SUPERSEDED Local Coverage Determination (LCD)

Intravenous Immune Globulin

L35891

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Document Note

Note History

Contractor Information

LCD Information

Document Information

Source LCD ID
N/A
LCD ID
L35891
Original ICD-9 LCD ID
Not Applicable
LCD Title
Intravenous Immune Globulin
Proposed LCD in Comment Period
N/A
Source Proposed LCD
DL35891
Original Effective Date
For services performed on or after 10/01/2015
Revision Effective Date
For services performed on or after 03/23/2023
Revision Ending Date
04/03/2024
Retirement Date
N/A
Notice Period Start Date
N/A
Notice Period End Date
05/17/2015
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Issue

Issue Description

Corrected the link for #3 in Bibliography section.

Issue - Explanation of Change Between Proposed LCD and Final LCD

CMS National Coverage Policy

Language quoted from CMS National Coverage Determinations (NCDs) and coverage provisions in interpretive manuals are italicized throughout the Local Coverage Determination (LCD). NCDs and coverage provisions in interpretive manuals are not subject to the LCD Review Process (42 CFR 405.860[b] and 42 CFR 426 [Subpart D]). In addition, an administrative law judge may not review an NCD. See §1869(f)(1)(A)(i) of the Social Security Act.

Unless otherwise specified, italicized text represents quotation from one or more of the following CMS sources:

Medicare Claims Processing Transmittal 507, CR 3745, dated March 18, 2005
CMS Manual System, Pub 100-03, Medicare National Coverage, Chapter 1, Section 250.3
CMS Manual System, Pub 100-04, Medicare Claims Processing, Chapter 17, Section 80.6
CMS Manual System, Pub. 100-04, Medicare Claims Processing, Transmittal 1482, CR 5980, dated March 21, 2008
Transmittal 1261 (Change Request 5635, dated 06/01/2007)
Transmittal 2045, Change Request 7147, dated September 10, 2010
Social security Act Section 1861 (t) (2) (b)

CMS Transmittal 2662, Change Request 8237, dated March 1, 2013. Update of the Ambulatory Surgical Center (ASC) Payment System.

Coverage Guidance

Coverage Indications, Limitations, and/or Medical Necessity

Intravenous Immune Globulin (IVIG) is a solution of human immunoglobulin specifically prepared for intravenous infusion. Immunoglobulin contains a broad range of antibodies that specifically act against bacterial and viral antigens.

The use of intravenous immune globulin should be reserved for patients with serious defects of antibody function. The goal is to provide immunoglobulin G (IgG) antibodies to those who lack them.IVIG infusion may have other effects beyond simple antibiody replacement. Coverage will be provided for intravenous immune globulin when it is used in treatment of the following conditions:

1.Primary Humoral Immunodeficiency Syndromes

IVIG is indicated for the treatment of patients with primary immunodeficiency syndromes such as common variable immunodeficiency (CVID), congenital agammaglobulinemia (X-linked agammaglobulinemia), severe combined immunodeficiency (SCID), X-linked immunodeficiency with hyperimmunoglobulin M (IgM), and Wiskott-Aldrich syndrome to replace or boost immunoglobulin G (IgG).

Common variable immunodeficiency (CVID), also known as acquired hypogammaglobulinemia, adult-onset hypogammaglobulinemia, and dysgammaglobulinemia, is characterized by reduced serum immunoglobulins, impaired antibody responses, and heterogenous clinical features. It is a rare syndrome, affecting one in 50,000 to one in 200,000 people. In most patients, the onset is in the second or third decade of life. The most common clinical presentation of CVID is an increased susceptibility to infection. Because patients with CVID are predisposed to chronic lung disease and pulmonary deterioration as a result of chronic or subclinical infection, early recognition of the diagnosis and initiation of the IVIG therapy are critical. Patients with CVID can also develop a variety of autoimmune and inflammatory disorders and are also at risk for inflammatory bowel disease.

Once the diagnosis of CVID is suspected based on clinical presentation, laboratory confirmation should be made. A low serum IgG level is the most consistent laboratory abnormality in CVID, with most patients having concurrent deficiencies of IgA and IgM. However, there are rare instances when a patient will have normal IgG levels. Therefore, the serum immunoglobulin measurement alone does not establish a diagnosis of CVID. A definitive diagnosis of CVID is established when a patient does not demonstrate an antibody response or rejection to immunization with protein antigens (e.g., tetanus) or carbohydrate antigens (e.g., pneumococcal capsular polysaccharides such as Pneumovax).

The following diagnostic evidence is required to support a diagnosis of CVID:

  • Laboratory reports demonstrating an IgG level of less than 400 mg/dl for the assay utilized, and lack of response to immunization (see below);


OR

  • An IgG level greater than or equal to 400mg/dl with evidence of recurrent severe infections with documented antibiotic therapy and lack of response to immunization (see below);
  • Laboratory reports demonstrating a lack of ability to produce an antibody response to a protein antigen (e.g., tetanus) or one of the polysaccharide antigens (e.g., Pneumococcal polysaccharide or H. Influenza type B). Two or more immunizations should have been given in the 12 months prior to laboratory assessment of antibody response. The exception maybe when a severe adverse reaction has occurred with the last immunization and two have been given over 12 month or longer interval. Pneumococcal titers are measured differently among different laboratories with some measuring 4, 5, 6, 12, or 14 serotypes. An adequate response of the serotypes tested should include a two to three fold increase in titers in at least 50 percent of the serotypes.



