MAUDE Adverse Event Report: ON-X LIFE TECHNOLOGIES, INC. ON-X PROSTHETIC MITRAL VALVE 25MM; HEART VALVE MECHANICAL

Model Number ONXM-25

Device Problem Insufficient Information (3190)

Patient Problems Aspiration/Inhalation (1725); Death (1802); Sepsis (2067)

Event Type  Death  

Manufacturer Narrative

This investigation is currently ongoing.Any additional information will be provided in the follow-up report.

Event Description

According to the case report, " a (b)(6)-year-old woman with severe rheumatic mitral stenosis, severe aortic stenosis, and severe tricuspid regurgitation underwent implantation of a 25 mm mitral and a19 mm aortic on-x valve, a de vega tricuspid annuloplasty, and maze procedure.The cardiopulmonary bypass and aortic cross-clamp times were 174 and 134 min, respectively.She had chronic atrial fibrillation, hypertension, and pacemaker placement for sick sinus syndrome, and was on warfarin, but denied any history of bleeding in the past.Her preoperative echocardiogram and right heart catheterization revealed severe pulmonary hypertension with pulmonary arterial systolic pressures of 75 mmhg and severe right ventricular dilatation.She came to the intensive care unit (icu)intubated and on high infusion rates of inotropic and vasopressor agents including epinephrine, norepinephrine, vasopressin, and milrinone.Despite multiple blood component therapy intraoperatively, she continued to be severely hypocoagulable, with thrombocytopenia, hypofibrinogenemia, and elevated international normalized ratio (inr) levels [figures 1 and 2].As her coagulation parameters began to normalize, she was started on subcutaneous heparin 5000 iu every 12 h for prophylaxis against deep vein thrombosis on postoperative day (pod) 8.However, neither antiplatelet therapy nor therapeutic heparinization was initiated due to the patient¿s precarious medical condition.Despite this, immediately after removal of the epicardial pacing wires on pod 9, she developed pericardial tamponade requiring emergent opening of the sternum.This led to progressive worsening of pulmonary hypertension, causing severe right heart failure and eventually biventricular failure, necessitating placement of an intra-aortic balloon pump and inhalational epoprostenol therapy.The patient developed renal failure which required continuous renal replacement therapy and compounded coagulopathy by causing consumptive thrombocytopenia and thrombocytopathia.Three weeks after surgery, she progressed to disseminated intravascular coagulopathy (dic) and was given multiple blood component transfusions including desmopressin, cryoprecipitate, and factor vii.After the dic was resolved, she exhibited waxing and waning coagulopathy and thrombocytopenia [figures 1 and 2].Interestingly, around 6 weeks into her icu stay, she developed profuse, life-threatening bleeding from the respiratory and upper gastrointestinal tracts and natural orifices in response to any attempts to initiate anticoagulation, even with prophylactic doses of heparin.Diagnostic bronchoscopy and upper and lower gastrointestinal endoscopies revealed extensive arteriovenous malformations (avms) throughout her respiratory and gastrointestinal tracts.Due to the lack of preoperative endoscopy and the fact that avms were not restricted to the colon, making a definitive diagnosis of heyde¿s syndrome with acquired von wille brand factor deficiency was difficult.However, there is also a possibility that some degree of aortic valve patient-prosthetic mismatch could have caused a variant of heyde¿s syndrome.The patient therefore received little or no anticoagulation for almost her entire hospital stay.During her 5 months in the icu, frequent transthoracic and transesophageal echocardiographic examinations revealed no valve thrombi.She was discharged to a long-term acute care facility on aspirin and warfarin with a subtherapeutic inr of 1.6, in view of her higher risk for bleeding.There was no history of thromboembolism and no further bleeding episodes.She died about 3 months later at an outside hospital due to pulmonary aspiration and sepsis.This investigation is relegated to the mitral valve.

Manufacturer Narrative

The manufacturing records for the onxm-25 serial number (b)(4) were reviewed and it was confirmed that all records were controlled, available for review, and met all specifications per the device master record.All lots passed functional testing and met release specifications.During the investigation no non-conformances or deviations were noted.The onxm-25 sn (b)(4) implanted (b)(6) 2013 as part of a double valve (aortic/mitral) procedure (with onxace-19 sn (b)(4)) for a (b)(6) year old female with a history of severe rheumatic mitral stenosis, severe aortic stenosis, severe tricuspid regurgitation, atrial fibrillation, hypertension, severe pulmonary hypertension with severe right ventricular dilatation, and a pacemaker for sick sinus syndrome.In addition to the double valve replacement, the patient also underwent tricuspid valve repair and a maze procedure.Referenced in an article by karkar am, et al.[karkar am, et al.2015j the patient in whom this valve was implanted suffered from multiple coagulopathies with the result that she was on minimum to no anticoagulation for most of her recovery period and yet the valve neither thrombosed nor showed any evidence of thrombosis at any time: "however, our patient remained off any type of anticoagulation for several months without any clinical evidence of valve thrombosis or embolism." her postoperative course was very complicated, however, and she died about 4 months postop at an outside hospital of pulmonary aspiration and sepsis.Among her postop complications were pericardial tamponade, pulmonary hypertension, severe right heart failure, biventricular failure, disseminated intravascular coagulopathy (dic), extensive arteriovenous malformations, possible heyde's syndrome, possible acquired von willebrand factor deficiency, renal failure, consumptive thrombocytopenia and thrombocytopathia.The authors do not attribute any of these events to the onxm valve.Unfortunately, despite their efforts, the patient died, which is a known risk for mechanical mitral valve recipients [instructions for use].The authors of this article attribute none of the complications experienced by neither the patient nor the patient's postoperative course, including the death, to the on-x mitral valve, but rather advance the idea that it provides a promising technology for high-risk patients.This complaint will be voided based on the findings of this investigation.

