carbonate supplements are a popular over‐the‐counter treatment for osteoporosis, dyspepsia, hypocalcemia, and hyperphosphatemia; these supplements provide both the calcium and alkali required for the development of milk‐alkali syndrome.

A 46‐year‐old man presented to the emergency department after his physician ordered outpatient laboratory tests to evaluate his fatigue. The patient was found to have acute renal failure and hypercalcemia. His serum creatinine was 3.6 mg/dL, increased from his baseline of 1.1 mg/dL several months prior, and his serum calcium was 14.9 mg/dL. Ten days prior to admission he developed increasing fatigue, decreased appetite, and decreased urine output, which he attributed to recent manual labor during summer. He reported taking an occasional calcium carbonate (Tums) for dyspepsia. He did not report pain or other complaints.

His medical history included hypertension and hyperlipidemia. He had a colonoscopy 1 year prior to presentation that was significant for a high‐grade dysplastic polyp and was currently due for repeat colonoscopy. His medications included clonidine, lisinopril, and aspirin. He had no recent medication changes. He had a 30 pack/year history of cigarette smoking and drank occasionally.

On physical exam, his temperature was 99.8F, blood pressure 97/48 mmHg, heart rate 89 beats per minute, respirations 20 breaths per minute, with a room air saturation of 97%. He had dry mucus membranes and the remainder of the physical exam was unremarkable.

In the emergency department laboratory testing revealed a creatinine of 4.6 mg/dL, serum total calcium of 15.9 mg/dL, serum bicarbonate level of 26 mmol/L, phosphate of 3.9 mg/dL, albumin of 4.4 gm/dL, and alkaline phosphatase of 92 IU/L. The urine specific gravity was 1.019 gm/mL (see Table 1 for the patient's complete admission laboratory values).

His intact parathyroid (PTH) hormone was 18.8 pg/mL (normal, 15‐65). PTH hormone‐related peptide (PTHrP) was <2.5 pmol/L. After reviewing these laboratory test results, we proceeded with further questioning, during which he admitted to taking approximately 15 to 20 Tums (>7.5 gm of calcium carbonate) daily for dyspepsia rather than the occasional Tums he had originally reported. Over the next 3 days, his calcium decreased to 8.4 mg/dL and his creatinine decreased to 1.6 mg/dL with intravenous hydration. His fatigue improved. His 25‐hydroxy vitamin D (25‐OH‐Vitamin D) level was 23 ng/mL (normal, 16‐74 ng/mL).

At his 1 week follow‐up, his calcium was 8.1 mg/dL, and his creatinine had returned to normal at 0.9 mg/dL. His intact PTH level was elevated at 240 pg/mL.

Discussion

Milk‐alkali syndrome is now believed to be the third most common reason for hypercalcemia hospital admission.2, 3 Malignancy and primary hyperparathyroidism are the only 2 causes of hypercalcemia more common than milk‐alkali syndrome in hospitalized patients; these must be excluded before making a definitive diagnosis of milk‐alkali syndrome. The differential diagnosis for hypercalcemia also includes other less common etiologies such as medications (hydrochlorothiazide and lithium), as well as familial hypocalciuric hypercalcemia, hyperthyroidism, Addison's disease, acromegaly, tertiary hyperparathyroidism, and vitamin D intoxication. Physicians often discover hypercalcemia incidentally on routine laboratory tests, and diagnostic workup should include a thorough history and physical examination, as well as further laboratory evaluation.

The diagnosis of milk‐alkali syndrome requires a history of increased calcium and alkali intake, but is otherwise a diagnosis of exclusion. Given the increasing consumption of nonprescribed calcium supplements, one should have a high index of suspicion for the diagnosis of milk‐alkali syndrome, as patients may not consider calcium carbonate to be hazardous or even a medication and thus may not report calcium carbonate consumption. Patients often view calcium carbonate as a benign treatment for dyspepsia. Its over‐the‐counter availability and economical price make it a common self‐treatment for minor dyspepsia or as prevention of osteoporosis. Calcium supplementation is increasingly added to many products, making it easy for patients to consume large quantities of calcium unknowingly. Of note, without the absorbable alkali supplied by the carbonate in calcium carbonate (Tums), milk‐alkali syndrome does not occur. The amount of calcium carbonate necessary to cause milk‐alkali syndrome is not well known, though it is speculated to be as little as 5 to 10 g of calcium in the form of calcium carbonate, especially in those with other risk factors for hypercalcemia such as chronic renal insufficiency or vomiting.2 Workup of hypercalcemia should entail careful questioning about medications, as well as over‐the‐counter supplements, vitamins, and foods.

