Hypercalcemia

Hypercalcemia refers to a serum calcium level higher than 2.8 mmol / l, ionized calcium higher than 1.4 mmol / l.

Hypercalcemic crisis is a life-threatening condition with a calcium higher than 4 mmol / l.

Etiology
YouTube video of hypercalcemia


 * Primary and tertiary hyperparathyroidism,
 * malignant tumors : malignant lymphomas, leukemia, osteolytic metastases, paraneoplastic expression,
 * other endocrinopathies : hyperthyroidism, Addison's disease, pheochromocytoma, acromegaly,
 * granulomatous diseases : sarcoidosis, tuberculosis, histoplasmosis, candidiasis, Wegener's granulomatosis, subcutaneous fat necrosis,
 * pharmaceuticals : thiazides, milk-alkali syndrome, cheese-alkali syndrom e, vitamin D, A intoxication, acetylsalicylic acid,
 * familial hypocalciuric hypercalcaemia,
 * Williams-Beuren syndrome,
 * Paget's disease,
 * immobilizers,
 * hypophosphatemia,
 * transplant rejection.

Clinical picture
Hypercalcemia is manifested by a wide GIT symptomatology - nausea, vomiting, metallic taste in the mouth, gastroduodenal ulcer disease, persistent constipation, pancreatitis. Within the kidney disease we find polyuria, polydipsia , nocturia , sometimes even symptoms of chronic or acute renal insufficiency. Hypercalcemia is also manifested in the CNS, we find headaches, disorders of consciousness. Neuromuscular symptoms include weakness, limb muscle pain. Cardiovascular symptoms include hypertension, arrhythmias , ECG changes ( shortening of the QT interval ). Changes on the ECG confirm the severity of hypercalcemia, which in extreme cases can also cause cardiac arrest in systole - we speak of the so-called " chemical death " at a calcium> 4 mmol / l. Other symptoms of hypercalcemia include pallor, cachectization during prolonged course and ray of the bones - a significant zone of temporary calcification, osteoporosis, metastatic calcifications.

Diagnosis
We determine the ionogram - ions: Ca, P, Na, Cl, Mg. The physiological level of serum phosphorus is 0.65–1.6 mmol infants 1.3–2.3 mmol / l. Decreased phosphorus or values ​​at the lower limit of normal are found in hyperparathyroidism and, conversely, increased phosphorus or at the upper limit of normal is found in hypervitaminosis D or thyrotoxicosis. A simple test is the S-Ca / SP ratio. If this index is> 27%, it indicates hyperparathyroidism , if it is lower, it indicates hypercalcemia from other causes. The next step is to determine ALP, including isoenzymes. Elevation of ALP in hypercalcemia indicates increased bone resorption (hyperparathyroidism, malignancy). Hyperchloremic acid-base balance for hyperparathyroidism MAC. Other detailed examinations include determination of urinary concentrations (U-Ca, UP, U-cAMP, U-citric acid), bone densitometry, determination of immunoreactive PTH. include Imaging methods wrist and forearm X-ray, S + P X-ray, parathyroid ultrasound, abdominal ultrasound, abdominal CT. The Ca / creatinine index (so-called Nordin index) from morning urine is helpful: in healthy children it is up to 0.6, in infants up to 1.0. At hypercalciuria the values ​​are higher, in hypocalciuria the value is <0.2. If sarcoidosis is suspected, we can also use the hydrocortisone test : we administer 100 mg of hydrocortisone daily for 7 days. If there is a decrease, resp. disappearance of hypercalcaemia, most likely sarcoidosis. should also be performed if hypercalcaemia is unclear Malignancy screening.

Therapy
In the treatment of acute hypercalcemia, we primarily administer saline 20 ml / kg iv within 60 minutes. The goal is hyperhydration, where we calculate the physiological daily fluid requirement as twice the norm. Following the bolus of saline, we administer the diuretic furosemide 1-2 mg / kg iv, ev. we repeat after 2-3 hours. In any case, we must carefully monitor fluid balances and consider the risk of hypokalaemia during drastic diuretic therapy. It follows from the above that in the next procedure, we supplement the circulating volume with diuresis losses and compensate for potassium losses.

A reduction in hypercalcaemia at symptomatic levels above 3 mmol / l or asymptomatic levels equal to or greater than 3.5 mmol / l is indicated. Acute dialysis is indicated, depending on the source, at levels above 4 mmol / l, possibly above 4.5 mmol / l.

persists, hypercalcemia therapy as the next step corticoid - methylprednisolone 0.5–1 mg / kg iv, not more than 50 mg / day for 7–10 days. The effect of corticoids is to antagonize vitamin D, in addition, corticoids increase calcium transport to ICT by opening calcium channels and increase calcium binding to mitochondria. The greatest therapeutic effect of corticoids can be expected in sarcoidosis and hypervitaminosis D. In addition to corticoids, ketoconazole and chloroquine (blockade of 1,25- (OH) 2 D production) also cause a decrease in intestinal calcium resorption.

Previously, the administration of phosphates (13.6% KH 2 PO 4 ), which bind calcium and reduce its bone mobilization, was also recommended. However, with current hypercalcaemia, there is a risk of calcium phosphate precipitation in parenchymal organs. We therefore prefer to avoid the phosphorus.

In severe and refractory cases, calcitonin 5–10 IU / kg / 24 hours by infusion in 2 daily doses. Concomitant administration of corticosteroids reduces the rapidly increasing resistance to calcitonin treatment. Other options are bisphosphonates (also bisphosphonates; eg etindronate, diethylene diphosphonate) 7.5 mg / kg iv over 2 hours, which are administered daily for 3-6 days. We start treatment with diphosphonates only a few hours after the hypercalcemic crisis. EDTA has 15–50 mg / kg iv within 4 hours of rarity in hypercalcemic crisis in case of severe clinical symptoms (arrhythmias, disorders of consciousness) or resistance to the above treatment. Frequency and serious side effects (nephrotoxicity) are limited. In extreme cases, hemodialysis. Fluid balance and cardiac activity should be carefully monitored as part of monitoring.

Related articles

 * Hypocalcemia
 * Disorders of calcium-phosphate metabolism
 * Bone remodeling indicators, bone resorption markers
 * Pathophysiology of bone, calcium and phosphates

Source
Category : Clinical biochemistry, Pathophysiology, Patobiochemie, Internal Medicine, Oncology, Cardiology, Video articles
 * HAVRÁNEK, J.: Dysbalance ostatních iontů.