Download - 46 Electrolytes
Hypocalcaemia
Links : http://www.diseasesdatabase.com/links1.asp?glngUserChoice=6412
"Reduction of the blood calcium below normal. Manifestations include
hyperactive deep tendon reflexes, Chvostek's sign, muscle and
abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)"
Hypocalcaemia may be caused by or feature of the following ... _ Artifacts
Citrated blood sample
EDTA blood sample
Oxalate blood sample
Miscellaneous syndromes
Malabsorption syndrome
Osteomalacia
Proximal renal tubular acidosis
Renal failure, acute
Renal failure, chronic
Rhabdomyolysis
Biochemical abnormalities
Hyperphosphataemia
Hypomagnesemia
Mendelian inherited conditions
Kenny-Caffey-Linarelli syndrome
Autosomal dominant conditions
Osteopetrosis (malignant)
Pseudohypoparathyroidism type 1a
Pseudohypoparathyroidism type 1b
Autosomal recessive conditions
Cystinosis
Intestinal hypomagnesemia type 1
Metaphyseal dysplasia
Osteopetrosis (malignant)
Vitamin D dependent rickets type 1
Vitamin D dependent rickets type 2a
Nutritional conditions
Cow milk, baby feed
Malabsorption syndrome
Vitamin D deficiency
Endocrine conditions
Hyperparathyroidism, secondary
Hyperthyroidism
Hypoparathyroidism
Inflammatory conditions
Pancreatitis, acute
Bacteria and bacterial conditions
Neisseria meningiditis
Iatrogenic conditions
Blood transfusion and complications
Tumor lysis syndrome
Chemicals
Ethylene glycol
Drugs, hormones and mediators
Actinomycin D
Alendronate
Bumetanide
Cinacalcet
Dasatinib
Edetate disodium
Ethotoin
Foscarnet
Frusemide
Gallium nitrate
Mithramycin
Pamidronate
Phenytoin
Paraneoplastic AutoantibodiesParathyroid HormoneParathyroid Hormone IntroperativeParathyroid Related ProteinParietal Cell AntibodiesParoxysmal Nocturnal HemoglobinuriaPartial Thromboplastin TimeParvovirus B19 AntibodiesPenicillin AntibodyPeptide Nucleic Acid FISH for Blood
Culture IdentificationPernicious AnemiapHPhenobarbitalPhenytoinPhosphatidyl GlycerolPhosphorusPlasma Cell Enumeration by Flow
CytometryPlastic Blood Collection TubesPlatelet AggregationPlatelet AntibodyPlatelet CountPlatelet Function ScreenPneumococcus Urine AntigenPneumocystisPolycythemiaPorphyrinsPotassium SerumPotassium UrinePrealbuminPregnancy TestPreoperative Hemostasis TestingPreoperative TestingPrimidoneProcainamide & NacetylprocainamideProgesteroneProinsulinProlactinProstate Specific AntigenProstate Specific Antigen FreeProtein CProtein ElectrophoresisProtein Electrophoresis Spinal FluidProtein Electrophoresis UrineProtein SProtein Total SerumProtein Total Spinal FluidProtein Urine QuantitativeProthrombin Gene MutationProthrombin TimeProthrombin Time Significant ChangePsoriasis & T Cell MonitoringPTT or Plasma Thromboplastin TimePyruvate Kinase Screen RBC
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Potassium Serum
Potassium is the major intracellular cation, with a 20 fold greater concentration in the cellsthan in the extracellular fluid. Only 2% of total body potassium circulates in the plasma. Thesodium potassium ATPase pump is largely responsible for maintaining this important ratio. Thekidneys are also important in regulating potassium balance. Proximal tubules reabsorb nearlyall of the filtered potassium. Under the influence of aldosterone, additional potassium issecreted by the distal tubules and collecting ducts in exchange for sodium. Maintaining normalpotassium levels is important for regulation of neuromuscular excitability, cardiac contractilityand rhythm, extracellular volume, and acid base balance.
