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.

Friday, January 19, 2018

Coverage BLOOD LEAD NURSING ASSESSMENT VISITS


MDHHS covers up to two blood lead nursing assessment visits and in-home education visits for children determined to be lead burdened. If more than one child in the home has blood lead poisoning, the blood lead nursing assessment visits are covered for each child.

Blood lead nursing assessment visits must be provided in the child’s home. A Medicaidenrolled home health agency or an LHD may conduct the visits. This procedure is not covered under the Maternal Infant Health Program (MIHP). Blood lead nursing visits provided through a MHP are covered by the individual MHP.

The first blood lead nursing assessment visit focuses on:

* Assessment of the growth and developmental status of the child, including any symptomatology that may be present in the child.


* Behavioral assessment of the child, including any aggressiveness and/or hyperactivity.

* Nutritional assessment of the child.

* Assessment of typical family practices that may produce lead risk (e.g., hobbies, occupation, cultural practices).

* Limited physical identification of lead hazards within the dwelling.

* Identification and planning for testing of any other family member at risk for sequelae of lead hazard exposure.

* Education and information regarding lead hazards and ways to minimize those risks in the future.

* Development of a family plan of care to increase the safety of the child from lead hazards.

* Facilitating blood lead follow-up testing and treatment recommended by the PCP.

The second blood lead nursing assessment visit focuses on:

* Reinforcement of the educational information presented to the family during the first visit.

* Validation of the family’s ability to carry out activities to minimize risks of continued lead exposure.

* Modifications of the plan of care to minimize lead risks, as needed.

* Facilitating blood lead follow-up testing and treatment recommended by the PCP.


BLOOD LEAD RESOURCE DOCUMENTS

Providers are encouraged to obtain and review materials and resources concerning blood lead poisoning from the MDHHS Childhood Lead Poisoning Prevention Program. (Refer to the Directory Appendix for contact information.)

FEE-FOR-SERVICE (FFS)

 For beneficiaries younger than 2 years of age, a letter stressing the importance of well child visits is sent to the parent/guardian every six months as a reminder to schedule a well child visit with the PCP. The parent/guardian of the beneficiary is encouraged to schedule the well child visits recommended during those six months with the beneficiary’s PCP. For beneficiaries 2 years of age and older, if a claim for a well child visit has not been processed by Medicaid by the time the child is halfway to their next well child visit due date (according to the AAP periodicity schedule), the parent/guardian will receive a second letter. A list of FFS beneficiaries who did not have a claim for a well child visit processed will be generated and issued to each LHD. LHDs may assist Medicaid in informing parents/guardians of the EPSDT program, scheduling appointments, and arranging medical transportation options.

Friday, December 29, 2017

CHILDREN IN FOSTER CARE Coverage


Medical interventions, screenings, and various preventive health care services are to be up-to-date for all children in foster care. For purposes of this section, any reference to “child” or “children” in foster care includes any individual in foster care who is younger than 21 years of age. The care of children should be comprehensive, well-coordinated, and fully documented throughout their stay in foster care. All children in foster care younger than 21 years of age must receive a full medical examination and screening for potential mental health issues by a PCP within the first 30 days of entering foster care. All children in foster care are eligible for Medicaid from the first day of the month of entry into foster care.The PCP must verify the child in foster care’s eligibility and enrollment status. In case of difficulty  confirming Medicaid status, or of verifying Medicaid Health Plan enrollment, the PCP should contact the foster care worker or the local MDHHS office designee. The PCP must complete the health maintenance visit regardless of whether or not the child in foster care recently received a health maintenance visit prior to entry into the foster care system.

The PCP’s office staff should obtain the completed MDHHS "Consent to Routine, Non-surgical Medical Care and Emergency Medical or Surgical Treatment" form (DHS-3762) from the foster care parent, or consent from the child in foster care if the child is at least 18 years of age, before the child is seen by the PCP. This form provides the PCP with informed consent to routine, non-surgical medical care and emergency medical or surgical treatment and provides the child’s foster care worker’s or local MDHHS office designee’s contact information. This form does not grant informed consent for the physician to provide psychotropic medication treatment. The MDHHS "Psychotropic Medication Informed Consent" form (DHS-1643) must be completed to receive informed consent to provide psychotropic medication treatment. (Refer to the MDHHS website for copies of forms and form information. Refer to the Directory Appendix for website information.)

A child may be assigned to a new PCP upon entry into the foster care system, and it will be necessary for the child’s previous PCP to share the child’s health information with the new PCP. In an order placing a child in foster care, the court shall include an order that each of the child's medical providers release the child's medical records. The court order requires the parent(s) to provide names and contact information for all previous medical and mental health providers, and to sign a consent to release health information on the day of the court proceedings.

The supervising agency shall develop a medical passport for each child who comes under its care. The medical passport shall contain all medical information required by policy or law to be provided to the PCP and to the foster care parent. The medical passport includes a basic medical history, a record of all immunizations from the Michigan Care Improvement Registry (MCIR), a complete and regularly updated statement of medical appointments, prescribed medications, and any other information available to the foster care worker concerning the child's medical, physical, and mental health status. The medical passport should be shared with the child’s foster care parents and all medical providers even if the document is not complete or up to date. Updates to the medical passport should be shared with the foster care parents and medical providers when new information becomes available. If health information, including the medical passport, is not made available to the medical provider at or before the time of the medical examination, the medical provider should contact the foster care worker and/or the local MDHHS office designee (noted on the DHS-3762 form) to assist with obtaining the missing health information.

