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Hypocalcemia is frequently encountered in patients who are hospitalized. Presentations vary widely, from asymptomatic to life-threatening situations. A 70-kg person has approximately 1.2 kg of calcium in the body, most of which is stored as hydroxyapatite in bones (>99%). Less than 1% (5-6 g) of this calcium is located in the intracellular and extracellular compartments, with only 1.3 g located extracellularly. The total calcium concentration in the plasma is 4.5-5.1 mEq/L (9-10.2 mg/dL). Fifty percent of plasma calcium is ionized, 40% is bound to proteins (90% of which binds to albumin), and 10% circulates bound to anions (eg, phosphate, carbonate, citrate, lactate, sulfate). At a plasma pH of 7.4, each gram of albumin binds 0.8 mg/dL of calcium. This bond is dependent on the carboxyl groups of albumin and is highly dependent on pH. Acute acidemia decreases calcium binding to albumin, whereas alkalemia increases binding, which decreases ionized calcium. Clinical signs and symptoms are observed only with decreases in ionized calcium concentration (normally 4.5-5.5 mg/dL).
Ionized calcium is the necessary plasma fraction for normal physiologic processes. In the neuromuscular system, ionized calcium levels facilitate nerve conduction, muscle contraction, and muscle relaxation. Calcium is necessary for bone mineralization and is an important cofactor for hormonal secretion in endocrine organs. At the cellular level, calcium is an important regulator of ion transport and membrane integrity. The calcium turnover is estimated at 10-20 mEq/d. Approximately 500 mg of calcium are removed from the bones daily and replaced by an equal amount. Normally, the amount of calcium absorbed by the intestines is matched by urinary calcium excretion. Despite these enormous fluxes of calcium, the levels of ionized calcium remain stable because of the rigid control of parathyroid hormone (PTH) and vitamin D levels. Normocalcemia requires PTH and normal target-organ response to PTH. The parathyroid gland has a remarkable sensitivity to ionized serum calcium changes. These changes are recognized by the calcium-sensing receptor (CaSR), a 7transmembrane receptor linked to G-protein with a large extracellular amino-terminal region. Binding of calcium to the CaSR induces activation of phospholipase C and inhibition of PTH secretion. On the other hand, a slight decrease in calcium stimulates the chief cells of the parathyroid gland to secrete PTH. CaSR is crucial in PTH secretion. A loss of CaSR function leads to pathological states, such as familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. In renal failure, CaSR agonists suppress the progression of hyperparathyroidism and parathyroid gland growth. PTH stimulates osteoclastic bone reabsorption and distal tubular calcium reabsorption and mediates 1,25-dihydroxyvitamin D (1,25[OH]2 D) intestinal calcium absorption.
and mediates PTH-stimulated bone reabsorption. but it should be administered via central venous access. o • Administer 1-2 ampules 10% calcium gluconate (93 mg/10 mL) in 50-100 mL of D5W over 5-10 minutes. however. or malnutrition. • o PTH deficiency: Patients with hypoparathyroidism and pseudohypoparathyroidism can be managed initially with the oral administration of calcium supplements. nephrotic syndrome. whereas acidemia is protective. Patients with a decrease in total serum calcium may not have "true" hypocalcemia. can present with a dramatic picture of hypocalcemia. and how rapidly the hypocalcemia developed. the severity. Medical Care The treatment of hypocalcemia depends on the cause. In patients with severe hypoparathyroidism. A reduction in total serum calcium can result from a decrease in albumin secondary to liver disease. the presence of symptoms. • Acute hypocalcemia • o Promptly correct symptomatic or severe hypocalcemia with cardiac arrhythmias or tetany with parenteral administration of calcium salts. o Identify and treat the cause of hypocalcemia and taper the infusion. ionized calcium should be monitored. o Start oral calcium and vitamin D treatment early. Hypocalcemia causes neuromuscular irritability and tetany. Measure serum calcium every 4-6 hours to maintain serum calcium levels at 8-9 mg/dL. o Treatment with calcium and vitamin D for 1-2 days prior to parathyroid surgery may help prevent the development of severe hypocalcemia. The hypercalcemic effects of thiazide diuretics may offer some additional benefits. Alkalemia induces tetany due to a decrease in ionized calcium. remember that PTH deficiency impairs the conversion of . Patients with postparathyroidectomy hungry bone disease. regulates PTH release by the chief cells. o Patients with cardiac arrhythmias or patients on digoxin therapy need continuous ECG monitoring during calcium replacement because calcium potentiates digitalis toxicity. Calcium chloride 10% solution (273 mg/10-mL ampule) delivers higher amounts of calcium and is advantageous when rapid correction is needed. vitamin D treatment may be required. which is defined as a decrease in ionized calcium. Chronic hypocalcemia: Treatment of chronic hypocalcemia depends on the cause of the disorder.Vitamin D stimulates intestinal absorption of calcium. especially those with osteitis fibrosa cystica. If low albumin is also present. This pathophysiology is important in patients with renal failure who have hypocalcemia because rapid correction of acidemia or development of alkalemia may trigger tetany.