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Hypokalemia is defined as a plasma potassium concentration less than 3 meq/L. The primarymechanisms are excessive GI or urinary loss of potassium, increased cellular uptake, orinadequate dietary intake. GI loss results from vomiting, diarrhea, gastric suction, or intestinalfistula discharge. Diuretics, such as thiazides and furosemide, promote potassium secretion inthe distal tubules. Kidney disorders, such as renal tubular acidosis, cause excessive urinary lossof potassium. Hyperaldosteronism leads to excessive urinary secretion of potassium andmetabolic acidosis. Hypomagnesemia causes hypokalemia by promoting both urinary and fecalloss of potassium. Magnesium deficiency diminishes sodium potassium ATPase activity andenhances aldosterone secretion. Alkalemia and insulin are the two major causes of increasedcellular uptake of potassium. Alkalemia promotes intracellular loss of hydrogen ion. Topreserve electroneutrality, both potassium and sodium enter cells. Plasma potassium decreasesby 0.4 meq/L for every 0.1 unit rise in pH. Insulin promotes the entry of potassium into muscleand hepatocytes. Reduced dietary intake of potassium is a rare cause of hypokalemia, but maybe an important factor in patients taking diuretics.
Hyperkalemia occurs frequently in hospitalized patients with a reported incidence of 1 to 10%.A recent article investigated the causes of 242 episodes of hyperkalemia in 206 inpatients atthe University of Pittsburgh Medical Center between February 15 and June 30, 1996 (ArchIntern Med 1998; 158: 917-24). Hyperkalemia was defined as a critical plasma potassium levelof 6 meq/L or more. The incidence of hyperkalemia in this study was 2.3%. Approximately 2hyperkalemic episodes occurred per day during the study period. Most of the elevatedpotassium levels fell between 6.0 and 7.1 meq/L, but a few values were as high as 9.0 meq/L.Further investigation revealed that most cases of hyperkalemia were multifactorial in origin.
Cause % of Cases
Renal failure 77
Hyperglycemia 49
Potassium supplements/ TPN 15
Medications 63
Cyclosporine/ Tacrolimus 27
Beta Blockers 17
Trimethoprim 15
ACE inhibitors 15
Digoxin 14
NSAID 9
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K sparing diuretics 5
Heparin 5
Amphotericin 2
Succinylcholine 2
Pentamidine 1
Penicillin G 1
RBC transfusion 10
Rhabdomyolysis 5
Renal failure was present in more than two thirds of the patients. Hyperglycemia was thesecond most common contributor to hyperkalemia. Medications contributed to the developmentof hyperkalemia in 63% of cases. The drugs most often implicated are listed in the table.Heparin causes hyperkalemia by suppressing aldosterone.
Another recent study revealed that 194 of 1818 (11%) medical outpatients using angiotensinconverting enzyme (ACE) inhibitors developed hyperkalemia, which was defined as a potassiumlevel above 5.1 meq/L (Arch Intern Med 1998; 158:26-32). The majority of patients hadpotassium levels between 5.1 and 5.5 meq/L, but one fifth of the patients had higher levels.Independent risk factors for developing hyperkalemia included a serum creatinine level above1.5 mg/dL, BUN greater than 18 mg/dL, congestive heart failure, and the use of long actingACE inhibitors. Patients over the age of 70 with a BUN of 25 mg/dL or higher were more likelyto develop severe hyperkalemia (potassium > 6.0 meq/L).
Hyperkalemia can cause muscle weakness by decreasing the ratio of intra to extracellularpotassium, which alters neuromuscular conduction. Muscle weakness does not usually developuntil plasma potassium reaches 8 meq/L. Hyperkalemia disturbs cardiac conduction, which cancause arrhythmias. Plasma potassium levels between 6 and 7 meq/L may alter the ECG, whilelevels greater than 10 meq/L may precipitate cardiac arrest.
Factitious causes of hyperkalemia include:
In vitro hemolysisTraumatic phlebotomyToo small bore of needleButterfly needle w/ excessive syringe pressureVacutainer tubes placed directly on large bore catheterCollection with syringe and injection into Vacutainer tubesElevated platelet count0.15 mEq/L increase for every 100,000 cells/uL increaseElevated leukocyte countContamination with IV fluidsContamination with anticoagulant (K3EDTA concentration exceeds 15 mEq/L)Aged specimensMore accelerated at 4oC than at 25oCSerum sitting on clotRespun serum separator tube
Plasma is the preferred specimen for patients with platelet counts greater than 600,000/uL.Erroneously high potassium results are also produced by centrifugation of SST tubes in fixedangle centrifuges. Under these conditions, the separation gel does not form a complete barrierand potassium leaks out of red blood cells into the plasma during specimen storage.
Reference range is 3.6 to 5.0 mEq/L (Vitros analyzer). Levels < 3.0 and > 6.0 mEq/L areconsidered critical values. Serum potassium levels run slightly higher (0.4 mEq/L) than plasmalevels, even in patients with normal platelet counts.
Specimen requirement is one SST tube of blood. Hemolysis should be avoided because it willcause false elevation of potassium.