Manifestations of the milk‐alkali syndrome include renal failure, metabolic alkalosis, and volume contraction. Normally, the kidneys prevent hypercalcemia by excretion of excess calcium. Hypercalcemia can cause tubular damage and vasoconstriction of the renal afferent arteriole leading to acute renal failure.2, 4 Hypercalcemia can also cause nephrogenic diabetes insipidus, causing impaired renal concentrating ability, leading to increased sodium excretion and volume contraction.2 In addition, alkalosis further impairs calciuresis.2 Laboratory values usually reveal suppressed PTH and vitamin D levels due to hypercalcemia caused by exogenous intake of calcium.5 Hypercalcemia causes suppression of PTH, which can lead to hyperphosphatemia, as well as decreased conversion of vitamin D to the active 1,25‐dihyroxyvitamin‐D form.

The management of hypercalcemia due to milk‐alkali syndrome is supportive and includes saline hydration as well as withholding calcium carbonate. Management of hypercalcemia due to malignancy and hyperparathyroidism includes bisphosphonates with the addition of calcitonin if symptoms are severe.6, 7 There is no evidence that supports the use of bisphosphonates in the treatment of milk‐alkali syndrome. Loop diuretics are sometimes used to promote calciuresis, though evidence is lacking to support this, and it may worsen renal failure.6

In this case, a middle‐aged man took greater than the recommended dose of calcium carbonate for dyspepsia, which led to the development of acute renal failure and hypercalcemia. At first, the patient did not provide an accurate history of the extent of his calcium carbonate ingestion, leading us to focus on hyperparathyroidism or malignancy. With aggressive hydration and cessation of calcium carbonate, his renal function and serum calcium returned to baseline. Because we initially assumed occult malignancy as the most likely diagnosis, we gave the patient pamidronate. The patient did not have a significant alkalemia (serum bicarbonate level was normal). This was thought to be due to the patient's degree of renal failure causing a concomitant metabolic acidosis. The patient's follow‐up elevated PTH level may be explained by bisphosphonate administration or underlying primary hyperparathyroidism. Of note, decreasing calcium levels have also been speculated to be a cause of high PTH levels.8

In conclusion, physicians should have a high index of suspicion for milk‐alkali syndrome in patients with hypercalcemia. Calcium carbonate is responsible for most cases of milk‐alkali syndrome, and clinicians should inquire about the use of this supplement in all patients with hypercalcemia. Milk‐alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hospital admissions for hypercalcemia.

Historically, the milk‐alkali syndrome developed as an adverse reaction to the Sippy regimen of frequent feedings of milk, cream, and alkaline powders as treatment for peptic ulcer disease.1 The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. This syndrome seemingly disappeared when modern acid suppression therapies such as histamine‐2 blockers and proton pump inhibitors improved dyspepsia treatment. Over the past 20 years, milk‐alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased.2 Calcium carbonate supplements are a popular over‐the‐counter treatment for osteoporosis, dyspepsia, hypocalcemia, and hyperphosphatemia; these supplements provide both the calcium and alkali required for the development of milk‐alkali syndrome.

A 46‐year‐old man presented to the emergency department after his physician ordered outpatient laboratory tests to evaluate his fatigue. The patient was found to have acute renal failure and hypercalcemia. His serum creatinine was 3.6 mg/dL, increased from his baseline of 1.1 mg/dL several months prior, and his serum calcium was 14.9 mg/dL. Ten days prior to admission he developed increasing fatigue, decreased appetite, and decreased urine output, which he attributed to recent manual labor during summer. He reported taking an occasional calcium carbonate (Tums) for dyspepsia. He did not report pain or other complaints.

His medical history included hypertension and hyperlipidemia. He had a colonoscopy 1 year prior to presentation that was significant for a high‐grade dysplastic polyp and was currently due for repeat colonoscopy. His medications included clonidine, lisinopril, and aspirin. He had no recent medication changes. He had a 30 pack/year history of cigarette smoking and drank occasionally.

On physical exam, his temperature was 99.8F, blood pressure 97/48 mmHg, heart rate 89 beats per minute, respirations 20 breaths per minute, with a room air saturation of 97%. He had dry mucus membranes and the remainder of the physical exam was unremarkable.

In the emergency department laboratory testing revealed a creatinine of 4.6 mg/dL, serum total calcium of 15.9 mg/dL, serum bicarbonate level of 26 mmol/L, phosphate of 3.9 mg/dL, albumin of 4.4 gm/dL, and alkaline phosphatase of 92 IU/L. The urine specific gravity was 1.019 gm/mL (see Table 1 for the patient's complete admission laboratory values).

His intact parathyroid (PTH) hormone was 18.8 pg/mL (normal, 15‐65). PTH hormone‐related peptide (PTHrP) was <2.5 pmol/L. After reviewing these laboratory test results, we proceeded with further questioning, during which he admitted to taking approximately 15 to 20 Tums (>7.5 gm of calcium carbonate) daily for dyspepsia rather than the occasional Tums he had originally reported. Over the next 3 days, his calcium decreased to 8.4 mg/dL and his creatinine decreased to 1.6 mg/dL with intravenous hydration. His fatigue improved. His 25‐hydroxy vitamin D (25‐OH‐Vitamin D) level was 23 ng/mL (normal, 16‐74 ng/mL).