the dietary intake of phosphate should be lowered to 400-800 mg/d to prevent hyperphosphatemia. Surgical Care Parathyroidectomy (subtotal or total) may be indicated in certain patients with severe secondary hyperparathyroidism and renal osteodystrophy. In patients with hypocalcemia and chronic renal failure. initiate a workup to help diagnose the cause of hypocalcemia. they will primarily act as phosphate binders. postparathyroidectomy. In/Out Patient Meds . Calcitriol may be used. Treat nutritional rickets with vitamin D2. Further Inpatient Care • After correction of serum calcium. but it has the disadvantages of a higher price and the possibility of producing hypervitaminosis D with hypercalcemia. particularly in cases of vitamin D deficiency. direct the treatment at preventing further episodes of hypocalcemia and avoiding the complications of chronic hypocalcemia. Active vitamin D administration (calcitriol) enhances the absorption of calcium. However. Therefore. Following parathyroidectomy. Diet • • An increase in dietary calcium to greater than 1 g/d is an important part of the treatment of chronic hypocalcemia. These levels can be managed several ways. otherwise. For infants who are breastfed. First. Finally.o o vitamin D to calcitriol. Oral calcium preparations containing 1-2 g of elemental calcium per day can treat patients with a calcium deficiency.5-2 mcg of calcitriol or 1-alpha-hydroxyvitamin D3. adjust the dose to 30 mg/kg/d. the calcium in the dialysate bath can be increased. Hypocalcemia in patients on dialysis: Most patients on hemodialysis will be hypercalcemic. Further Outpatient Care • • After determining the cause for hypocalcemia. oral calcium supplements should be provided. Nutritional vitamin D deficiency from lack of sunlight exposure or poor oral intake of vitamin D: Ultraviolet light or sunlight exposure can treat these patients. patients may have considerable difficulty in maintaining appropriate calcium levels. patients should be seen in 5-7 days for follow-up determination of serum calcium. the most efficient treatment is the addition of 0. They must be given between meals.
such as paresthesias and muscle weakness. so they can obtain care prior to developing more severe symptoms.glucagon) . renal disease (calcium is excreted . the citrate binds with calcium so it is not usable in the body). abuse of laxatives or enemas Some drugs (glucocorticoids. loop diuretics. Transfer • Patients with hypocalcemia and renal failure may require transfer to a facility with hemodialysis available. Prognosis • Prognosis usually is favorable and depends on the cause and duration of hypocalcemia. massive blood transfusions (they put citrate in the blood to preserve it. or lactase deficiency. chrones disease or other malabsorptive disorders para-thyroid hormone deficiency. Patients with hypocalcemia associated with chronic renal failure often require phosphate binders and vitamin D supplementation. • o o Osteomalacia and rickets result from vitamin D deficiency. Osteitis fibrosis cystica and osteomalacia occur in patients with hypercalcemia and secondary hyperparathyroidism./dL) • • Inadequate calcium intake. Causes of Hypocalcemia (Serum levels below 4.• • Patients with hypocalcemia due to resistance to PTH generally will require longterm therapy with vitamin D and calcium supplementation. Patient Education • • The primary component of patient education involves dietary instruction in patients with hypocalcemia. Patients with chronic hypocalcemia should be informed about the early symptoms of hypocalcemia.Vitamin D.5mEq/l or 9 mg.phosphorus is retained) More Causes of Hypocalcemia • • some cancers. Complications • Complications of chronic hypocalcemia predominantly are those of bone disease. heparin.
