Wednesday, February 13, 2019

CPT 37243, 75894, 79445, S2095 - Metastatic Tumors of the Liver

Code Description CPT

37243 Vascular embolization or occlusion, inclusive of all radiological supervision and interpretation, intraprocedural roadmapping, and imaging guidance necessary to complete the intervention; for tumors, organ ischemia, or infarction.

75894 Transcatheter therapy, embolization, any method, radiological supervision and interpretation

79445 Radiopharmaceutical therapy, by intra-arterial particulate administration

S2095 Transcatheter occlusion or embolization for tumor destruction, percutaneous, any method, using ytrrium-90 microspheres


Radioembolization for Primary and Metastatic Tumors of the Liver

Introduction


Embolization is procedure to block blood flow. Combined with radiation, it is a way to treat cancer in the liver in some situations. In this procedure a catheter (a long, thin, hollow tube) is inserted in an artery near the groin. It’s threaded to the tumor’s blood supply. Tiny radioactive particles are released into the artery that feeds the tumor. The particles travel into the tumor and block off — embolize — the blood supply feeding the tumor, causing it to shrink. The radiation works to kill the cancer cells. The radiation dissipates in a few weeks and the particles stay in the liver permanently. The radiation usually doesn’t affect the healthy liver tissue around the tumor very much. This policy describes when radioembolization may be considered medically necessary.




Policy Coverage Criteria


Service Medical Necessity 


Radioembolization Radioembolization may be considered medically necessary in the following situations: * Treatment of primary hepatocellular carcinoma that is  unresectable and limited to the liver (size of 3cm or larger, and patient with good performance status)   OR * Treatment of primary hepatocellular carcinoma as a bridge to  liver transplantation OR * Treatment of primary intrahepatic cholangiocarcinoma in  patients with unresectable tumors OR * Treatment of hepatic metastases from neuroendocrine tumors  (carcinoid and noncarcinoid) with diffuse and symptomatic disease when systemic therapy has failed to control symptoms. (symptoms related to excess hormone production)  OR * Treatment of unresectable hepatic metastases 

o From breast, colorectal or melanoma (ocular or cutaneous)       AND  o That are progressive and unresectable in patients with liver dominant disease
AND o That are refractory to chemotherapy or are not candidates  for chemotherapy   Service Investigational  Radioembolization Radioembolization is considered investigational for all other hepatic metastases except as noted in the Medical Necessity section above. 


Service Investigational

Documentation Requirements


Radioembolization is considered investigational for all other indications not described in the Medical Necessity section above.

The patient’s medical records submitted for review for all conditions should document that medical necessity criteria are met. The record should include office visit notes that contain the relevant history and physical supporting ANY of the following situations: * Patient with primary liver cancer that cannot be removed by surgery and limited to the liver  (size of 3 cm or larger, and patient with good performance status) * Treatment for hepatocellular carcinoma before a liver transplant *
Treatment of primary   intrahepatic cholangiocarcinoma that cannot be removed by surgery * Treatment of hepatic metastases from neuroendocrine tumors (carcinoid and noncarcinoid)  with diffuse and symptomatic disease when systemic therapy has failed to control symptoms (symptoms related to excess hormone production)

* Treatment of hepatic metastases that cannot be removed by surgery: o From breast, colorectal, or melanoma (ocular or cutaneous)

AND o That are progressive and unresectable in patients with liver dominant disease ND * Has failed chemotherapy or are not candidates for chemotherapy




Related Information


In general, radioembolization is used for unresectable hepatocellular carcinoma that is greater than 3 cm.

There is little information on the safety or efficacy of repeated radioembolization treatments or about the number of treatments that should be administered.

Radioembolization should be reserved for patients with adequate functional status (Eastern Cooperative Oncology Group Performance Status 0-2), adequate liver function and reserve, Child-Pugh class A or B, and liver-dominant metastases.

Symptomatic disease from metastatic neuroendocrine tumors refers to symptoms related to excess hormone production.

Definition of Terms

Child-Pugh Score: This score is used to assess the prognosis of chronic liver disease, usually cirrhosis. 

Eastern Cooperative Oncology Group (ECOG): The ECOG performance status is used to assess the patient’s disease progression and how the disease impacts the patient’s activities of daily living (ADLs). http://www.ecog.org/  (Accessed September 2018)


Description

Radioembolization (RE), also referred to as selective internal radiotherapy, delivers small beads (microspheres) impregnated with yttrium 90 intra-arterially via the hepatic artery. The microspheres, which become permanently embedded, are delivered to tumors preferentially, because the hepatic circulation is uniquely organized, whereby tumors greater than 0.5 cm rely on the hepatic artery for blood supply while the normal liver is primarily perfused via the portal vein. Radioembolization has been proposed as a therapy for multiple types of primary and metastatic liver tumors.

Background

Treatments for Hepatic and NeuroEndocrine Tumors


The use of external-beam radiotherapy and the application of more advanced radiotherapy approaches (eg, intensity-modulated radiotherapy) may be of limited use in patients with multiple diffuse lesions due to the low tolerance of normal liver to radiation compared with thehigher doses of radiation needed to kill the tumor.

Various nonsurgical ablative techniques have been investigated that seek to cure or palliate unresectable hepatic tumors by improving locoregional control. These techniques rely on extreme temperature changes (cryosurgery or radiofrequency ablation), particle and wave physics (microwave or laser ablation), or arterial embolization therapy including chemoembolization, bland embolization, or radioembolization.

Radioembolization

Radioembolization, (radiotherapy in older literature) delivers small beads (microspheres) impregnated with yttrium 90 intra-arterially via the hepatic artery. The microspheres, which become permanently embedded, are delivered to tumors preferentially because thehepatic circulation is uniquely organized, whereby tumors greater than 0.5 cm rely on the hepatic arteryfor blood supply while normal liver is primarily perfused via the portal vein. Yttrium-90 is a pure beta-emitter with a relatively limited effective range and short half-life that helps focus the radiation and minimize its spread. Candidates for radioembolizationare initially examined by hepatic angiogram to identify and map the hepatic arterial system. At that time, a mixture of technetium 99-labeled albumin particles is delivered via the hepatic artery to simulate  microspheres. Single-photon emission computed tomography is used to detect possible shunting of the albumin particles into gastrointestinal or pulmonary vasculature.

