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.
Failure to diagnose milk-alkali syndrome is usually related to a failure to obtain a full history of OTC medications. [38] 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. [13] Patients discharged without a specific diagnosis are likely to continue excess intake of calcium carbonate and develop hypercalcemia again.
Three different progressive stages have been noticed. First, the toxemia (acute) stage occurs within 2-30 days after calcium ingestion begins and clinically patients present with irritability, vertigo, apathy, headaches, weakness, muscle aches, and/or vomiting. Second, the intermediate stage, or Cope syndrome, clinically has the above symptoms along with conjunctivitis. Third, the chronic stage, or Burnett syndrome, manifests as soft tissue calcification including conjunctivitis, band keratopathy of the cornea, musculoskeletal deposits, and nephrocalcinosis. [39]
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:
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Fatigue
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Depression
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Malaise
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Confusion/mental status changes
GI symptoms may include the following:
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Nausea
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Vomiting
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Constipation
Genitourinary symptoms and signs may include the following:
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Urinary frequency
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Renal tubular defects
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Renal failure
Cardiac symptoms and signs may include the following:
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Electrocardiographic changes (short QT/QTc interval) [40]
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Hypercalcemia can occasionally produce J (or Osborn) waves, which are typically seen in hypothermia. However, Osborn waves due to hypothermia and other conditions like haloperidol overdose and active cardiac ischemia are associated with prolonged QT/QTc interval in contrast to short QT/QTc interval in hypercalcemia. [4]
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Arrhythmias
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The hospital course of a patient with milk-alkali syndrome who, during treatment, developed symptomatic hypocalcemia with a markedly elevated serum parathyroid hormone level (PTH). Thirty days after discharge, the calcium and PTH levels were normal.
Tables
| Mean Age | 59.8 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 | 17. 2mg/dL (4.30mmol/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,
[12] as well as additional patients reported by Gibbs and Lee, 1992;
[15] Nakanishi et al, 1992
[16] ; Brandwein and Sigman, 1994
[17] ; Campbell et al, 1994
[18] ; Duthie et al, 1995
[19] ; Spital and Freedman, 1995
[20] ; Fiorino, 1996
[21] ; Lin et al, 1996
[22] ; Muldowney and Mazbar, 1996
[23] ; Sulkin and Krentz, 1999
[24] ; Camidge and Peaston, 2000
[25] ; George and Clark, 2000
[26] ; Vanpee et al, 2000
[27] ; Liu et al, 2002
[28] ; Robertson, 2002
[29] ; Morton, 2002
[30] ; Kleinig and Torpy, 2004
[6] ; Picolos et al, 2005
[13] ; Gordon et al, 2005
[31] ; Addington et al, 2006
[10] ; Verburg et al, 2006
[32] ; Ennen and Magann, 2006
[33] ; Caruso et al, 2007
[34] ; Dinnerstein et al, 2007
[35] ; Javid et al, 2007; Kaklamanos and Perros, 2007
[36] ; Shah et al, 2007
[37] ; Irtiza-Ali et al, 2008
[7] ; and Jousten and Guffens, 2008.
[8]
Two of the patients were pregnant. |
