Milk-Alkali Syndrome Clinical Presentation
- Author: R Hal Scofield, MD; Chief Editor: George T Griffing, MD more...
History
Milk-alkali syndrome is a diagnosis of history and of exclusion; other potential causes of hypercalcemia must be eliminated. A careful history of all medicines, including OTC medications, should be obtained. This includes actual inspection of bottles to determine ingredients, when needed.
In the author's experience, failure to diagnose milk-alkali syndrome is usually related to a failure to obtain a full history of OTC medications. Moreover, in a series of 11 patients with milk-alkali syndrome, only 5 had the diagnosis made while hospitalized. The remaining 6 were diagnosed only with chart review in retrospect.[7] Patients discharged without a specific diagnosis are likely to continue excess intake of calcium carbonate and develop hypercalcemia again.
No specific or characteristic physical findings are described for milk-alkali syndrome; the signs and symptoms are those of hypercalcemia from any cause. Central nervous system symptoms may include the following:
- Fatigue
- Depression
- Malaise
- Confusion/mental status changes
GI symptoms may include the following:
- Nausea
- Vomiting
- Constipation
Genitourinary symptoms may include the following:
- Urinary frequency
- Renal tubular defects
- Renal failure
Cardiac symptoms may include the following:
- Electrocardiographic changes (short QT interval)[32]
- Arrhythmias
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| Mean Age | 51 Years (Range, 24-95 y) |
| Sex | 35 men and 43 women |
| Calcium source | Calcium carbonate in all but 1 |
| Ingestion of bicarbonate | In 7 patients |
| Ingestion of milk | In 20 patients (plus one who ate yogurt) |
| Mean serum calcium | 15.1mg/dL (3.75mmol/L) (range, 11.1-27.5mg/dL) |
| High serum phosphorus | In 12 patients |
| Permanent renal insufficiency | In 20 of 57 patients eligible for evaluation |
| Parathyroid exploration | In 3 patients |
| Hypocalcemia with treatment | In 16 patients |
| *These data are derived from the 7 patients reported, plus the 28 reviewed in Beall and Scofield, 1995,[6] as well as additional patients reported by Gibbs and Lee, 1992;[9] Nakanishi et al, 1992[10] ; Brandwein and Sigman, 1994[11] ; Campbell et al, 1994[12] ; Duthie et al, 1995[13] ; Spital and Freedman, 1995[14] ; Fiorino, 1996[15] ; Lin et al, 1996[16] ; Muldowney and Mazbar, 1996[17] ; Sulkin and Krentz, 1999[18] ; Camidge and Peaston, 2000[19] ; George and Clark, 2000[20] ; Vanpee et al, 2000[21] ; Liu et al, 2002[22] ; Robertson, 2002[23] ; Morton, 2002[24] ; Kleinig and Torpy, 2004[2] ; Picolos et al, 2005[7] ; Gordon et al, 2005[25] ; Addington et al, 2006[5] ; Verburg et al, 2006[26] ; Ennen and Magann, 2006[27] ; Caruso et al, 2007[28] ; Dinnerstein et al, 2007[29] ; Javid et al, 2007; Kaklamanos and Perros, 2007[30] ; Shah et al, 2007[31] ; Irtiza-Ali et al, 2008[3] ; and Jousten and Guffens, 2008.[4] Two of the patients were pregnant. | |

