Tuesday, January 17, 2017

CPT 43257, 43499, 49999 - Endoscopic treatment of GERD

Procedure  Codes and Description

Group 1 Codes:

43257 ESOPHAGOGASTRODUODENOSCOPY, FLEXIBLE, TRANSORAL; WITH DELIVERY OF THERMAL ENERGY TO THE MUSCLE OF LOWER ESOPHAGEAL SPHINCTER AND/OR GASTRIC CARDIA, FOR TREATMENT OF GASTROESOPHAGEAL REFLUX DISEASE

43499 UNLISTED PROCEDURE, ESOPHAGUS

43999 UNLISTED PROCEDURE, STOMACH

49999 UNLISTED PROCEDURE, ABDOMEN, PERITONEUM AND OMENTUM


Coverage Indications, Limitations, and/or Medical Necessity

Benefits are not available for endoluminal treatment for Gastroesophageal Reflux Disease (GERD) using the Stretta® procedure, the Bard EndoCinch™ Suturing System, Plicator™, EsophyX™ or similar treatments as these procedures are not considered reasonable and necessary for the diagnosis or treatment of an injury or disease.

Currently, these procedures are considered non-covered due to the fact that current peer-reviewed literature does not support the efficacy of the services. Claims will be denied as "not proven effective."

The Stretta® procedure is an endoluminal treatment for GERD in which radiofrequency energy is delivered to smooth muscle of the lower esophageal sphincter (LES). A flexible catheter equipped with special needle electrodes for precise energy delivery is placed by mouth into the esophagus and carefully controlled radiofrequency energy is then delivered to the LES and gastric cardia, creating thermal lesions. The manufacturer maintains that the changes that occur immediately, and over time, result in a "tighter" LES and a less compliant gastric cardia. Additionally, the interruption of nerve pathways in the LES area is believed to reduce the incidence of inappropriate LES "relaxations," leading to an improvement in GERD symptoms. Substantial peer-reviewed evidence to fully support these assumptions remains to be published.

The Bard EndoCinch™ Suturing System and the Plicator™ are intended for use in endoscopic placement of suture(s) in the soft tissue of the esophagus and stomach and for approximation of tissue for treatment of symptomatic gastroesophageal reflux disease.

EsophyX™ is a device for performing transoral incisionless fundoplication surgery for treating gastroesophageal reflux disease. This procedure reconstructs the valve at the top of the stomach that helps prevents acid reflux.

These procedures are promising for treatment of patients in whom proton pump inhibitor therapy fails. Clinical data from various studies are emerging. At this time, open-label studies or patient registries with short term follow-ups are the dominant source of data. The overwhelming preponderance of reviewers remains equivocal in their support and have called for randomized controlled trials with long-term follow-ups. In the absence of evidence from such studies, and in the absence of wide acceptance, endoscopic treatments for GERD are not proven effective. Therefore, they are not reimbursable even though some of the treatments may have associated CPT™ or OPPS codes.


Bill Type Codes:

Contractors may specify Bill Types to help providers identify those Bill Types typically used to report this service. Absence of a Bill Type does not guarantee that the policy does not apply to that Bill Type. Complete absence of all Bill Types indicates that coverage is not influenced by Bill Type and the policy should be assumed to apply equally to all claims.
N/A

Revenue Codes:

Contractors may specify Revenue Codes to help providers identify those Revenue Codes typically used to report this service. In most instances Revenue Codes are purely advisory. Unless specified in the policy, services reported under other Revenue Codes are equally subject to this coverage determination. Complete absence of all Revenue Codes indicates that coverage is not influenced by Revenue Code and the policy should be assumed to apply equally to all Revenue Codes.

N/A

Sunday, January 15, 2017

cpt code 22510, 22514, 22515


Procedure Codes And Description

Group 1 Paragraph: N/A

Group 1 Codes:

22510 PERCUTANEOUS VERTEBROPLASTY (BONE BIOPSY INCLUDED WHEN PERFORMED), 1 VERTEBRAL BODY, UNILATERAL OR BILATERAL INJECTION, INCLUSIVE OF ALL IMAGING GUIDANCE; CERVICOTHORACIC

22511 PERCUTANEOUS VERTEBROPLASTY (BONE BIOPSY INCLUDED WHEN PERFORMED), 1 VERTEBRAL BODY, UNILATERAL OR BILATERAL INJECTION, INCLUSIVE OF ALL IMAGING GUIDANCE; LUMBOSACRAL

22512 PERCUTANEOUS VERTEBROPLASTY (BONE BIOPSY INCLUDED WHEN PERFORMED), 1 VERTEBRAL BODY, UNILATERAL OR BILATERAL INJECTION, INCLUSIVE OF ALL IMAGING GUIDANCE; EACH ADDITIONAL CERVICOTHORACIC OR LUMBOSACRAL VERTEBRAL BODY (LIST SEPARATELY IN ADDITION TO CODE FOR PRIMARY PROCEDURE)

22513 PERCUTANEOUS VERTEBRAL AUGMENTATION, INCLUDING CAVITY CREATION (FRACTURE REDUCTION AND BONE BIOPSY INCLUDED WHEN PERFORMED) USING MECHANICAL DEVICE (EG, KYPHOPLASTY), 1 VERTEBRAL BODY, UNILATERAL OR BILATERAL CANNULATION, INCLUSIVE OF ALL IMAGING GUIDANCE; THORACIC

22514 PERCUTANEOUS VERTEBRAL AUGMENTATION, INCLUDING CAVITY CREATION (FRACTURE REDUCTION AND BONE BIOPSY INCLUDED WHEN PERFORMED) USING MECHANICAL DEVICE (EG, KYPHOPLASTY), 1 VERTEBRAL BODY, UNILATERAL OR BILATERAL CANNULATION, INCLUSIVE OF ALL IMAGING GUIDANCE; LUMBAR