Reimbursement will not be provided for the initiation or continuation of intravenous immune globulin therapy based solely on a low IgG value, there must be a demonstrated lack of ability to produce an adequate antibody response to protein or carbohydrate antigens. There is no scientific rationale for IVIG therapy and it will be considered not medically reasonable and necessary, when used in patients with normal humoral immunity but with recurrent infections. The use of IVIG for recurrent viral upper respiratory infection will not be considered medically reasonable and necessary. Sinopulmonary disease which merits the use of IVIG is defined as a documented pneumonia, bronchiectasis, chronic bronchitis, recurrent bacterial or mycoplasma bronchitis, pneumonitis and documented episodes of acute bacterial sinusitis requiring extensive and/or recurrent courses of antibiotics. The goal of using IVIG therapy in this situation to prevent progressive lung disease and avoid other serious bacterial infections including meningitis, sepsis, solid organ abscess, osteomylitis, or other bacterial infection of sufficient severity to merit hospitalization

When IVIG is indicated in immunodeficient individuals (as defined above), with recurrent or chronic bacterial sinusitis, the medical record must document findings diagnostic of, or highly suggestive of, recurrent or chronic bacterial sinus infection. Such findings may include, but are not limited to, fever, unilateral purulent nasal discharge and unilateral facial pain." Absence of these findings will not preclude the use of IVIG, however, documentation will be considered insufficient to justify medical necessity when antibiotic therapy is prescribed routinely during the first few days of symptoms in the absence of these findings, or in the instance where antibiotic therapy is prescribed by phone without the benefit of an examination by a physician (or qualified non-physician practitioner). The fact that antibiotic therapy is prescribed for an episode of sinusitis will not be considered, in and of itself, evidence of bacterial sinus infection. IVIG is never indicated and therefore not reasonable and necessary for the treatment of simple viral rhinosinusitis, even in immunodeficient individuals and even if recurrent. Recurrent rhinosinustis is defined as the occurrence of four or more episodes of acute rhinosinustis per year with interim symptom resolution. Chronic sinusitis is defined as an episode of rhinosinustis that persists for greater than 12 weeks.

Patients who have been receiving long term IVIG therapy for Primary Humoral Immunodeficiency Syndromes may have undergone diagnostic testing in the remote past, the results of which may no longer be available. Repeat testing for the purpose of re-confirming the diagnosis is not necessary. Similarly, repeat testing with new technology, not available at the time or original testing for the purpose of diagnostic confirmation is also not necessary. The medical record must document that the patient has been receiving long term IVIG therapy .

Dosage Guidelines:

The dosing regimen for patients with CVID is not standardized, but is based primarily on the clinical response. Generally, checking trough levels of IgG and functional antibody levels are not medically necessary more frequently than every 3-6 months. A patient will generally receive initial IVIG doses of 400-600 mg/kg every 3-4 weeks titrating the dose and interval to achieve serum trough levels of at least 400 mg/dl or 300 mg/dl above the baseline IgG level. Documentation should support the rationale for a serum trough level greater than 300 mg above the baseline IgG. IVIG replacement in these patients is usually life-long.

Maintenance doses exceeding the 400-600 mg/kg range may be covered, but only if the desired clinical response to 400-600 mg/kg is clearly documented as inadequate as evidenced by serum trough levels below 400mg/dl.


  • Congenital agammaglobulinemia (X-linked agammaglobulinemia) is an inherited deficiency that appears in the first 3 years of life and occurs in one out of 10,000 people. Quantitative immunoglobulins show marked deficits or absence of all five immunoglobulin classes. Peripheral blood B-lymphocytes are usually absent.
  • Severe combined immunodeficiency (SCID) is a rare and fatal inherited syndrome that has an incidence of approximately one in 1,000,000 people. The typical case involves an infant less than one year of age. The lymphocyte counts are significantly below normal, the levels of B- and T-lymphocytes are absent or below normal, the lymphocyte response to mitogen is absent or below normal, and the quantitative measurements of IgG, IgA, and IgM show marked deficits.
  • X-linked immunodeficiency with hyperimmunoglobulin M (IgM) is similar to X-linked agammaglobulinemia, however, these patients sometimes have lymphoid hyperplasia. The concentrations of serum IgG, IgA, and IgE are very low, whereas the serum IgM concentration is either normal or, more frequently, greatly elevated and polyclonal.
  • Wiskott-Aldrich syndrome is an X-linked recessive syndrome characterized by eczema, thrombocytopenia purpura with normal-appearing megakaryocytes but small defective platelets, and undue susceptibility to infection. Patients usually present during infancy. Survival beyond the teens is rare.


For congenital agammaglobulinemia (X-linked agammaglobulinemia), severe combined immunodeficiency (SCID), X-linked immunodeficiency with hyperimmunoglobulin M (IgM), and Wiskott-Aldrich syndrome, the dosage variability is based on a patient’s condition and disease type, providers must adhere to the current clinical standard of practice and recommended dosage in current literature. Any time there is a departure from the standard dosing, the rationale for this must be documented in the medical record.

Dosage Guidelines:

  • A patient will generally receive initial IVIG doses of 400-600 mg/kg every 3-4 weeks titrating the dose and interval to achieve serum trough levels of at least 500 mg/dl or 300 mg/dl above the baseline IgG level. IVIG replacement in these patients is usually life-long.
  • Maintenance doses exceeding the 400-600 mg/kg range may be covered, but only if the desired clinical response to 400-600 mg/kg is clearly documented as inadequate as evidenced by serum trough levels below 400mg/dl.


 2. IVIG in Children with Human Immunodeficiency Virus (HIV) Disease who do not have ITP

IVIG may be medically necessary to reduce significant bacterial infections when all three primary criteria and one of the secondary criteria are met:

Primary criteria:

1.Age less than 13 years
2.IgG level less than 400 mg/dl
3.Entry CD4+ lymphocyte cell count is greater than or equal to 200/mm3

Secondary criteria:

1.Two or more bacterial infections in a 1-year period despite antibiotic chemoprophylaxis with TMP-SMZ or another active agent

2.The child has received two doses of measles vaccine and lives in a region with a high prevalence of measles

3.The child has chronic bronchiectasis whose immunological response is suboptimal to antimicrobial and pulmonary therapy

4.The child has immune abnormalities with symptomatic or asymptomatic HIV, as evidenced by a lack of ability to produce an antibody response to immunization with protein antigens (e.g., tetanus) or carbohydrate antigens (e.g., pneumococcal capsular polysaccharides. such as, Pneumovax).

Dosage guideline: For pediatric (HIV) Infection is 400-mg/kg body weight given every 28 days to prevent serious bacterial infection. Claims reimbursed with dosages in larger or decreased frequency of administration are subject to medical review, like any service.

5. Neurological Disorders

IVIG is indicated for the treatment of patients with neurological disorders such as Guillain-Barre’ syndrome, relapsing-remitting multiple sclerosis, chronic inflammatory demyelinating polyneuropathy (and variant syndromes such as Multifocal Motor Neuropathy), myasthenia gravis, refractory polymyositis, and refractory dermatomyositis. However, it is noted that not all patients with these diagnoses require treatment with IVIG.