Currently 2 commercial forms of yttrium-90 microspheres are available: a glass sphere, (TheraSphere) and a resin sphere (SIR-Spheres). Noncommercial forms are mostly used outside the United States. While the commercial products use the same radioisotope (yttrium-90) and have the same target dose (100 Gy), they differ in microsphere size profile, base material (ie, resin vs glass), and size of commercially available doses. The physical characteristics of the active and inactive ingredients affect the flow of microspheres during injection, their retention at the tumor site, spread outside the therapeutic target region, and dosimetry calculations. The  Food and Drug Administration (FDA) granted premarket approval of SIR-Spheres for use in combination with 5-floxuridine chemotherapy by hepatic arterial infusion to treat unresectable hepatic metastases from colorectal cancer. In contrast, TheraSphere’s glass sphere was approved under a humanitarian device exemption for use as monotherapy to treat unresectable hepatocellular carcinoma. In 2007, this humanitarian device exemption was expanded to include patients with hepatocellular carcinoma who have partial or branch portal vein thrombosis. For these reasons, results obtained with 1 product do not necessarily apply to other commercial (or non-commercial) products (see Regulatory Status section). 

Thursday, January 17, 2019

CPT 43647,43648, 43881, 43882, E0765 - laparoscopy gastric nerostimulaor

Coding Code Description CPT

43647 Laparoscopy, surgical; implantation or replacement of gastric neurostimulator electrodes, antrum
43648 Laparoscopy, surgical; revision or removal of gastric neurostimulator electrodes, antrum
43881 Implantation or replacement of gastric neurostimulator electrodes, antrum, open
43882 Revision or removal of gastric neurostimulator electrodes, antrum, open

HCPCS

E0765 FDA approved nerve stimulator, with replaceable batteries, for treatment of nausea and vomiting
L8680 Implantable neurostimulator electrode, each
L8685 Implantable neurostimulator pulse generator, single array, rechargeable, includes extension
L8686 Implantable neurostimulator pulse generator, single array, nonrechargeable, includes extension
L8687 Implantable neurostimulator pulse generator, dual array, rechargeable, includes extension
L8688 Implantable neurostimulator pulse generator, dual array, nonrechargeable, includes extension

Introduction
Gastroparesis is a condition in which the normal movement of food from the stomach to the small intestine is drastically slowed or has stopped. This can lead to nausea and vomiting.

Gastric electrical stimulation (GES) is a treatment that sends weak electrical signals to the nerves and smooth muscles in the lower stomach. This treatment helps decrease nausea and vomiting caused by gastroparesis. A small battery-powered device is surgically placed in the skin in the lower belly area. Wires are then placed in the area to be stimulated. This policy discusses when GES may be considered medically necessary. It has also been proposed as a treatment for obesity. The one published medical study that looked at using GES for obesity did not show it improved weight loss. GES for obesity is considered investigational (unproven) because more medical studies are needed.

 Note: The Introduction section is for your general knowledge and is not to be taken as policy coverage criteria. Therest of the policy uses specific words and concepts familiar to medical professionals. It is intended for providers. A provider can be a person, such as a doctor, nurse, psychologist, or dentist. A provider also can be a place where medical care is given, like a hospital, clinic, or lab. This policy informs them about when a service may be covered.


Service Medical Necessity Gastric electrical stimulation

Gastric electrical stimulation may be considered medically necessary in the treatment of chronic, intractable nausea and vomiting secondary to gastroparesis of diabetic or idiopathic etiology when ALL of the following criteria are met:

* Significantly delayed gastric emptying as documented by standard scintigraphic imaging of solid food AND
* Patient is refractory or intolerant of prokinetic medications and antiemetic medications AND
* Patient’s nutritional status is sufficiently low that total parenteral nutrition is likely to become medically necessary Gastric electrical stimulation is investigational for the treatment of obesity and all other indications.

Documentation Requirements

The medical records submitted for review should document that medical necessity criteria are met. The record should include clinical documentation of ALL of the following:
* Member has chronic, intractable nausea and vomiting secondary to gastroparesis (inability to empty food) caused by diabetes or for an unknown reason
* Significantly delayed gastric emptying confirmed by standard scintigraphic imaging (gastric emptying scan) of solid food
* Member has not responded or is intolerant to the use of prokinetic (antireflux) and antiemetic (antinausea and vomiting) medications
* The need for parenteral nutrition is likely to become medically necessary because of member’s inadequate nutritional status.




Description

Gastric electrical stimulation (GES) is performed using an implantable device designed to treat chronic drug-refractory nausea and vomiting secondary to gastroparesis of diabetic, postsurgical or idiopathic etiology. The device may be referred to as a gastric pacemaker.

Background

Gastric electrical stimulation (GES, also referred to as gastric pacing) has been investigated primarily as a treatment for gastroparesis. Currently available devices consist of a pulse generator which can be programmed to provide electrical stimulation at different frequencies.

The pulse generator is connected to intramuscular stomach leads, which are implanted during laparoscopy or open laparotomy (see Regulatory Status section). Gastroparesis is a chronic disorder of gastric motility characterized by delayed emptying of a solid meal from the stomach. Symptoms include bloating, distension, nausea, and vomiting.