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Paraneoplastic AutoantibodiesParathyroid HormoneParathyroid Hormone IntroperativeParathyroid Related ProteinParietal Cell AntibodiesParoxysmal Nocturnal HemoglobinuriaPartial Thromboplastin TimeParvovirus B19 AntibodiesPenicillin AntibodyPeptide Nucleic Acid FISH for Blood
Culture IdentificationPernicious AnemiapHPhenobarbitalPhenytoinPhosphatidyl GlycerolPhosphorusPlasma Cell Enumeration by Flow
CytometryPlastic Blood Collection TubesPlatelet AggregationPlatelet AntibodyPlatelet CountPlatelet Function ScreenPneumococcus Urine AntigenPneumocystisPolycythemiaPorphyrinsPotassium SerumPotassium UrinePrealbuminPregnancy TestPreoperative Hemostasis TestingPreoperative TestingPrimidoneProcainamide & NacetylprocainamideProgesteroneProinsulinProlactinProstate Specific AntigenProstate Specific Antigen FreeProtein CProtein ElectrophoresisProtein Electrophoresis Spinal FluidProtein Electrophoresis UrineProtein SProtein Total SerumProtein Total Spinal FluidProtein Urine QuantitativeProthrombin Gene MutationProthrombin TimeProthrombin Time Significant ChangePsoriasis & T Cell MonitoringPTT or Plasma Thromboplastin TimePyruvate Kinase Screen RBC
Potassium Urine
In healthy individuals, nearly all potassium filtered by the kidney is reabsorbed. Potassiumexcretion reflects distal tubule secretion of potassium, which is stimulated by aldosterone andthe rate of potassium entry into the plasma from the diet and from cells. Urine potassiumlevels are generally helpful only in evaluation of patients with unexplained hypokalemia. Urinepotassium levels between 0 and 10 mEq/L suggest the GI tract is the source of potassium loss,while levels >10 mEq/L suggest renal potassium loss.
Reference range is 25 - 123 mEq/24 hr.
Specimen requirement is a 24-hour urine collection in a container without preservative.Specimen should be refrigerated during and after the collection.
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Calcium Ionized
Low ionized calcium levels are common in critically ill patients with sepsis, renal failure, cardiacfailure, pulmonary failure, post-surgery or burns. Monitoring of ionized calcium is particularlyimportant in the unconscious or anesthetized patient, in whom unrecognized changes incalcium homeostasis may result in serious cardiovascular dysfunction with little of no priorwarning signs. Decreased ionized calcium levels between 3 and 4 mg/dL are usually welltolerated, but the risk of cardiac arrest increases when ionized calcium levels approach 2.5mg/dL. An ionized calcium level below 2.8 mg/dL is a reasonable threshold to begin calciumreplacement therapy. Patients with hypotension or low cardiac output may require calciumreplacement when ionized calcium falls below 3.2 to 3.6 mg/dL. Replacement therapy shouldbe monitored with Ionized calcium levels.
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Measurement of ionized calcium may also be helpful in evaluating neonatal hypocalcemia, andfor monitoring hypo- or hypercalcemia associated with malignancy and pancreatitis. Ionizedcalcium is valuable in establishing a diagnosis of hyperparathyroidism, especially in borderlinecases where total calcium levels may be normal but ionized calcium increased.
In these clinical situations, total calcium is often difficult to interpret or misleading due todecreased albumin and other proteins, acid-base disturbances, and transfusion of citratedblood. Alterations in serum albumin during an acute illness may change the total serumcalcium by as much as 30%. Nomograms and formulas for indirect prediction of free calciumlevels are inaccurate and may under-diagnose hypocalcemia. The percentage of protein boundcalcium may vary from 30 to 50% during illness. Acute acidosis decreases protein binding,while acute alkalosis increases it. Free fatty acids often increase during illness and afteradministration of heparin, isproterenol and insulin. They increase calcium binding to albumin.Changes in the concentration of anions such as phosphate, bicarbonate, and citrate alsochange ionized calcium levels. Transfusion of large numbers of blood components, containingexcess citrate, may chelate calcium. Total calcium levels may only be slightly decreased, eventhough ionized calcium levels are markedly decreased.
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Reference range is 4.5 - 5.3 mg/dL. Critical values are < 3.5 mg/dL and >6.5 mg/dL.
Specimen requirement is one SST tube of blood. Tourniquet time should not exceed oneminute. The tube must remained capped and should be transported in wet ice. Hemolysis willfalsely lower ionized calcium values.
