Description of Event or Problem · 0
IT HAS COME TO MY ATTENTION A DEVICE RELATED DEATH WAS NOT REPORTED TO THE FDA. AN ARTICLE DETAILING HOW THE DEVICE WAS USED WAS PUBLISHED (HTTPS://DOI.ORG/10.1016/J.INAT.2017.07.012). I REPORT IT NOW TO CLOSE THE REGULATORY GAP BETWEEN THE FDA RECOGNIZING DEATHS CAUSED BY A NOW ADULTERATED MEDICAL DEVICE (GIVEN THE ABSENCE OF PMA SUBMITTED BY (B)(6) 2019 FOR CLASS III USE AND THE ABSENCE OF "SPECIAL CONTROLS" NECESSARY TO PREVENT DEATH OF PEOPLE LIVING WITH CLASS II INDICATIONS SUBMITTED TO THE FDA BY THE FINAL RULING'S (B)(6) 2019 DEADLINE.) INFO COPIED VERBATIM "THE PATIENT'S PRE-ECT EXAMINATION DOCUMENTED DECREASE IN AFFECT, MOOD, ANXIETY, VOICE INFLECTION, RATE OF SPEECH AND SPEECH CONTENT, AND PSYCHOMOTOR ACTIVITY. THE PATIENT UNDERWENT 2 ROUNDS OF ECT STIMULATIONS. STIMULATION 1 CONSISTED OF BIFRONTAL STIMULATION FOR 6 S AT 90 HZ, 0.8 AMPS, 0.37 MSEC. HYPERVENTILATION WAS USED. THE CHARGE WAS 319 MC; ENERGY: 69.8 J; STATIC IMPEDANCE: 530 O, DYNAMIC IMPEDANCE: 267 O. THE PATIENT HAD A PERIPHERAL SEIZURE AT 21 S AND CENTRAL SEIZURES AT 27 S; POSTICTAL SUPPRESSION WAS PRESENT. STIMULATION 2 WAS AUGMENTED WITH 125 MG INTRAVENOUS CAFFEINE AND HYPERVENTILATION. AGAIN, BIFRONTAL STIMULATION WAS USED FOR 7 S AT 100 HZ, 0.8 AMPS, 0.37 MSEC. THE CHARGE WAS 414 MC; ENERGY: 77.6 J; STATIC IMPEDANCE: 480 O, DYNAMIC IMPEDANCE: 236 O. THERE WAS A PERIPHERAL SEIZURE AT 71 S AND CENTRAL SEIZURES AT 128 S; POSTICTAL SUPPRESSION WAS IMMEDIATE. DURING RECOVERY IN THE POSTANESTHESIA CARE UNIT, THE PATIENT BECAME AGITATED AND RECEIVED 5 MG MIDAZOLAM, 2 MG LORAZEPAM, AND 5 MG HALOPERIDOL. SHE HAD A TONIC-CLONIC SEIZURE LASTING 10 MIN. AN IMMEDIATE COMPUTED TOMOGRAPHY (CT) SCAN REVEALED A LARGE LEFT BASAL GANGLIA INTRAPARENCHYMAL HEMORRHAGE WITH INTRAVENTRICULAR EXTENSION (FIG. 1A). UPON IDENTIFICATION OF HEMORRHAGE, THE NEUROSURGERY SERVICE WAS CONSULTED. THE PATIENT WAS INTUBATED AND TRANSFERRED TO THE INTENSIVE CARE UNIT, WHERE SHE WAS NOTED TO BE LOCALIZING BILATERALLY BUT WEAKER ON THE RIGHT SIDE. THE PATIENT'S PUPILS WERE EQUAL, ROUND, AND REACTIVE TO LIGHT. DURING THE PREPARATION FOR VASCULAR IMAGING, THE PATIENT SUDDENLY EXPERIENCED PULSELESS ELECTRICAL ACTIVITY. AFTER 30 MIN OF RESUSCITATION, A NORMAL RHYTHM RESUMED. AN EXTERNAL VENTRICULAR DRAIN WAS PLACED, AND INTRACRANIAL PRESSURES WERE NOTED TO BE ELEVATED OVER 60 MMHG. THE PATIENT'S POSTRESUSCITATION EXAMINATION WAS CONSISTENT WITH THE ADMISSION EXAMINATION. EN ROUTE TO THE CT SCANNER, THE PATIENT DEVELOPED PUPILLARY ASYMMETRY, WHICH