Basic Metabolic Panel (Calcium, total), 80048
CPT coding guidelines indicate that a Basic Metabolic Panel (Calcium, total), CPT code 80048 should not be reported in conjunction with 80053. If a submission includes CPT 80048 and CPT 80053, only CPT 80053 will be reimbursed. There are 2 configurations for a Basic Metabolic Panel (Calcium, total), CPT code 80048:
A submission that includes 5 or more of the following laboratory component codes by the same individual physician or other health care professional for the same patient on the same date of service is a reimbursable service as a Basic Metabolic Panel (Calcium, total), CPT code 80048.
Panel Code – 80048
Effective January 1, 2008, the CPT Editorial Panel created a new code 80047 Basic metabolic panel (Calcium, ionized) which is an automated multi-channel chemistry (AMCC) code and is currently included in the automated multi-channel chemistry code (AMCC) Panel Payment Algorithm. The new code 80047 is comprised of eight component test codes (see table below). Also, new code 80047 is not a replacement for code 80048 Basic metabolic panel. Both codes 80048 and 80047 are included in the 2008 clinical laboratory fee schedule.
In order to determine payment for the new code 80047, using the AMCC Panel Payment Algorithm, existing code 82330, Calcium; ionized, will be added as an AMCC panel code. Payment code ATP23 has also been included in the clinical laboratory fee schedule data file to correspond to the AMCC panel code addition.
CPT code 80047 Basic metabolic panel (Calcium, ionized) comprises:
• Calcium; ionized (82330)
• Carbon dioxide (82374)
• Chloride (82435)
• Creatinine (82565)
• Glucose (82947)
• Potassium (84132)
• Sodium (84295)
• Urea Nitrogen (BUN) (84520)
For ESRD dialysis patients, CPT code 82330 Calcium; ionized shall be included in the calculation for the 50/50 rule as defined in Pub. 100-04, Chapter 16, Section 40.6. When CPT code 82330 is billed as a substitute for CPT code 82310, Calcium; total, it shall be billed with modifier CD or CE. When CPT code 82330 is billed in addition to CPT 82310, it shall be billed with CF modifier.
CPT panel code 80047 cannot be billed for services ordered through an ESRD facility. All tests billed for services ordered through an ESRD facility must be billed individually, not in an organ disease panel.
Basic Metabolic Panel (Calcium, total), 80048
CPT coding guidelines indicate that a Basic Metabolic Panel (Calcium, total), CPT code 80048 should not be reported in conjunction with 80053. If a submission includes CPT 80048 and CPT 80053, only CPT 80053 will be reimbursed. There are 2 configurations for a Basic Metabolic Panel (Calcium, total), CPT code 80048:
1. A submission that includes 5 or more of the following laboratory Component Codes by the Same Individual Physician or Other Health Care Professional for the same patient on the same date of service is a reimbursable service as a Basic Metabolic Panel (Calcium, total), CPT code 80048.
Panel Code Code Description Must contain 5 or more of the following Component Codes for the same patient on the same date of service
82310 Calcium; total
82374 Carbon Dioxide (bicarbonate)
82435 Chloride; blood
82565 Creatinine; blood
82947 Glucose; quantitative, blood (except reagent strip)
84132 Potassium; serum, plasma or whole blood
84295 Sodium; serum, plasma or whole blood
84520 Urea nitrogen (BUN)
A submission that includes an Electrolyte Panel, CPT code 80051 plus 1 or more of the following laboratory component codes by the same individual physician or other health care professional for the same patient on the same date of service is a reimbursable service as a Basic Metabolic Panel (Calcium, total) CPT code 80048.
Panel Code – 80048
Code Description
Includes the following panel:
. 80051 – Electrolyte Panel
.Plus 1 or more of the following component codes for the same patient on the same date of service:
.82310 – Calcium; total
.82565 – Creatinine; blood
.82947 – Glucose; quantitative, blood (except reagent strip)
.84520 – Urea nitrogen; quantitative
UHC Guideline
Organ or Disease-Oriented Laboratory Panel Codes
The Organ or Disease-Oriented Panels as defined in the CPT book are codes 80047, 80048, 80050, 80051, 80053, 80055, 80061, 80069, 80074, and 80076. According to the CPT book, these panels were developed for coding purposes only and are not to be interpreted as clinical parameters. UnitedHealthcare Community Plan uses CPT coding guidelines to define the components of each panel.
UnitedHealthcare Community Plan also considers an individual component code included in the more comprehensive Panel Code when reported on the same date of service by the Same Individual Physician or Other Health Care Professional. The Professional Edition of the CPT ® book, Organ or DiseaseOriented Panel section states: “Do not report two or more panel codes that include any of the same constituent tests performed from the same patient collection. If a group of tests overlaps two or more panels, report the panel that incorporates the greater number of tests to fulfill the code definition and report the remaining tests using individual test codes.”