Must have Vit D to absorb calcium (added to milk) Your patient who has serum calcium of 8. green leafy veggies Treatment of Hypocalcemia • pre-manapausal women should have 1000mg/day .post 1500 to prevent osteoporosis. restlessness. bleeding tendencies Tetany . Treatment of Hypocalcemia • • • Calcium gluconate or calcium chloride IV (causes sloughing if infiltrates) Oral calcium suppliments (Tums. cramping. dietary history. radiation or injury to the neck. use of vitamin D suppliments or calcium medication Assess for S/S of hypocalcemia Possible nursing diagnoses • Risk for injury related to tetany secondary to hypocalcemia .Symptoms of Hypocalcemia • • • Tingling of hands. lack of concentration.grimacing.Calcium channels are too open letting impulses go through too fast diarrhea (intestinal motility). feet. or around the mouth laryngeal spasm. fingers. hyperactive reflexes (Chvostek’s sign tapping the facial nerve causes facial twitch) Symptoms of hypocalcemia • • severe flexion of the wrist and ankle joints when circulation is interrupted for a few minutes(Trousseau’s sign) . calcium lactate) Increased calcium in diet .4 states that she hates milk • what could you suggest to help her improve the serum calcium level (you cannot order medication of any kind) Nursing Process • • Take a history for hypoparathyroidism. muscle twitching.overuse of laxatives or anticids.milk. cheese.
Approximately 40% of the calcium is bound to protein. Pathophysiology Plasma calcium is maintained within the reference range by a complex interplay of 3 major hormones. Calcium enters the body through the small intestine and eventually is excreted via the kidney. Treatment of the elevated calcium level may resolve the crisis. although marked elevation of serum calcium. primarily albumin. and small intestine sites to maintain appropriate calcium levels. These 3 hormones act primarily at bone. and calcitonin. bones. The reference range of serum calcium levels is 8. calcitriol. usually more than 14 mg/dL. Other causes of elevated calcium are less common and usually are not considered until malignancy and parathyroid disease are ruled out. the calcium elevation is caused by increased intestinal calcium absorption. The causes are divided into PTH-mediated hypercalcemia and non–PTH-mediated hypercalcemia. This is mediated by the PTH-induced calcitriol . PTH-mediated hypercalcemia Primary hyperparathyroidism originally was the disease of "stones. kidney. 1. calcitriol). Hypercalcemia can result from a multitude of disorders." In most primary hyperparathyroidism cases. This entire system is controlled through a feedback loop. and abdominal groans. For hypercalcemia to develop. The remaining 10% is complexed to anions. the normal calcium regulation system must be overwhelmed by an excess of PTH. Hypercalcemic crisis does not have an exact definition. parathyroid hormone (PTH). is associated with acute signs and symptoms of hypercalcemia.4 mg/dL. individual hormones respond as needed to increase or decrease the serum calcium concentration. while 50% is ionized and is in physiologic active form. with somewhat higher levels present in children.• • Altered nutrition less than body requirements related to inadequate intake of calcium or vitamin D avoid use laxatives (especially ones containing phosphates) or antacids containing magnesium hypercalcemia Background Hypercalcemia is a disorder that most commonly results from malignancy or primary hyperparathyroidism.7-10. some other serum factor that can mimic these hormones. Bone can act as a storage depot. or a huge calcium load.25-dihydroxyvitamin D (ie.
