MAUDE Adverse Event Report: PHILIPS/RESPIRONICS, INC. REMSTAR PRO C-FLEX AUTOIQ SYSTEM ONE; VENTILATOR, NON-CONTINUOUS (RESPIRATOR)

Device Problem Adverse Event Without Identified Device or Use Problem (2993)

Patient Problems Dizziness (2194); Convulsion/Seizure (4406); Epistaxis (4458); Unspecified Respiratory Problem (4464); Unspecified Eye / Vision Problem (4471)

Event Date 06/08/2012

Event Type  Injury  

Event Description

Two 2 million safe driving miles with (b)(6) 2012.Put mask on while sitting on bed.Got up and exited passenger side of semi.My wife was driving about 60 near (b)(6).My grand daughter pulled the hose off mask.I got road rash, fractured pelvic, crushed right wrist, 3 fractured ribs, concussion, and black eyes showed up from where face or nose mask saved my nose from road rash.I have accident report, hospital records and been on total disability sense i lost my job in 2012.Started cpap (b)(6) 2012.After a healing period from (b)(6) 2012.I had a grand maul seizure (b)(6) 2012 the day i was hoping to try to go back to work.Sleep center kept telling me i just needed to get used to device.Increased levels of ros cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space.In hyperoxia, multiple signaling pathways determine the pulmonary cellular response: apoptosis, necrosis, or repair.Understanding the effects of o2 administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation.1.Introduction when administering supplemental oxygen (o2) to treat hypoxemia associated with acute and chronic conditions, o2 toxicity by overexposure may be present.[1].Suboptimal use of o2 is reflected in prescription and treatment errors that exceed those related to antibiotics [2¿4].The alveolar epithelial and alveolar capillary endothelial cells are vulnerable targets for o2-free-radical-induced injury caused by hyperoxia.In acute lung injury (ali) caused by hyperoxia, hyperpermeability of the pulmonary microvasculature causes flooding of the alveolus with plasma extravasations leading to pulmonary edema and abnormalities in the coagulation and fibrinolysis pathways promoting fibrin deposition [5, 6].Type ii alveolar epithelial cells are injured by o2 free radicals leading to impairment of surfactant production [7].Thus, the maximum positive biological benefit for this life essential but toxic molecule exists along a dose-response, deficiency¿toxicity continuum 2.Pathophysiology of oxygen toxicity hyperoxia is a state of excess supply of o2 in tissues and organs.Oxygen toxicity occurs when the partial pressure of alveolar o2 (pao2) exceeds that which is breathed under normal conditions.With continuous exposure to supraphysiologic concentrations of o2, a state of hyperoxia develops.Under hyperoxic pathological conditions, a large influx of reactive o2 species (ros) are produced.In intracellular and extracellular biological systems, the mass effect of ros elevation, caused by o2 overexposure, disrupts the balance between oxidants and antioxidants, and this disruption of homeostasis can result in damage to cells and tissues [8¿11].Exposure time, atmospheric pressure, and "fractio" the formation of fluid in the lungs causes a feeling of shortness of breath combined with a burning of the throat and chest, and breathing becomes very painful [12].The reason for this effect in the lungs but not in other tissues is that the air spaces of the lungs are directly exposed to the high o2 pressure.Oxygen is delivered to the other body tissues at almost normal partial pressure of o2 (po2) because of the hemoglobin-o2 buffer system [13¿15].Toxicity also occurs when the ata is high (1.6¿4) and the high fio2 exposure time is short.This type of exposure is referred to as high pressure o2 poisoning or the paul bert effect and is toxic to the central nervous system (cns).Central nervous system toxicity results in seizures followed by coma in most people within 30 to 60 minutes.Seizures often occur without warning and are likely to be lethal.Other symptoms include nausea, muscle twitching, dizziness, disturbances of vision, irritability, and disorientation.I've found fraud in testing.Sleep walking, death and blindness cases.All this not talked about.Call center for sleep point kept telling me i was doing good.Dizzy nose bleeds, drove at night because my eyes would hurt, at er was told i had nasal polyps.Which are soft, painless, noncancerous growths on the lining of your nasal passages or sinuses.They hang down like teardrops or grapes.They result from chronic inflammation and are associated with asthma, recurring infection, allergies, drug sensitivity or certain immune disorders.Er doctor said to quit cpap.Do more sleep studies.All were worse.But due to dot rules i was required to use cpap to keep cdl.(air force use a mouth years ago.) fda safety report id # (b)(4).

• Brand Name: REMSTAR PRO C-FLEX AUTOIQ SYSTEM ONE
• Type of Device: VENTILATOR, NON-CONTINUOUS (RESPIRATOR)
• Manufacturer (Section D): PHILIPS/RESPIRONICS, INC.
• MDR Report Key: 14676822
• MDR Text Key: 293960854
• Report Number: MW5110274
• Device Sequence Number: 1
• Product Code: BZD
• Combination Product (y/n): N
• Reporter Country Code: US
• Number of Events Reported: 1
• Summary Report (Y/N): N
• Report Source: Voluntary
• Reporter Occupation: Patient
• Type of Report: Initial
• Report Date: 06/09/2022

1 Device was Involved in the Event

1 Patient was Involved in the Event

• Date FDA Received: 06/10/2022
• Is this an Adverse Event Report?: Yes
• Is this a Product Problem Report?: Yes
• Device Operator: Lay User/Patient
• Device Expiration Date: 02/28/2014
• Was Device Available for Evaluation?: Yes
• Patient Sequence Number: 1
• Treatment: B12; CITALOPRAM 20MG ; D3; DIVALPROEX DR 500MG; LEVETIRACETAM 1000MG; PACE MAKER; VIT C
• Patient Outcome(s): Hospitalization; Life Threatening; Disability
• Patient Age: 61 YR
• Patient Sex: Male
• Patient Weight: 136 KG
• Patient Ethnicity: Non Hispanic
• Patient Race: White