Hypocalcemia

Hypocalcemia is a serum concentration of total calcium <8.8 mg / dl (<2.20 mmol / L) in normal plasma protein concentrations or serum concentration of ionized calcium <4.7 mg / dl (<1.17 mmol / l). The causes are hypoparathyroidism, vitamin D deficiency and kidney diseases. The clinical symptoms are paresthesias, tetany and, in severe cases, seizures, encephalopathy and heart failure. The diagnosis is the determination of the serum calcium value with adjustment for serum albumin concentration. The treatment consists of the administration of calcium and the treatment of the underlying disease. Occasionally, vitamin D is additionally administered.

(See also overview of disorders of calcium concentration and hypokalemia in newborns.)

Hypocalcemia is a serum concentration of total calcium <8.8 mg / dl (<2.20 mmol / L) in normal plasma protein concentrations or serum concentration of ionized calcium <4.7 mg / dl (<1.17 mmol / l). The causes are hypoparathyroidism, vitamin D deficiency and kidney diseases. The clinical symptoms are paresthesias, tetany and, in severe cases, seizures, encephalopathy and heart failure. The diagnosis is the determination of the serum calcium value with adjustment for serum albumin concentration. The treatment consists of the administration of calcium and the treatment of the underlying disease. Occasionally, vitamin D is additionally administered. (See also overview of disorders of calcium concentration and hypokalemia in newborns.) Etiology hypocalcemia can have many causes, including hypoparathyroidism Pseudohypoparathyroidism vitamin D deficiency and dependency Kidney Diseases Hypoparathyroidism The Hypoparathyroidism is characterized by hypocalcemia and hyperphosphatemia and often causes chronic tetany , Hypoparathyroidism results from a lack of parathyroid hormone (PTH), which in turn can result in autoimmune diseases and after accidental removal or damage to parathyroid glands during thyroidectomy. A temporary hypoparathyroidism often occurs after subtotal thyroidectomy, but a permanent hypoparathyroidism occurs 3% carried out by experienced surgeons thyroid surgery on in. " Symptoms of hypocalcemia usually show up about 24 to 48 hours after surgery. but it can take months or years. PTH deficiency is more common after radical thyroidectomy due to a tumor or after surgery to the parathyroid glands (subtotal or total parathyroidectomy). Risk factors for severe hypocalcaemia after subtotal parathyroidectomy are severity of preoperative hypercalcemia removal of a large adenoma Elevated alkaline phosphatase Chronic kidney disease idiopathic hypoparathyroidism is an unusual, sporadic or inherited condition in which the parathyroid glands are missing or atrophied. The manifestation occurs in childhood. The parathyroid glands occasionally and thymic aplasia and anomalies of the arteries of the aortic arch (DiGeorge syndrome) are missing are present. Other inheritäre forms are autoimmune polyendokrines syndromes with mucocutaneous candidiasis associated autoimmune hypoparathyroidism and X-linked recessive idiopathic Hypoparathyreoidismus.Pseudohypoparathyreoidismus As Pseudohypoparathyroidism refers to a rare group of disorders that are characterized not by a hormone deficiency, but by a target organ resistance to PTH. The genetic transmission of these disorders is complex. Type Ia Pseudohypoparathyroidism (hereditary osteodystrophy by Albright) is caused by a mutation in the ?1-stimulatory G protein of Adenylatcyclasekomplexes (GNAS1). This leads to a lack of normal response to PTH, which would be a renal phosphaturia or elevation of cAMP in urine. Patients are usually hypocalcemic and hyperphosphatemic. Secondary hyperparathyroidism and hyperparathyreoide bone disease can occur. Related disorders are short stature, a round face, decreased intelligence with calcification of the basal ganglia, shortened metacarpal and metatarsal bones, mild hypothyroidism and other subtle endocrine changes. Since only the maternal allele for GNAS1 is expressed in the kidneys, have patients whose diseased gene from the father, although many of the somatic stigmata of the disease, but no hypocalcemia, hyperphosphatemia, and not any secondary hyperparathyroidism. This fact is sometimes called pseudo-Pseudohypoparathyroidism. The type II Pseudohypoparathyroidism is less known. Affected patients have a hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism, but show none of the other associated disorders. The type II Pseudohypoparathyroidism is even more rare than type I. In affected patients exogenous PTH results in an increase of cAMP in the urine, but does not increase serum calcium levels or the phosphate concentration in urine. Intracellular