Reversible cerebral vasoconstriction syndrome (RCVS) caused by over-the-counter calcium supplement ingestion.

A 59-year-old woman was found unresponsive at home. Initial neurologic examination revealed aphasia and right-sided weakness. Laboratory results demonstrated a serum calcium level of 17.3 mg/dL (corrected serum calcium for albumin concentration was 16.8 mg/dL). Extensive workup for intrinsic aetiology of hypercalcemia was unrevealing. Further discussion with family members and investigation of the patient's home for over-the-counter medications and herbal supplements revealed chronic ingestion of calcium carbonate tablets. CT angiogram of the brain revealed multifocal intracranial vascular segmental narrowing, which resolved on a follow-up cerebral angiogram done 2 days later. These findings were consistent with reversible cerebral vasoconstriction syndrome.Appropriate blood pressure control with parenteral agents, calcium channel blockade with nimodipine and supportive care therapies resulted in significant improvement in neurologic status. By discharge, patient had near-complete resolution of neurologic symptoms.

[Granulomatous pleuritis and chylothorax caused by calcite inhalation in a Galgo Español dog]. / Granulomatöse Pleuritis und Chylothorax durch Kalzitinhalation bei einem Galgo Español.

A 6-year-old, male Galgo Español dog was presented with severe dyspnea. Radiography and ultrasonography revealed pleural effusion. Approximately 4 l of a milky and slightly reddish fluid were aspirated and drained from the thoracic cavity. Clinical chemistry examination of the fluid indicated a modified transudate with a high amount of triglycerides. On cytological examination, degenerated neutrophilic granulocytes, small lymphocytes, macrophages and chylomicrons were found. A chest tube was placed and computed tomography was performed, which indicated thickening of parietal and visceral pleura and enlargement of the sternal lymph node without abnormal findings in the lungs. During subsequent thoracoscopy disseminated proliferative masses, appearing as small white nodules, covering nearly the entire pleural surface were found and biopsies were taken for further analysis. Histopathologic diagnosis was a granulomatous pleuritis with intralesional birefringent foreign material. Energy dispensive x-ray emission analysis was used to determine the origin of the material. Scanning electron microscopy revealed high amounts of calcium containing foreign material (calcite) within the granulomas. An extended clinical history of the dog gave evidence that the animal had lived next to a construction site 15 months earlier and may well have inhaled the calcium-containing dust. Treatment with prednisolone was initiated, however the dog developed gastro-intestinal side effects and treatment was stalled after 10 weeks. Dyspnea and liquidothorax re-occurred 4 months later. A further attempt of immunosupressive treatment was commenced, using a combination of prednisolone and ciclosporine, which again was not tolerated by the patient. The dog finally developed pneumonia and was euthanized by the owner's request.

Calcium carbonate toxicity: the updated milk-alkali syndrome; report of 3 cases and review of the literature.

OBJECTIVE: To describe 3 patients with calcium carbonate-induced hypercalcemia and gain insights into the cause and management of the milk-alkali syndrome. METHODS: We report the clinical and laboratory data in 3 patients who presented with severe hypercalcemia (corrected serum calcium > or = 14 mg/dL) and review the pertinent literature on milk-alkali syndrome. RESULTS: The 3 patients had acute renal insufficiency, relative metabolic alkalosis, and low parathyroid hormone (PTH), PTH-related peptide, and 1,25-dihydroxyvitamin D concentrations. No malignant lesion was found. Treatment included aggressive hydration and varied amounts of furosemide. The 2 patients with the higher serum calcium concentrations received pamidronate intravenously (60 and 30 mg, respectively), which caused severe hypocalcemia. Of the 3 patients, 2 were ingesting acceptable doses of elemental calcium (1 g and 2 g daily, respectively) in the form of calcium carbonate. In addition to our highlighted cases, we review the history, classification, pathophysiologic features, and treatment of milk-alkali syndrome and summarize the cases reported from early 1995 to November 2003. CONCLUSION: Milk-alkali syndrome may be a common cause of unexplained hypercalcemia and can be precipitated by small amounts of orally ingested calcium carbonate in susceptible persons. Treatment with hydration, furosemide, and discontinuation of the calcium and vitamin D source is adequate. Pamidronate treatment is associated with considerable risk for hypocalcemia, even in cases of initially severe hypercalcemia.

The milk-alkali syndrome caused by betelnuts in oyster shell paste.

BACKGROUND: The carcinogenic effect of betelnut chewing leading to oral cancer is well known. Betelnut chewing may also affect the autonomic nervous system. In this report, we present another potential hazard of betelnuts, milk-alkali syndrome. CASE REPORT: Two patients who had chewed a large quantity of betelnuts developed hypercalcemia, metabolic alkalosis, and renal insufficiency. They ingested a large amount of calcium carbonate from a local special paste used for betelnut preparation, the main ingredient of which is ground oyster shell. The symptoms and metabolic abnormalities disappeared promptly after abstinence from betelnut chewing and administration of saline solution. Improvement of renal function was observed in both patients. Analysis of the calcium content of the paste suggested that the patients might have ingested 9 g and 6 g of calcium carbonate per day, respectively. CONCLUSION: This is the first report of milk-alkali syndrome not caused iatrogenically, but by recreational usage of oyster shell preparations of betelnuts.

Undisclosed self-medication--a clinical pitfall.

Over-the-counter medication may produce side-effects or precipitate hospital admission. Our patient's self-medication, initially not admitted, led to much mental and physical morbidity.

Suspected ammonium nitrate fertiliser poisoning in cattle.

The occurrence of a suspected mixed ammonia and nitrate fertiliser poisoning that led to acute illness and fatalities in cattle is described. The circumstances leading to the incident included the method of application of the fertiliser, low rainfall and the absence of subsequent irrigation of the fertilised pastures. The clinical and gross post mortem findings, principally dehydration and fluid distension of the rumen, were not pathognomonic. The complex of nitrate, nitrite and ammonia toxicity is discussed.