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Calcium, Total
Plasma calcium exists in the blood in three forms; 50% is ionized, 40-45% is protein bound,and 5-10% is complexed to anions such as bicarbonate, citrate, sulfate, phosphate, andlactate. Plasma ionized calcium is the biologically active moiety. Total calcium levels aremaintained between 8.8 and 10.2 mg/dL. Parathyroid hormone and vitamin D regulate normalplasma calcium levels by their actions on kidney, intestine, and bone ion transport.
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The main causes of hypercalcemia are primary hyperparathyroidism, malignant disease, andchronic renal failure. The differential diagnosis of hypercalcemia depends on the clinical setting.Overall, primary hyperparathyroidism and malignancy account for 80 - 90% of hypercalcemiacases. However, primary hyperparathyroidism is the cause of ~60% of ambulatory cases andof ~25% of inpatient cases, whereas malignancy causes ~35% of ambulatory cases and 65%of inpatient cases.
Malignancies can raise serum calcium levels by either direct bone destruction or secretion ofcalcemic factors. Patients with squamous cell carcinoma of the lung, metastatic breast cancer,multiple myeloma, and renal cell carcinoma are most prone to hypercalcemia. These tumorsmay produce PTH related protein (PTH-rp) which binds to PTH receptors, but is not detected bystandard intact PTH immunoassays. Specific assays for PTH-rp are available.
The prevalence of hyperparathyroidism in the general population is 1 to 2 cases per 1000people, but is more frequent in the elderly and in women. The most common pathologicallesion is a single parathyroid adenoma (85% of cases) or chief cell hyperplasia (10%).Parathyroid carcinoma occurs in 1 to 3% of cases. Hyperparathyroidism also occurs in multipleendocrine neoplasia type 1 and 2A. Patients identified by laboratory screening are commonlyasymptomatic. Presentation with kidney stones is unusual today, but 5% of patients withkidney stone disease have primary hyperparathyroidism. Finding an elevated PTH level in apatient with hypercalcemia makes the diagnosis.
The signs and symptoms of hypercalcemia are summarized in the following table.
Mental Neurological & Skeletal GI & Urological
Fatigue Reduced muscle tone Nausea
Obtundation Muscle weakness Vomiting
Apathy Myalgia Polyuria
Lethargy Pain Polydipsia
Confusion Deep tendon reflexes Dehydration
Disorientation Anorexia
Coma Constipation
Evaluation of hypercalcemia usually begins with measurement of total calcium. If total calciumis markedly elevated, an ionized calcium level is usually not needed. Slightly to moderatelyelevated total calcium should be confirmed by measurement of ionized calcium. The patient'shistory may indicate the cause, such as; immobilization for more than a week, drug therapy,hyperthyroidism, adrenal insufficiency, or familial hypocalciuric hypercalcemia. If time permits,
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total calcium levels should be repeated two more times to rule out a transient cause ofhypercalcemia before undertaking a complete work-up. If hypercalcemia is still evident, serumalbumin and total protein should be determined. Calcium levels should be corrected forelevated albumin levels (see below). If total protein is high, but albumin is normal or low, amonoclonal gammopathy should be ruled out by serum protein electrophoresis. Serumchloride, phosphorus and intact PTH are also useful in diagnosing the most frequent causes ofhypercalcemia; malignancy and hyperparathyroidism. Serum chloride is mildly elevated inprimary hyperparathyroidism.
Test Hyperparathyroidism Malignancy
Total calcium (mg/dL) <12.4 >12.4
Chloride (meq/L) >103 <103
Phosphorus normal to low normal
Chloride : phosphorus ratio 29 or greater <29
Intact PTH elevated suppressed
PTH-rp normal elevated
Calcitriol elevated low
Hypocalcemia most commonly results from PTH deficiency or failure to produce 1,25 dihydroxyvitamin D. The most common causes of hypoparathyroidism are parathyroid or thyroid surgeryand parathyroid infiltration by cancer, sarcoid, amyloid or hemochromatosis. Acute illnessessuch as pancreatitis, hepatic failure, sepsis, and various medications can also causehypocalcemia. The normal response to a fall in the plasma ionized calcium level is increasedPTH secretion and 1,25 dihyroxy vitamin D synthesis, leading to increased calcium absorptionfrom the intestine and increased resorption from bone and kidneys.
Some drugs are associated with hypocalcemia. Gentamicin and cisplatin cause renalmagnesium loss, which leads to hypocalcemia. Heparin therapy releases fatty acids that bindcalcium ions and cause transient hypocalcemia. Anticonvulsants such as dilantin andphenobarbital induce the microsomal oxidase pathway which accelerates inactivation of vitaminD. Loop diuretics such as furosemide enhance renal calcium excretion. Phosphate salts bind upcalcium ions causing hypocalcemia.
