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Additional information was received from a healthcare provider (hcp) via a clinical study regarding an autopsy report.The autopsy was performed on (b)(6) 2017 at 11:00 hours.The final anatomic diagnosis were as follows: pulmonary artery and inferior vena cava with intimal tears; bilateral serosanguineous pleural effusions (1600 ml right side and 600 ml left side); serosanguineous pericardial effusion (250ml) with pericardial hematoma; right ventricular myocardium with hypertrophy; no evidence of myocardial ischemia; pulmonary arterioles with intimal hyperplasia and plexiform lesions; no arteritis seen; no pulmonary infarcts and no pulmonary embolus identified; and brain with mild global hypoxic ischemic changes and venous angioma (5mm) in left thalamus.Both grossly and microscopically intimal tears and associated tissue reaction were noted in pulmonary artery and in inferior vena cava.These were associated with serosanguineous pleural effusion and pericardial effusion.Also noted were rib fractures.The presence of rib fractures confounds the determination of cause of the tears and effusion.While these may be seen secondarily to resuscitation process, accurate assessment of cause of tears is uncertain.No embolus is identified in pulmonary vessels or vena cava.Presence of pulmonary arteriolar intimal hyperplasia and right ventricular hypertrophy is concurrent with reported history of pulmonary hypertension.Cutaneous sequelae of neurofibromatosis are noted, grossly.Examination of the sections from heart and vascular system shows coronary arteries with minimal calcified atherosclerosis, no active thrombosis and no significant occlusion of vessels.The right ventricular myocardium shows patchy fibrosis and adipocytic metaplasia.There was no morphologic evidence of overt myocardial ischemia in either ventricle.Sections form the interior vene cava and the pulmonary artery, from the region of grossly noted tears showed focally eroded intimal layer with focal early thrombus formation and reactive and reparative processes involving all layers of these vessels.No acute or granulomatous arteritis, no significant dissection and no aneurysms identified.Sections from the lung parenchyma showed mild emphysematous changes and thickened walls of pulmonary arterioles.Evaluation with vvg stain supports the diagnosis of areas of cellular and acellular intimal hyperplasia with rare plexiform lesions.No significant arteritis was identified.A small focus of atypical adenomatous hyperplasia was also noted in the lung parenchyma.On microscopic examination of the brain, cortical lamination was preserved.The hippocampus, brainstem, and cerebellum demonstrated normal architecture.Scattered red neurons were present in the neocortex and hippocampus with loss of purkinje neurons in the cerebellum, suggested of global hypoxic ischemic changes, likely pre-terminal.The substantia nigra and locus ceruleus were well pigmented.The sampled meninges and ependymal lining were unremarkable.The cord plexus demonstrated some calcifications.Numerous corpora amylacea were present along the ventricular system.The chest plate showed multiple rib fractures and was removed to demonstrate a large amount of bloody fluid (mostly blood) that measured 600 ml in the left pleural space, 1600 ml in the right pleural space and 250 ml in the pericardial sac.It was noted that the pericardial sac was ruptured and there was also a small rupture in the inferior vena cava.The heart had shifted to the left and was in a slightly abnormal position.The implantable device was carefully removed in one piece and demonstrated the catheter tip to be located normally in the superior vena cava.The pulmonary artery was opened and showed no evidence of a pulmonary embolus.There was a 7cm circumferential tear in the pulmonary artery intima located at the bifurcation.The heart was removed and weight (b)(6).The epicardial surface was smooth and without discoloration.Abundant pericardial fat was noted.The coronary artery ostia were probe patent and sectioning the coronary arteries showed focal non-obstructive calcified arteriosclerosis of the right coronary artery.No thrombi or areas of stenosis were seen.The vascular pattern was right dominant.The heart was serially sectioned from apex to base to demonstrate homogenous brown myocardium with no evidence of recent or remote infarcts.The right ventricular wall was noticeably thick, measuring 0.8 to 1 cm in thickness.The endocardial lining is smooth and showed no fibrosis.The atria and atrial appendages appeared normal and showed no evidence of a thrombus.The heart valves were anatomically normal and showed no vegetations or focal lesions.The aorta showed atherosclerotic plaques in the arch and descending portion.The left and right lungs were removed and weighed (b)(6) respectively.The pleural surfaces were pink, pale and smooth.The pulmonary arteries were opened further and showed no evidence of a pulmonary embolus.The bronchi were patent and showed glistening pink mucosa.Both lungs showed subcrepitant pale p aerenchyma without any overt lesions.The brain was removed and weighed (b)(6) fresh and would be fixed prior to further examination.A portion of dorsal cerebral dura is available for examination and showed no epidural or subdural hemorrhage.The superior sagittal sinus was patent.The leptomeninges were thin and translucent without subarachnoid hemorrhage.The cerebral gyral pattern was of normal anatomic configuration and showed no atherosclerosis.No