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Your reader barcode: Your last name:. Cite this Email this Add to favourites Print this page. You must be logged in to Tag Records. In the Library Request this item to view in the Library's reading rooms using your library card. Details Collect From In this volume, Dr. Steinberg has offered the reader a unique opportunity to share his many years of experience in caring for the immobilized patient.
His careful attempt to explore the pathophysiologic effects of immobilization on a number of organ systems, combined with a host of practical aspects with regard to patient care, is unique and refreshing.
This text should command the re spect of any physician faced with the vicissitudes and frus trations of caring for the immobilized. The final chapter de tailing "The Psychological Aspects of Immobilization," by Hammer and Kenan, offers the reader considerable insight into the essentials and value of occupational and physical therapy. It should prove most valuable to physicians as well "Asher, R. Milk-alkali syndrome is a syndrome of hypercalcemia, metabolic alkalosis, hypercalciuria and renal failure which occurs usually occurs in patients consuming large quantities typically at least mg elemental calcium per day of absorbable calcium containing-antacids, such as calcium carbonate.
Hypercalcemia occurs as a result of passive intestinal calcium absorption exceeding the ability of the kidney to clear the calcium. The hypercalcemia is reversible with hydration and reduction of calcium intake, though the resulting renal damage may be permanent. The immobilization activates osteoclastic bone resorption and suppresses osteoblastic bone resorption, leading to loss of calcium from the skeleton, hypercalcemia and reduced bone mineral density.
The syndrome is associated with hypercalciuria as well, and this, together with chronic urinary catheterization, leads to urinary tract infection and severe calcium nephrolithiasis. Restoring active weight bearing is the most effective treatment, if possible, though bisphosphonates and hydration are an alternative therapy.
Renal failure is a risk factor for hypercalcemia. In patients with chronic renal failure, hypercalcemia may occur as a result of calcitriol treatment, use of phosphate-binding agents, excessive calcium intake from supplements or diet, or immobilization. Hypercalcemia in patients with chronic renal failure may also result from tertiary hyperparathyroidism. Transient rebound hypercalcemia has been described during the resolution phase of acute renal failure due to rhabdomyolysis as serum phosphate concentrations decline. Chronic total parenteral nutrition TPN in patients with short bowel syndrome has been associated with hypercalcemia.
This is sometimes related to large amounts of calcium, vitamin D or aluminum in the TPN solution, but in other cases, the mechanism is unexplained. High calcium from parenteral or enteral feeding combined with reduced calcium clearance due to renal insufficiency can also cause hypercalcemia similar to milk-alkali syndrome. In these cases, the amount of calcium bound to proteins may be elevated though ionized calcium will be normal.
Patients display an elevation in total serum calcium without symptoms or signs of hypercalcemia or evidence of hypercalciuria. Since ionized calcium levels are normal, these patients do not require treatment of hypercalcemia. Medications to lower calcium can result in hypocalcemic seizures despite normal measured total calcium. End-stage liver disease has been noted to cause hypercalcemia which reverses with successful liver transplant. The underlying mechanism is unknown. Manganese intoxication in patients who drink water from contaminated wells has been described as a cause of hypercalcemia.
Severe dietary phosphate restriction in animals causes hypophosphatemia associated with hypercalcemia. Although this has not been documented in humans, hypophosphatemia is often associated with hypercalcemia in cancer, hyperparathyroidism, and other causes of hypercalcemia.
Anecdotally, treatment of hypercalcemia may be more successful once hypophosphatemia is corrected. Total serum calcium: As mentioned above, the total serum calcium concentration is comprised of ionized serum calcium and serum calcium bound to proteins, mainly albumin, and anions, such as phosphate, sulfate, carbonate or citrate. Ionized calcium is the only physiologically active form, but it is not routinely measured.
CKS is only available in the UK
The total calcium level should be adjusted for albumin levels as described above. Hypercalcemia is present when the adjusted total calcium level is greater than two standard deviations above the normal mean in a particular laboratory often Albumin:Since albumin is the main protein to which calcium is bound, a person with hypoalbuminemia may have hypercalcemia despite measured calcium in the normal range. Using an albumin level, an adjusted calcium level can be calculated and compared to the total calcium reference range.