cAMP is resistance to vermutet.Vitamin D deficiency and dependence vitamin D deficiency and dependence will be discussed in full elsewhere. Vitamin D is absorbed through foods that are rich in vitamin D naturally or have been fortified with vitamin D,. It is also in the skin formed as reaction to sunlight (UV light). A vitamin D deficiency may be caused by insufficient dietary intake or by decreased absorption at a hepatobiliary disease or intestinal malabsorption. A vitamin D deficiency can be caused by changes in vitamin D metabolism caused by various drugs (eg., By phenytoin, phenobarbital, rifampin), or be triggered by reduced formation in the skin due to lack of sunlight , Even at the age synthesis capacity of the skin decreases. The decreased synthesis in the skin is an important cause of the acquired vitamin D deficiency in people who spend a long time in closed rooms, who live in northern or southern climates and completely conceal their bodies or frequently use sunscreen. Accordingly, a subclinical vitamin D deficiency is widespread, especially during the winter months in temperate climates in the elderly. Older residents are particularly at risk because their skin has a reduced synthetic capacity, they are exposed to malnutrition and rarely a sunlight. Most people with a deficiency exhibit both a decreased synthesis in the skin as well as malnutrition. However, most doctors think that the considerable risks of skin cancer that has not yet proven risk of excessively low vitamin D levels predominate, therefore it is not recommended to increase the sunlight or not to use a sun block; Vitamin D supplements are available for patients with concerns are available. Vitamin D dependency arises from the inability to convert vitamin D to its active form or reduced responsiveness of the end effectors to a reasonable level of active vitamin. The type I of the vitamin D-dependent rickets (pseudo vitamin D deficiency rickets) is an autosomal recessive disorder that lies a mutation in the gene coding for the enzyme 1-alpha-hydroxylase is based. The 1-alpha-hydroxylase, which is normally expressed in the kidneys, is used to convert inactive vitamin D to the active form calcitriol. In type II vitamin D-dependent rickets the target organs can not respond to calcitriol. Vitamin D deficiency, hypocalcemia, and severe hypophosphatemia are the result. Muscle weakness, pain and the typical bone deformities part of the symptoms. Kidney disease renal tubular diseases, including acquired proximal renal tubular acidosis caused by nephrotoxins (e.g., as by heavy metals, especially cadmium) is caused, and the distal renal tubular acidosis, produce severe hypocalcaemia. This is caused by a pathological renal loss of calcium and a decreased renal conversion of vitamin D to the active 1,25 (OH) 2D. Renal failure may lead to a reduced formation of 1,25 (OH) 2D cause due to Direct cell damage of the kidneys Suppression of 1-alpha-hydroxylase (for vitamin D conversion required) of by hyperphosphatemia Other reasons Other causes of hypocalcaemia Magnesiumdepletion are ( can cause a relative PTH deficiency and a Endorganresistenz to PTH, usually when serum magnesium levels are <1.0 mg / dl [<0.5 mmol / l]; magnesium substitution increases PTH levels and improved renal calcium conservation) Acute pancreatitis (if from the inflamed pancreas liberated products of lipolysis calcium chelates) hypoproteinemia (reduces the protein-bound part of the serum calcium; hypocalcemia due to decreased protein binding is asymptomatic - because ionized calcium is unaffected, as this state was spurious Hypocalcemia called) syndrome of hungry bone (persistent hypocalcemia and hypophosphatemia after surgical or medical correction of medium to severe hyperparathyroidism in patients whose serum calcium concentrations has been supported by a high bone turnover, which was induced by highly elevated PTH - a syndrome hungry bone was by parathyroidectomy, after renal transplantation, and only rarely in patients with end stage renal disease, who were treated with calcimimetics described) septic shock ((by suppression of PTH release and decreased conversion of 25 (OH) D to 1.25 OH) 2D cause) hyperphosphatemia (via largely unknown mechanisms to hypocalcemia; Patients with renal failure and subsequent phosphate retention are particularly vulnerable) drugs, including anti-epileptic drugs (eg., Phenytoin, phenobarbital) and rifampicin that affects vitamin D metabolism, and medicines for the treatment of hypercalcemia transfusion of> 10 units of citrate-anticoagulated blood and use of X-ray contrast agents that the divalent ion-chelating agent ethylene diamine tetraacetate (EDTA; it can reduce the concentration of