The laboratory evaluation of a low total plasma calcium level should include measurement ofionized calcium, magnesium, and phosphorus levels. Low ionized calcium rules out artefactualcauses of hypocalcemia, such as hypoalbuminemia. Abnormally high or low magnesium levelsshould be excluded because they can inhibit PTH secretion. A low serum phosphorus level isconsistent with vitamin D deficiency, while a high level suggests chronic renal failure orpseudohypoparathyroidism. Measurement of intact PTH levels helps to differentiate betweenconditions caused by PTH and vitamin D defects. The demonstration of an inappropriately lowintact PTH level in the presence of hypocalcemia is consistent with the diagnosis ofhypoparathyroidism. Serum 25-hydroxyvitamin D levels can be measured to confirm vitamin Ddeficiency.
Total calcium levels are effected by changes in plasma protein concentrations. Most of theprotein bound fraction of calcium is bound to albumin; each 1 g/dL of albumin binds 0.8 mg/dLof calcium. Three formulas have been used to correct calcium for decreased serum albuminlevels:
%Calcium bound = 8 (albumin) + 2(globulin) + 3
Corrected calcium = measured Calcium /0.6 + [total protein/8.5]
Corrected calcium = Calcium - albumin + 4
Each formula will give a slightly different value for corrected calcium. A better approach is todirectly measure ionized calcium levels.
Two of the four approved gadolinium based magnetic resonance (MR) imaging contrast agents,gadodiamide (Omniscan) and gadoversetamide (OptiMARK), have recently been shown tointerfere with calcium measurements on some chemistry analyzers, resulting in falsely lowvalues. Patients with normal renal function may have spuriously low calcium measurements upto 24 hours after administration of these contrast agents, but patients with renal insufficiencymay be affected for up to 4.5 days. However, the Vitros chemistry analyzers used throughoutthe Saint Luke's Health System are not adversely affected (Am J Clin Pathol 2004;121:282-92).
Reference range is 8.8 - 10.2 mg/dL. Calcium levels less than 6.0 mg/dL or greater than 13.0mg/dL are considered critical values.
Specimen requirement is one SST tube or one green top (heparin) tube of blood. Prolongedvenous stasis should be avoided because it can produce artefactual hypercalcemia.
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Acid and BaseDisorders
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PotassiumDisorders
Urine CalciumAka: Hypercalciuria, Hypocalciuria
I. NormalA. Women: Urine
Calcium <250 mgper 24 hours
B. Men: UrineCalcium <300 mgper 24 hours
II. IncreasedA. Associated
Hypercalcemia1. Primary
Hyperparathyroidism2. Hypervitaminosis D3. Sarcoidosis4. Bone metastases5. Multiple Myeloma6. Corticosteroids7. Prolonged immobilization8. Paget's Disease
B. No Associated Hypercalcemia1. Increased Calcium intake2. Idiopathic hypercalciuria3. Renal tubule acidosis4. X-Linked Hypercalciuria (Dent's Disease)
III. DecreasedA. HypoparathyroidismB. Pseudo-HypoparathyroidismC. Vitamin D DeficiencyD. Low Calcium dietE. Familial hypocalciuric HypercalcemiaF. Renal osteodystrophyG. Medications
1. Thiazide Diuretics2. Oral Contraceptives
Hypercalciuria (C0020438)
Definition(CSP)
abnormally high calcium in the urine; may be due tohyperabsorption of calcium, with the formation ofcalcium oxalate or calcium phosphate renal stones.
Definition(MSH)
Excretion of abnormally high level of CALCIUM in theURINE, greater than 4 mg/kg/day.