22515 PERCUTANEOUS VERTEBRAL AUGMENTATION, INCLUDING CAVITY CREATION (FRACTURE REDUCTION AND BONE BIOPSY INCLUDED WHEN PERFORMED) USING MECHANICAL DEVICE (EG, KYPHOPLASTY), 1 VERTEBRAL BODY, UNILATERAL OR BILATERAL CANNULATION, INCLUSIVE OF ALL IMAGING GUIDANCE; EACH ADDITIONAL THORACIC OR LUMBAR VERTEBRAL BODY (LIST SEPARATELY IN ADDITION TO CODE FOR PRIMARY PROCEDURE)


Group 2 Codes:

0200T PERCUTANEOUS SACRAL AUGMENTATION (SACROPLASTY), UNILATERAL INJECTION(S), INCLUDING THE USE OF A BALLOON OR MECHANICAL DEVICE, WHEN USED, 1 OR MORE NEEDLES, INCLUDES IMAGING GUIDANCE AND BONE BIOPSY, WHEN PERFORMED

0201T PERCUTANEOUS SACRAL AUGMENTATION (SACROPLASTY), BILATERAL INJECTIONS, INCLUDING THE USE OF A BALLOON OR MECHANICAL DEVICE, WHEN USED, 2 OR MORE NEEDLES, INCLUDES IMAGING GUIDANCE AND BONE BIOPSY, WHEN PERFORMED


Coverage Indications, Limitations, and/or Medical Necessity

This LCD applies to all types of and methods involving any procedure affecting vertebral augmentation, such as balloon reduction and augmentation, vertebroplasty.

In the US, more than one quarter of the population age 50 years or older experiences one vertebral fracture in the later years of life. Fractured vertebral bodies may produce intractable pain. Vertebral augmentation procedures are some of the invasive treatments that may be employed to address pain refractory to non-invasive therapeutic modalities. The percutaneous injection of medical cement or polymethylmethacrylate (PMM) or other material FDA-approved for this purpose into the vertebral body may reduce pain and improve function. One type of vertebral augmentation procedure, e .g. Kyphoplasty, also includes fracture reduction by expanding the intrabody space with a device such as a balloon. Following reduction, the bone cement is injected.

Indication

There is only one indication for these procedures: treatment of acute (< 4 months of symptoms) and painful compression fracture(s), regardless of etiology, in a patient without contraindication due to neurological deficits:

The fracture may be demonstrated by plain film, CT or by MRI. The findings must correlate unequivocally with the site of the patient’s pain as demonstrated by physical examination.

Acuity may be established by history, MRI and/or nuclear medicine bone scan.

Pain must be predominantly related to the demonstrated fracture(s), of moderate to severe intensity (e.g., pain level at least 6 on VAS 1-10), such that the patient cannot perform basic activities of daily living (ADLs), such as ambulation, sitting, bathing, transfers.

Pain must be refractory to conservative measures employed for reasonable periods of time, such as medication management with appropriate titration. 
o Generally, procedures are not medically reasonable and necessary when performed immediately after the fracture occurs. Exceptions will not be allowed unless the medical record establishes a clear rationale for the exception. For example, “adequate pain control impairs basic ADLs” or "is associated with respiratory compromise.”

If pain may be due to one or more conditions, prior to any vertebral augmentation procedure, an appropriately comprehensive pain assessment and consequent pain management treatment plan must be instituted. Other probable causes of pain must be reasonably excluded. The treatment plan must begin with the least invasive approach that addresses identified pain generators; potentially, an implantable pump for analgesia or surgical stabilization in a patient with concurrent instability.

An interval assessment by the proceduralist is an absolute requirement if the procedure is performed by any provider other than the diagnostician who performed the pain assessment and developed the plan of care. The proceduralist must document the rationale for proceeding with treatment in the medical record.

The medical record must contain a detailed operative procedure narrative report. “Boilerplate” or other non-specific “canned” reports does not fulfill this requirement.

While treatment of only one to two levels would be anticipated, treatment of no more than three (3) vertebral levels within the range of T1-L5 may be covered and reimbursed during the entire episode of pain caused by or related to an acute compression fracture(s), regardless of the number of fractures. Hence, if more than three acute fractures are present, alternative therapies must be employed. Treatment of three levels may be subject to pre- or post-pay review.

o Exceptions: steroid-induced osteoporosis and multiple myeloma when conservative measures have been demonstrated to be inadequate in the specific patient and result in the inability to perform basic ADLs.
Procedures must be performed with real-time CT or fluorscopic imaging guidance, Images of final trocar placement and appearance of the vertebral body at the end of the procedure must be available on request.

The medical record must contain assessment of patient condition and response to treatment at one month, three months and 6 months post-procedure unless the patient is enrolled in a registry. Telephone follow-up with documentation of outcomes is acceptable. Documentation of at least two (2) unsuccessful and reasonable attempts to contact the patient may substitute for the 3 or 6 month follow-up evaluations.

Enrollment in a registry with an outcomes documentation schedule consistent with that described in this LCD is an acceptable substitute for medical records’ follow-up documentation. Any acceptable registry must be compliant with the principles established in AHRQ’s “Registries for Evaluating Patient Outcomes: A User’s Guide”. (See bibliography.) Noridian knows of one such registry currently available for enrollment.
The link to the registry is: http://www.benchmarketmedical.com/VCF-Registry/ This homepage describes the registry as well as registration resources.
No percutaneous vertebral augmentation procedure, such as sacroplasty, is indicated for treatment of lesions of the sacrum or coccyx. The CPT Category III codes, 0200T and 0201T, are non-covered.