For reimbursement purposes, UnitedHealthcare Community Plan differs from the CPT book’s inclusion of the specific number of Component Codes within an Organ or Disease-Oriented Panel. UnitedHealthcare Community Plan will deny the individual Component Codes and require the provider to submit the more comprehensive Panel Code. as set forth more fully in the tables below. The tables for CPT codes 80047, 80048, 80050, 80051, 80053, 80061, 80069, 80074 and 80076 identify the Component Codes that UnitedHealthcare Community Plan will require the submission of the specific panel.
Basic Metabolic Panel (Calcium, total), 80048
CPT coding guidelines indicate that a Basic Metabolic Panel (Calcium, total), CPT code 80048 should not be reported in conjunction with 80053. If a submission includes CPT 80048 and CPT 80053, only CPT 80053 will be reimbursed. There are 2 configurations for a Basic Metabolic Panel (Calcium, total), CPT code 80048:
1. A submission that includes 5 or more of the following laboratory Component Codes by the Same Individual Physician or Other Health Care Professional for the same patient on the same date of service is a reimbursable service as a Basic Metabolic Panel (Calcium, total), CPT code 80048.
Panel Code Component Code Code Description
80048 Basic Metabolic Panel (Calcium, total), 80048 Must contain 5 or more of the following Component Codes for the same patient on the same date of service
82310 Calcium; total
82374 Carbon Dioxide (bicarbonate)
82435 Chloride; blood
82565 Creatinine; blood
82947 Glucose; quantitative, blood (except reagent strip)
84132 Potassium; serum, plasma or whole blood
84295 Sodium; serum, plasma or whole blood
84520 Urea nitrogen (BUN)
Indications and Limitations of Coverage and/or Medical Necessity
Two of the panel codes are similar in that they include laboratory studies that evaluate the bodyys effectiveness in carrying on its metabolic processes. The component tests included in one or both of the metabolic panels are: Carbon dioxide, chloride, creatinine, glucose, potassium, sodium, urea nitrogen, albumin, bilirubin, calcium, alkaline phosphatase, total protein, and aspartate aminotransferase.
The indications for the metabolic panels are the indications for each individual test. Brief descriptions of the component laboratory tests follow:
Albumin is the most abundant protein in human plasma, representing 40% to 60% of the total protein. It is synthesized in the liver. The chief biological functions of albumin are to transport and store a wide variety of ligands, to maintain the plasma oncotic pressure, and to serve as a source of endogenous amino acids.
Hyperalbuminemia is of little diagnostic significance except in dehydration. Hypoalbuminemia, however, is very common in many conditions such as liver disease; tissue damage and inflammation; malabsorption syndromes; malnutrition; protein loss in urine, feces, or through skin due to burns; and ascites.
Bilirubin, total or direct, is one of a number of tests useful in the assessment of liver function. Bilirubin is produced from the catabolism of the heme molecule.
A number of inherited and acquired diseases affect one or more of the steps involved in the production, uptake, storage, metabolism, and excretion of bilirubin. The most commonly occurring form of unconjugated hyperbilirubinemia is physiological jaundice of the newborn. Both conjugated and unconjugated bilirubin are retained in hepatobiliary diseases. When any portion of the biliary tree becomes blocked or abnormally permeable, biliary passage of bilirubin and of all other components of bile is retarded. Examples of these conditions include sclerosing cholangitis; primary biliary cirrhosis; sarcoidosis; hepatic carcinomas; carcinoma of the head of the pancreas, common bile duct, or ampulla of Vater; choledocholithiasis; and common duct strictures.
Calcium is found in three main body compartments: bone, soft tissue, and extracellular fluid. In blood, virtually all of the calcium is in plasma. The concentration of calcium as well as inorganic phosphate and magnesium in plasma is dependent on the balance between rates of bone mineral deposition, bone resorption, intestinal absorption, and renal clearance. Parathyroid hormone and 1,25-dihydroxyvitamin D are the two primary regulators of these processes and the concentration of these ions in plasma.
Alkalosis leads to an increase in binding and a decrease in free calcium; conversely, acidosis leads to a decrease in binding and an increase in free calcium. A decrease in the serum free calcium concentration causes increased neuromuscular excitability and tetany; whereas an increased concentration reduces neuromuscular excitability. Calcium is also important in muscle contraction and is a second messenger affecting enzyme activity and hormone secretion.
Carbon Dioxide is transported in the blood in several forms. The most abundant and important is bicarbonate in the plasma. Alterations of bicarbonate dissolved in plasma are characteristic of acid-base imbalance. The nature of the imbalance cannot, however, be inferred from the carbon dioxide value itself; its value has significance only in the context of other electrolytes and pH that have been determined simultaneously.