Concepts Disease or Syndrome (T047)
Pathology andLaboratory Medicine
Chapter
A-a GradientABG InterpretationAnion GapArterial Blood GasBase ExcessCalculated PaCO2Excess Anion GapFractional Excretionof BicarbonatePaO2Urinary Anion Gap
Serum CalciumUrine Calcium
Serum ChlorideUrine Chloride
Fluid Deprivation TestHare-Hickey Test
Serum Magnesium
HyperuricemiaSerum AldolaseUric AcidUrine Uric Acid
Blood Urea NitrogenCreatinine ClearanceRenal FunctionSerum CreatinineUrine Creatinine
Serum Phosphorus
Fractional Excretionof PotassiumSerum PotassiumTranstubularPotassium Gradient
MacrocytosisMagnesiumMalaria Blood SmearManganeseMean Platelet VolumeMenorrhagia Coagulation WorkupMercuryMetanephrines for PheochromocytomaMetapneumovirusMethanol PoisoningMethemoglobinMethicillin Resistant Staphylococcus
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Magnesium
Magnesium is the fourth most abundant cation in the body, behind sodium, potassium, andcalcium. It is the second most prevalent intracellular cation after potassium. The normal bodymagnesium content is approximately 1000 mmol or 25 g, of which about half is in bone andthe other half is intracellular in soft tissue and muscle. Less than 1% of the total bodymagnesium is present in blood. Magnesium is essential for the function of many importantenzymes, including reactions involving ATP synthesis and DNA replication and transcription.Magnesium is also required for cellular energy metabolism, membrane stabilization, nerveconduction, calcium channel activity and ion transport. Magnesium deficiency results in avariety of metabolic abnormalities and clinical consequences.
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GI absorption and renal excretion regulate total body magnesium levels. The average dailydietary intake is about 325 mg and intestinal absorption is inversely proportional to the amountingested. Most magnesium is absorbed in the ileum and colon. Cereal, grains, nuts legumes,and chocolate are relatively rich in magnesium. Vegetables, fruits, meats and fish haveintermediate amounts and dairy products are low in magnesium. The kidney is the majorexcretory organ for magnesium. Approximately 70% of plasma magnesium is filtered throughthe glomerular membrane. Only about 6% of filtered magnesium (120 mg) is excreted dailyinto the urine, because of reabsorption in the Loop of Henle. The major regulator of tubularreabsorption is the plasma magnesium concentration. Hypermagnesemia inhibits andhypomagnesemia stimulates renal transport.
Serum magnesium exists in three states: approximately 60% is ionized (free), 33% is proteinbound, and 7% is complexed to phosphate, citrate, and other anions. Approximately 75% ofthe protein bound fraction is bound to albumin and 25% to globulins. Serum magnesiumconcentration does not correlate very well with tissue magnesium levels. Serum levels areuseful for assessing acute changes in magnesium states, especially in patients with cardiacarrhythmias, acute onset of seizures, and diabetic ketoacidosis.
Hypomagnesemia is found in 12 to 20% of hospitalized patients and up to 65% of patients inintensive care units. The usual reason is loss of magnesium from the GI tract or the kidney.The causes of magnesium depletion can be remembered as the "D" factors:
Diarrhea: Lower GI secretions are rich in magnesium. Diarrhea, malabsorption, bowelresection, steatorrhea and acute pancreatitis are common causes of magnesiumdepletion.Diuretics: Loop diuretics can rapidly induce magnesium wasting. Long term thiazidediuretics can also cause hypomagnesemia.Diabetes: This is the most common cause probably due to glycosuria and osmoticdiuresis.Drugs: mostly nephrotoxic drugs such as aminoglycosides, amphotericin B, cyclosporine,cisplatin, foscarnet, pentamidine.Delivery: Magnesium normally declines by 10% in pregnancy and further during labor.Severe depletion is associated with eclampsia.Denuded Skin: Burns are associated with a general loss of electrolytes.Dietary: Hypomagnesemia becomes evident after 7 days of dietary magnesiumrestriction. Clinical signs are observed after 42 days.Drinking: Alcohol inhibits renal tubular reabsorption of magnesium. Thirty percent ofalcoholics admitted to the hospital have low magnesium.
Hypocalcemia is common in patients with severe hypomagnesemia, usually appearing when theserum magnesium level is less than 1.0 mEq/L. PTH levels are usually low and rise rapidlyfollowing magnesium replacement. Hyokalemia also frequently accompanies hypomagnesemia.It does not respond to potassium replacement until the magnesium deficit is corrected.
Hypermagnesemia is rare and usually iatrogenic. The most common causes are IV magnesiumand magnesium containing cathartics or antacids. Patient most at risk are the elderly and thosewith bowel disorders or renal insufficiency. Clinical manifestations include hypotension,
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bradycardia, respiratory depression, depressed mental status, and ECG abnormalities.
Reference range is 1.4 - 2.0 mEq/L.. Levels below 1.0 mEq/L are considered critical values.
Specimen requirement is one SST tube of blood.
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Sodium Urine
Dietary intake greatly influences the urinary excretion of sodium. The rate of sodium excretionduring the night is only one fifth of the peak rate during the day, indicating a large diurnalvariation. Measurement of urinary sodium is helpful in the differential diagnosis ofhyponatremia and hypernatremia.