Contraindications

Absence of a confirmed fracture or fracture more than 4 months unless there is evidence of edema on MRI. Symptoms that cannot be directly related to a specific acute fracture(s).

Prophylactic treatment for osteoporosis of the spine or for chronic back pain unrelated to compression fractures. All prophylactic procedures will be denied.

Symptomatic foraminal stenosis, other spinal degenerative disease, facet arthropathy, or other significant coexistent spinal or bony pain generators that account for the predominant portion of the patient’s pain. These conditions require treatment before reimbursement for vertebral augmentation procedures may be considered. Following adequate address of other pain generators accounting for most of the patient’s pain, residual disabling pain localized to the compression fracture may allow payment for vertebroplasty or vertebral augmentation procedures.

Investigational procedures such as performance of a vertebral augmentation procedure concurrent with an open spinal surgical procedure.

Unstable fracture or requirement for stabilization procedure in same or adjacent spinal region.

Presence of painful metastases to areas other than the spine unless radiotherapy and other conservative measures have failed to relieve the pain due to the compression fracture.

Presence of any other condition described as a contraindication in the FDA labeling.


Special Considerations

Bone biopsy done at the same level as Vertebral Augmentation is part of the primary procedure and is not be separately payable consistent with CPT Manual instructions.

In and of themselves, vertebral augmentation procedures do not require inpatient admission and the procedures do not appear on the Inpatient Only list.



Provider Qualifications

Patient safety and quality of care mandate that healthcare professionals who perform Facet Joint Injections, Medial Branch Blocks, and Facet Joint Radiofrequency Neurotomy percutaneous vertebral augmentation procedures are appropriately experienced and/or trained to provide and manage the services. The CMS Manual System, Pub. 100-8, Program Integrity Manual, Chapter 13, Section 5.1 (http://www.cms.hhs.gov/manuals/downloads/pim83c13.pdf) underscores this point and states that "reasonable and necessary" services must be "ordered and/or furnished by qualified personnel." Services will be considered medically reasonable and necessary only if performed by appropriately experienced and/or formally trained providers. 

The following training requirement applies only to those providers who have not provided these specific interventional pain management services on a regular basis (at least one time per month) during the ten years prior to the effective date of this LCD as may be established by claims billings. 

A basic requirement of payment is training and/or credentialing by a formal residency/fellowship program and/or other training program that is accredited by a nationally-recognized body and whose core curriculum includes the performance and management of the procedures addressed in this policy. (Recognized accrediting bodies include only those whose program accreditation gains the trainee eligibility to sit for a healthcare-related licensing exam or licensing itself, which in turn allows the licensee to perform these procedures. At a minimum, training must cover and develop an understanding of anatomy and drug pharmacodynamics and kinetics, the technical performance of the procedure(s) and utilization of the required associated imaging modalities, and the diagnosis and management of potential complications from the intervention. 

The following credentialing requirement applies to all providers of the services addressed in this policy. If the practitioner works in a hospital facility at any time and/or is credentialed by a hospital for any procedure, the practitioner must be credentialed to perform the same procedure in the outpatient setting.


Bill Type Codes:
Contractors may specify Bill Types to help providers identify those Bill Types typically used to report this service. Absence of a Bill Type does not guarantee that the policy does not apply to that Bill Type. Complete absence of all Bill Types indicates that coverage is not influenced by Bill Type and the policy should be assumed to apply equally to all claims.
011x Hospital Inpatient (Including Medicare Part A)
012x Hospital Inpatient (Medicare Part B only)
013x Hospital Outpatient
022x Skilled Nursing - Inpatient (Medicare Part B only)
023x Skilled Nursing - Outpatient
071x Clinic - Rural Health
072x Clinic - Hospital Based or Independent Renal Dialysis Center
085x Critical Access Hospital

Revenue Codes:

Contractors may specify Revenue Codes to help providers identify those Revenue Codes typically used to report this service. In most instances Revenue Codes are purely advisory. Unless specified in the policy, services reported under other Revenue Codes are equally subject to this coverage determination. Complete absence of all Revenue Codes indicates that coverage is not influenced by Revenue Code and the policy should be assumed to apply equally to all Revenue Codes.

032X Radiology - Diagnostic - General Classification
033X Radiology - Therapeutic and/or Chemotherapy Administration - General Classification
036X Operating Room Services - General Classification
040X Other Imaging Services - General Classification
045X Emergency Room - General Classification
049X Ambulatory Surgical Care - General Classification
050X Outpatient Services - General Classification
051X Clinic - General Classification
076X Specialty Services - General Classification
096X Professional Fees - General Classification