When severe and chronic, gastroparesis can be associated with dehydration, poor nutritional status, and poor glycemic control in diabetics. While most commonly associated with diabetes, gastroparesis is also found in chronic pseudo-obstruction, connective tissue disorders, Parkinson disease, and psychological pathologic conditions. Some cases may not be associated with an identifiable cause, and are referred to as idiopathic gastroparesis. Treatment of gastroparesis includes prokinetic agents such as cisapride and metoclopramide, and antiemetic agents such as metoclopramide, granisetron, or ondansetron. Severe cases may require enteral or total parenteral nutrition. GES has also been investigated as a treatment of obesity. It is used to increase a feeling of satiety with subsequent reduction in food intake and weight loss. The exact mechanisms resulting in changes in eating behavior are uncertain but may be related to neurohormonal modulation and/or stomach muscle stimulation.

Summary of Evidence

For individuals who have gastroparesis who receive gastric electrical stimulation (GES), the evidence includes randomized controlled trials (RCTs) and systematic reviews. Relevant outcomes are symptoms and treatment-related morbidity. Five crossover RCTs have been published. A 2017 meta-analysis of these 5 RCTs did not find a significant benefit of GES on the severity of symptoms associated with gastroparesis. Patients generally reported improved symptoms at follow-up whether or not the device was turned on, suggesting a placebo effect. The evidence is insufficient to determine the effects of the technology on health outcomes.

A Hayes Medical Technology Directory report analyzed the evidence (n=10 studies) for GES for the treatment of gastroparesis. The report evaluated controlled studies (n=7studies/18-241 patients) and uncontrolled studies (n=3 studies/131-233 patients). The controlled trials included RCTs (n=3 studies), prospective (n=2), and retrospective studies (n=2). Patients were selected who had symptomatic gastroparesis refractory to medical treatment with diagnoses of diabetic gastric neuropathy or idiopathic gastroparesis. Exclusion criteria included the structural cause of symptoms, psychogenic vomiting, chemical dependency, previous gastric surgery, and pregnancy. Outcomes measured were gastroparesis symptom severity and gastric retention assessed by scintigraphy. Additional outcomes included the need for nutritional support, and changes in antiemetic and/or prokinetic medications. Follow-up timeframe varied among studies, the longest follow-up being four years. The report found poor to fair quality evidence indicating that GES may improve gastroparesis symptoms and gastric emptying as well as decrease the need for nutritional support in some patients with refractory gastroparesis. Overall, GES was found to be safe with the device removal rate ranging from 7%-12% in most studies, primarily due to lack of symptom improvement. It was noted that despite the low quality of the supportive evidence, GES may be an option for patients with debilitating gastroparesis that is refractory to medical treatment (Hayes, 2016 update).

Overall, the evidence for gastric electrical stimulation is not very strong. However, this Premera policy requires that the patient has tried and failed other treatments and that their nutritional status is so depleted that total parenteral nutrition (TPN) may soon become medically necessary. TPN is invasive and not without its own risks. Therefore, even though the evidence for gastric electrical stimulation is not strong and the Enterra Therapy System had only been approved by the FDA under a Humanitarian Device Exemption (HDE), GES may be helpful and allow the patient to avoid the risks associated with receiving ongoing TPN.

For individuals who have obesity who receive GES, the evidence includes 1 published RCT. Relevant outcomes are change in disease status and treatment-related morbidity. The SHAPE trial did not show significant improvement in weight loss with GES compared to sham stimulation. The evidence is insufficient to determine the effects of the technology on health outcomes.

Thursday, December 20, 2018

cpt 43201, 43210, 43236,43257 -Transesophageal Endoscopic Therapies

CPT Coding - Code Description

43201 Esophagoscopy, flexible, transoral; with directed submucosal injection(s), any substance

43210 Esophagogastroduodenoscopy, flexible, transoral; with esophagogastric fundoplasty, partial or complete, includes duodenoscopy when performed

43236 Esophagogastroduodenoscopy, flexible, transoral; with directed submucosal injection(s), any substance

43257
Esophagogastroduodenoscopy, flexible, transoral; with delivery of thermal energy tothe muscle of lower esophageal sphincter and/or gastric cardia, for treatment of gastroesophageal reflux disease

43499 Unlisted procedure, esophagus



Transesophageal Endoscopic Therapies for Gastroesophageal Reflux Disease

Introduction

GERD — gastroesophageal reflux disease — is a long-term medical condition. It’s a digestive problem that affects the ring of muscles between the esophagus (the tube that carries swallowed food to the stomach) and the stomach. When food is swallowed, the muscles at the end of the esophagus open so food can pass into the stomach. The muscles then close to prevent acid and stomach contents from backing up into the esophagus. In GERD, however, the ring of muscles is too weak, and acid can leak back up into the esophagus. GERD is usually treated with changes to lifestyle and diet, or medications, or in some cases a surgery called fundiplication. A number of other treatments have been studied. These include a procedure that is done through the mouth that wraps the upper part of the stomach around the esophagus, the use of radiofrequency energy to try to improve the barrier between the stomach and the esophagus, and the placement of implants or fillers in the esophagus. These procedures are investigational (unproven). More studies are needed to determine if they are as effective as other standard treatments.

Note: The Introduction section is for your general knowledge and is not to be taken as policy coverage criteria. The rest of the policy uses specific words and concepts familiar to medical professionals. It is intended for providers. A provider can be a person, such as a doctor, nurse, psychologist, or dentist. A provider also can

be a place where medical care is given, like a hospital, clinic, or lab. This policy informs them about when a service may be covered. Policy Coverage Criteria Service Investigational

Transoral incisionless fundoplication (TIF)

Transoral incisionless fundoplication (TIF)(ie, Esophyx®) is considered investigational as a treatment of gastroesophageal reflux disease.

Transesophageal radiofrequency  Transesophageal radiofrequency to create submucosal thermal lesions of the gastroesophageal junction (ie, Stretta® procedure) is considered investigational as a treatment of gastroesophageal reflux disease.

Endoscopic submucosal implantation of a prosthesis or injection of a bulking agent

Endoscopic submucosal implantation of a prosthesis (ie, Gatekeeper™ Reflux Repair System) or injection of a bulking agent (eg, polymethylmethacrylate beads [PMMA], zirconium oxide spheres [ie, Durasphere®]) is considered investigational as a treatment of gastroesophageal reflux disease.