IVIG therapy will only be considered medically reasonable and necessary for these neurological disorders when there is evidence of rapid progression of the disease or relapse or when other forms of treatment have failed or are contraindicated. The physician must document the rationale for the choice of therapy and consider disease activity, concurrent illness, venous access, side effects and drug availability in the decision of which therapy to prescribe and in what sequence.

For each of these diseases, the diagnosis of the disorder must be unequivocal. There must be clinical (history, quantitative examination), electrophysiological motor-sensory nerve conductions, electromyography (EMG), cerebrospinal fluid (CSF), and when necessary, biopsy (muscle-nerve) data to support the diagnosis. This must be clearly documented in the medical record and conclusions based upon this information must be consistent with accepted standards of care, in order for IVIG treatment to be considered reasonable and necessary.

Once IVIG treatment is initiated, meticulous documentation of progress is required. If there is initial improvement, and continued treatment is necessary, quantitative assessment to monitor the progress is required (e.g., ADL measurements). Changes in these parameters must be clearly documented. Subjective or experiential improvement alone is insufficient to either continue IVIG or to expect coverage.

There must be evidence of an attempt to wean the dosage when improvement has occurred. This “weaning” may be either a reduction in the frequency of administration and/or a reduction in dosage. There must be an attempt to stop the IVIG infusion if improvement is sustained with dosage reduction. If improvement does not occur with IVIG, then IVIG therapy is not indicated and should be discontinued. Generally, objective clinical improvement should occur within three months of the start of the IVIG therapy. If objective clinical improvement does not occur within this time frame, further administration of IVIG will be considered not medically reasonable and necessary.

Maintenance dosing for neurologic disorders should be individualized such that the minimum dose required to maintain clinical response is used for those patients who require chronic therapy. Where it is necessary to administer larger doses than noted in the dosage guidelines, the medical record must document that such higher doses are required to maintain response. Such documentation must include evidence that lower doses are not efficacious in producing the needed functional response for any individual patient.

  • Guillain-Barre’ syndrome is an acute, frequently severe, and fulminant inflammatory demyelinating polyneuropathy that occurs at a rate of approximately one case in a million per month. An infection generally precedes the onset of neuropathy by 1 to 3 weeks. A small proportion occurs within 1 to 4 weeks of a surgical procedure. The clinical features include ascending paralysis, hyporeflexia or areflexia, parasthesias, and elevated spinal fluid protein levels. Pain, particularly in the back and extremities may be reported in up to two thirds of cases. Electrophysiologic evidence includes prolonged or absent F waves and absent H reflexes. Increased distal latencies, conduction blocks with temporal depression of motor responses also occur followed by slowing of nerve conduction velocities. Intravenous administration of high-dose immunoglobulin given over 5 days has been proven effective.


Dosage Guidelines: 1,000 mg/kg body weight daily for two days; or 400 mg/kg body weight daily for five days.


  • Multiple Sclerosis that is relapsing-remitting is characterized by unpredictable recurrent attacks of neurological dysfunction. Attacks generally evolve over days to weeks and may be followed by complete, partial, or no recovery. Patients with a relapsing-remitting course experience no progression of neurological impairment between attacks. The age of onset is generally between 15 and 60 years. IVIG has not as yet been shown to be clinical benefit in patients with progressive forms of multiple sclerosis. IVIG will be covered for the treatment of multiple sclerosis only when there is clear documentation of relapsing remitting disease.


Dosage Guidelines: Usual dosing is 200-400 mg/kg every 4 weeks.

  • Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) includes a group of chronic progressive or relapsing, inflammatory demyelinating peripheral neuropathies that are manifested by physiological abnormalities such as partial conduction block,slowed nerve conduction velocities manifested by prolonged distal motor latencies and/or delayed or absent F waves, or dispersion of compound muscle action potentials. Clinical features include chronic progressive or relapsing symmetric weakness with sensory loss and high spinal fluid protein levels. In addition, IVIG may be approved for CIDP patients, who had no response or an inadequate response to corticosteroids, who have experienced unacceptable side effects to the use of corticosteroids and dosage reduction is not clinically feasible or have contraindications to steroids. The physician will be required to substantiate the contraindication(s) in the medical record.



Dosage Guidelines for:

  • Initial therapy - 400 mg/kg body weight per day for five days
  • Maintenance therapy - 250-400 mg/kg body weight no more frequently than every two weeks.


 6. Myasthenia gravis is a disorder of neuromuscular transmission characterized by fluctuating weakness and fatigability. It is attributed to blockage of the acetylcholine receptor at the neuromuscular end-plates by anti-acetylcholine receptor autoantibodies. The diagnosis of myasthenia gravis is confirmed by a positive Tensilon test. Anticholinesterase drugs or thymectomy are generally the first treatments for this condition

IVIG is indicated in those patients with myasthenia gravis who have failed to respond to, or have intolerable side effects to acetylcholinesterase inhibitors, are either refractory to corticosteroids over a 6 week period; have been unable to successfully taper corticosteroids below moderately high doses; or develop severe side effects due to steroid therapy; and have also failed at least one immunosuppressive agent (e.g., azathiprime, Methotrexate, cyclophosphamide, cyclosporine). Thymectomy must be considered in patients who have evidence of thymoma prior to the use of IVIG. IVIG will be considered medically reasonable and necessary as a first line therapy for Myasthenic crisis or preoperatively for planned thymectomy. Length of treatment with IVIG will vary due to the remittent and recurrent nature of this condition.

Dosage Guidelines: At this time, there is no clearly established dozing regimen, although many studies have reported success with a dose of 400 mg/kg weight per day for five days.

7. Polymyositis and dermatomyositis are conditions in which the skeletal muscle is damaged by a nonsuppurative inflammatory process dominated by lymphocytic infiltration. Polymyositis begins acutely or insidiously with muscle weakness, tenderness, and discomfort. Proximal muscles more often than distal muscles are affective. Dermatomyositis involves characteristic skin changes that may precede or follow the muscle syndrome and include a localized or diffuse erythema, maculopapular eruption, scaling eczematoid dermatitis, or rarely, an exfoliative dermatitis. The classic lilac-colored (heliotrope) usually manifested on the eyelids, bridge of the nose, cheeks (butterfly distribution), forehead, chest, elbows, knees and knuckles, and around the nailbeds. Periorbital edema is frequent.