ICD-10 Codes that Support Medical Necessity


ICD-10 CODE DESCRIPTION
M48.53XA Collapsed vertebra, not elsewhere classified, cervicothoracic region, initial encounter for fracture
M48.53XD Collapsed vertebra, not elsewhere classified, cervicothoracic region, subsequent encounter for fracture with routine healing
M48.53XG Collapsed vertebra, not elsewhere classified, cervicothoracic region, subsequent encounter for fracture with delayed healing
M48.53XS Collapsed vertebra, not elsewhere classified, cervicothoracic region, sequela of fracture
M48.54XA Collapsed vertebra, not elsewhere classified, thoracic region, initial encounter for fracture
M48.54XD Collapsed vertebra, not elsewhere classified, thoracic region, subsequent encounter for fracture with routine healing
M48.54XG Collapsed vertebra, not elsewhere classified, thoracic region, subsequent encounter for fracture with delayed healing
M48.54XS Collapsed vertebra, not elsewhere classified, thoracic region, sequela of fracture
M48.55XA Collapsed vertebra, not elsewhere classified, thoracolumbar region, initial encounter for fracture
M48.55XD Collapsed vertebra, not elsewhere classified, thoracolumbar region, subsequent encounter for fracture with routine healing
M48.55XG Collapsed vertebra, not elsewhere classified, thoracolumbar region, subsequent encounter for fracture with delayed healing
M48.55XS Collapsed vertebra, not elsewhere classified, thoracolumbar region, sequela of fracture
M48.56XA Collapsed vertebra, not elsewhere classified, lumbar region, initial encounter for fracture
M48.56XD Collapsed vertebra, not elsewhere classified, lumbar region, subsequent encounter for fracture with routine healing
M48.56XG Collapsed vertebra, not elsewhere classified, lumbar region, subsequent encounter for fracture with delayed healing
M48.56XS Collapsed vertebra, not elsewhere classified, lumbar region, sequela of fracture
M48.57XA Collapsed vertebra, not elsewhere classified, lumbosacral region, initial encounter for fracture
M48.57XD Collapsed vertebra, not elsewhere classified, lumbosacral region, subsequent encounter for fracture with routine healing
M48.57XG Collapsed vertebra, not elsewhere classified, lumbosacral region, subsequent encounter for fracture with delayed healing
M48.57XS Collapsed vertebra, not elsewhere classified, lumbosacral region, sequela of fracture
M80.08XA Age-related osteoporosis with current pathological fracture, vertebra(e), initial encounter for fracture
M80.08XD Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with routine healing
M80.08XG Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with delayed healing
M80.08XK Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with nonunion
M80.08XP Age-related osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with malunion
M80.08XS Age-related osteoporosis with current pathological fracture, vertebra(e), sequela
M80.88XA Other osteoporosis with current pathological fracture, vertebra(e), initial encounter for fracture
M80.88XD Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with routine healing
M80.88XG Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with delayed healing
M80.88XK Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with nonunion
M80.88XP Other osteoporosis with current pathological fracture, vertebra(e), subsequent encounter for fracture with malunion
M80.88XS Other osteoporosis with current pathological fracture, vertebra(e), sequela
M84.58XA Pathological fracture in neoplastic disease, other specified site, initial encounter for fracture
M84.58XD Pathological fracture in neoplastic disease, other specified site, subsequent encounter for fracture with routine healing
M84.58XG Pathological fracture in neoplastic disease, other specified site, subsequent encounter for fracture with delayed healing
M84.58XK Pathological fracture in neoplastic disease, other specified site, subsequent encounter for fracture with nonunion
M84.58XP Pathological fracture in neoplastic disease, other specified site, subsequent encounter for fracture with malunion
M84.58XS Pathological fracture in neoplastic disease, other specified site, sequela
M84.68XA Pathological fracture in other disease, other site, initial encounter for fracture
M84.68XD Pathological fracture in other disease, other site, subsequent encounter for fracture with routine healing
M84.68XG Pathological fracture in other disease, other site, subsequent encounter for fracture with delayed healing
M84.68XK Pathological fracture in other disease, other site, subsequent encounter for fracture with nonunion
M84.68XP Pathological fracture in other disease, other site, subsequent encounter for fracture with malunion
M84.68XS Pathological fracture in other disease, other site, sequela
S22.010A Wedge compression fracture of first thoracic vertebra, initial encounter for closed fracture
S22.010B Wedge compression fracture of first thoracic vertebra, initial encounter for open fracture
S22.010D Wedge compression fracture of first thoracic vertebra, subsequent encounter for fracture with routine healing
S22.010G Wedge compression fracture of first thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.010K Wedge compression fracture of first thoracic vertebra, subsequent encounter for fracture with nonunion
S22.010S Wedge compression fracture of first thoracic vertebra, sequela
S22.011A Stable burst fracture of first thoracic vertebra, initial encounter for closed fracture
S22.011B Stable burst fracture of first thoracic vertebra, initial encounter for open fracture
S22.011D Stable burst fracture of first thoracic vertebra, subsequent encounter for fracture with routine healing
S22.011G Stable burst fracture of first thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.011K Stable burst fracture of first thoracic vertebra, subsequent encounter for fracture with nonunion
S22.011S Stable burst fracture of first thoracic vertebra, sequela
S22.018A Other fracture of first thoracic vertebra, initial encounter for closed fracture
S22.018B Other fracture of first thoracic vertebra, initial encounter for open fracture
S22.018D Other fracture of first thoracic vertebra, subsequent encounter for fracture with routine healing
S22.018G Other fracture of first thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.018K Other fracture of first thoracic vertebra, subsequent encounter for fracture with nonunion
S22.018S Other fracture of first thoracic vertebra, sequela
S22.020A Wedge compression fracture of second thoracic vertebra, initial encounter for closed fracture
S22.020B Wedge compression fracture of second thoracic vertebra, initial encounter for open fracture
S22.020D Wedge compression fracture of second thoracic vertebra, subsequent encounter for fracture with routine healing
S22.020G Wedge compression fracture of second thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.020K Wedge compression fracture of second thoracic vertebra, subsequent encounter for fracture with nonunion
S22.020S Wedge compression fracture of second thoracic vertebra, sequela
S22.021A Stable burst fracture of second thoracic vertebra, initial encounter for closed fracture
S22.021B Stable burst fracture of second thoracic vertebra, initial encounter for open fracture
S22.021D Stable burst fracture of second thoracic vertebra, subsequent encounter for fracture with routine healing
S22.021G Stable burst fracture of second thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.021K Stable burst fracture of second thoracic vertebra, subsequent encounter for fracture with nonunion
S22.021S Stable burst fracture of second thoracic vertebra, sequela
S22.028A Other fracture of second thoracic vertebra, initial encounter for closed fracture
S22.028B Other fracture of second thoracic vertebra, initial encounter for open fracture
S22.028D Other fracture of second thoracic vertebra, subsequent encounter for fracture with routine healing
S22.028G Other fracture of second thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.028K Other fracture of second thoracic vertebra, subsequent encounter for fracture with nonunion
S22.028S Other fracture of second thoracic vertebra, sequela
S22.030A Wedge compression fracture of third thoracic vertebra, initial encounter for closed fracture
S22.030B Wedge compression fracture of third thoracic vertebra, initial encounter for open fracture
S22.030D Wedge compression fracture of third thoracic vertebra, subsequent encounter for fracture with routine healing
S22.030G Wedge compression fracture of third thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.030K Wedge compression fracture of third thoracic vertebra, subsequent encounter for fracture with nonunion
S22.030S Wedge compression fracture of third thoracic vertebra, sequela
S22.031A Stable burst fracture of third thoracic vertebra, initial encounter for closed fracture
S22.031B Stable burst fracture of third thoracic vertebra, initial encounter for open fracture
S22.031D Stable burst fracture of third thoracic vertebra, subsequent encounter for fracture with routine healing
S22.031G Stable burst fracture of third thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.031K Stable burst fracture of third thoracic vertebra, subsequent encounter for fracture with nonunion
S22.031S Stable burst fracture of third thoracic vertebra, sequela
S22.038A Other fracture of third thoracic vertebra, initial encounter for closed fracture
S22.038B Other fracture of third thoracic vertebra, initial encounter for open fracture
S22.038D Other fracture of third thoracic vertebra, subsequent encounter for fracture with routine healing
S22.038G Other fracture of third thoracic vertebra, subsequent encounter for fracture with delayed healing
S22.038K Other fracture of third thoracic vertebra, subsequent encounter for fracture with nonunion
S22.038S Other fracture of third thoracic vertebra, sequela
S22.040A Wedge compression fracture of fourth thoracic vertebra, initial encounter for closed fracture
S22.040B Wedge compression fracture of fourth thoracic vertebra, initial encounter for open fracture