Evidence Review Description


Transesophageal endoscopic therapies are being developed for the treatment of gastroesophageal reflux disease (GERD). A variety of procedures are being evaluated, including transesophageal (or transoral) incisionless fundoplication (TIF), application of radiofrequency  (RF) energy, and injection/implantation of prosthetic devices or bulking agents. Background

GERD is a common disorder characterized by heartburn and other symptoms related to reflux of stomach acid into the esophagus. Nearly all individuals experience such symptoms at some point in their lives; a smaller number have chronic symptoms and are at risk for complications of GERD. The prevalence of GERD has been estimated to be 10% to 20% in the Western world, with a lower prevalence in Asia.1

Pathophysiology


The pathophysiology of GERD involves excessive exposure of the esophagus to stomach acid, which occurs for several reasons. There can be an incompetent barrier between the esophagus and stomach, either due to dysfunction of the lower esophageal sphincter (LES) or incompetence of the diaphragm (eg, a hiatal hernia). Another mechanism is abnormally slow

clearance of stomach acid. In this situation, delayed clearance leads to an increased reservoir of stomach acid and a greater tendency to reflux.

In addition to troubling symptoms, some patients will have more serious disease, which results in complications such as erosive esophagitis, dysphagia, Barrett esophagus, and esophageal carcinoma. Pulmonary complications may result from aspiration of stomach acid into the lungs and can include asthma, pulmonary fibrosis and bronchitis, or symptoms of chronic hoarseness, cough, and sore throat.

Treatment Guidelines on the management of GERD emphasize initial medical management. Weight loss, smoking cessation, elevating the head of the bed, and elimination of food triggers are all recommended in recent practice guidelines.1 Proton pump inhibitors (PPIs) have been shown to be the most effective medical treatment. In a 2010 Cochrane systematic review, PPIs demonstrated superiority to H2-receptor agonists and prokinetics in both network metaanalyses and direct comparisons.

2 Surgical Treatment

The most common surgical procedure used for GERD is laparoscopic Nissen fundoplication. Fundoplication involves wrapping a portion of the gastric fundus around the distal esophagus to increase LES pressure. If a hiatal hernia is present, the procedure also restores the position of the LES to the correct location. Laparoscopic fundoplication was introduced in 1991 and has been rapidly adopted because it avoids complications associated with an open procedure. Although fundoplication results in a high proportion of patients reporting symptom relief, complications can occur and sometimes require conversion to an open procedure. Patients who have relief of symptoms of GERD after fundoplication may have dysphagia or gas-bloat syndrome (excessive gastrointestinal gas).

Other Treatment Options

Due in part to the high prevalence of GERD, there has been interest in creating a minimally invasive transesophageal therapeutic alternative to open or laparoscopic fundoplication or chronic medical therapy. Three types of procedures have been investigated.

1. Transesophageal endoscopic gastroplasty (gastroplication, TIF) can be performed as an outpatient procedure. During this procedure, the fundus of the stomach is folded and then held in place with staples or fasteners that are deployed by the device. The endoscopic procedure is designed to recreate a valve and barrier to reflux

2. Radiofrequency (RF) energy has been used to produce submucosal thermal lesions at the gastroesophageal junction. (This technique has also been referred to as the Stretta procedure.) Specifically, RF energy is applied through 4 electrodes inserted into the esophageal wall at multiple sites both above and below the squamocolumnar junction. The mechanism of action of the thermal lesions is not precisely known but may be related to ablation of the nerve pathways responsible for sphincter relaxation or may induce a tissuetightening effect related to heat-induced collagen contraction and fibrosis.

3. Submucosal injection or implantation of a prosthetic or bulking agent to enhance the volume of the lower esophageal sphincter has also been investigated. One bulking agent, pyrolytic carbon-coated zirconium oxide spheres (Durasphere®), is being evaluated.

The Gatekeeper™ Reflux Repair System (Medtronic, Shoreview, MN) uses a soft, pliable, expandable prosthesis made of a polyacrylonitrile-based hydrogel. The prosthesis is implanted into the esophageal submucosa, and with time, the prosthesis absorbs water and expands, creating bulk in the region of implantation.

U.S. Food and Drug Administration (FDA)product code: DQX. Endoscopic submucosal implantation of polymethylmethacrylate beads into the lower esophageal folds has also been investigated.

Summary of Evidence

For individuals who have GERD and hiatal hernia of 2 cm or less that is not controlled by PPIs who receive TIF (eg, EsophyX), the evidence includes 2 RCTs comparing TIF with PPI therapy, nonrandomized studies comparing TIF with fundoplication, and case series with longer term follow-up. Relevant outcomes are symptoms, change in disease status, quality of life, medication use, and treatment-related morbidity. The highest quality RCT (RESPECT) was a sham-controlled together with PPI therapy while the other RCT (TEMPO) compared TIF with maximum PPI therapy. Both trials found a significant benefit of TIF on the primary outcome measure in about 65% of patients, but the sham-controlled trial found improvement in 45% of the sham-

controlled group and no benefit on secondary subjective outcome measures. The nonblinded RCT found significant improvements in subjective measures but no difference in objective outcome measures when compared with PPI therapy. Together, these trials suggest a strong placebo effect of the surgery and a modest benefit of TIF in patients whose symptoms are not controlled by PPIs. For these patients, the most appropriate comparator is laparoscopic fundoplication. Studies comparing TIF with fundoplication have limitations that include earlier TIF procedures and unequal groups at baseline and are inadequate to  determine relative efficacy. The evidence is insufficient to determine the effects of the technology on health outcomes.

