Pulmonary Embolism: when insurers say no, reviewers often say yes

Where the denial was overturned

Nature of Statutory Criteria/Case Summary: An enrollee has requested authorization and coverage for Prothrombin (Factor II) G20210A gene mutation testing (CPT 81240). Stroke is caused by one of several pathophysiologic processes involving the blood vessels of the brain. The process may be intrinsic to the vessel, as in thrombosis seen in a hypercoagulable state. Stroke evaluation involves brain imaging, cardiac testing, and laboratory studies. The records provided for review document that this patient underwent a comprehensive neurological evaluation and patent foramen ovale closure. Despite the exhaustive work-up and medical evaluations, the patient sustained a subsequent stroke and etiology remained cryptogenic. Coinciding with the patient’s brain ischemia there was diagnosis of unprovoked pulmonary embolism.

Findings: The physician reviewer found that Nature of Statutory Criteria/Case Summary: A patient has requested reimbursement for a Factor V Leiden gene test and/or F2 Prothrombin gene test. Deep venous thrombosis and pulmonary embolism or arterial thromboses may be caused by hereditary thrombophilias. The increased risk is worth knowing, especially in situations of prolonged immobility. The complications may be prevented by appropriate interventions and the avoidance of certain drugs like estrogens, which are prothrombic. There are several known genetic mutations that can cause thrombophilia. The Prothrombin (F2) G20210A mutation increases risk of deep venous thrombosis nearly 20-fold in compound heterozygous patients with Factor V Leiden. Similarly, patients with hyperhomocysteinemia (MTHFR variants) and Factor V Leiden are at greatly increased risk for deep venous thrombosis.

Where the denial was upheld

Nature of Statutory Criteria/Case Summary: An enrollee has requested authorization and coverage for genetic testing. This patient has a personal history of bilateral upper lobe pulmonary emboli and a family history of breast cancer, blood disorder, and malignant melanoma. The patient’s provider has recommended genetic testing to determine the presence of mutations in diagnosing and treating the patient. As noted in the medical literature, patients with inherited thrombophilia have a genetic tendency for venous thrombosis. The most common inherited thrombophilias are the factor V Leiden (FVL) mutation and the prothrombin gene mutation (PGM), which together account for up to 60% of cases of an inherited hypercoagulable state.

Nature of Statutory Criteria/Case Summary: An enrollee has requested authorization and coverage for the medication Pradaxa. The American College of Chest Physicians (ACCP) 2016 guideline recommends long-term (first 3 months) anticoagulant therapy for patients with DVT of the leg or PE and no cancer. The ACCP suggests Pradaxa (dabigatran), and other medications over vitamin K antagonist (VKA) therapy (all Grade 2B). The ACCP states that several of the direct oral anticoagulants (DOAC) are equally effective. At this time, there are reversal agents available: Praxbind for Pradaxa. These reversal agents are noted to be effective in rapidly reversing the anticoagulant effect of DOACs.In this case, the patient meets the 2016 ACCP criteria for extended anticoagulation based upon recurrent VTE of legs and pulmonary embolism.

These outcomes come from California’s external review program — an independent physician panel whose decision binds the insurer. Every state has an equivalent, and internal appeals succeed even more often. If your care for pulmonary embolism was denied, the published record says the denial is worth fighting.