Thursday, January 12, 2017

CPT CODE 81479, 81403, 81311 -Metastatic Melanoma

Procedure Codes and Description

Group 1 Codes:

81311 NRAS (NEUROBLASTOMA RAS VIRAL [V-RAS] ONCOGENE HOMOLOG) (EG, COLORECTAL CARCINOMA), GENE ANALYSIS, VARIANTS IN EXON 2 (EG, CODONS 12 AND 13) AND EXON 3 (EG, CODON 61)

81479 UNLISTED MOLECULAR PATHOLOGY PROCEDURE

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)

Coverage Indications, Limitations, and/or Medical Necessity

Indications:

This is limited coverage policy for genetic testing of tumor tissue for somatic mutations in the NRAS gene (81311). Noridian will cover NRAS testing for metastatic colorectal cancer, per NCCN guidelines (Version 3.2014). 

All other NRAS testing is non-covered.

Background:

RAS oncogene is a superfamily of signal transduction proteins, which are proteins that communicate signals between the cells. DNA mutations in the RAS family genes turns the signals on permanently such that the cells divide nonstop, leading to cancer. Three of this family’s proteins, HRAS, KRAS, and NRAS are important in tumors and encode 21kD proteins called p21s.

Previous studies have shown that targeting oncogenic NRAS-driven melanomas requires decrease in both pERK and pAKT downstream of RAS-effectors for efficacy, which could be achieved by either targeting both BRAF and CRAF or BRAF and PIK3CA simultaneously in NRAS mutant tumor cells.

Colorectal Cancer:

Multiple signaling pathways are involved in colorectal cancer pathogenesis. The epidermal growth factor receptor (EGFR) plays a key role in activation of these pathways and is commonly overexpressed in metastatic colorectal cancer (mCRC). Consequently, EGFR is a target of anticancer therapies. Two of these drugs, cetuximab and panitumumab, are monoclonal antibodies that block EGFR action. The 2013 NCCN Clinical Practice Guidelines for Colon Cancer describes a recent study by Douillard et al [2013] which reported that 17% of 641 patients from the PRIME trial without KRAS exon 2 mutations were found to have mutations in exons 3 and 4 of KRAS or mutations in exons 2, 3, and 4 of NRAS. A predefined retrospective analysis of a subset of these patients showed that progression free survival (PFS) and overall survival (OS) were decreased in those who received panitumumab plus FOLFOX compared to those who received FOLFOX alone. For this reason the FDA indication for panitumumab was recently updated to state that panitumumab is not indicated for the treatment of patients with NRAS mutation-positive disease in combination with oxaliplatin-based chemotherapy.

In chemotherapy-refractory patients, fewer than 10% of patients who harbor one of these mutations respond to EGFR immunotherapy. The American Society of Clinical Oncology (ASCO) and the National Comprehensive Cancer Network (NCCN) both recommend KRAS mutation testing prior to prescribing EGFR antagonist therapy for patients with mCRC and state that alternative therapy should be prescribed when mutations are detected. 

However, NCCN Colorectal Guidelines (Version 3.2014) recommend “All patients with metastatic colorectal cancer should have tumor tissue genotyped for RAS mutations (KRAS and NRAS). At the very least, exon 2 KRAS mutation status should be determined. Whenever possible, non-exon 2 KRAS mutation status and NRAS mutation status should also be determined. Patients with any known KRAS mutation (exon 2 or non-exon-2) or NRAS mutation should not be treated with either cetuximab or panitumumab.” Consequently, Noridian is expanding coverage of NRAS to patients with metastatic colorectal cancer. 

Metastatic Melanoma:

The NRAS gene encodes a protein that helps control cell division. Approximately 15% to 20% of melanomas harbor an oncogenic NRAS mutation. NRAS mutations can occur in all melanoma subtypes, but may be slightly more common in skin with chronic sun damage or in nodular melanomas. In addition, NRAS mutations are not found in tumors with BRAF mutations.