For individuals who have GERD and hiatal hernia of 2 cm or less that is controlled by PPIs who receive TIF (eg, EsophyX), the evidence includes 2 RCTs and observational studies with longer term follow-up. Relevant outcomes are symptoms, change in disease status, quality of life, medication use, and treatment-related morbidity. A sham-controlled trial found that the time to resume PPI therapy was longer following TIF and the remission rate was higher, indicating that TIF is more effective than no therapy. The nonblinded RCT found a benefit of TIF compared with continued PPI therapy for subjective measures, but not for the objective measures of pH normalization and esophagitis. These results raise questions about a possible placebo effect for the procedure. Also, observational studies have indicated a loss of treatment effectiveness over time. Adverse events associated with the procedure (eg, perforation) may be severe. At present, the available evidence does not support the use of this intervention in patients whose symptoms are adequately controlled by medical therapy. The evidence is insufficient to determine the effects of the technology on health outcomes.

For individuals who have GERD who receive endoscopic radiofrequency energy (eg, Stretta), the evidence includes 4 small RCTs, a nonrandomized comparative study, and observational studies with longer term follow-up. Relevant outcomes are symptoms, change in disease status, quality of life, medication use, and treatment-related morbidity. The RCTs report improvements in symptoms and quality of life following treatment with RF energy compared with sham controls, however, objective measures of GERD and a meta-analysis of these studies found no significant improvement in outcomes, raising questions about the mechanism of the symptom relief. Symptom relief is reported to be lower than after fundoplication, and reoperations greater. Larger RCTs with longer follow-up, preferably compared with fundoplication, are needed to better define the risks and benefits of this procedure. The evidence is insufficient to determine the effects of the technology on health outcomes.

For individuals who have GERD who receive esophageal bulking agents, the evidence includes an RCT and case series. Relevant outcomes are symptoms, change in disease status, quality of life, medication use, and treatment-related morbidity. The RCT for a single product was  terminated early due to lack of efficacy, while other products have only case series to support use. High-quality data from large RCTs are needed to compare bulking procedures with both sham controls and with the currently accepted treatments for GERD (ie, drug therapy, laparoscopic fundoplication). Well-designed trials should use standardized outcome measures to examine whether subjective improvement (eg, discontinuation of medication therapy, GERD– Health-Related Quality of Life scores) is supported by objective improvement (eg, esophageal acid exposure). The evidence is insufficient to determine the effects of the technology on health outcomes.

Wednesday, November 28, 2018

CPT 81403, 81405, 81406, 81047 - Molecular Pathology, Gnetic Testing dilated cardiomyopathy

Code Description CPT

81403 Molecular pathology procedure, Level 4 (eg, analysis of single exon by DNA sequence analysis, analysis of >10 amplicons using multiplex PCR in 2 or more independent reactions, mutation scanning or duplication/deletion variants of 2-5 exons) –Includes: PLN (phospholamban) (eg, dilated cardiomyopathy, hypertrophic cardiomyopathy), full gene sequence

81405 Molecular pathology procedure, Level 6 (eg, analysis of 2-5 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of 6-10 exons, or characterization of a dynamic mutation disorder/triplet repeat by Southern blot analysis)

–Includes: ANKRD1 (ankyrin repeat domain 1) (eg, dilated cardiomyopathy), full gene sequence; TPM1 (tropomyosin 1 [alpha]) (eg, familial hypertrophic cardiomyopathy), full gene sequence; TNNC1 (troponin C type 1 [slow]) (eg, hypertrophic  cardiomyopathy or dilated cardiomyopathy), full gene sequence

81406 Molecular pathology procedure, Level 7 (eg, analysis of 11-25 exons by DNA sequence  analysis, mutation scanning or duplication/deletion variants of 26-50 exons, cytogenomic array analysis for neoplasia) –Includes: LDB3 (LIM domain binding 3) (eg, familial dilated cardiomyopathy, myofibrillar myopathy), full gene sequence; LMNA (lamin A/C) (eg, Emery-Dreifuss muscular dystrophy; [EDMD1, 2 and 3] limb-girdle muscular dystrophy; [LGMD] type  1B, dilated cardiomyopathy; [CMD1A], familial partial lipodystrophy; [FPLD2]), full gene sequence; TNNT2 (troponin T, type 2 [cardiac]) (eg, familial hypertrophic cardiomyopathy), full gene sequence

81407 Molecular pathology procedure, Level 8 (eg, analysis of 26-50 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of >50 exons, sequence Code Description analysis of multiple genes on one platform) –Includes: MYH6 (myosin, heavy chain 6, cardiac muscle, alpha) (eg, familial dilated cardiomyopathy), full gene sequence; MYH7 (myosin, heavy chain 7, cardiac muscle, beta) (eg, familial hypertrophic cardiomyopathy, Liang distal myopathy), full gene sequence; SCN5A (sodium channel, voltage-gated, type V, alpha subunit) (eg, familial dilated cardiomyopathy), full gene sequence 81439 Inherited cardiomyopathy (eg, hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy) genomic sequence analysis panel, must include sequencing of at least 5 genes, including DSG2, MYBPC3, MYH7, PKP2, and TTN



If a genetic sequencing panel (GSP) is performed that does not meet the criteria in code 81439, the relevant tier 2 codes above would be reported for the specific genes tested, and the unlisted molecular pathology code would be reported 1 time for the remaining genes in the panel that lack a specific CPT. Related Information





Genetic Testing for Dilated Cardiomyopathy

Introduction

Dilated cardiomyopathy is a condition in which the left ventricle (the main pumping chamber of the heart) becomes enlarged and can no longer pump effectively. This can lead to heart failure, as well as cause an abnormal rhythm of the heart. It has been found that sometimes dilated cardiomyopathy seems to run in families, and in these cases it may be caused by a genetic problem. Doing genetic tests to see if a genetic problem has caused a person’s dilated cardiomyopathy is still investigational. Testing people who do not have any known heart problems to see if they are at risk for developing dilated cardiomyopathy is also investigational. Medical studies have not shown that this type of testing helps to manage the care of patients. For this reason, genetic testing for dilated cardiomyopathy is still considered to be unproven (investigational).