Diagnostic studies to support a diagnosis of polymyositis or dermatomyositis include an elevated creatine phosphokivase (CPK), an abnormal electromyography (EMG), and/or an abnormal muscle biopsy. The differential diagnosis of polymyositis and dermatomyositis includes other entities which may cause muscle weakness including drug induced myopathy, necrotizing myopathy, hypothyroidism, HIV infection, myasthenia gravis, inherited metabolic myopathies and the muscular dystrophies. Diagnostic studies, along with the history and physical examination must clearly document the diagnosis to be polymyositis or dermtomyositis.

IVIG is indicated in those patients with polymyositis or dermatomyositis who are either refractory to corticosteroids over a 6 week period administered as Prednisone 1 mg/kg or equivalent; have been unable to successfully taper corticosteroids below moderately high doses even with the addition of other immunosupressive agents; or develop severe side effects due to steroid therapy; and have also failed at least one immunosuppressive agent (e.g., azathioprime, Methotrexate, cyclophosphamide, cyclosperine). Patients who fail to show a response to initial therapies are considered to have resistant disease. Resistant disease is defined by a lack of normalization of the serum creatine kinase (CK) by 4-6 weeks and/or a failure to regain muscle strength in three months. Before treatment with IVIG, consideration should be given to alternative diagnoses. Length of treatment with IVIG will vary due to the remittent and recurrent nature of these conditions. The need for continuation of IVIG must be documented and would be demonstrated by continued decreased muscle strength, elevated CPKs, and/or EMG abnormalities.

Dosage Guidelines: 1,000 mg/kg body weight daily for two days every four weeks or 400mg/kg body weight for five days every four weeks in patients intolerant of high-dose therapy.

Note: For patients who are unable to tolerate corticosteroid or immunosuppressive agents, or in the rare instance that these agents are contraindicated for the patient, treatment for polymyositis or dermatomyositis will be covered only if medical record documentation clearly indicates the reason that the patient cannot take the corticosteroid or immunosuppressive agent

Other Disorders

a. Chronic Lymphocytic Leukemia

Chronic lymphocytic leukemia is a disorder of accumulation of mature-appearing lymphocytes in blood marrow and other organs. The symptoms usually develop gradually and include fatigue, shortness of breath with activity, weight loss, or frequent infections of the skin, lungs, kidneys, or other sites. Recurrent infections are a frequent complication.

IVIG is indicated for the prevention of recurrent bacterial infections and an immunoglobulin G (IgG) level of less then 600 mg/dl in patients with hypogammaglobulinemia associated with B-cell chronic lymphocytic leukemia (CLL) in order to help correct the patient’s immunity deficiency.

Dosage guideline for this disease process is 400 mg/kg body weight given every 3 – 4 weeks.

b. Hematopoetic Stem Cell Transplantation (HSCT)

IVIG is indicated to prevent the risk of acute graft-versus-host disease, associated interstitial pneumonia (infectious or idiopathic) and infections (e.g., cytomegalovirus infections [CMV], varicella-zoster virus infection, and recurrent bacterial infection) after HSCT in patients 20 years of age or older during the first 100 days after transplantation. It is not indicated in HSCT patients younger than 20 years of age, nor is it recommended for autologous transplants.

Dosage guideline is 500 mg/kg body weight given on days –7 and –2 pre-transplantation, then weekly through day 90 post-transplantation.

c .Kawasaki Disease (mucocutaneous Lymph Node Syndrome)

Kawasaki disease is an acute childhood vasculitis, the diagnosis of which is made based on clinical criteria. These criteria include fever of at least five (5) days duration and at least four (4) of the following: (1) polymorphic exanthem, (2) changes in the oropharynx such as fissured lips and strawberry tongue without discrete lesions, (3) changes in the extremities such as edema of the hands and feet and erythema of the palms and soles, (4) bilateral conjunctival infection without exudate, and (5) cervical lymphadenopathy, often singular and unilateral. IVIG is indicated for the treatment of Kawasaki disease when used in conjunction with aspirin.

Dosage guideline: 400 mg/kg body weight for four (4) consecutive days or a single infusion of 2,000 mg/kg body weight.

d. Autoimmune Hemolytic Anemia

Autoimmune hemolytic anemia is an acquired anemia induced by the binding of autoantibodies and/or a complement to the red cells. Signs and symptoms may include, but are not limited to, weakness, fatigue, exertional dyspnea, pallor, jaundice, tachycardia, splenomegaly, hepatomegaly, and anemia. In the majority of patients, this disease can be controlled by steroid therapy alone, by splenectomy or by a combination of these.

In this condition, intravenous immune globulin is indicated only for those patients who have failed to respond to other forms of therapy and/or require rapid cessation of hemolysis due to severe or life threatening manifestations of this condition. Other therapies showing treatment efficacy include corticosteroids, immunosuppressive and cytotoxic agents and monoclonal antibodies such as Rituximab. Duration of treatment is generally a short course of 3-5 weeks. Realizing dosage may vary based on patient’s individual situation; dosage must be in keeping with the recommended current literature and standard of practice.

Dosage guidelines: Realizing dosage may vary based on a patient’s individual situation, the dosage must be in keeping with the recommended dosage in current literature and the standard of practice. Any time there is a departure from the standard dosing, the rationale for this must be documented in the medical record.

e. Autoimmune Neutropenia

Autoimmune neutropenia is a hematologic disorder in which there is a decreased number of neutrophilic leukocytes in the blood due to an autoimmune mechanism. The disease is usually benign and self-limiting, and treatment beyond antibiotics is not frequently required. Occasionally, however, it is marked by repeated infection. IVIG may be recommended for the treatment of an absolute neutrophil count less than 800mm with recurrent bacterial infections.

Dosage guidelines are 1 to 2 g/kg of IVIG over 1 to 2 days.

f. Autoimmune Mucocutaneous Blistering Diseases

Effective October 1, 2002, IVIG is covered for the treatment of biopsy-proven (1) Pemphigus Vulgaris, (2) Pemphigus Foliaceus, (3) Bullous Pemphigoid, (4) Mucous Membrane Pemphigoid (a.k.a., Cicatricial Pemphigoid), and (5) Epidermolysis Bullosa Acquista for the following patient subpopulations:

1. Patients who have failed conventional therapy such as corticosteroids (prednisone at not less than 1 mg/kg or equivalent), azathioprine or mycophenolate mofetil;

2. Patients in whom conventional therapy is otherwise contraindicated; or

3. Patients with rapidly progressive disease in whom a clinical response could not be affected quickly enough using conventional agents. In such situations IVIG therapy would be given along with conventional treatment(s) and the IVIG would be used only until the conventional therapy could take effect.