Event Description

According to the case report, " a (b)(6)-year-old woman with severe rheumatic mitral stenosis, severe aortic stenosis, and severe tricuspid regurgitation underwent implantation of a 25 mm mitral and a19 mm aortic on-x valve, a de vega tricuspid annuloplasty, and maze procedure.The cardiopulmonary bypass and aortic cross-clamp times were 174 and 134 min, respectively.She had chronic atrial fibrillation, hypertension, and pacemaker placement for sick sinus syndrome, and was on warfarin, but denied any history of bleeding in the past.Her preoperative echocardiogram and right heart catheterization revealed severe pulmonary hypertension with pulmonary arterial systolic pressures of 75 mmhg and severe right ventricular dilatation.She came to the intensive care unit (icu)intubated and on high infusion rates of inotropic and vasopressor agents including epinephrine, norepinephrine, vasopressin, and milrinone.Despite multiple blood component therapy intraoperatively, she continued to be severely hypocoagulable, with thrombocytopenia, hypofibrinogenemia, and elevated international normalized ratio (inr) levels [figures 1 and 2].As her coagulation parameters began to normalize, she was started on subcutaneous heparin 5000 iu every 12 h for prophylaxis against deep vein thrombosis on postoperative day (pod) 8.However, neither antiplatelet therapy nor therapeutic heparinization was initiated due to the patient¿s precarious medical condition.Despite this, immediately after removal of the epicardial pacing wires on pod 9, she developed pericardial tamponade requiring emergent opening of the sternum.This led to progressive worsening of pulmonary hypertension, causing severe right heart failure and eventually biventricular failure, necessitating placement of an intra-aortic balloon pump and inhalational epoprostenol therapy.The patient developed renal failure which required continuous renal replacement therapy and compounded coagulopathy by causing consumptive thrombocytopenia and thrombocytopathia.Three weeks after surgery, she progressed to disseminated intravascular coagulopathy (dic) and was given multiple blood component transfusions including desmopressin, cryoprecipitate, and factor vii.After the dic was resolved, she exhibited waxing and waning coagulopathy and thrombocytopenia [figures 1 and 2].Interestingly, around 6 weeks into her icu stay, she developed profuse, life-threatening bleeding from the respiratory and upper gastrointestinal tracts and natural orifices in response to any attempts to initiate anticoagulation, even with prophylactic doses of heparin.Diagnostic bronchoscopy and upper and lower gastrointestinal endoscopies revealed extensive arteriovenous malformations (avms) throughout her respiratory and gastrointestinal tracts.Due to the lack of preoperative endoscopy and the fact that avms were not restricted to the colon, making a definitive diagnosis of heyde¿s syndrome with acquired von wille brand factor deficiency was difficult.However, there is also a possibility that some degree of aortic valve patient prosthetic mismatch could have caused a variant of heyde¿s syndrome.The patient therefore received little or no anticoagulation for almost her entire hospital stay.During her 5 months in the icu, frequent transthoracic and transesophageal echocardiographic examinations revealed no valve thrombi.She was discharged to a long-term acute care facility on aspirin and warfarin with a subtherapeutic inr of 1.6, in view of her higher risk for bleeding.There was no history of thromboembolism and no further bleeding episodes.She died about 3 months later at an outside hospital due to pulmonary aspiration and sepsis.This investigation is relegated to the mitral valve.

Manufacturer Narrative

This investigation is currently ongoing.Any additional information will be provided in the follow-up report.Date of first bleeding episode (tamponade) on (b)(6) 2013 later multiple episodes of oral/nasal, transrectal and transvaginal bleeding episodes.