Note: The Introduction section is for your general knowledge and is not to be taken as policy coverage criteria. The rest of the policy uses specific words and concepts familiar to medical professionals. It is intended for providers. A provider can be a person, such as a doctor, nurse, psychologist, or dentist. A provider also can be a place where medical care is given, like a hospital, clinic, or lab. This policy informs them about when a service may be covered.

Testing Investigational  Genetic testing for dilated cardiomyopathy

Genetic testing for dilated cardiomyopathy is considered investigational in all situations. Coding

There are several listings of genetic tests performed for dilated cardiomyopathy in the CPT Tier 2 molecular pathology codes listed below.


Genetics Nomenclature Update

The Human Genome Variation Society nomenclature is used to report information on variants found in DNA and serves as an international standard in DNA diagnostics (see Table 1). TheSociety’s nomenclature is recommended by the Human Variome Project, the Human Genome Organization, and by the Human Genome Variation Society itself.

The American College of Medical Genetics and Genomics and the Association for Molecular Pathology standards and guidelines for interpretation of sequence variants represent expert opinion from both organizations, in addition to the College of American Pathologists. These recommendations primarily apply to genetic tests used in clinical laboratories, including genotyping, single genes, panels, exomes, and genomes. Table 2 shows the recommended standard terminology—“pathogenic,” “likely pathogenic,” “uncertain significance,” “likely benign,” and “benign”—to describe variants identified that cause Mendelian disorders.

Table 1. Nomenclature to Report on Variants Found in DNA Previous Updated Definition  Mutation Disease-associated variant Disease-associated change in the DNA sequenceVariant Change in the DNA sequence Familial variant Disease-associated variant identified in a proband for use in subsequent targeted genetic testing in first-degree relatives Table 2. ACMG-AMP Standards and Guidelines for Variant Classification

Variant Classification Definition

Pathogenic Disease-causing change in the DNA sequence Likely pathogenic Likely disease-causing change in the DNA sequence Variant of uncertain significance Change in DNA sequence with uncertain effects on disease Likely benign Likely benign change in the DNA sequence Benign Benign change in the DNA sequence American College of Medical Genetics and Genomics; AMP: Association for Molecular Pathology

Genetic Counseling

Experts recommend formal genetic counseling for patients who are at risk for inherited disorders and who wish to undergo genetic testing. Interpreting the results of genetic tests and understanding risk factors can be difficult for some patients; genetic counseling helps individuals understand the impact of genetic testing, including the possible effects the test results could have on the individual or their family members. It should be noted that genetic counseling may alter the utilization of genetic testing substantially and may reduce inappropriate testing; further, genetic counseling should be performed by an individual with experience and expertise in genetic medicine and genetic testing methods.


Description

Dilated cardiomyopathy (DCM) is characterized by progressive left ventricular enlargement and systolic dysfunction, leading to clinical manifestations of heart failure. There are a variety of causes of DCM, including genetic and nongenetic conditions. Genetic forms of DCM are heterogeneous in their molecular basis and clinical expression. Genetic testing for DCM has potential utility in confirming a diagnosis of genetic DCM, and as a prognostic test in family members when familial DCM is present.

Background

Dilated Cardiomyopathy


Dilated cardiomyopathy (DCM) is defined as the presence of left ventricular enlargement and dilatation in conjunction with significant systolic dysfunction. DCM has an estimated prevalence of 1 in 2700 in the United States.1

The age of onset for DCM is variable, ranging from infancy to the eighth decade, with most individuals developing symptoms in the fourth through sixth decades.2

Diagnosis

Primary clinical manifestations of DCM are heart failure and arrhythmias. Symptoms of heart failure, such as dyspnea on exertion and peripheral edema, are the most common presentation of DCM. These symptoms are generally gradual in onset and slowly progressive over time. Progressive myocardial dysfunction also may lead to electrical instability and arrhythmias. Symptoms of arrhythmias may include light-headedness, syncope, or sudden cardiac arrest.

Many underlying conditions can cause DCM, including3 :
* Ischemic coronary artery disease
* Toxins
* Metabolic conditions
* Endocrine disorders
* Inflammatory and infectious diseases
* Infiltrative disorders
* Tachycardia-mediated cardiomyopathy

Therefore, when a patient presents with DCM, a workup is performed to identify underlying causes, especially those treatable. The standard workup consists of clinical exam, blood pressure monitoring, electrocardiography, echocardiography, and workup for coronary artery disease as warranted by risk factors. Extensive workup including cardiac magnetic resonance imaging, exercise testing, right-sided catheterization with biopsy, and 24-hour ECG monitoring will uncover only a small number of additional etiologies for DCM.4 Approximately 35% to 40% of DCM cases are thus determined to be idiopathic after a negative workup for secondary causes.3 This has traditionally been termed idiopathic dilated cardiomyopathy (IDC). Clustering of IDC within families has been reported, leading to the conclusion that at least some cases of DCM have a genetic basis. Familial DCM is diagnosed when 2 closely related family members have IDC in the absence of underlying causes. Penetrance of familial DCM is variable and age-dependent, often leading to lack of appreciation of the familial component.

Treatment

Treatment of DCM is similar to that for other causes of heart failure. This includes medications to reduce fluid overload and relieve strain on the heart, and lifestyle modifications such as salt restriction. Patients with clinically significant arrhythmias also may be treated with antiarrhythmic medications, pacemaker implantation, and/or an automatic implantable cardiac defibrillator. Automatic implantable cardiac defibrillator placement for primary prevention also may be performed if criteria for low ejection fraction and/or other clinical symptoms are present. End-stage DCM can be treated with cardiac transplantation.