Dosage guidelines: 2,000 mg/kg body weight per month divided into 1 to 5 doses.

In addition, IVIG for the treatment for autoimmune mucocutaneous blistering diseases must be used only for short-term therapy and not as a maintenance therapy.

g. Multiple Myeloma

IVIG is indicated in patients with multiple myeloma to reduce the incidence of recurrent bacterial infection when the patient is in the plateau phase of the disease and there is evidence of immunodeficiency as indicated by a serum IgG level <600mg/dl and a history of one documented, serious bacterial infection requiring IV antibiotic therapy in the previous six months or two or more such infections in the previous one year. IVIG will also be considered medically necessary when there has been a failure to mount an appropriate IgG humoral response to pneumococcal vaccine. IVIG therapy is not considered medically reasonable and necessary during primary induction chemotherapy or during a relapse of the disease


IVIG is considered medically reasonable and necessary for the following off-label indications:

  • Stiff-man syndrome. Please refer to the utilization guidelines and documentation requirements for specific criteria related to coverage.
  • Hypogammaglobulinemia with NNI (non neutropenic infection) induced by certain agents (All criteria must be met):

1. Recent treatment with rituximab in combination with cytotoxic chemotherapy
2. Laboratory proven hypogammaglobulinemia and an absolute neutrophil count over 1,000.
3. Acute infection requiring hospitalization or an infection lasting over 2 weeks in spite of antibiotics or an infection relapsing immediately after discontinuation of antibiotics.
4. Dose: 400-600 mg/kg one time that can be repeated at a standard interval based on laboratory assessment of IG levels and persistence of non neutropenic infection.

h. Chronic Graft versus Host Disease (GVHD)

 

IVIG is indicated in patient with chronic GVHD who meet all of the following criteria

 

  1. Laboratory proven hypogammaglobulinemia with IgG levels <400 mg/dl.

  2. At least one acute infection requiring hospitalization and/or parenteral antibiotics

  3. Confirmed diagnosis of chronic GVHD

  4. At least 100 days post transplant.

 

 

Summary of Evidence


Expansion of coverage to treat secondary hypogammaglobulinemia to any medication that may cause this laboratory finding

The literature reviewed shows the following evidence

 

  1. There is an association between the administration of certain pharmaceuticals and the development of hypogammaglobulinemia.

  2. Not all forms of secondary hypogammaglobulinemia confer an increased risk of infection

  3. There is insufficient evidence to conclude that IVIG reduces the incidence or severity of infection in patients with drug induced secondary hypogammaglobulinemia.

 

 

Adding coverage for IVIG for hematopoietic stem cell transplantation (HSCT)

 

  1. The evidence is sufficient to conclude that the complications of stem cell transplantation are independent of the source of stem cells.

 

 

Adding coverage for IVIG for hypogammaglobulinemia for Graft vs. Host Disease (GVHD)

 

  1. There is sufficient evidence to conclude that patients who require ongoing immunosuppression for the treatment of chronic GVHD are at increased risk when compared to their peers who do not require such treatment.

  2. There is sufficient evidence that such patients who are hypogammaglobulinemic (IgG < 400 mg/d)  and have experienced one serious infection may benefit from treatment of IVIG

  3. There is insufficient evidence that prophylactic treatment of HSCT patients with IVIG provides a benefit in the absence of hypogammaglobulinemia





 

Analysis of Evidence (Rationale for Determination)

1.Use of IVIG for the treatment of secondary hypogammaglobulinemia induced by various medications.

 

While evidence from the peer reviewed medical literature documents an association between various agents which suppress the immune system and low immunoglobulin levels, the literature does not address whether this finding equates to a higher incidence of serious and/or life threatening infections or that the administration of immune globulin offers a beneficial effect by reducing either the frequency of said infections, or the morbidity/mortality associated with them

 

2.Use of IVIG for hypogammaglobulinemia associated with hematopoetic stem cell transplant (HSCT).

The Infectious Disease Society of America (IDSA) in their guideline for preventing infectious complications among HSCT recipients, defines HSCT to include any stem cell transplant, regardless of type or source.  While there are differences in the risks and complications of HSCT between different sources, the effects on immune function are similar.  In light of this, CGS will no longer cover indications for bone marrow transplant (BMT) recipients only, but will extend the same coverage currently in place of BMT recipients, to all HSCT receipients.

 

 

3. Use of IVIG  for hypogammaglobulinemia associated with complications of HSCT such as graft vs. host disease (GVHD). 

 

The ISDA guidelines provides a summary of evidence which supports that risk of infection is, among other things, related to the presence or absence of GVHD.  Patients with chronic GVHD, who require ongoing immunosuppressive therapy to prevent complications of GVHD, may have ongoing impaired immunity as demonstrated by any number of objective tests.  This being said, the ISDA does not recommend routine administration of IVIG during the first 100 days post transplant and indicates that IVIG treatment as prophylaxis “may be considered” in patients with IgG levels <400 mg/dl.  We note the quality of evidence on their scale (graded CIII) does not meet the reasonable and necessary criteria of 1862(a)(1)(A) which supports the decision not to add this indication as covered.  The same applies to routine prophylaxis in the absence of confirmed hypogammaglobulinemia in patients >100 days post transplant.  There is however, support for the use of IVIG in patients with chronic GVHD with confirmed hypogammaglobulinemia (IgG < 400 mg/dl) and who have experienced at least one serious infection.

 

 

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Requestor Information
This request was MAC initiated.
Requestor Name Requestor Letter
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Contact for Comments on Proposed LCD

Coding Information

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Code Description
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Revenue Codes

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CPT/HCPCS Codes

Group 1

Group 1 Paragraph

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Group 1 Codes

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ICD-10-CM Codes that Support Medical Necessity

Group 1

Group 1 Paragraph:

N/A

Group 1 Codes:

N/A

N/A

ICD-10-CM Codes that DO NOT Support Medical Necessity

Group 1

Group 1 Paragraph:

N/A

Group 1 Codes:

N/A

N/A

Additional ICD-10 Information

General Information

Associated Information
Documentation Requirements

Medical record documentation maintained by the treating physician must clearly document the medical necessity to initiate intravenous immune globulin therapy and the continued need thereof. Required documentation of medical necessity includes but is not limited to:


  • History and physical; supporting physician rationale (current within the last 12 months)
  • Physicians orders not more than 30 days old to date of service specifying dose, frequency, administration route and duration office/progress note(s); that clearly document the necessity for both initiation and continuation of IVIG
  • ICD-10-CM diagnosis codes supporting medical necessity must be submitted with each claim. Claims submitted without such evidence will be denied as not medically necessary.
  • Documentation supporting the diagnosis
  • A copy of applicable lab and procedure test results
  • An accurate weight in kilograms should be documented prior to each infusion since the dosage is based mg/kg/dosage; and
  • Prior failed conventional therapies or documentation that conventional therapy is contraindicated
  • Medication administration records
  • Each order (which must not be more than 30 days old) should be accompanied by documentation in the record as to the response to the prior infusions in order for ongoing therapy to be considered medically reasonable and necessary.



