Intended for healthcare professionals

Rapid response to:

Practice Lesson of the week

Milk alkali syndrome without the milk

BMJ 2007; 335 doi: https://doi.org/10.1136/bmj.39247.754676.BE (Published 23 August 2007) Cite this as: BMJ 2007;335:397

Rapid Response:

Evaluation of Milk Alkali Syndrome

I have seen a dozen cases of milk alkali syndrome over the course of
a few years.
Whenever I write my diagnosis as milk alkali syndrome, I get some raised
eyebrows, as the primary care physicians and nurses know that the patient
is not a milk drinker.
I admit that, for this reason, I do like the term “calcium alkali
syndrome" suggested by the authors.

There are a few diagnostic pearls that the authors failed to mention:
1. You have to pull out history of calcium intake “like a tooth” from
hospitalized patients who are frequently obtunded by hypercalcemia.
Asking about calcium is not enough.
Most calcium supplements might not have the word “calcium” in the name;
such as Tums, Rolaids, and Oyster shells to name a few in the United
States. It is probably wise to ask what supplements and herbs, or vitamins
do they take. Whether, they take any medications over the counter for
heartburn since most patients take calcium carbonate for this purpose.
2. The calcium supplement need not be calcium carbonate to cause milk
alkali syndrome.
3. Any calcium supplement overdose even citrate could cause milk alkali
syndrome provided that there is alkalosis. For example any calcium
supplement would cause milk alkali syndrome in conjunction with diuretic
use or history of vomiting.
4. Chloride is of high diagnostic yield. The authors failed to mention
serum chloride level in the case presentation.
In primary hyperparathyroidism serum chloride level is usually high, or
high normal (=> 106 mmol/L_.
In milk alkali syndrome or malignancy-induced hypercalcemia, serum
chloride level is typically
< 100 mmol/L. In this setting, patients who look healthy most likely
have milk alkali syndrome, and the sick ones (with weight loss, anemia,
renal dysfunction, and constitutional symptoms) need to be evaluated for
malignancy.

5. The authors should have not specified the type of IV fluids. The
preferred IV fluid is an adequate volume of 0.9% saline (barring cardiac
decompensation). In the renal tubules, calcium follows sodium in excretion
into the urine.
6. Using IV pamidronate was a rush to judgment in this case and was
unnecessary in this patient or in any milk alkali syndrome case. Milk
alkali syndrome is not caused by bone resorption, so you do not need IV
pamidronate to prevent bone resorption. Discontinuation of calcium
supplements, correction of alkalosis and copious IV hydration are the only
measures that are needed in “calcium alkali syndrome”.

Competing interests:
None declared

Competing interests: No competing interests

27 August 2007
Shirwan A. Mirza, MD, FACP, FACE
Chairman: Department of Medicine, Consultant Endocrinologist
Auburn, New York, 13021