bioavailable ionized calcium, while the total serum calcium concentrations remain unchanged) containing infusion of gadolinium (can apparently reduce the calcium concentration) Although one might expect, that the excessive secretion of calcitonin results in a Kalzämie, did calcitonin has little effect on serum calcium. For example, low serum calcium levels rarely occur in patients with high levels of circulating calcitonin due to a medullary thyroid cancer does not occur. Symptoms and complaints Hypocalcaemia runs often asymptomatic. Evidence of the existence of hypoparathyroidism stem more from the clinical manifestations of the underlying disease (eg. As short stature, round face, decreased intelligence, calcification of the basal ganglia in Type Ia Pseudohypoparathyroidism). The major clinical manifestation of hypocalcemia is characterized by disturbances of cellular membrane potential, which leads to neuromuscular irritability. Typical neurological manifestations include muscle spasms of the legs and back. A creeping hypocalcemia can trigger a light, diffuse encephalopathy. This should be considered in patients with unexplained dementia, depression or psychosis. Occasionally papilledema is observed. A severe hypocalcemia with serum calcium levels of <7 mg / dl (<1.75 mmol / L) may result in hyperreflexia, tetany, laryngospasm and generalized seizures. Tetany is characteristically initiated by the hypocalcemia, but may be caused to ionized calcium in the serum without the presence of hypocalcemia by a reduction in the fraction z. Ie as part of alkalosis, at a hyperventilation. Tetany is characterized by: Sensory symptoms consisting of paresthesias of the lips, tongue, fingers and feet Karpopedalspasmen that can be long lasting and painful Generalized muscle pain spasms of the facial muscles tetany can obviously be latent with spontaneous symptoms or. In the latter case it takes a provocative tests to elicit them. Latent tetany occurs (1.75-2.20 mmol / l) at less severe calcium deficiency with serum calcium concentrations in the range of 7-8 mg / dl. The Chvostek- and Trousseau signs are to be triggered for the identification of latent tetany very easy on the patient. The Chvostek sign is an irrepressible twitching of the facial muscles, which is triggered by tapping on the facial nerve on the cheek in front of the ear. It appears at ? 10% of all healthy and in most patients with acute hypocalcemia, but is not detectable unfortunately for chronic hypocalcemia often. The Trousseau character is the triggering of Karpalspasmen by the inhibition of blood flow to the hand by means of a tourniquet, or a blood pressure cuff is inflated to 20 mmHg for 3 minutes over the systolic blood pressure on the forearm. The Trousseau sign also occurs in alkalosis, hypomagnesemia, hypokalemia and 6% of healthy subjects with no electrolyte imbalance auf.Andere manifestations in the setting of chronic hypocalcemia occurred many other disorders such. As a dry, flaky skin, brittle nails and brittle hair on. Candida infections can occasionally be seen in the context of hypocalcemia, but typically occur in an idiopathic hypoparathyroidism. Cataracts develop during prolonged hypocalcemia and are not reversible even after correction of serum calcium levels. Diagnostic assessment or determination of ionized calcium (the physiologically active form of calcium) Occasionally further tests, including measurement of magnesium, PTH, phosphate, alkaline phosphatase and vitamin D concentrations in blood as well as cAMP and phosphate concentrations in the urine can hypocalcemia in patients are accepted with characteristic neurological manifestations or cardiac arrhythmias, but is often discovered as an incidental finding. Hypocalcemia is referred to <8.8 mg / dl (<2.20 mmol / l) at a total serum calcium levels. Since a reduction of plasma proteins to the lowering of the total calcium concentration, but not necessarily also to decrease the amount of ionized calcium may result in the serum, the amount should be judged to ionized calcium in function of the albumin concentration (estimation of the concentration of ionized calcium). Suspicion of a reduction in the ionized calcium requires a direct measurement, even when normal values ??for the total concentration of calcium present. A serum-ionized calcium concentration <4.7 mg / dl (<1.17 mmol / l) is low. Hypocalcemic patients should be subjected to an investigation of renal function. In the laboratory, BUN, creatinine, serum phosphate, magnesium and alkaline phosphatase be determined. Estimating the concentration of ionized calcium The concentration of ionized calcium can be assessed by routine laboratory tests usually with sufficient accuracy. In