Increases in total carbon dioxide occur in metabolic alkalosis due to severe vomiting, hyperkalemic states, or excessive intake of alkali, as well as in respiratory acidosis, especially when compensated. Decreases are associated with renal failure, renal tubular acidosis which coexist in hyperchloremia, diarrhea, states of poor tissue perfusion, and respiratory alkalosis.
Chloride is the major extracellular anion and is significantly involved in maintenance of water distribution, osmotic pressure, and anion-cation balance in the extracellular fluid compartment.
Hypochloremia is observed in chronic pyelonephritis and metabolic acidoses caused by conditions such as diabetic ketoacidosis or renal failure. In addition, persistent gastric suction and prolonged vomiting result in significant loss of chloride ions. Other conditions associated with hypochloremia include hyperaldosteronism, bromide intoxication, and cerebral salt- wasting after head injury. Hyperchloremia occurs with dehydration, renal tubular acidosis, acute renal failure, metabolic acidosis associated with prolonged diarrhea and loss of sodium bicarbonate, diabetes insipidus, adrenocortical hyper function, hyperparathyroidism, and salicylate intoxication. Extremely high dietary intake of salt and over treatment with saline solutions are also causes of hyperchloremia.
Creatinine is a metabolic by-product of muscle contraction. The amount of endogenous creatinine produced is proportional to muscle mass and varies with age and sex. Daily excretion of creatinine can be 10% to 30% greater as a result of dietary intake of creatine and creatinine in meats. The excretion rate in any one person, in the absence of renal disease, is relatively constant and parallels endogenous production.
Creatinine clearance is performed by obtaining urine specimens over a period of time and also a blood specimen at sometime during that collection period. Estimations of creatinine clearance can be obtained from the plasma creatinine level. In patients with advanced renal failure, plasma creatinine levels are used as an adjunct to managing the administration of potentially toxic drugs that are cleared by the kidneys.
Plasma creatinine levels are used in conjunction with a plasma urea
determination in discriminating between prerenal and postrenal increases in blood urea.
Hyperglycemia or an elevation in blood glucose is produced by a group of metabolic disorders of carbohydrate metabolism called diabetes mellitus. A subclass of the condition includes patients in whom hyperglycemia is due to a specific underlying disorder, such as pancreatic disease with endocrine insufficiency; hormonal disorder; certain genetic syndromes; insulin receptor abnormalities; or the administration of hormones or drugs known to cause hyperglycemia.
Blood glucose testing is performed to diagnose hypoglycemia, to diagnose hyperglycemia, and to aid in the management of diabetes mellitus. Blood glucose testing is not paid for by Medicare when performed for screening purposes in asymptomatic individuals.
Alkaline Phosphatase (ALP) is present in practically all tissues of the body, especially at or in the cell membranes, and it occurs at particularly high levels in intestinal epithelium, kidney tubules, bone (osteoblasts), liver, and placenta. Although the precise metabolic function of the enzyme is not yet understood, the enzyme is closely associated with the calcification process in bone.
Serum ALP measurements are of particular interest in the investigation of hepatobiliary disease and bone disease associated with increased osteoblastic activity. The response of the liver to any form of biliary obstruction is to synthesize more ALP. Among the bone diseases, the highest levels of serum ALP activity are encountered in Pagets disease (osteitis deformans) as a result of the action of the osteoblastic cells as they try to rebuild bone that is reabsorbed by the uncontrolled activity of osteoclasts. Moderate rises are observed in osteomalacia. Very high enzyme levels are present in patients with osteogenic bone cancer. Secondary deposits in bone from malignancies in other sites vary in the extent to which they stimulate osteoblastosis and the ensuing elevation in the serum levels of ALP.
Potassium is the major cation within the cell. The intracellular potassium concentrations are considerably higher than serum potassium levels. This ratio is the most important determinant in maintaining membrane electrical potential in excitable neuromuscular tissue.
The serum potassium level is a blood test which reveals the bodys (serum) potassium level and is helpful in diagnosing potassium imbalances as related to medical conditions (such as complications of diabetes mellitus, complications of acute renal failure, hypokalemia and/or hyperkalemia).
This test is also utilized to monitor the efficacy of medical interventions or treatments specific to the condition under treatment.
Sodium ions are the major cations of extracellular fluid and play a major role in maintaining the normal distribution of water and the osmotic pressure in the extracellular fluid compartment. The average diet contains many times more than the body requirement of sodium. The excess is excreted by the kidneys.
Hyponatremia may be the result of excessive sweating, prolonged vomiting, persistent diarrhea, or salt-losing enteropathies. Renal loss due to diminished tubular reabsorption may be caused by inappropriate choice, dose, or use of diuretics; by primary or secondary deficiency of aldosterone, and other mineralocorticoids; or severe polyuria.