RESPONDED TO MANNITOL. REPEAT CT DEMONSTRATED INTERVAL INCREASE IN THE SIZE OF THE INTRAPARENCHYMAL HEMORRHAGE (NOT SHOWN). COMPUTED TOMOGRAPHIC ANGIOGRAPHY DID NOT DEMONSTRATE A STRUCTURAL VASCULAR CAUSE RESPONSIBLE FOR THE PATIENT'S HEMORRHAGE (FIG. 1B¿D). THE PATIENT WAS TAKEN FOR AN EMERGENT HEMICRANIECTOMY AND EVACUATION OF THE HEMATOMA. THE PROCEDURE WAS UNEVENTFUL, BUT DURING THE CLOSURE OF THE SKIN, THE PATIENT EXPERIENCED RECURRENT PULSELESS ELECTRICAL ACTIVITY, REQUIRING OVER 30 MIN OF RESUSCITATION. AGAIN, NORMAL RHYTHM WAS RESTORED. THE PATIENT'S POSTOPERATIVE EXAMINATION WAS CONSISTENT WITH BRISK LOCALIZATION ON THE LEFT SIDE AND BRISK WITHDRAWAL ON THE RIGHT SIDE. A FORMAL DIAGNOSTIC CEREBRAL ANGIOGRAM DID NOT DEMONSTRATE ANY UNDERLYING VASCULAR CAUSE RESPONSIBLE FOR THE PATIENT'S HEMORRHAGE (FIG. 2). SIMILARLY, A MAGNETIC RESONANCE IMAGING STUDY DID NOT REVEAL TUMOR OR OTHER CAUSES RESPONSIBLE FOR THIS HEMORRHAGE (FIG. 3). DESPITE AGGRESSIVE MEDICAL THERAPY, THE PATIENT DEVELOPED SEVERE PULMONARY EDEMA THAT WAS RECALCITRANT TO THERAPEUTIC INTERVENTIONS. ULTIMATELY, AFTER FAMILY DISCUSSION, THE DECISION WAS MADE TO WITHDRAW CARE. THE PATIENT DIED 12 DAYS AFTER THE ORIGINAL HEMORRHAGE." PLEASE NOTE, THE FIRST SEIZURE LASTED 21 SECONDS (WITHIN STANDARD PRACTICE FOR "CLINICALLY EFFECTIVE" SEIZURE DURATION (DEPENDING ON THE ARTICLE INVOLVED). RATHER THAN LET THAT GO, AND BECAUSE THERE ARE NO "SPECIAL CONTROLS" ABOUT WHEN AND HOW TO RESTIMULATE AFTER HAVING ALREADY HAD A 21 SECOND SEIZURE (DUMPING POTASSIUM) USING (69.8 JOULES), THE DOCTOR FILLED THE PATIENT WITH CAFFEINE (A KNOWN HYPOKALEMIC AGENT), PUMPED THE OXYGEN IN TO THE POINT OF HYPERCAPNIA, UPPED THE ELECTRICAL FIELD STRENGTH DOSE, AND GAVE THE PATIENT ANOTHER SHOCK WITH A LARGER ENERGY DOSE (77.6 JOULES). DUMPING MORE POTASSIUM. THREE EVENTS DUMPING POTASSIUM IN AN OTHERWISE HEALTHY INDIVIDUAL. LOW POTASSIUM IS A PLAUSIBLE REASON FOR THE 10 MINUTE TONIC-CLONIC SEIZURE WHICH OCCURRED IMMEDIATELY AFTER THE INITIAL TWO SEIZURES. 10 MINUTE SEIZURE WITHOUT FOLLOWING THE EMERGENCY MEDICINE GOLD STANDARD PRACTICES FOR SEIZURES, DUMPING MORE POTASSIUM. BOTH CAFFEINE AND ELECTRICITY AT SUCH HIGH FIELD STRENGTHS CAUSES TACHYCARDIA. ECT CAN CAUSE THE CEREBRAL PERFUSION TO SPIKE 300-400% BASELINE. THIS PATIENT RUPTURED A HEMORRHAGE AND ULTIMATELY WAS KILLED BY PHYSICIANS WITHOUT FORMAL SUBSPECIALITY TRAINING IN BIOPHYSICS, ELECTRICAL INJURY, EPILEPSY, OR CHANNELOPATHIES. THEY ARBITRARILY CHOOSE AN "EFFECTIVE" ELECTRICAL ENERGY DOSE TWICE IN ONE PROCEDURE BECAUSE THEY