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Urine Sodium Concentration in Patients with Hyponatremia
Fluid Volume Urinary Sodium Causes
Hypovolemia >20 Renal losses due to diuretics, aldosterone deficiency, salt
losing nephropathy, osmotic diuresis, ketonuria, RTA
<20 Extra renal losses due to vomiting, diarrhea, third spacing of
fluids from burns, pancreatitis, trauma
Euvolemia >20 Cortisol deficiency, hypothyroidism, stress, drugs, SIADH
Hypervolemia >20 Acute or chronic renal failure
<20 Nephrotic syndrome, cirrhosis, cardiac failure
Urine Sodium Concentration in Patients with Hypernatremia
Fluid Volume Urinary Sodium Causes
Hypovolemia <20 Excess sweating, burns, diarrhea, fistulas
>20 Renal disease, urinary tract obstruction, osmotic or loop
diuretics
Euvolemia Variable Diabetes insipidus, hypodipsia, Insensible losses, respiratory,
dermal
Hypervolemia >20 Primary hyperaldosteronism, Cushing's syndrome, hypertonic
dialysis, hypertonic sodium bicarbonate, sodium chloride tablets
Reference range is 43 - 217 mEq/24 hours.
Specimen requirement is a 24 hour urine collection in a container without preservative.Specimen should be refrigerated during an after the collection.
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Sodium, Serum
Sodium is the most abundant cation in the extracellular fluid. Serum sodium with itsaccompanying anions accounts for most of the osmotic activity of the plasma. Serum sodiumand osmolality are controlled by two separate but related systems. Serum sodium ismaintained by a feedback loop involving the kidney and adrenal glands. A decrease in serumsodium concentration or in blood pressure results in the release of renin by the kidney. Renincatalyzes the conversion of angiotensinogen to angiotensin I, which in turn is converted toangiotensin II by angiotensin converting enzyme in the lung. Angiotensin II stimulates thedistal convoluted tubule in the kidney to retain sodium and water, thereby removing thestimulus to renin secretion.
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Serum osmolality is maintained by a feedback system involving the hypothalamus, pituitarygland, and the kidney. An increase in serum osmolality is sensed by osmoreceptors located inthe anterior hypothalamus resulting in release of antidiuretic hormone (ADH) from the posteriorpituitary gland. ADH acts on the distal nephron to cause retention of water, which reducesserum osmolality and removes the stimulus to ADH secretion. Conversely, a decrease in serumosmolality inhibits ADH release, and excess water is excreted in the urine until serumosmolality returns to normal.
Hyponatremia is the most common electrolyte abnormality in hospitalized patients and isdefined as a serum sodium concentration less than 135 mEq/L. Symptoms are due to therelative excess of water that results in overhydration of cells. The severity of symptomsdepends on the degree of hyponatremia and the rate at which it develops. A patient with mildhyponatremia (sodium >125 mEq/L) may be asymptomatic or experience malaise and nausea.As the hyponatremia worsens, headaches, lethargy, confusion, and a decreasing level ofconsciousness may develop. Seizures and coma usually occur only if there is a suddendecrease in sodium to less than 120 mEq/L.
Hyponatremia can be categorized by its effect on blood volume. The initial evaluation ofhyponatremia should include measurement of plasma osmolality, electrolytes, glucose andBUN. When serum osmolality is reduced, the next step is to determine the extracellular fluidvolume of the patient. If it is reduced, hyponatremia is defined as depletional. The patient haslost sodium and water, and the sodium loss is proportionately greater than the water loss.Measurement of urinary sodium concentration helps to identify the site of sodium and fluidloss. Urinary sodium concentration greater than 20 mEq/L indicates renal loss of sodium whileurinary sodium concentration less than 20 mEq/L indicates extrarenal loss. The most commoncauses are thiazide diuretics; prolonged vomiting or diarrhea; third spacing of fluids secondaryto burns, pancreatitis or trauma; potassium depletion, and aldosterone deficiency.
Euvolemic hyponatremia is the most commonly encountered sodium disorder in hospitalizedpatients. It typically indicates a problem with water balance. The most common etiologies areinappropriate ADH secretion, severe hyperglycemia, polydipsia, adrenal (cortisol) insufficiency,and pregnancy. The syndrome of inappropriate ADH secretion (SIADH) is the commonest causeof hyponatremia in hospital patients and is associated with malignancies, pulmonary disease,CNS disorders, and HIV infection. Hyponatremia is common after surgery and is characterizedby high levels of circulating ADH. Hyperglycemia accounts for 15% of hyponatremia ininpatients. Plasma sodium falls by 1.6 mEq/L for every 100 mg/dL increase in plasma glucose.Drug induced hyponatremia can be caused by drugs that stimulate the release of ADH orpotentiate its action. Drugs causing hyponatremia include psychoactive agents (fluoxetine,sertraline, thiothixene, haloperidol, and amitriptyline), some anti-cancer agents (vincristine,vinblastine, and high dose cyclophosphamide), and carbamazepine, bromocriptine, lorcainide,chlorpropamide, and IV vasopressin.