Event Description

According to the case report, " a (b)(6) woman with severe rheumatic mitral stenosis, severe aortic stenosis, and severe tricuspid regurgitation underwent implantation of a 25 mm mitral and a 19 mm aortic on-x valve, a de vega tricuspid annuloplasty, and maze procedure.The cardiopulmonary bypass and aortic cross-clamp times were 174 and 134 min, respectively.She had chronic atrial fibrillation, hypertension, and pacemaker placement for sick sinus syndrome, and was on warfarin, but denied any history of bleeding in the past.Her preoperative echocardiogram and right heart catheterization revealed severe pulmonary hypertension with pulmonary arterial systolic pressures of 75 mmhg and severe right ventricular dilatation.She came to the intensive care unit (icu) intubated and on high infusion rates of inotropic and vasopressor agents including epinephrine, norepinephrine, vasopressin, and milrinone.Despite multiple blood component therapy intraoperatively, she continued to be severely hypocoagulable, with thrombocytopenia, hypofibrinogenemia, and elevated international normalized ratio (inr) levels [figures 1 and 2].As her coagulation parameters began to normalize, she was started on subcutaneous heparin 5000 iu every 12 h for prophylaxis against deep vein thrombosis on postoperative day (pod) 8.However, neither antiplatelet therapy nor therapeutic heparinization was initiated due to the patient¿s precarious medical condition.Despite this, immediately after removal of the epicardial pacing wires on pod 9, she developed pericardial tamponade requiring emergent opening of the sternum.This led to progressive worsening of pulmonary hypertension, causing severe right heart failure and eventually biventricular failure, necessitating placement of an intra-aortic balloon pump and inhalational epoprostenol therapy.The patient developed renal failure which required continuous renal replacement therapy and compounded coagulopathy by causing consumptive thrombocytopenia and thrombocytopathia.Three weeks after surgery, she progressed to disseminated intravascular coagulopathy (dic) and was given multiple blood component transfusions including desmopressin, cryoprecipitate, and factor vii.After the dic was resolved, she exhibited waxing and waning coagulopathy and thrombocytopenia [figures 1 and 2].Interestingly, around 6 weeks into her icu stay, she developed profuse, life-threatening bleeding from the respiratory and upper gastrointestinal tracts and natural orifices in response to any attempts to initiate anticoagulation, even with prophylactic doses of heparin.Diagnostic bronchoscopy and upper and lower gastrointestinal endoscopies revealed extensive arteriovenous malformations (avms) throughout her respiratory and gastrointestinal tracts.Due to the lack of preoperative endoscopy and the fact that avms were not restricted to the colon, making a definitive diagnosis of heyde¿s syndrome with acquired von wille brand factor deficiency was difficult.However, there is also a possibility that some degree of aortic valve patient-prosthetic mismatch could have caused a variant of heyde¿s syndrome.The patient therefore received little or no anticoagulation for almost her entire hospital stay.During her 5 months in the icu, frequent transthoracic and transesophageal echocardiographic examinations revealed no valve thrombi.She was discharged to a long-term acute care facility on aspirin and warfarin with a subtherapeutic inr of 1.6, in view of her higher risk for bleeding.There was no history of thromboembolism and no further bleeding episodes.She died about 3 months later at an outside hospital due to pulmonary aspiration and sepsis.This investigation is relegated to the mitral valve.

• Brand Name: ON-X PROSTHETIC MITRAL VALVE 25MM
• Type of Device: HEART VALVE MECHANICAL
• Manufacturer (Section D): ON-X LIFE TECHNOLOGIES, INC.; 1300 e. anderson ln., bldg. b; austin TX 78752
• Manufacturer (Section G): ON-X LIFE TECHNOLOGIES, INC.; 1300 e. anderson ln., bldg. b; austin TX 78752
• Manufacturer Contact: rochelle maney ; 1655 roberts blvd; kennesaw, GA 30144
• MDR Report Key: 6954168
• MDR Text Key: 89468256
• Report Number: 1649833-2017-00079
• Device Sequence Number: 1
• Product Code: LWQ
• Combination Product (y/n): N
• Reporter Country Code: US
• PMA/PMN Number: P000037
• Number of Events Reported: 1
• Summary Report (Y/N): N
• Report Source: Manufacturer
• Source Type: health professional,literatur
• Reporter Occupation: Physician
• Type of Report: Initial,Followup,Followup
• Report Date: 01/02/2018

1 Device was Involved in the Event

1 Patient was Involved in the Event

• Date FDA Received: 10/17/2017
• Is this an Adverse Event Report?: Yes
• Is this a Product Problem Report?: No
• Device Operator: Physician
• Device Model Number: ONXM-25
• Was Device Available for Evaluation?: No
• Is the Reporter a Health Professional?: Yes
• Distributor Facility Aware Date: 09/18/2017
• Date Manufacturer Received: 09/18/2017
• Was Device Evaluated by Manufacturer?: Yes
• Is the Device Single Use?: Yes
• Is This a Reprocessed and Reused Single-Use Device?: No
• Type of Device Usage: Initial
• Patient Sequence Number: 1
• Patient Outcome(s): Death
• Patient Age: 57 YR