HAD NO SPECIAL CONTROLS OR PMA TO REASONABLY GUARANTEE SAFE USE OF THIS DEVICE. THE HOSPITAL & DOCTORS SHOULD BE INVESTIGATED FOR NOT FILING NOTICE OF DEATH USING THIS DEVICE. THERE ARE STILL NO RECORD OF PMA OR SPECIAL CONTROLS IN PLACE TO PREVENT THIS FROM HAPPENING TO ANOTHER BELOVED FAMILY MEMBER ON THIS DEVICE, OR ANY OTHER ECT DEVICE USED FOR CLASS II OR CLASS III INDICATIONS. THE FDA SHOULD BE INVESTIGATED FOR THEIR NEGLIGENCE IN ENFORCING THEIR OWN RULING. HTTPS://WWW.FEDERALREGISTER.GOV/D/2018-27809/P-215 AND HTTPS://WWW.FEDERALREGISTER.GOV/D/2018-27809/P-217. THE PATIENT'S FAMILY HISTORY WAS SIGNIFICANT FOR DEPRESSION, ANXIETY, AND SCHIZOPHRENIA. THE PATIENT HAD NO SIGNIFICANT SOCIAL HISTORY. HER MEDICAL HISTORY WAS NOTABLE FOR ASTHMA, DEPRESSION, DIABETES MELLITUS, AND CHRONIC HEADACHES. THE PATIENT'S MEDICATIONS INCLUDED BUPROPION XL (300 MG DAILY), CLONAZEPAM (2 MG THREE TIMES PER DAY), FLUVOXAMINE (200 MG DAILY), LAMOTRIGINE (100 MG DAILY), PROPRANOLOL (20 MG DAILY), AND QUETIAPINE (50 MG DAILY). PLEASE NOTE SHE HAD NO PERSONAL HISTORY OF CARDIAC EVENTS, NO FAMILY HISTORY OF HEMORRHAGIC STROKES, NO DOCUMENTED HISTORY OF RISK FACTORS COMMON TO PEOPLE HOW HAVE SPONTANEOUS 10 MINUTE GRAND MAL SEIZURES, CARDIAC ARREST, BUT PLEASE NOTE "ACUTE POST STIMULUS BRADYCARDIA AND ASYSTOLE ARE COMMON DURING ECT, A VERY OBVIOUS SITE INVOLVED BY STIMULATION DURING ECT IS THE TRIGEMINAL AREA... HYPERCAPNIA... LIGHT GENERAL ANESTHESIA, YOUNGER [NON-GERIATRIC] AGE, AND A STRONG AND/OR LASTING PROVOKING STIMULUS [ARE] PREDISPOSING FACTORS FOR THE OCCURRENCE OF THE TRIGEMINOCARDIAC REFLEX, UNILATERAL AND BILATERAL ELECTRODE PLACEMENT RESULTED IN MORE PRONOUNCED ASYSTOLE AND BRADYCARDIA THAN BIFRONTAL STIMULATIONS... THE TRIGEMINAL NERVE IS MORE DIRECTLY STIMULATED BY THE ELECTRODE PLACEMENT IN RIGHT UNILATERAL AND BILARERAL STIMULATION" (SARTORIUS A, KELLNER CH, SEBASTIAN K. THE TRIGEMINOCARDIAC REFLEX IN ELECTROCONVULSIVE THERAPY. THE JOURNAL OF ECT 2022;38(4):257¿58 DOI: 10.1097/YCT.0000000000000859. IT IS EXTREMELY CONCERNING THAT THE PHYSICIANS INVOLVED DID NOT NOTE ANY CAPNOGRAPHY DETAILS DURING THE PROCEDURE OR AFTERWARDS (END TIDAL CO2, BLOOD PRESSURE, BLOOD PERFUSION, HEART RATE, ETC), BUT CAPNOGRAPHY IS NOT A STANDARD PRACTICE IN ECT THOUGH GENERAL ANESTHESIA WITH PARALYTIC REQUIRES IT TO MONITOR CRITICAL VITALS. ALSO NOTE THESE PHYSICIANS DID NOT HAVE EQUIPMENT NECESSARY TO IDENTIFY NON-CONVULSIVE STATUS EPILEPTICUS (A KNOWN ADVERSE EVENT), PROVIDE EMERGENCY SEIZURE MEDICINE (GLUCOSE, INTUBATION, ETC) DURING 10M SZER.