Hypercalcemia symptoms

Ca " concentration, termed hypocalcemia, excitabihty increases. If this condition is not corrected, the symptoms of tetany, ie, muscular spasm, tremor, and even convulsions, can appear. Too great an increase in Ca " concentration, hypercalcemia, may impair muscle function to such an extent that respiratory or cardiac failure may occur. 

Sodium and water retention may also occur with androgen or anabolic steroid administration, causing die patient to become edematous, hi addition, otiier electrolyte imbalances, such as hypercalcemia, may occur. The nurse monitors the patient for fluid and electrolyte disturbances (see Chap. 58 for signs and symptoms of electrolyte disturbance). 

Contact the primary health care provider if the following occur nausea, vomiting, anorexia, constipation, abdominal pain, dry mouth, thirst, or polyuria (symptoms of hypercalcemia). 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

Therapeutic options for the treatment of hypercalcemia should be directed toward the level of corrected serum calcium and the presence of symptoms. Adequate treatment of mild or asymptomatic hypercalcemia may be achieved on an outpatient basis with nonpharmacologic measures. Moderate to severe or symptomatic hypercalcemia almost always requires pharmacologic intervention. 

Are there any presenting signs or symptoms that are consistent with possible hypercalcemia ... 

What treatment plan would you outline to manage LP s hypercalcemia based on the calcium level and his signs and symptoms ... 

Therapeutic options for the treatment of hypercalcemia should be directed toward the level of corrected serum calcium and the presence of symptoms (Fig. 96-5). Hypercalcemia may be classified as mild [corrected calcium equal to 10.5-11.9 g/dL (2.6-3 mmol/L)], moderate [12-13.9 g/dL (3-3.5 mmol/L)], and severe [greater than 14 g/dL (3.5 mmol/L)].26 Adequate treatment of mild or asymptomatic hypercalcemia may be achieved on an outpatient basis with nonpharmacologic measures. Moderate to severe or symptomatic hypercalcemia almost always requires pharmacologic intervention. 

Calciuric therapy in the form of hydration is a key component of the treatment of hypercalcemia, regardless of severity or presence of symptoms.28 Mild or asymptomatic patients may be encouraged to increase oral fluid intake (3-4 L/day). Patients with moderate to severe or symptomatic hypercalcemia should receive normal saline at 200 to 500 mL/hour according to dehydration and cardiovascular status. Patients should be encouraged to ambulate as much as possible because immobility enhances... 

Multiple pharmacologic interventions are available for the treatment of hypercalcemia (Table 96-10). Furosemide 20 to 40 mg/day may be added to hydration once rehydration has been achieved to avoid fluid overload and enhance renal excretion of calcium. Although effective in relieving symptoms, hydration and diuretics are temporary measures that are useful until the onset of antiresorptive therapy thus hydration and antiresorptive therapy should be initiated simultaneously. 

Assess the patient s symptoms to determine the need for laboratory studies. Determine if absence of symptoms in the presence of mild hypercalcemia warrants conservative outpatient management. 

The approach to hypercalcemia depends on the degree of hypercalcemia, acuity of onset, and presence of symptoms (Fig. 78-2). 

Milk-alkali syndrome Milk-alkali syndrome, an acute illness with symptoms of headache, nausea, irritability, and weakness, or a chronic illness with alkalosis, hypercalcemia and, possibly, renal impairment, has occurred following the concurrent use of high-dose calcium carbonate and sodium bicarbonate. Hypophosphatemia Prolonged use of aluminum-containing antacids may result in hypophosphatemia in normophosphatemic patients if phosphate intake is not adequate. 

Calcipotriol is a vitamin D3 derivative which is used as a topical agent in the treatment of psoriasis. Although not completely elucidated its mechanism of action seems to be based on inhibition of the proliferation and stimulation of the differentiation of epidermal keratinocytes. Adverse effects include irritation of the skin but also urticarial reactions. Calcipotriol has 100 fold less vitamin D activity as its active vitamin D3 metabolite calcitriol. However, calcipotriol in overdose can cause symptoms of hypercalcemia. 

The hypercalcemia resulting from hypervitaminosis D is responsible for toxic symptoms such as muscle weakness, bone pain, anorexia, ectopic calcification, hypertension, and cardiac arrhythmias. Toxicity in infants can result in mental and physical retardation, renal failure, and death. 

Assess the patient for signs and symptoms of hypercalcemia, including constipation, deep bone or flank pain, excessive thirst, hypotonicity of muscles, increased urine output, nausea and vomiting, and renal calculi... 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

This rather common disease, if associated with symptoms and significant hypercalcemia, is best treated surgically. Oral phosphate and bisphosphonates have been tried but cannot be recommended. Asymptomatic patients with mild disease often do not get worse and may be left untreated. The calcimimetic agent cinacalcet, discussed previously, has been approved for secondary hyperparathyroidism and is in clinical trials for the treatment of primary hyperparathyroidism. If such drugs prove efficacious, medical management of this disease will need to be reconsidered. 

Clearly, the dosage of a calcium supplement must be determined by the specific needs of each individual. Excessive doses must also be avoided because they may produce symptoms of hypercalcemia, including constipation, drowsiness, fatigue, and headache. As hypercalcemia becomes more pronounced, confusion, irritability, cardiac arrhythmias, hypertension, nausea and vomiting, skin rashes, and pain in bones and muscle may occur. Hypercalcemia is a cause for concern because severe cardiac irregularities may prove fatal. 

Idiopathic hypercalcemia of infancy was first described as such by Lightwood in 1952 (L3). In the same year Fanconi and Girardet (F2) and Schlesinger et al. (SI) described two children in whom hypercalcemia was first recognized at the age of approximately 20 months but who had exhibited symptoms at a much earlier age. In both of these children the hypercalcemia was associated with mental retardation, cranial abnormalities, and cardiac murmurs. 

In severe cases the appearance has been described as elfin, and Schles-inger et al. have indicated specific features to be prominent epicanthic folds, an overhanging upper lip and underdevelopment of the bridge of the nose and the mandible (S2). As noted above, in severe cases described in the literature there has usually been a very considerable interval—of the order of 6 months to years—between the onset of symptoms and the diagnosis of hypercalcemia. In these cases dwarfism and mental retardation have been features, osteosclerosis has been much more marked, cardiac systolic murmurs have, frequently been found, hypertension has occurred in some cases, squint has been common, and transient facial paresis has been noted. In such cases the skull circumference is usually less than normal and craniostenosis can occur. 

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