The medical evaluation must follow the AAP periodicity schedule and Medicaid EPSDT policy. The examination should be completed according to the recommendations for the nearest or most appropriate periodic examination age. The PCP will assess the child for medical, dental, developmental, and mental health needs. The full medical evaluation will include an immunization review, health history, and physical examination. The medical examination and screenings should be documented for the initial and for all subsequent well child visits and will become a part of the child’s medical record. PCPs may reference the age appropriate MDHHS Well Child Exam form and use their own Well Child Exam form or electronic medical record (EMR) if the form or EMR contains all of the elements of the AAP periodicity schedule. (Refer to the Directory Appendix for AAP and MDHHS website information.)

All children who are 3 years of age or older at the time of entry into foster care will receive a dental examination within 90 days of entry into foster care unless the child had a dental exam in the six months prior to foster care placement. It is the responsibility of the foster care parent to take the child to the dentist.

A developmental/behavioral assessment must be completed according to the recommendations of the AAP. A developmental/behavioral assessment includes developmental screening, autism screening, developmental surveillance, psychosocial/behavioral assessment, alcohol and drug use assessment, and depression screening. Screening for these potential developmental/behavioral issues is accomplished by using an objective validated and standardized screening tool and should be completed with the assistance of a person who knows the child best. This may be the child’s biological parent, foster care parent, caregiver, or other adult who knows the child. The foster care worker is available to assist the provider in identifying the person who knows the child best. The psychosocial/behavioral assessment is required at each scheduled well child visit and may be accomplished by surveillance or by using a validated and standardized screening tool such as the ASQ-SE or PSC with appropriate action to follow if the assessment is positive. PCPs should use a validated and standardized screening tool for all children in foster care and for children with mental health conditions. The use of validated and standardized screening tools improves the detection rate of social-emotional problems of children in foster care compared to the reliance on subjective clinical judgment (i.e., surveillance).

The foster care worker is trained in the use of the ASQ-SE and PSC. If the physician chooses to use either of these tools, the foster care worker is available to assist in completing the screening tool and ensure that it is made available to the medical provider for scoring and for incorporation into the treatment plan. The individual accompanying the child to the medical examination should present the completed screening tool to the PCP at the initial appointment or for any other periodic examinations. The PCP is responsible for scoring and interpreting the results of the screening tool and proposing recommendations regarding follow-up. (Refer to the Directory Appendix for foster care resources.) The PCP will recommend to the foster care worker, the birth parents, and the foster care parents (when applicable) when the child in foster care may benefit by visiting with a mental health professional. The child will be referred for a prompt follow-up assessment by an appropriate medical, dental, developmental, or mental health professional for any further identified health needs.

Thursday, October 5, 2017

Payment for hospital, Therapeutic leave days - revenue code 0185, 0813

HOSPITAL LEAVE DAYS

For Hospital Leave Days, Medicaid will pay to hold a beneficiary’s bed only when the facility’s total available bed occupancy is at 98 percent or more on the day the beneficiary leaves the facility. Facilities at 97.50 percent occupancy may round up to 98 percent. Facilities may not round up 97.45 percent – 97.49 percent to 98 percent. Hospital leave days are limited to a total of 10 days per admission to the hospital for emergency medical treatment. The patient must return to the nursing facility in 10 or fewer days in order for the nursing facility to bill for hospital leave days. When billing, the facility must use:

* Revenue Code 0185; and

* Occurrence Span Code 74, with dates representing the leave days.



THERAPEUTIC LEAVE DAYS

 Therapeutic leave days are limited to a total of 18 days during a 365-day period. When billing, the facility must use:

* Revenue Code 0183; and

* Occurrence Span Code 74, with dates representing leave days.


BILLED FACILITY DAYS

Day of Admission Medicaid reimburses the day of admission if the beneficiary is counted in the facility census (e.g., if they are in the facility at midnight). Day of Discharge Medicaid does not reimburse the day of discharge unless the discharge is due to the resident's death. When billing, the facility must indicate “20” (expired) as the Patient Status Code. A discharge due to death is counted in the facility census.

Hospital Leave Days * If the resident is expected to be in the hospital for 10 days or fewer and dies while in the hospital, the nursing facility may bill for the hospital leave days up to the day before the resident died.

* For Medicaid to pay for hospital leave days, Medicaid must have been paying for the nursing facility stay before the beneficiary was admitted to the hospital.

* If the resident returns to the nursing facility under Medicare coverage, the facility may bill for the hospital leave days if the emergency hospitalization was for ten days or fewer.

* A resident is counted in the facility census if he is in the facility at midnight. If the resident is out of the facility on hospital leave at midnight, that day must be counted as a hospital leave day. If the resident returns to the nursing facility from the hospital, then is readmitted to the hospital for the same condition that he was hospitalized for previously, the 10-day period of Medicaid reimbursed hospital leave days continues if the resident was not counted in the facility census for that day. If, given the circumstances above, the resident was counted in the facility census, a new 10-day period of Medicaid reimbursed hospital leave days may begin.

One-Day Stay A nursing facility is reimbursed for a one-day stay if a Medicaid beneficiary is admitted to the facility and, the same day, is discharged from the facility due to death, return home, or transfer to another institution that is not a Medicaid-enrolled provider. The one-day stay does not apply to a beneficiary admitted to a nursing facility if, later that
day, the beneficiary is discharged and transferred to another nursing facility or an inpatient hospital and, at midnight, the second facility or hospital claims the beneficiary in its daily census.

Outpatient and Emergency Room

A beneficiary who goes to the hospital for outpatient or emergency room services is not discharged from the nursing facility because the beneficiary is not admitted to the inpatient hospital. The beneficiary should be included in the census of the nursing facility, and this day may be billed to Medicaid even if the beneficiary was being treated at midnight in the hospital outpatient or emergency room.

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