The expansion of extracellular volume also increases the renal calcium clearance. the chronicity. and the underlying cause of the problem. In mild-to-moderate elevations of calcium. and histoplasmosis. Emergency Department Care The treatment of hypercalcemia depends on the level. Non–PTH-mediated hypercalcemia Hypercalcemia associated with malignancy commonly is the result of multiple myeloma.synthesis that enhances calcium absorption. Iatrogenic disorders of calcium levels may increase secondary to the ingestion of many medications. In PTHmediated hypercalcemia. or lung cancer and is caused by increased osteoclastic activity within the bone. Because of PTH-mediated absorption of calcium at the distal tubule. Hypercalcemia of this disorder may remain mild for long periods because some parathyroid adenomas respond to the feedback generated by the elevated calcium levels. berylliosis. few treatment options may be available in the ED. Prehospital Care Prehospital care is primarily supportive with management of the ABCs. immediately begin IV hydration. leprosy. The increase in serum calcium results in an increase in calcium filtration at the kidney. less calcium is excreted than might be expected. The rate of fluid therapy is based upon the following: o o o o o o • o o Degree of hypercalcemia Severity of dehydration . A physical evaluation to help delineate the source of the elevation is always appropriate. If a patient has a history of hypercalcemia and displays evidence of acute hypercalcemia. breast. coccidioidomycosis. bones do not play an active role because most of the PTHmediated osteoclast activity that breaks down bone is offset by hypercalcemic-induced bone deposition. tuberculosis. Granulomatous disorders with high levels of calcitriol may be found in patients with sarcoidosis. • Initial goals of treatment • • Stabilization and reduction of the calcium level Adequate hydration Increased urinary calcium excretion Inhibition of osteoclast activity in the bone Discontinuation of pharmacologic agents associated with hypercalcemia Treatment of the underlying cause (when possible) The initial step in the care of severely hypercalcemic patients is hydration with saline. Hydration helps decrease the calcium level through dilution. as is a subsequent timely follow-up visit.
Patients in this group who present with severe elevations of calcium may require urgent dialysis. Bisphosphates . Further Inpatient Care • • Serum calcium level generally responds to fluids and Lasix. The drug regimen most appropriate for each individual depends on the cause of the elevation and usually is not managed by the ED physician. . this therapy has no effect on the principle pathologic process causing hypercalcemia. Patients with malignancy may require surgery. This may also prevent volume overload during therapy. Dialysis is necessary to correct hypercalcemia in patients with renal failure. For those patients with malignancy as the cause of their hypercalcemia. or radiation treatment. depending on the severity of the hypercalcemia. a cure may not be possible. avoid thiazide diuretics because they increase the reabsorption of calcium. o Hydration is ineffective in patients with kidney failure because diuresis is impossible.These agents will inhibit osteoclast activity for up to a month. o Consultations • • • Patients with renal failure or heart failure may not be able to tolerate fluid hydration or some of the other medications. Appropriate consultation should be undertaken. o In contrast to loop diuretics. the patient may not need therapy for the hypercalcemia itself.Vigilance to prevent volume overload is critical.• Ability of the patient to tolerate rehydration . furosemide) may be used with hydration to increase calcium excretion. This referral may be urgent. Further Outpatient Care • • • • Patients with primary hyperparathyroidism who present with symptoms of severe or moderate elevations of calcium levels should be referred for parathyroidectomy. but surgery usually does not need to be performed on an urgent basis. however. Additional therapy must be added to the temporizing treatment described above. chemotherapy. Patients with primary hyperparathyroidism may require surgery to eliminate the condition. If this is accomplished. Patients with mild-to-moderate elevations of calcium who have no symptoms may be evaluated on an outpatient basis and usually are treated medically. The ideal scenario finds a treatable underlying cause for hypercalcemia and allows the physician to attend to this primary process. Treatment of the underlying disease must be addressed. Consult a nephrologist immediately in such cases. Loop diuretics o • • A loop diuretic (eg.