Hyponatremia is common in metabolic acidosis (diabetic ketoacidosis). Dilutional hyponatremia is secondary to excessive retention of water and occurs in edema, ascites from chronic cardiac failure, uncontrolled diabetes, hepatic cirrhosis, nephrotic syndrome, and malnutrition.
Proteins have numerous biological functions that are important and varied. Enzymes catalyze biochemical transformations essential to metabolism; protein, poly peptides, and oligopeptide hormones regulate metabolism; antibodies and components of the complement system protect against infection. Plasma proteins maintain the oncotic pressure of plasma; they transport hormones, vitamins, metals, and drugs, often serving as reservoirs for their release and use; apoliproteins solubilize lipids; hemoglobin carries oxygen; protein coagulation factors control hemostasis.
Most proteins, with the exception of immunoglobulins and protein hormones, are synthesized in the liver. Disease often alters the amount and proportions of plasma proteins in body fluids in characteristic ways.
The two general causes in alterations of serum total protein are a change in the volume of plasma water and a change in the concentration of one or more of the specific proteins in the plasma. Hyperproteinemia is noted in dehydration due to inadequate water intake or to excessive water loss, as in severe vomiting, diarrhea, Addison’s disease, or diabetic acidosis. Increases in plasma water volume is reflected as relative hypoproteinemia and physiologically when a recumbent position is assumed.
Urea is the major nitrogen-containing metabolic product of protein catabolism in humans. More than 90% of urea is excreted through the kidneys, with the remaining lost primarily through the gastrointestinal tract and skin. In a normal kidney, 40% to 70% of the urea moves passively out of the renal tubule and into the interstitium, ultimately to re-enter plasma.
A wide variety of renal diseases with different permutations of glomerular, tubular, interstitial, or vascular damage can cause an increase in plasma urea concentration. However, the usefulness of urea as an independent indicator of renal function is limited by the variability of its blood levels as a result of nonrenal factors. Mild dehydration, high protein diet, increased protein catabolism, muscle wasting as in starvation, reabsorption of blood proteins after gastrointestinal hemorrhage, treatment with cortisol or its synthetic analogs, and decreased perfusion of the kidneys may cause an increased blood urea that is called prerenal. Postrenall increases in blood urea is caused by conditions that obstruct urine outflow through the ureters, bladder, or urethra. The principle clinical utility of plasma urea determination lies in its measurement in conjunction with the measurement of plasma creatinine and in discrimination between prerenal and postrenal increases in blood urea.
Aspartate aminotransferase (AST) are a group of enzymes that are involved in the metabolism of amino acids. Isoenzyme of AST are present in the cytoplasm and the mitochondria of cells. Severe tissue damage and even a mild degree of liver tissue injury results in the release of mitochondrial isoenzyme.
In viral hepatitis and other forms of liver disease associated with hepatic necrosis, levels of serum AST are elevated even before the clinical signs and symptoms of disease, such as jaundice appear. Moderately increased levels of AST activity may also be observed in extrahepatic cholestasis. Levels observed in cirrhosis vary with the status of the cirrhotic process. Elevations also occur in patients with primary or metastatic carcinoma of the liver. AST levels are also elevated in other conditions such as myocardial infarction, progressive muscular dystrophy, pulmonary emboli, acute pancreatitis, crushed muscle injuries, gangrene, and hemolytic disease.
Alanine Aminotransferase (ALT) are part of a group of enzymes that are involved in the metabolism of amino acids. ALT is found primarily in the liver, although significant amounts are also present in the kidney. ALT is thought to be predominantly nonmitochondrial.
The chief application of a determination of this serum enzyme is in the diagnosis of hepatocellular disease. It has been postulated that, in mild hepatocellular injury, when the hepatocyte plasma but not the mitrochondrial membrane is damaged, cytoplasmic ALT and AST are released into the serum. With more severe hepatocellular injury, mitochondrial membrane damage may result in the release of mitochondrial AST, elevating the AST/ALT ratio. Since ALT is found primarily in the liver, in patients with myocardial infarction, elevations of the serum levels of ALT are only slight or absent.
The ratio of AST to ALT, or DeTitus quotient, is normally 1 or slightly more. An abnormal AST/ALT ratio can be used in diagnosing a variety of conditions such as alcoholic liver disease, viral hepatitis, and metastatic carcinoma to the liver.
Limitations of coverage include ordering a metabolic panel test when one or more of its component tests are not medically necessary and reasonable in the management of the patients condition. In this case, individual tests should be ordered by the physician specific for the patients needs. In addition, the test must be ordered by a physician treating the patient or non-physician practitioners (within their scope of practice) treating the patient.
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