Several studies have been carried out to examine whether mutations in BRAF and NRAS confer different pathological features and clinical behavior. The effect of these mutations on clinical outcome remains uncertain with previous studies reporting conflicting
results.

The NRAS protein is a GTPase which can lead to the activation of other proteins (such as AKT and MEK) that are also in pathways that help regulate cell division. In theory, drugs that inhibit AKT or MEK also have the potential to counteract the effects of NRAS mutations, although NRAS targeting therapies are still in clinical trials. In addition, pathways that help regulate cell division also include other proteins that could potentially be targeted such as PI3K and mTOR.

Melanomas can be tested for NRAS mutations with targeted sequencing. There are several manufacturers of targeted genetic tests that can detect NRAS mutations in melanoma tumor samples. The prognostic significance of NRAS mutations is still not well understood and further investigation of the histologic types of melanoma with specific NRAS mutations in a larger series is necessary to validate these apparent impacts on patient outcomes. In smaller subsets of cutaneous melanoma, other activating mutations have been described, including NRAS, c­KIT, and CDK4.

Other Cancers:

Other neoplastic diseases in which NRAS mutations have been reported in the primary literature include: myeloid leukemia, bladder cancer, liver cancer, and proliferative thyroid lesions.

Schulten et al [2­013] directly sequenced mutational hotspot regions encompassing codons 12, 13, and 61 of the RAS genes in 381 cases of thyroid lesions. In addition, the putative NRAS hotspot region encompassing codon 97 was sequenced in 36 thyroid lesions. Schulten and team found mutations in 16 out of 57 patients.

Kompier et al [2010] reports that although they have been reported, NRAS mutations are not common in bladder cancer.

Although NRAS mutations have been identified in the above tumor types, evidence in the primary literature is limited with regard to the clinical utility of NRAS mutation testing and its impact on management and survival. There is currently insufficient evidence to demonstrate clinical utility of NRAS testing in these tumor types.

NRAS Testing in relation to Noonan syndrome diagnosis:

Noonan syndrome is a common autosomal dominant condition with an incidence of 1/1,000 to 1/2,500 people. Unlike the somatic tumor mutations discussed above, Noonan syndrome may be caused by a germline mutation in the NRAS gene which would be present in every cell of the body. Noonan syndrome is characterized by a number of phenotypic findings including distinctive facial features, short stature, heart defects, cryptorchidism, lymphedema, and coagulation defects, among others. Several syndromes have features that overlap clinically with Noonan syndrome including cardiofaciocutaneous syndrome, Costello syndrome, LEOPARD syndrome and Noonan-­like syndrome with loose anagen hair. The genetic etiologies of these conditions can also overlap with Noonan syndrome.

Several of these disorders have been referred to as neurocardiofacialcutaneous syndromes, RASopathies or Ras/MAPK pathway disorders and have a shared pathway of genetic function.

They are characterized by facial dysmorphism, cardiac disease, reduced growth, skeletal and ectodermal defects and variable cognitive deficits. They also share a predisposition to development of malignancies.

Overall, approximately 75% of individuals with Noonan syndrome will have an identifiable mutation with gene panel testing. To date, NRAS mutations have been found in four individual case reports which suggests that NRAS testing for Noonan syndrome is unlikely to yield positive results. The clinical features appear to be typical with no particular or distinctive phenotype observed suggesting that mutation testing targeted to select individuals is not feasible.

Genotype­phenotype correlations have emerged that can help to direct medical management for those affected with an associated condition, but not specifically for NRAS mutations. For instance, mutations in the SOS1 gene have been associated with an increased chance for ectodermal involvement, development of certain solid tumors, pulmonary stenosis, and atrial and ventricular septal defects; with an associated decreased prevalence of cognitive defects, short stature, and hypertrophic cardiomyopathy.

Medical management recommendations are available for many of the Noonan syndrome spectrum disorders. Overlapping features result in overlapping medical management recommendations, typically guided by clinical features.


RBC phenotyping

This policy provides limited-coverage for molecular phenotyping of erythrocyte antigens performed on the HEA BeadChip™ (Immucor, Warren, NJ), a single nucleotide polymorphisms (SNP)-based microarray test. This high-throughput molecular assay received FDA PMA approval in May, 2014 and is the only IVD- approved molecular test to characterize human red blood cell (RBC) antigens. 

Many clinically significant antigens are encoded by alleles defined by SNPs. This assay identifies 35 antigens and 3 phenotypic variants across 11 blood groups (Rh, Kell, Duffy, Kidd, MNS, Lutheran, Dombrock, Landsteiner-Wiener, Diego, Colton and Scianna). Genomic DNA targets isolated from whole blood are amplified and fluorescent signals are interpreted by online software as specific alleles and probable antigen phenotype. This test does not evaluate patient antibody status. 

For more than ten years, RBC genotyping has been applied mainly to mass screen donors in blood centers. American Rare Donor Program, a consortium of the American Red Cross and American Association of Blood Banks (AABB) accredited immunohematology reference laboratories have used molecular genotype information for several years to identify antigen negative blood units from donor for patients with antibodies. Blood centers also use molecular technology to genotype donors for certain antigens (eg, Dombrock) that are hard to ascertain because of antisera unavailability or weak potency. 

Hemagglutination is the most common serologic method of determining a RBC phenotype. In this technique, the patient’s RBCs are tested with antisera specific for the antigens of interest. However, hemagglutination testing cannot be used if a patient has a positive direct antiglobuin test (DAT), or if direct agglutination typing sera is not available for the antigen. In addition, serologic phenotyping is invalid in the transfused patient who may have persistent donor RBCs in circulation. Because molecular genotyping is not subject to the limitations of serologic testing, it has become a useful tool in large hospital transfusion services. 