Genetic DCM

Genetic DCM has been proposed as a newer classification that includes both familial DCM and some cases of sporadic IDC. The percentage of patients with sporadic DCM that has a genetic basis is not well characterized. Most disease-associated variants are inherited in an autosomal dominant fashion, but some autosomal recessive, X-linked, and mitochondrial patterns of inheritance also are present.5

In general, genotype-phenotype correlations are either not present or not well-characterized.

There have been some purported correlations between certain disease-associated variants and


the presence of arrhythmias. For example, patients with conduction system disease and/or a family history of sudden cardiac death may be more likely to have disease-associated variants in the LMNA, SCN5A, and DES genes.1 Kayvanpour et al (2017) performed a meta-analysis of genotype-phenotype associations in DCM.6

The analysis included 48 studies (total N=8097 patients) and found a higher prevalence of sudden cardiac death, cardiac transplantation, and ventricular arrhythmias in LMNA and PLN disease-associated variant carriers and increasing penetrance with age of DCM phenotype in subjects with TTN-truncating variants. There may be interactions between genetic and environmental factors that lead to the clinical manifestations of DCM. A genetic variant may not in itself be sufficient to cause DCM, but may predispose to developing DCM in the presence of environmental factors such as nutritional deficiencies or viral infections.2

It also has been suggested that DCM genetics may be more  complex than simply single-gene variants, with low-penetrance variants that are common in the population contributing to a cumulative risk of DCM that includes both genetic and environmental factors.

Genetic Testing for DCM

Approximately 30% to 40% of patients referred for genetic testing will have a disease-associated variant identified.5 Disease-associated variants linked to DCM have been identified in more than 40 genes of various types and locations. The most common genes involved are those that code for titin (TTN), myosin heavy chain (MYH7), troponin T (TNNT2), and alpha-tropomyosin (TPM1).

These 4 genes account for approximately 30% of disease-associated variants identified in cohorts of patients with DCM.5 A high proportion of the identified disease-associated variants are rare, or novel, variants, thus creating challenges in assigning the pathogenicity of discovered variants.2

Some individuals with DCM will have more than 1 DCM-associated variant.1

The frequency of multiple disease-associated variants is uncertain, as is the clinical significance. Summary of Evidence

For individuals who have signs and/or symptoms of dilated cardiomyopathy (DCM) who receive comprehensive genetic testing, the evidence includes case series reporting clinical validity.

Relevant outcomes are overall survival, test accuracy and validity, symptoms, change in disease status, functional outcomes, quality of life, and treatment-related morbidity. There is a large degree of uncertainty with clinical validity. The percentage of patients with idiopathic DCM who have a genetic variant (clinical sensitivity) is relatively low, in the range of 10% to 50%. Clinical specificity of DCM-associated variants is unknown, but DCM-associated variants in the same  genes have been reported in 1% to 3% of patients without DCM. Because of the suboptimal clinical validity, the accuracy of assigning variants as disease-associated or benign may also be suboptimal. The clinical usefulness of genetic testing for diagnosing DCM has not been demonstrated. For a patient who is diagnosed with idiopathic DCM, the presence of a DCMassociated variant will not change treatment or prognosis. The evidence is insufficient to determine the effect of the technology on health outcomes.

For individuals who are asymptomatic with a first-degree relative who has DCM and a known familial variant who receive targeted genetic testing for a known familial variant, the evidence includes case series reporting test accuracy and clinical value. Relevant outcomes are test accuracy and validity, symptoms, morbid events, functional outcomes, quality of life, and treatment-related morbidity. For an individual at risk due to genetic DCM in the family, genetic testing can identify whether a familial variant has been inherited. However, it is uncertain how knowledge of a familial variant improves outcomes for an asymptomatic individual. The uncertain clinical validity of predictive testing makes it unclear whether actions taken as a result of testing will improve outcomes. Early treatment based on a genetic diagnosis is unproven. The evidence is insufficient to determine the effect of the technology on health outcomes. Ongoing and Unpublished Clinical Trials
Practice Guidelines and Position Statements British Society of Echocardiography

Guidelines from the British Society of Echocardiography (2017) have presented diagnostic criteria for assessing dilated cardiomyopathy (DCM) with echocardiography, recommending that caregivers regularly administer echocardiograms to individuals with potential genetic risk, particularly those related to an individual with idiopathic DCM.53 The guidelines did not address the use of genetic testing in cases of DCM.

Sunday, November 4, 2018

CPT 81229, 81313, 81539, 81541 - Oncology, cytogenomic - Prostate cancer


Code Description CPT

81229 Cytogenomic constitutional (genome-wide) microarray analysis; interrogation of genomic regions for copy number and single nucleotide polymorphism (SNP) variants for chromosomal abnormalities

81313 PCA3/KLK3 (prostate cancer antigen 3 [non-protein coding]/kallikrein-related peptidase 3 [prostate specific antigen]) ratio (eg, prostate cancer)

81479 Unlisted molecular pathology procedure

81539 Oncology (high-grade prostate cancer), biochemical assay of four proteins (Total PSA, Free PSA, Intact PSA, and human kallikrein-2 [hK2]), utilizing plasma or serum,

81541 Oncology (prostate), mRNA gene expression profiling by real-time RT-PCR of 46 genes (31 content and 15 housekeeping), utilizing formalin-fixed paraffin-embedded tissue, algorithm reported as a disease-specific mortality risk score (new code effective 1/1/18)


Genetic and Protein Biomarkers for the Diagnosis and Cancer Risk Assessment of Prostate Cancer

Introduction


A biomarker is a chemical in the body. Certain biomarkers can show when something unusual is going on with certain bodily processes. One of the most commonly known and tested biomarkers is prostate specific antigen (PSA). Higher levels of PSA in the blood indicate a problem with the prostate. The difficulty is that the PSA test doesn’t tell us what kind of problem is affecting the prostate – whether it’s simply an enlarged prostate or cancer. If the PSA is high, the usual next step is a biopsy. A biopsy is taking small bits of tissue to see if cancer is present. Other biomarker tests have been developed in recent years with the hope of telling doctors which patients should have a biopsy and who can skip it. Published medical studies about these newer prostate biomarker tests are contradictory. That means some studies show the tests detect what they’re supposed to and other studies don’t. At this time, there is not enough medical evidence to show that newer prostate cancer biomarker tests are effective.