In addition, medical record documentation maintained by the treating physician for claims billed with a diagnosis of CVID must include the following: the initial presenting IgG levels and evidence that the patient has been vaccinated with Pneumovax and has had pre-and post-vaccine pneumococcal antibody titers performed to demonstrate the lack of ability to produce an antibody response to protein or carbohydrate antigens.

Documentation must include dual diagnoses listed for the underlying condition that demonstrates the medical necessity for intravenous immune globulin therapy.

Documentation must include a statement regarding lack of response to protein antigen.

For patients with HIV disease and ITP the medical record must specifically reflect that the patient has a platelet count of less than 30,000 and is actively bleeding. This must be supported by applicable lab results.

When IVIG is indicated in immunodeficient individuals (as defined above), with recurrent or chronic bacterial sinusitis, the medical record must document findings diagnostic of, or highly suggestive of, recurrent or chronic bacterial sinus infection. Such findings may include, but are not limited to, fever, unilateral purulent nasal discharge and unilateral facial pain." Absence of these findings will not preclude the use of IVIG, however, documentation will be considered insufficient to justify medical necessity when antibiotic therapy is prescribed routinely during the first few days of symptoms in the absence of these findings, or in the instance where antibiotic therapy is prescribed by phone without the benefit of an examination by a physician (or non-physician practitioner). IVIG is never indicated and therefore not reasonable and necessary for the treatment of simple rhinosinusitis, even in immunodeficient individuals and even if recurrent. The administration of antibiotics in and of itself will not be considered evidence of bacterial rhinosinustis. The medical record must substantiate the use of prolonged and/or recurrent antibiotic therapy in the treatment of these infections. Radiographic documentation of mucosal thickening of the paranasal sinuses, in and of itself, is not specific to bacterial sinusitis and as a sole finding will not be consideration sufficient documentation to support the use of IVIG.

For stiff-man syndrome documentation must support that the patient is under the care of a physician who is competent in the diagnosis of the syndrome. The current defined criteria for the diagnosis must be met.. Patient would have demonstrated failed conservative treatment (such as benzodiazapines). The record must show the patients response to therapy after initial treatment (0 and 1 month). Documentation must support objective response for continued coverage each month or at longer intervals.

All documentation must support the criteria for coverage as set forth in the "Indications and Limitations of Coverage and/or Medical Necessity" section of this policy.

Utilization Guidelines

Where no dosage guidelines are provided in this LCD and that realizing dosage may vary based on a patient’s individual situation, the dosage must be in keeping with the recommended dosage in current literature and the standard of practice. Initial and/or maintenance doses of IVIG may be administered as a single infusion or may be divided and administered over several days. Any time there is a departure from the standard dosing(either dose or frequency of administration), the rationale for this must be documented in the medical record.