Prognosis is excellent when the underlying cause is treatable and treatment is initiated promptly. Consider transfer if this is unavailable at the initial treatment center.• • Patients may require ongoing treatment for calcium elevation. consider transferring patients with normal kidney function who are being treated for severe hypercalcemia. and it is not always successful. • o o Prognosis is very poor with malignancy that has progressed into development of hypercalcemia. This type of treatment can be frustrating and difficult. Avoid salt restriction. If no intensivist or physician familiar with the inpatient treatment of hypercalcemia is available. Deterrence/Prevention • • • • • Avoid prolonged bedrest for patients known to have rapid bone turnover. Prognosis • The prognosis of patients with hypercalcemia depends upon the etiology of the elevation. Worsening hypercalcemia is common in patients with known metastatic disease who are too ill to ambulate. This should be anticipated and treated before the patient becomes symptomatic. Transfer • Transfer may be considered in a number of situations. Causes of Hypercalcemia (Serum levels over 10. diuretics. Mobilize patients as quickly as possible to minimize bone loss.5mg/dL) • • • • • Excessive intake of Vitamin D Excessive intake of milk or alkaline antacids hyperthyroidism or some cancers immobility or reduced renal function thiazide diuretics (HTZ) . Consider elective surgical procedures for patients with Paget disease after therapy has been initiated for calcium elevation. Patients at risk for hypercalcemia should have scheduled appointments with ongoing evaluation to monitor for development or progression of the disease. • o o If a patient presents with severe hypercalcemia and renal failure. and other causes of volume depletion and dehydration in patients with active or potential hypercalcemia. emergency dialysis is necessary.
kidney stones and bone pain Treatment of Hypercalcimia • • IV normal saline. hyperparathyroidism. depression Gastrointestinal problems: decreased peristalsis. lethargy. In cases of hyperparathyroidism. diagnose and treat the hyperthyroidism or cancer Your patient has a serum calcium of 10. slurred speech. Assess for S/S or hypercalcemia • Possible Nursing Diagnoses • • Constipation related to decreased intestinal motility Risk for injury related to muscle weakness incoordination. immobility. Use of medications (glucocorticoids. and renal failure. lack of coordination. hyperthyroidism. absent deep tendon reflexes.muscle weakness. memory lapses and confusion Treatment Return to top Treatment is directed at the cause of hypercalcemia whenever possible. calcium or vit D supliments & antacids. If your hypercalcemia is mild and caused by primary hyperparathyroidism. and impaired memory. and constipation. cancer. surgery may be needed to remove the abnormal parathyroid gland and cure the hypercalcemia.6 • name 4 behaviors that if present could indicate hypercalcemia Nursing Process • Obtain history of health problems associated with hypercalcemia. loop diuretics treat the cause . your health care provider will follow you closely over time. anorexia.thiazide diuretics. nausea. . confusion. vomiting.Symptoms of Hypercalcemia • • • Decreased neuromuscular irritability .stop taking too much vitamin D. foods containing calcium. puritis (itching).
rather than to the hypercalcemia. .Severe hypercalcemia that causes symptoms and requires a hospital stay is treated with the following: • • • • • Calcitonin Dialysis Drugs that stop bone breakdown and absorption by the body. Patients with hypercalcemia due to conditions such as cancer or granulomatous disease may not do well due to the disease itself. such as pamidronate or etidronate (bisphosphonates) Fluids through a vein (intravenous fluids) Glucocorticoids (steroids) Return to top Outlook (Prognosis) How well you do depends on the cause of hypercalcemia. Possible Complications Gastrointestinal • • • Return to top Hypertension Pancreatitis Peptic ulcer disease Kidney • • • • Calcium deposits in the kidney (nephrocalcinosis) Dehydration Kidney failure Kidney stones Psychological • • Depression Difficulty concentrating or thinking Skeletal • • • Bone cysts Fractures Osteoporosis The complications of long-term hypercalcemia are uncommon today. Patients with mild hyperparathyroidism or hypercalcemia with a treatable cause (for example. primary hyperparathyroidism or dietary hypervitaminosis D) may not have complications.
You can avoid hypercalcemia from calcium and vitamin D supplements by contacting your health care provider for advice if you are taking supplements without a prescription.When to Contact a Medical Professional Return to top Contact your physician or health care provider if you have: • • • Family history of hypercalcemia Family history of hyperparathyroidism Symptoms of hypercalcemia Return to top Prevention Most causes of hypercalcemia cannot be prevented. Women over the age of 50 should see their health care provider regularly and have their blood calcium screened periodically. .
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