Note: The Introduction section is for your general knowledge and is not to be taken as policy coverage criteria. The rest of the policy uses specific words and concepts familiar to medical professionals. It is intended for providers. A provider can be a person, such as a doctor, nurse, psychologist, or dentist. A provider also can be a place where medical care is given, like a hospital, clinic, or lab. This policy informs them about when a service may be covered.

Test Investigational Genetic and protein biomarkers

The following genetic and protein biomarkers for the diagnosis of prostate cancer are considered investigational:
* Candidate gene panels
* Gene hypermethylation testing (eg, ConfirmMDx®)
* Kallikrein markers (eg, 4Kscore™ Test)
* Mitochondrial DNA mutation testing (eg, Prostate Core Mitomics Test™)
* PCA3 testing
* Prostate Health Index (phi)
* SelectMDx
* TMPRSS fusion genes

Single nucleotide polymorphisms testing Single nucleotide polymorphisms (SNPs) testing for cancer risk assessment of prostate cancer is considered investigational.

Note: Prolaris and Oncotype DX Prostate, gene expression analysis tests for prostate cancer management, are addressed in a separate medical policy (see Related Policies).

Coding


Related Information

Genetic Counseling


Experts recommend formal genetic counseling for patients who are at risk for inherited disorders and who wish to undergo genetic testing. Interpreting the results of genetic tests and understanding risk factors can be difficult for some patients. Genetic counseling helps individuals understand the impact of genetic testing, including the possible effects the test results could have on the individual or their family members. It should be noted that genetic counseling may alter the utilization of genetic testing substantially and may reduce inappropriate testing. Further, genetic counseling should be performed by an individual with experience and expertise in genetic medicine and genetic testing methods.

Evidence Review

Background


Various genetic and protein biomarkers are associated with prostate cancer. These tests have the potential for determining which men should undergo prostate biopsy or rebiopsy after a prior negative biopsy. This evidence review addresses these types of tests for cancer risk assessment. Testing to determine cancer aggressiveness after a tissue diagnosis of cancer is addressed in a related policy (see Related Policies).

Prostate Cancer

Prostate cancer is the second most common cancer in men with a predicted 161,360 cases and 26,700 deaths expected in the United States in 2017.

1 Prostate cancer is a complex, heterogeneous disease, ranging from microscopic tumors that are unlikely to be life-threatening to aggressive tumors which can metastasize, leading to morbidity or death. Early localized disease can usually be treated with surgery and radiotherapy, and active surveillance may be adopted in men whose cancer is unlikely to cause major health problems during their lifespan or for whom the treatment might be dangerous. In patients with inoperable or metastatic disease, treatment consists of hormonal therapy and possibly chemotherapy. The lifetime risk of being diagnosed with prostate cancer for men in the United States is approximately 16%, but the risk of dying of prostate cancer is 3%.2 African American men have the highest prostate cancer risk in the United States; the incidence of prostate cancer is about 60% higher and the mortality rate is more than 2 to 3 times greater than that of white men.3 Although the lifetime risk of being diagnosed with prostate cancer is 16%, autopsy results have suggested that about 30% of men age 55 and 60% of men age 80 who have died of other causes have incidental prostate cancer.

4 This indicates that many cases of prostate cancer are present but are unlikely to pose a threat during a man’s life expectancy. Grading

The most widely used grading scheme for prostate cancer is the Gleason system.5

It is an architectural grading system ranging from 1 (well differentiated) to 5 (poorly differentiated); the score is the sum of the primary and secondary patterns. A Gleason score of 6 is low-grade prostate cancer that usually grows slowly; 7 is an intermediate grade; 8 to 10 is high-grade cancer that grows more quickly. Ten-year survival stratified by Gleason score has been estimated from the Surveillance, Epidemiology, and End Results to be about 98% for scores 2 through 6, 92% for score 7 with primary pattern 3 and secondary pattern 4 (3+4), 77% for score 7 (4+3), and 70% for scores 8 to 10.6

Numerous genetic alterations associated with the development or progression of prostate cancer have been described. These molecular markers have been used to help decide which men should undergo prostate biopsy or rebiopsy after an initial negative biopsy.

Summary of Evidence

For individuals who are being considered for an initial prostate biopsy or a repeat biopsy who receive testing for genetic and protein biomarkers of prostate cancer, the evidence includes systematic reviews and meta-analyses and primarily observational studies. Relevant outcomes are overall survival, disease-specific survival, test accuracy, test validity, other test performance measures, resource utilization, hospitalizations, and quality of life. The evidence supporting clinical utility varies by test but has not been directly shown for any biomarker test. In general, the performance of biomarker testing for predicting biopsy referrals compared with clinical examination, including the ratio of free or unbound PSA to total PSA, is lacking. Procedures for referrals for biopsy based on clinical examination vary, making it difficult to quantify performance characteristics for this comparator. There is also considerable variability in biopsy referral practices based on clinical examination alone, and many of the biomarker tests do not have standardized cutoffs to recommend biopsy. Therefore, to determine whether the tests improve the net health outcome, prospective comparative data are needed on how test results are expected to be used vs how they are actually being used in practice. Many test validation populations have included men with positive digital rectal exam, PSA level outside of the gray zone (between 3 or 4 ng/mL and 10 ng/mL), or older men for whom the information from PSA test results are to be informative. African American men have a high burden of morbidity and mortality, but have not been well represented in these study populations. It is unclear how to monitor men with low biomarker risk scores who continue to have symptoms or high or rising PSA levels. Comparative studies of the many biomarkers are lacking, and it is unclear how to use the tests in practice, particularly when test results are contradictory. The evidence is insufficient to determine the effects of the technology on health outcomes.

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