For stiff man syndrome initial coverage is limited to up to 2g of immune globulin per kilogram of body weight per month.
Sources of Information
N/A
Bibliography
  1. American Society of Hematology. (Online 2006). Idopathic thrombocytopenic purpura: a practice guideline developed by explicit methods for the American Society of Hematology. Available: http://www.hematology.org/policy/guidelines/idiopathic.cfm
  2. Ammann A, Ashman RF, Buckley RH et al. Use of Intravenous y-Globulinin Antibody Immunodeficiency:Results of a Multicenter Controlled Trial. Clin lmmunol lmmunopathol 1982;22:60-67.
  3. Besada E.Risk factors and adverse events poorly predict infections and hypogammaglobulinemia in granulomatosis with polyangiitis patients receiving rituximab. Autoimmune Diseases 2016; Article ID 8095695,http://dx.doi.org/10  .1155/2016/8095695
  4. Brannagan III, T.H. (2002). Intravenous gammaglobulin (IVIg) for treatment of CIDP and related immune-mediated neuropathies. Neurology. 59(12 Suppl 6):S33-40
  5. Cabanillas,F.,Liboy,I.,Pavia,O.,Rivera,E.(2006).High incidence of non-neutropenic infections induced by rituximab plus fludarabine and associated with hypogammaglobulinemia: A frequently unrecognized and easily treatable complication.Annals of Oncology,17(9),1424-1427.doi:10.1093/annonc/mdl141
  6. Caso, J.A.A., et al. (1999). Effect of highly active antiretroviral therapy on thrombocytopenia in patients with HIV infection. The New England Journal of Medicine, 341(16), 1239-1240.
  7. Casulo C, Maragulia J, Zelenetz AD. Incidence of hypogammaglobulinemia in patients receiving rituximab and the use of intravenous immunoglobutin for recurrent infections. Clin Lymphoma Mye1oma Leuk 2013; 13:106-111.
  8. Cervetti G, Carulli G, Galimberti S Et al. Reduction of immunoglobulin levels during imatinib therapy of chronic myeloid leukemia . Leuk Res 2008; 32:191-192.
  9. Chapel HM,Lee M, Hargreaves R Et al.Randomized trial of intravenous immune globulin as prophylaxis against infection in plateau-phase multiple myeloma.The UK Group for lmmunoglobulin Replacement Therapy in Multiple Myeloma. Lancet  1994;343:1059-1063.
  10. Conley, M.E., Notarangelo, L.D., & Etzioni, A. (1999). Diagnostic criteria for primary immunodeficiencies. Clinical Immunology, 93 (3), 190-197.
  11. Cooperative Group for the Study of lmmunoglobulin in Chronic Lymphocytic Leukemia.Intravenous immunoglobulin for the prevention of infection in chroniclymphocytic leukemia. N EnglJ Med 1988; 319:902-907.
  12. Corales R,Chua J, Mawhoter S Et al. Significant post-transplant hypogammaglobulinemia in six heart transplant recipients: an emerging clinical phenomenon? Transpl Infect Dis 2000;2:133-139.
  13. Dalakas, M.C., Fujii, M., et al. (2001). High dose intravenous immune globulin for stiff-person syndrome. N Engl J Med 2001; 345:1870-1876.
  14. Duraisingham SS,Buckland M,Dempster J Et al. Primary vs.secondary antibody deficiency: clinical features and infection outcomes if immunoglobulin replacement.PLOS ONE 2014; 9: e100324.doi: 0.1371
  15. Griffiths H, Brennan V, Lea J Et al. Crossover study of immunoglobulin replacement therapy in patients with low grade B-cell tumors. Blood 1989; 73:366-368 .
  16. Kado R, Sanders G, McCune WJ. Diagnostic and therapeutic consideration in patients with hypogammaglobulinemia after rituximab therapy. Curr Opin Rheumatol 2017; 29:228-233 .
  17. Keven K,Sahin M,Kutlay S Et al. lmmunoglobulin deficiency in kidney allograft recipients: comparative effects of mycophenolate mofetil and azathioprine.TransplInfect Dis 2003:5:181-186
  18. Levy R,Mahevas M,Galicier L Et al. Profound symptomatic hypogammaglobulinemia : a rare late complication after rituximab treatment for immune thrombocytopenia.Report of 3 cases and systematic review of the literature. Autoimmunity Reviews 2014; 13:1055 1063.
  19. Majhail NS, Rizzo JD, Lee SJ et al. Recommended screening and preventive practices for long-term survivors after hematopoietic cell transplantation. Biol Blood Marrow Transplant 2012; 18:348-371. Pages 348,350,353, and 354 provided.
  20. Makatsori M,Kiani-Alikhan S, Manson AL et al. Hypogammaglobulinemia after rituximab treatment· incidence and outcomes.Q J  Med 2014;  107:821-828.
  21. Maury S, Mary J-Y, Rabian C Et al. Prolonged immune deficiency following allogeneic stem cell transplantation:risk factors  and complications in adult  patients.Br J  Haematol 2001;115:630-641.
  22. Musto P, Brugiatelli M,Carotenuto M. Prophylaxis against infections with intravenous immunoglobulins in multiple myeloma. Br J Haematol 1995; 89:945-946.
  23. National Cancer Institute. NCI Dictionary of Cancer Terms
  24. National Coverage Determination (NCD) for Intravenous Immune Globulin for the Treatment of Autoimmune Mucocutaneous Blistering Diseases (250.3).
  25. Norlin A-C,Sairafi 0,Mattsson J Et al. Allogeneic stem cell transplanta tion:low immunoglobulin levels associated with decreased surviva l. Bone Marrow Transplantation 2008; 41:267-273.
  26. Ochs HD, Fischer SH,Wedgewood RJ.Modified Immune Globulin: It's Use in the Prophylactic Treatment of Patients with Immune Deficiency.J Clin lmmunol 1982; 2 (April Supplement).22s - 30s.
  27. Ofatumumab (Arzerra•) package insert. 8/2016. Pages 1,9,and 10 provided.
  28. Orange, J.S. et al. (2006). Use of intravenous immunoglobulin in human disease: A review of evidence by members of the Primary Immunodeficiency Committee of the American Academy of Allergy, Asthma and Immunology. Journal of Allergy and Clinical Immunology. 117(4). S525-44.
  29. Pamukcuoglu M,Emmez H,Tunccan OG et al. Brain abscess caused by Nocardia cyriacigeorgica in two patients with multiple myeloma : novel agents, new spectrum of infections.Hematology 2014; 19:158-162.
  30. Rajala HLM, El Missiry M,Ruusila A Et al. Tyrosine kinase inhibitor therapy-induced changes in humoral immunity in patients with chronic myeloid leukemia.J Cancer Res Clin Oncol 2017;143:1543-1554.
  31. Ratko, T.A., Ehmann, W.C., Foulke, G.E., Givner, L.B., Kahaleh, B., Sacher, R.A., Samaha, F.J., Wingard, J.R., & Yocum, D.E. (1999). UHC recommendations for the off-label use of standard intravenous immunoglobulin preparations. [On-line]. Available: http://www.guideline.gov.
  32. Roberts DM,Jones RB,Smith RM et al.lmmunoglobulin G replacement for the treatment of infective complications of rituximab-associated hypogammaglobulinemia in autoimmune disease: a case series.J Autoimmunity 2015; 57:24-29.
  33. Santachiara R, Maffei R, Martinelli S et al. Development of hypogamma gl obul i nemia i n patients treated with i matinib for chroni c myeloid l eukemi a or gastrointestinal stroma l tumor . Haematologica 2008; 93:1252-1255 .
  34. Shortt J, Spencer A.Adjuvant rituximab causes prolonged hypogammaglobulinemia following autologous stem cell transplant for non-Hodgkin's lymphoma. Bone Marrow Transplantation 2006; 38:433-436 .
  35. Silverman, M.A. (2005) Idiopathic Thrombocytopenic Purpura [Online], Available: http://www.emedicine.com/EMERG.topic282.htm. The Association of Community Cancer Centers. (1999). United States pharmacopeia drug information: Oncology drug information (3rd ed.). Englewood, CO: Micromedex, Inc.
  36. Srivastave S,Wood P.Secondary antibody-deficiency - causes and approach to diagnosis.Clinical Medicine 2016; 16:571-576.
  37. Stapp, J. & Marshall, G. (2000). Fulfillment of diagnostic criteria in Kawasaki disease. South Medical Journal, 93(1), 44-47.
  38. Stasi R,Pagano A, Stipa E Et al. Rituximab chimeric anti-CD20 monoclonal antibody treatment for adults with chronic idiopathic thrombocytopenic purpura.  Blood 2001;98:952-957.
  39. Steegmann JL, Moreno G, A laez C et al. Chronic myeloid l eukemia patients resistant to or i ntolerant of i nterferon al pha and subsequentl y treated with i matinib show reduced i mmunog l obuli n l evels and hypogammagl obulinemia. Haematologica 2003;88:762-768.
  40. Tomblyn M, Chiller T, Et al. Guidelines for Preventing Infections Complications among Hematopoietic Cell Transplantation Recipients: A Global Perspecitve, Biol Blood Marrow Transplant 15: 1143-1238 (2009)
  41. Trivedi, D.H. et al. (2003). Immunologic Disorders. Journal of Allergy and Clinical Immunology, 111(2).
  42. The Leukemia and Lymphoma Society. (2000). Chronic lymphocytic leukemia (CLL). [On-line]. Available: http://www.leukemia.org.
  43. The United States Pharmacopeia Drug Information. (1999). United States pharmacopeia drug information book (19th ed.). (Vol. I). Englewood, CO: Micromedex, Inc.
  44. Truven Health Analytics MicroMedex .Immune Globulin ·Prevention of Bacterial Infections in Hematopoietic Cell Transplantation.5/12/2016.
  45. U.S. Food and Drug Administration (FDA) website prescribing information and approval letter for Bivigam, Immune Globulin (2012).
  46. U.S. Food and Drug Administration (FDA) website prescribing information and approval letter for Gammaplex, Immune Globulin (2009).
  47. Yu, Z., & Lennon, V.A. (1999). Mechanism of intravenous immune globulin therapy in antibody-mediated immune diseases. The New England Journal of Medicine, 340(3), 227-228.