At his 1 week follow‐up, his calcium was 8.1 mg/dL, and his creatinine had returned to normal at 0.9 mg/dL. His intact PTH level was elevated at 240 pg/mL.

Discussion

Milk‐alkali syndrome is now believed to be the third most common reason for hypercalcemia hospital admission.2, 3 Malignancy and primary hyperparathyroidism are the only 2 causes of hypercalcemia more common than milk‐alkali syndrome in hospitalized patients; these must be excluded before making a definitive diagnosis of milk‐alkali syndrome. The differential diagnosis for hypercalcemia also includes other less common etiologies such as medications (hydrochlorothiazide and lithium), as well as familial hypocalciuric hypercalcemia, hyperthyroidism, Addison's disease, acromegaly, tertiary hyperparathyroidism, and vitamin D intoxication. Physicians often discover hypercalcemia incidentally on routine laboratory tests, and diagnostic workup should include a thorough history and physical examination, as well as further laboratory evaluation.

The diagnosis of milk‐alkali syndrome requires a history of increased calcium and alkali intake, but is otherwise a diagnosis of exclusion. Given the increasing consumption of nonprescribed calcium supplements, one should have a high index of suspicion for the diagnosis of milk‐alkali syndrome, as patients may not consider calcium carbonate to be hazardous or even a medication and thus may not report calcium carbonate consumption. Patients often view calcium carbonate as a benign treatment for dyspepsia. Its over‐the‐counter availability and economical price make it a common self‐treatment for minor dyspepsia or as prevention of osteoporosis. Calcium supplementation is increasingly added to many products, making it easy for patients to consume large quantities of calcium unknowingly. Of note, without the absorbable alkali supplied by the carbonate in calcium carbonate (Tums), milk‐alkali syndrome does not occur. The amount of calcium carbonate necessary to cause milk‐alkali syndrome is not well known, though it is speculated to be as little as 5 to 10 g of calcium in the form of calcium carbonate, especially in those with other risk factors for hypercalcemia such as chronic renal insufficiency or vomiting.2 Workup of hypercalcemia should entail careful questioning about medications, as well as over‐the‐counter supplements, vitamins, and foods.

Manifestations of the milk‐alkali syndrome include renal failure, metabolic alkalosis, and volume contraction. Normally, the kidneys prevent hypercalcemia by excretion of excess calcium. Hypercalcemia can cause tubular damage and vasoconstriction of the renal afferent arteriole leading to acute renal failure.2, 4 Hypercalcemia can also cause nephrogenic diabetes insipidus, causing impaired renal concentrating ability, leading to increased sodium excretion and volume contraction.2 In addition, alkalosis further impairs calciuresis.2 Laboratory values usually reveal suppressed PTH and vitamin D levels due to hypercalcemia caused by exogenous intake of calcium.5 Hypercalcemia causes suppression of PTH, which can lead to hyperphosphatemia, as well as decreased conversion of vitamin D to the active 1,25‐dihyroxyvitamin‐D form.

The management of hypercalcemia due to milk‐alkali syndrome is supportive and includes saline hydration as well as withholding calcium carbonate. Management of hypercalcemia due to malignancy and hyperparathyroidism includes bisphosphonates with the addition of calcitonin if symptoms are severe.6, 7 There is no evidence that supports the use of bisphosphonates in the treatment of milk‐alkali syndrome. Loop diuretics are sometimes used to promote calciuresis, though evidence is lacking to support this, and it may worsen renal failure.6

In this case, a middle‐aged man took greater than the recommended dose of calcium carbonate for dyspepsia, which led to the development of acute renal failure and hypercalcemia. At first, the patient did not provide an accurate history of the extent of his calcium carbonate ingestion, leading us to focus on hyperparathyroidism or malignancy. With aggressive hydration and cessation of calcium carbonate, his renal function and serum calcium returned to baseline. Because we initially assumed occult malignancy as the most likely diagnosis, we gave the patient pamidronate. The patient did not have a significant alkalemia (serum bicarbonate level was normal). This was thought to be due to the patient's degree of renal failure causing a concomitant metabolic acidosis. The patient's follow‐up elevated PTH level may be explained by bisphosphonate administration or underlying primary hyperparathyroidism. Of note, decreasing calcium levels have also been speculated to be a cause of high PTH levels.8

In conclusion, physicians should have a high index of suspicion for milk‐alkali syndrome in patients with hypercalcemia. Calcium carbonate is responsible for most cases of milk‐alkali syndrome, and clinicians should inquire about the use of this supplement in all patients with hypercalcemia. Milk‐alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hospital admissions for hypercalcemia.