As early as 1999, Legler et al demonstrated disparate molecular Rh phenotyping in 7 of 27 patients compared to serologic typing. Soon afterwards, Reid and others demonstrated that DNA from blood samples could be used to genotype patients who had recently been transfused. Castilho et al confirmed the unreliability of serologic testing when they showed that 6 of 40 molecular genotypes differed from serologic phenotypes in multiply transfused sickle cell anemia (SCA) patients, and in 9 of 10 alloimmunized thalassemic patients. A number of investigators have replicated these findings, most notably Bakanay et al when they demonstrated genotypic and phenotypic discrepancies in 19 or 37 multi-transfused patients in multiple alleles. The discrepancies aided in the selection of antigen-matched blood products and improved RBC survival, ultimately improving patient care. A recent case report by Wagner emphasizes the usefulness of molecular testing over serologic testing in chronically transfused patients. 

In a prospective observational study, Klapper et al. used the HEA BeadChip™ to provide extended human erythrocyte antigen (xHEA) phenotyped donor units and recipient patient samples. XHEA-typed units were assigned to pending transfusion requests using a web-based inventory management system to simulate blood order processing at four hospital transfusion services. The fraction of requests filled (FF) in 3 of 4 sites was > 95% when matching for ABO, D and known alloantibodies, with a FF of > 90% when additional matching for C, c, E, e, and K antigens. The most challenging requests came from the fourth site where the FF was 62 and 51% respectively, even with a limited donor pool. 

In a prospective observational study by Da Costa et al, 21 of 35 sickle cell anemia (SCA) patients had discrepancies or mismatches, mainly in the Rh, Duffy, Jk and MNS blood groups, between the genotype profile and the serologically-matched blood unit for multiple antigens. These authors report that their genotype-matching program resulted in elevated hemoglobin levels, increased time between transfusions and prevented the development of new alloantibodies. 

Two recently published papers have shown the feasibility of routinely applying molecular blood banking techniques in a hospital transfusion service. Routine RBC testing has been implemented in a large tertiary care hospital in Los Angeles, CA to maximize efficient use of blood units. Patients with warm or cold reacting autoantibodies, patients with SCA and patients with antibodies that could not be identified were molecularly genotyped and received molecularly matched blood from the hospital’s genotyped donor inventory. 

At a large hospital in Cleveland, OH, pre-transfusion molecular typing is performed on chronically transfused patients, patients with autoantibodies, multiple antibodies, when no antigen specific antibody is available for testing and to solve laboratory discrepancies. They authors note that the major benefit of molecular typing is its application for patients who cannot be typed by serology due to an unsuitable sample. Valid results can be obtained even when they have been transfused within a few days of testing or have been massively transfused. Samples selected for molecular testing were based on an algorithm. 

Two recent research studies have demonstrated that treatment with daratumumab, a CD38 monoclonal antibody, can bind to CD38 expressed on the surface of red blood cells (RBCs) and interferes with serologic testing, thereby preventing cross-match. False-positive reactions may persist for 2 to 6 months after infusion. 

Medicare will cover pretransfusion molecular testing using the HEA BeadChip™ assay for the following categories of patients:
Long term, frequent transfusions anticipated to prevent the development of alloantibodies (e.g. sickle cell anemia, thalassemia or other reason);

Autoantibodies or other serologic reactivity that impedes the exclusion of clinically significant alloantibodies (e.g. autoimmune hemolytic anemia, warm autoantibodies, patient recently transfused with a positive DAT, high-titer low avidity antibodies, patients about to receive or on daratumumab therapy, other reactivity of no apparent cause);

Suspected antibody against an antigen for which typing sera is not available; and

Laboratory discrepancies on serologic typing (e.g. rare Rh D antigen variants)

Medicare does not expect molecular testing to be performed on patients undergoing surgical procedures such as bypass or other cardiac procedures, hip or knee replacements or revisions, or patients with alloantibodies identifiable by serologic testing that are not expected to require long term, frequent transfusions. 

The medical necessity for molecular RBC phenotying must be documented in the patient’s medical record.

ICD-10 CODE DESCRIPTION

C90.00 Multiple myeloma not having achieved remission
C90.01 Multiple myeloma in remission
C90.02 Multiple myeloma in relapse
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency
D53.9 Nutritional anemia, unspecified
D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G6PD] deficiency
D55.1 Anemia due to other disorders of glutathione metabolism
D55.2 Anemia due to disorders of glycolytic enzymes
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemias due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified
D56.0 Alpha thalassemia
D56.1 Beta thalassemia
D56.2 Delta-beta thalassemia
D56.3 Thalassemia minor
D56.5 Hemoglobin E-beta thalassemia
D56.8 Other thalassemias
D56.9 Thalassemia, unspecified
D57.00 Hb-SS disease with crisis, unspecified
D57.01 Hb-SS disease with acute chest syndrome
D57.02 Hb-SS disease with splenic sequestration
D57.1 Sickle-cell disease without crisis
D57.20 Sickle-cell/Hb-C disease without crisis
D57.211 Sickle-cell/Hb-C disease with acute chest syndrome
D57.212 Sickle-cell/Hb-C disease with splenic sequestration
D57.219 Sickle-cell/Hb-C disease with crisis, unspecified
D57.3 Sickle-cell trait
D57.40 Sickle-cell thalassemia without crisis
D57.411 Sickle-cell thalassemia with acute chest syndrome
D57.412 Sickle-cell thalassemia with splenic sequestration
D57.419 Sickle-cell thalassemia with crisis, unspecified
D57.80 Other sickle-cell disorders without crisis
D57.811 Other sickle-cell disorders with acute chest syndrome
D57.812 Other sickle-cell disorders with splenic sequestration
D57.819 Other sickle-cell disorders with crisis, unspecified
D58.0 Hereditary spherocytosis
D58.1 Hereditary elliptocytosis
D58.9 Hereditary hemolytic anemia, unspecified
D59.0 Drug-induced autoimmune hemolytic anemia
D59.1 Other autoimmune hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified
D60.0 Chronic acquired pure red cell aplasia
D60.1 Transient acquired pure red cell aplasia
D60.8 Other acquired pure red cell aplasias
D60.9 Acquired pure red cell aplasia, unspecified
D61.01 Constitutional (pure) red blood cell aplasia
D61.09 Other constitutional aplastic anemia
D61.1 Drug-induced aplastic anemia
D61.2 Aplastic anemia due to other external agents
D61.3 Idiopathic aplastic anemia
D61.89 Other specified aplastic anemias and other bone marrow failure syndromes
D63.0 Anemia in neoplastic disease
D63.1 Anemia in chronic kidney disease
D63.8 Anemia in other chronic diseases classified elsewhere
D64.0 Hereditary sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to disease
D64.2 Secondary sideroblastic anemia due to drugs and toxins
D64.3 Other sideroblastic anemias
D64.4 Congenital dyserythropoietic anemia
D64.89 Other specified anemias