 

 

Other Contractors LCDs:

 

 

  • Local Coverage Determination (LCD): Drugs and Biologicals: Immune Globulin Intravenous (IVIg) (L34256)
  • Local Coverage Determination (LCD): Immune Globulin Intravenous (IVIg) (L34074)
  • Local Coverage Determination (LCD): Immune Globulin Intravenous (IVIg) (L34314)
  • Local Coverage Determination (LCD): Intravenous Immune Globulin (L34007)
  • Local Coverage Determination (LCD): Intravenous Immune Globulin IVIG) (L35093)
  • Future Local Coverage Determination (LCD): Intravenous Immune Globulin (L34580)

Revision History Information

Revision History Date Revision History Number Revision History Explanation Reasons for Change
03/23/2023 R21

R21

Revision Effective: 03/23/2023

Revision Explanation: Annual review, no changes were made.

At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Other (Annual Review)
03/24/2022 R20

R20

Revision Effective: 03/24/2022

Revision Explanation: Annual review, no changes were made.

At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Other (Annual Review)
02/03/2022 R19

R19

Revision Effective: 02/03/2022

Revision Explanation: Corrected link for #3 in Bibliography section.

At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Other (corrected link)
04/01/2021 R18

R18

Revision Effective: 04/01/2021

Revision Explanation: Annual review, no chnages made.

At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Other (Annual Review)
09/19/2019 R17

R17

Revision Effective: N/A

Revision Explanation: Annual review, removed ITP details since there is a separate policy for ITP.

03/25/2020:At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Other (Annual Review)
09/19/2019 R16

R16

Revision Effective: 09/19/2019 Revision Explanation: Converted policy into new policy template that no longer includes coding section based on CR 10901. For Approval, no changes.

09/13/2019:At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Revisions Due To Code Removal
09/19/2019 R15

R15

Revision Effective: 09/19/2019 Revision Explanation: Converted policy into new policy template that no longer includes coding section based on CR 10901.

09/12/2019:At this time 21st Century Cures Act will apply to new and revised LCDs that restrict coverage which requires comment and notice. This revision is not a restriction to the coverage determination; and, therefore not all the fields included on the LCD are applicable as noted in this policy.

  • Revisions Due To Code Removal
08/01/2019 R14

Revision#:R14
Revision Effective: 08/01/2019
Revision Explanation: Removed coding from LCD based on instructions in CR 10901.

  • Other (Code Migration)
03/01/2018 R13

Revision#:R13
Revision Effective: N/A
Revision Explanation: Annual review no changes made.

  • Other (Annual Review)
03/01/2018 R12

Revision#:R12
Revision Effective: N/A
Revision Explanation: changed title of B. from Bone Marrow Transplantation (BMT) to Hematopoetic Stem Cell Transplantation (HSCT), added section H and added new ICD-10 codes; D89.810, D89.811, d89.812, D89.813, T86.5, and Z94.84. Converted to 21st century format. Annual review was done during this time as well

  • Reconsideration Request
01/01/2017 R11 Revision#:R11
Revision Effective: N/A
Revision Explanation: Annual review no changes made.
  • Other (Annual review)
01/01/2017 R10 Revision#:R10
Revision Effective: 01/01/2017
Revision Explanation: Added D80.3 to list of ICD-10 codes
  • Reconsideration Request
10/01/2016 R9 Revision#:R9
Revision Effective: 10/01/2016
Revision Explanation: Added G61.82 to list of ICD-10 codes
  • Revisions Due To ICD-10-CM Code Changes
04/01/2016 R8 Revision#:R8
Revision Effective: 04/01/2016
Revision Explanation: Corrected typographical error in associated information, ICD-9 to ICD-10.
  • Typographical Error
04/01/2016 R7 Revision#:R7
Revision Effective: 04/01/2016
Revision Explanation: Added clarifying language in text for indications and limitations.
  • Reconsideration Request
10/01/2015 R6 Revision#:R6
Revision Effective: 10/01/2015
Revision Explanation: Added G61.0 as it was left out in error
  • Typographical Error
10/01/2015 R5 Revision#:R5
Revision Effective: N/A
Revision Explanation: Annual review no changes made at this time.
  • Other (Annual Review)
10/01/2015 R4 Revision#:R3
Revision Effective: 10/01/2015
Revision Explanation: Correcting typo that was in revision 2 Added ICd-10 code T86.11-T86.13, T86.19, Z48.22, Z76.82, and Z94.0. Z48.0 should have been Z48.22.
  • Typographical Error
10/01/2015 R3 Revision#:R3
Revision Effective: 10/01/2015
Revision Explanation: Added clarifying language in the indications and limitation section concerning humoral immunodeficiency.
  • Reconsideration Request
10/01/2015 R2 Revision#:R2
Revision Effective: 10/01/2015
Revision Explanation: AddedICd-10 code T86.11-t86.13, T86.19, Z48.0, Z76.82, and Z94.0.
  • Reconsideration Request
10/01/2015 R1 Revision#:r1
Revision Effective: 10/01/2015
Revision Explanation: Added notice period dates.
  • Provider Education/Guidance
N/A

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Public Versions
Updated On Effective Dates Status
03/29/2024 04/04/2024 - N/A Currently in Effect View
03/13/2023 03/23/2023 - 04/03/2024 Superseded You are here
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