Hypervolemic hyponatremia is nearly always a problem of water overload, which causesedema. Total body sodium is increased, but total body water is increased even more. The mostcommon causes are congestive heart failure, cirrhosis, advanced renal failure, and nephroticsyndrome. In congestive heart failure, impaired perfusion of the kidney causes retention ofsodium and water, with water retained in excess of sodium. In renal failure, the impaired
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kidney is unable to excrete normal amounts of water. Hypoalbuminemia due to cirrhosis ornephrotic syndrome decreases oncotic pressure and causes water to leave the intravascularspace, resulting in decreased blood pressure. Homeostatic mechanisms lead to retention ofwater in the extracellular fluid compartment.
Approach to Diagnosis of Hyponatremia
Pseudohyponatremia is an artifactual hyponatremia most commonly caused by severehypertriglyceridemia (>1500 mg/dL), or less often, by severe hyperproteinemia (>10 g/dL).Sodium is most commonly measured with an ion specific electrode (ISE). Two types of ISEexist; indirect and direct. Sodium is dissolved only in the water portion of plasma. Whentriglyceride or protein levels are extremely high, they occupy more space in a given volume ofplasma, resulting in a decreased in the percentage of water with its sodium content.Consequently, an artifactually low sodium concentration is obtained because less sodium ispresent in a given volume of plasma, even though the concentration of sodium in the waterphase is unaltered. Pseudohyponatremia can occur when sodium is measured with an indirectISE, which is the method used by most automated chemistry analyzers. This phenomenon isnot seen when sodium is measured with an instrument that uses direct ISE, such as point ofcare instruments and blood gas analyzers. These instruments use whole blood, instead ofplasma, and do not require predilution of the sample. Pseudohyponatremia can be confirmedby measuring sodium on an instrument using direct ISE and also measuring serum osmolalityand comparing the result to a calculated osmolality. In a patient with hyponatremia, anincreased osmolal gap suggests the presence of pseudohyponatremia.
Hypernatremia is far less common than hyponatremia. Patients at highest risk include infants,elderly patients, patients with altered mental status, uncontrolled diabetics, and hospitalizedpatients receiving hypertonic infusions, tube feedings, osmotic diuretics, lactulose, ormechanical ventilation. Hypernatremia always reflects a hyperosmolar state so CNS symptomsare prominent. The signs and symptoms include; altered mental status, lethargy, irritability,restlessness, seizures, muscle twitching, hyerreflexia, spasticity, fever, nausea, laboredrespiration, and intense thirst. In adults, a plasma sodium level above 160 mEq/L is associatedwith a 60 to 75% mortality.
Hypernatremia usually results from excessive loss of water relative to sodium. Loss ofhypotonic fluid may be secondary to kidney disease or profuse sweating or diarrhea. The renalconcentrating mechanism is the first line of defense against water depletion andhyperosmolarlity. Thirst is an important backup defense. Measurement of urine osmolality ishelpful in evaluating the cause of hypernatremia Urine osmolality is normal or low after renalloss and increased after extrarenal losses. Patients fall into three broad categories.
Urine osmolality < 300 mOsm/kg
Diabetes insipidus (central or nephrogenic)
Urine osmolality 300 to 800 mOsm/kg
Defect in ADH release -DiureticsOsmotic diuresis
Urine osmolality >800 mOsm/kg
Excess intake of sodiumInsensible water loss - infants, dementia, fever, burns, heat exposureGI loss of hypotonic fluidLoss of thirst
Sodium levels above 160 mEq/L are unusual and may be due to a preanalytical error.Vacutainer tubes containing a sodium based anticoagulant such as sodium heparin, sodium
fluoride, sodium citrate, or sodium EDTA can markedly elevate plasma sodium levels. Cardiacpatients whose specimen are collected from catheters containing benzalkonium heparin canalso have falsely elevated heparin levels.
Reference range is 134 - 144 mEq/L. Sodium concentrations < 120 mEq/L or >155 mEq/L areconsidered critical values.
Specimen requirement is one SST tube of blood.
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