Milk-alkali syndrome may be classified as the following: acute (toxemic form), subacute (Cope’s syndrome), and chronic (Burnett’s syndrome).

In all types of milk-alkali syndrome there are increases in calcium, BUN, creatinine, and there are normal or increased phosphorus. Milk-alkali syndrome may be classified as the following:^[1]

• The acute or toxemic form occurs about one week after treatment with milk and alkali.
• They have symptoms of acute hypercalcemia such as:
  • Headache, dizziness
  • Lethargy
  • Nausea, vomiting
  • Anorexia  
  • Weakness
  • Mental changes such as psychosis

• Acute renal insufficiency

• Metabolic alkalosis
• Withdrawal of milk and alkali resolves the symptoms and renal function to normal, rapidly.

• Usually seen in patients that have taken milk and alkali intermittently for years.
• Patients have symptoms of both acute and chronic hypercalcemia and respond to medication withdrawal with gradual improvement. Renal function improves gradually but significantly.

• Patients have a long history of high milk and alkali consumption.
• They have symptoms of chronic hypercalcemia such as:
  • Occasional nausea, vomiting, anorexia and mental changes  
  • Asthenia  
  • Polyuria
  • Polydipsia
  • Pruritus
  • Myalgia
• Metastatic calcifications (band keratopathy and nephrocalcinosis)
• Laboratory abnormalities are similar to those in the acute syndrome, but the response to the withdrawal of milk and alkali is quite different.
• Myalgia and pruritus improves slowly as calcium level slowly normalizes.
• Calcium levels resolve to a normal level, gradually and some abnormal calcification decrease.
• There is usually minimal or no improvement in renal function, as many patients continue to have chronic renal failure.^[2][3]