Hypoalbuminemia the measured serum calcium level is low often, which is mainly an expression of a low concentration of protein-bound calcium, while ionized calcium may be normal. The measured total serum calcium takes g per 1 / dl off or zugenommenem albumin to about 0.8 mg / dl (0.2 mmol / l) or off. Thus, it should reduce the measured serum calcium value of 1.6 mg / dl (0.4 mmol / l) an albumin concentration of 2.0 g / dl (normal value 4.0 g / dl). Accordingly, an increase in the serum proteins, as occurs in multiple myeloma, increasing the total serum calcium level. Acidosis increased ionized calcium by reduced protein binding, while a alkalosis ionized calcium decreased. Clinical Calculator: Calcium Correction in Hypoalbuminemia clinical computer: Calcium Correction in hypoalbuminemia (SI units) If no cause is obvious (. Eg alkalosis, renal failure, drug or massive blood transfusion), further testing is required (see table: Typical laboratory findings in diseases hypocalcaemia). Additional tests begin with the determination of serum concentrations of magnesium, phosphate, PTH, alkaline phosphatase and sometimes vitamin D levels (25 (OH) D and 1,25 (OH) 2D). Phosphate and cAMP concentrations in the blood are measured in suspected pseudohypoparathyroidism. The PTH concentration should be determined with an assay for the intact molecule. Because hypocalcemia is the main stimulus of PTH secretion, PTH should normally increases in response in hypocalcemia. So low or low-normal PTH levels are suggestive of a hypoparathyroidism. A non-measurable PTH levels indicates an idiopathic hypoparathyroidism. A high PTH concentration is an indication of a pseudohypoparathyroidism or a disturbance of vitamin D metabolism. A hypoparathyroidism is the further characterized by a high serum phosphate and normal values ??for alkaline phosphatase. In type I-pseudohypoparathyroidism in spite of an increased concentration of circulating PTH cAMP and phosphate in urine are missing. A challenge test in which a parathyreoidaler extract or recombinant human PTH is injected, does not increase the cAMP content in serum and urine. Patients with type Ia Pseudohypoparathyroidism have very often skeletal deformities such. B. metacarpale a small stature and a shortening of the first, fourth and fifth Os. Patients with type Ib disease show renal manifestations without skeletal deformities. When vitamin D deficiency osteomalacia or rickets may be, usually with typical skeletal abnormalities on radiographs. The diagnosis of vitamin D deficiency and dependence and the measurement of vitamin D concentrations will be discussed elsewhere. Typical laboratory results in diseases surgical hypocalcaemia disorder finding hypoparathyroidism PTH low or low-normal PO4 normal serum or high PO4 in urine low serum alkaline phosphatase normal idiopathic hypoparathyroidism PTH not measurable PO4 serum high PO4 in urine low serum alkaline phosphatase normal type Ia pseudohypoparathyroidism (hereditary osteodystrophy by Albright) PTH hoc h PO4 in serum highly No cAMP in urine or PO4 excretion increased, even after injection of parathyroid extract or PTH skeletal and other abnormalities type 1b-Pseudohypoparathyroidism PTH increased high PO4 in serum highly No cAMP in urine or PO4 excretion, also after injection of parathyroid extract or PTH No skeletal abnormalities type II pseudohypoparathyroidism PTH high PO4 in serum highly No cAMP or PO4 in the urine injection of PTH increases cAMP in the urine, but not PO4 urinary vitamin D concentrations normal or high vitamin D PTH deficiency high PO4 in serum alkaline phosphatase low high 25 (OH) D * low hereditary vitamin D-dependent rickets type I PTH high PO4 low serum alkaline phosphatase high X-ray evidence of rickets 25 (OH) D in the serum of normal 1,25 (OH) 2D in serum low hereditary vitamin D-dependent rickets type II PTH high PO4 low serum alkaline phosphatase high X-ray evidence of rickets 25 (OH) D in the serum of normal or high 1,25 (OH) 2D normal or high * The measurement of serum -25 (OH) D and 1,25 (OH) 2D may be helpful to distinguish between a vitamin D-deficient and vitamin D-dependent to distinguish n states. 