If significant abnormalities in the level of bound calcium are expected, an ionized calcium may be a more precise reflection of biologically active calcium. Ionized calcium: Ionized calcium is the physiologically active form of calcium. Since estimates of adjusted total calcium are not always reliable, measurement of ionized calcium should be considered if abnormalities in the level of bound calcium are expected. Calcium-binding immunoglobulins in rare cases of multiple myeloma may cause misleading elevated total serum calcium levels with a normal ionized calcium level. Phosphorus: Calcium and phosphorus metabolism are closely related.
Serum phosphorus may be elevated in vitamin-D mediated hypercalcemia and renal failure and tends to be low in hyperparathyroidism and HHM.
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Patients with hypercalcemia and hyperphosphatemia are at risk of precipitation of calcium-phosphate salts in soft tissues such as the kidney, cardiac conduction system, cornea, and basal ganglia. This most commonly occurs when the calcium-phosphate product is above Parathyroid hormone PTH : Although ectopic hyperparathyroidism is very rare, coexisting primary hyperparathyroidism and cancer is fairly common.
PTH may be mildly elevated in FHH as well; a 24 hour urinary calcium is useful for further evaluation in this situation. It may be helpful to measure PTHrP if the diagnosis of HHM cannot be made on clinical grounds or if the cause of hypercalcemia is unknown. Vitamin D metabolites:1,25 OH 2 vitamin D should be measured when 1,25 OH 2 vitamin D-secreting tumors or granulomatous disorders are considered in the differential diagnosis.
Basic metabolic profile: Creatinine, blood urea nitrogen, bicarbonate and chloride can be checked to evaluate renal function and hydration status. Endocrine-Related Cancer In: Favus M, ed. In: Rosen CJ,ed.
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Primer on the metabolic bone diseases and disorders of mineralmetabolism, 7th Ed. Endocrinology, 6thEd. Philadelphia: Saunders Elsevier; Bone imaging studies such as a skeletal survey or a bone scan may be useful when assessing skeletal tumor burden in patients with known cancer and hypercalcemia. Thyroid stimulating hormone TSH and free T4 may be checked to exclude hyperthyroidism as a cause of hypercalcemia. Management of hypercalcemia should be directed toward the underlying cause or combination of causes. For patients with cancer, the most effective long-term therapy is eradication of the tumor.
Of course, sometimes treatment of hypercalcemia must begin before a diagnosis is made or before antineoplastic treatment has its effect. Many patients with malignancy-associated hypercalcemia have dehydration and reduced renal function due to nephrogenic diabetes insipidus and decreased oral hydration from anorexia, nausea, and vomiting. The dehydration leads to a decrease in glomerular filtration rate, which further impairs renal calcium clearance.
Renal calcium clearance may be increased by increasing the glomerular filtration rate GFR using aggressive hydration with saline, taking into account the level of dehydration as well as renal function, cardiovascular status, and severity of hypercalcemia. The patient should be watched carefully for signs of fluid overload. Thiazide diuretics should be discontinued because they stimulate renal calcium reabsorption. Once the patient is adequately volume resuscitated and GFR is normal, a loop diuretic such as furosemide may be added to block renal calcium absorption and permit increased administration of saline.
In patients with HHM, local osteolysis, and PTH-secreting tumors hypercalcemia is primarily due to accelerated bone resorption. Treatment in these patients should include agents that block bone resorption, such as the intravenous bisphosphonates, zoledronate or pamidronate. If hypercalcemia is mild, it may be reasonable to wait to see the magnitude of calcium decrease with hydration first, though antiresorptive therapy with a bisphosphonate should be administered soon after discovery of hypercalcemia in patients with serum calcium above Limiting oral calcium intake is not important in HHM and LOH, since intestinal calcium absorption is already low as a result of the low 1,25 OH 2 vitamin D concentrations and because cachexia is common in these patients.
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Patients with 1,25 OH 2 vitamin D-secreting tumors have hypercalcemia primarily due to increased GI absorption of calcium.