Thursday, November 24, 2016

Insurance requests for medical records



1. Insurance  staff members conduct medical review of claims and seek the advice of qualified and, typically, practicing professionals when necessary. Contracting providers agree to accept the decisions made as a result of those reviews and to follow the appeals procedures established by this Policy Memo.

2. The entire review process itself includes the development of guidelines that relate to specific provisions of members' contracts; the processing of claims based on guidelines and medical records when indicated; the retrospective review of claim determinations; and the appeal process. Insurance  seeks the advice of clinical professionals at appropriate points throughout the entire review process.


3. Contracting providers must submit all pertinent and complete medical records to Insurance  within the time frame specified by Insurance  when records are needed for the initial review of a claim or when records are requested for an audit. In most instances, Insurance  will allow 30 calendar days for the production of the requested records. In certain unusual circumstances as determined solely by Insurance , Insurance  will require providers to submit medical records without advance notice. In such cases, a Insurance  representative will visit the provider's office during business hours and secure the requested records immediately. The provider agrees to provide the requested records immediately. Members' contracts permit Insurance  to obtain medical records without a signed patient release.



4. The ordering/referring provider shall also provide medical records to the performing provider when requested for the purpose of medical necessity review. Additional documentation that is not a part of the medical record and that was not provided at the time of the initial request will not be accepted. Only records created contemporaneous with treatment will be considered pertinent. Services denied for failure to submit documentation are not eligible for provider appeal, and are a provider write-off.

5. If Insurance  determines that the patient services provided by the contracting provider are not medically necessary, the claim is denied and is a write-off to the provider. If the services are requested by the patient after being advised by the provider of the lack of medical necessity and the daily record or patient chart has been documented to that effect and a written waiver is obtained by the provider before the service being rendered, charges for the services will be the patient's responsibility.

Thursday, November 17, 2016

Medical Record Signature policy

Signature Requirements

In the content of health records, each entry must be authenticated by the author. Authentication is the process of providing proof of the authorship signifying knowledge, approval, acceptance or obligation of the documentation in the health record, whether maintained in a paper or electronic format accomplished with a handwritten or electronic signature. Individuals providing care for the patient are responsible for documenting the care. The documentation must reflect who performed the service.

a. The handwritten signature must be legible and contain at least the first initial and full last name along with credentials and date. A typed or printed name must be accompanied by a handwritten signature or initials with credentials and date.

b. An electronic signature is a unique personal identifier such as a unique code, biometric, or password entered by the author of the electronic medical record (EMR) or electronic health record (EHR) via electronic means, and is automatically and permanently attached to the document when created including the author’s first and last name, with credentials, with automatic dating and time stamping of the entry. After the entry is electronically signed, the text-editing feature should not be available for amending documentation. Example of an electronically signed signature: “Electronically signed by John Doe, M.D. on MM/DD/YYYY at XX:XX A.M.”

c. A digital signature is a digitized version of a handwritten signature on a pen pad and automatically converted to a digital signature that is affixed to the electronic document. The digital signature must be legible and contain the first and last name, credentials, and date.

d. Rubber stamp signatures are not permissible. This provision does not affect stamped signatures on claims, which remain permissible.

4. Corrections in the Medical Record


If the original entry in the medical record is incomplete, contracting providers shall follow the guidelines below for making a correction, addendum, or amendment. Signature requirements as defined above apply to all corrections in the medical record.

a. Errors in paper-based records:

To add an addendum or amendment to paper-based records, draw a single line in ink through the incorrect entry, print the word "error" at the top of the entry, the reason for the change, the correct information, and authenticate the error by signing (including credentials) the notation with the date and time. Entries should not be antedated (assigned a date earlier than the current date). Errors must never be blocked out or erased.

b. Electronic medical records/Electronic health records:

i. Addendum

An addendum is new documentation used to add information to an original entry that has already been signed. Addenda should be timely with date and time of the addendum. Write “addendum” and state the reason for the addendum referring back to the original entry.

Complete the addendum as soon after the original note as possible. Identify any sources of information used to support the addendum. Entries should not be antedated (assigned a date earlier than the current date).


ii. Amendment

An amendment is documentation meant to clarify or provide additional information within the medical record in conjunction with a previous entry. An amendment is made after the original documentation has been completed and signed by the provider.

All amendments should be timely with the date and time of the amended documentation. Write “amendment” and document the clarifying information referring back to the original entry.

Complete the amendment as soon after the original note as possible. Entries should not be antedated (assigned a date earlier than the current date).

Most read colonoscopy CPT codes