1,25 (OH) 2D 1,25-dihydroxycholecalciferol or = calcitriol; 25 (OH) D = inactive vitamin D; PO4 = phosphate, PTH = parathyroid hormone. A severe hypocalcemia may affect the ECG. The ECG typically shows a prolongation of the QTc and the ST interval. Changes in the repolarization phase such. As an inversion or worsening of the T wave, can also be observed. The ECG may show an arrhythmia or cardiac block formation in patients with severe hypocalcemia. However, a study on isolated hypocalcemia does not require the creation of an EKG. Intravenous treatment with calcium gluconate tetany Oral calcium postoperatively hypoparathyroidism oral calcium and vitamin D in chronic tetany hypocalcemia Upon the occurrence of tetany, 10 ml of a 10% Kalziumglukonatlösung over 10 minutes i.v. administered. The improvement may be impressive, but may only last for a few hours. Repeated bolus doses or continuous, over the next 24 h lasting infusion of 1 liter of a 5% dextrose solution, 20-30 mL of 10% calcium gluconate were added, may be necessary. Calcium infusions may occur in patients who are receiving Glykosidtherapie, cause damage and should be carried out slowly and under continuous ECG monitoring to test for hypokalemia. If a tetany is associated with a hypomagnesemia, it can temporarily respond to the administration of calcium, or potassium; a lasting improvement is, however, only be achieved by a substitution of magnesium, usually with 10% of magnesium sulfate (MgSO4-) solution (1 g / 10 ml) iv followed by magnesium salts orally (z. B. magnesium gluconate 500-1000 mg po 3 times daily). Tips and risks calcium infusions may occur in patients who are receiving Glykosidtherapie, cause damage and should be carried out slowly and under continuous ECG monitoring to test for hypokalemia. Transient hypoparathyroidism When transient hypoparathyroidism after a thyroid surgery or partial parathyroidectomy oral calcium substitution is sufficient: It can 1-2 grams of elemental daily calcium as calcium gluconate (90 mg elemental calcium / 1 g) or calcium carbonate (400 mg elemental calcium / 1 g) become. Hypocalcaemia may run particularly heavy and prolonged after subtotal parathyroidectomy particularly in patients with renal disease or in patients where a large tumor was removed. Postoperatively, a prolonged parenteral calcium administration may be necessary. I.v. Substitution with amounts of up to 1 g of calcium (z. B. 111 ml of calcium gluconate, the 90 mg of elemental calcium / 10 ml contains) per day for 5-10 days may be required before an oral calcium and vitamin D supplementation sufficient is. Increased serum alkaline phosphatase may indicate a rapid absorption of calcium in the bones in such patients. 1-2 may Daily g: the need for large amounts of parenteral calcium does not decrease as long as the concentrations of alkaline phosphatase increased sind.Chronische hypocalcemia In chronic hypocalcemia, substitution of oral Calcium and occasionally vitamin D supplementation is usually sufficient elemental calcium as calcium gluconate or calcium carbonate are added. In patients without renal failure Vitamin D is given as an oral standard substitution (eg., 800 IU of cholecalciferol 1 times / day). A vitamin D therapy is not effective, if not sufficient quantities of calcium and phosphate (hypophosphatemia: treatment) are taken with food or as a medicament. In patients with renal calcitriol or another 1,25 (OH) 2D analog is used because it requires by the kidney, these drugs any metabolic change. Patients with hypoparathyroidism have difficulty in converting cholecalciferol to its active form and usually need also calcitriol, usually 0.5-2 mcg p.o. 1 time / day. Pseudohypoparathyroidism can be treated with oral sometimes alone Kalziumsubsitution. This requires Calcitrioldosen of 1-3 mcg / day. Among the vitamin D analogues (usually 0.8-2.4 mg po 1 time / day for several days, then 0.2-1.0 mg 1 times / day) include dihydrotachysterol and Salcidiol (eg . B. 4000-6000 IU po 1 times / week). In the application of vitamin D analogues, especially when longer acting calcidiol, a vitamin D poisoning with severe symptomatic hypercalcemia may be a complication. Serum calcium levels should be measured 1 time determined in the week. When the calcium levels have stabilized, a measurement at an interval of 1-3 months is sufficient. The maintenance dose of calcitriol or its analog dihydrotachysterol usually decreases over time. Summary causes of hypocalcemia are hypoparathyroidism, pseudohypoparathyroidism, vitamin D deficiency and kidney failure. A mild hypocalcemia may be asymptomatic or cause muscle cramps. Severe hypocalcemia (serum calcium levels <7 mg / dL [<1.75 mmol / L]) can hyperreflexia, tetany (paresthesias of the lips, tongue, fingers and feet, Karpopedal- and / or facial spasms, muscle pain) or generalized seizures lead , The diagnosis is made by means of estimation or determination of ionized (not all) of serum calcium. Normally, the serum concentrations of magnesium, phosphate, PTH, alkaline phosphatase, and occasionally vitamin D levels are determined. Calcium gluconate iv can be given to patients with tetany; the other patients are treated with oral calcium supplementation.

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