aneurysms were identified.There was no evidence of cingulate gyrus, uncal, cerebellar tonsillar or central herniation.The brainstem and cerebellum have a normal external appearance.Serial coronal sections of the cerebral hemisphere revealed cortical and subcortical gray and white matter structures to be of normal configuration without hemorrhage, infarcts, or mass lesions.The basal ganglia, thalamus, amygdalae, hippocampal formations and mamillary bodies were bilaterally of normal size, color, and consistency.The ventricular system was of normal caliber and was symmetrical.Serial sections of the brainstem and cerebellum revealed no lesions and showed that the substantia nigra and locus ceruleus were well pigmented.Examination of the central nervous system demonstrated an 1100-g, normally developed brain without significant atrophy.Sectioning demonstrated a continuous, even cortical ribbon and robust white matter.The ventricular system was not dilated.No masses, ifarcts, herniation or lesions were identified.The hcp thought that he could not explain either of the intimal tear was from trauma due to cpr.He also did not think that they would have caused hemodynamic embarrassment as they were specifically limited to the intima of the blood vessel and that he specifically remembered that the media was intact and therefore the tear was not a through and through tear of the vessel.Additionally, the reactive in repair to have changes that he noted at the site of those intimal tear is could not have occurred postmortem and therefore it was likely that those proceeded the patient's death and the body was in the process of healing these intimal tears.The stairs were unexplained.Additionally, he noted a bloody left pleural effusion as well as a pericardial hematoma and fusion, both of which he attributed to cpr.He did not have an explanation for the bloody right-sided pleural effusion.
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Additional information received from a healthcare provider (hcp) via a clinical study indicated the patient had hearing impairment and was unable to hear the non-critical alarm at implant, but could hear the critical alarm.The husband could hear both and he was usually with her.They refreshed hearing the alarms with the patient throughout the study and recently.It was noted a motor stall occurred at 4:57 pm.The site confirmed that an alarm was not reported by anyone during that time, but the patient was an inpatient at the hospital.The doctor indicated the logs showed a motor stall at 4:59 pm with a recovery at 5:08 pm.Printouts from the refill on (b)(6) 2017 showed no entries that suggested motor stall on that printout, however, it was seen on the printout after the patient's death.The doctor saw the patient around 1:34 pm and cardiac arrest was called at 22:29.The patient was noted to have vfib, however the doctor said there was no vf on telemetry, instead bradycardia.The loop recorder was interrogated, showed the af that was known, but no evidence of a ventricular arrhythmia.There was no afib from the time of the recorder being implanted to the time of the next emergency room visit.The doctor recommended reporting the event with an unknown relationship at that time.It was later reported the physician was still awaiting full autopsy results.The doctor's opinion about the suspected cause of death was either "stroke associated with afib or interruption of prostacyclin therapy." it was later reported the patient had a previous medical history of neurofibromatosis (didn¿t know type), pulmonary arterial hypertension, tia (transient ischemic attack) x2 in 2015 and 2016, hypothyroidism, recent shortness of breath, remote history of migraines.The patient presented with left leg weakness on (b)(6) 2017.The patient noted at 02:00 am that morning she had left arm and leg pain,(also reported as left hemiparesis) which was new.The patient's speech was slurred, had left eye twitching and was disoriented.She awoke at 04:00 am and walked to a bedside commode without difficulty, but then could not remember how to get back to her bed.She awoke her husband, who led her back to the bed and noted that she could not lift her leg into bed, which was usually not a problem from her.He denied noting any facial droop at that time.On admission, code grey was initiated, but did not reveal any abnormal lesions.She denied loss of consciousness, fall, or seizure activity, but reported a severe headache with left eye pain, chills, and shaking.She then complained of neck pain.Review of systems also found lightheadedness.The patient's home medication list included letairis 10mg daily, cialis 40mg, atorvastatin 20mg daily, levalbuterol 1.25mg/3ml, levothyroxine 50 mcg, lomotil 2.5mg- 0.025mg, tramadol 50mg, flonase 50mcg/inh, loratadine, ambrisentan, fluticasone, tadalafil and oxygen 5l at home.The patient's past medical history also included pulmonary arterial hypertension, hypoxemia, diarrhea due to drug, and thyroid carcinoma.The patient's past surgical history included two c-sections (1971 <(>&<)> 1974), tah in 1976, gallbladder in 2007, tonsils, cardiac cath 2015 and one after.The patient was a former cigarette smoker (less than 10 per day) and quit in 1970.At the time of the physician's evaluation, dysarthria had almost completely resolved, and she no longer had a left facial droop.She no longer had left arm weakness either, but was having left leg weakness, although the husband was telling the doctor that it was related to her old stroke.The patient had a very severe headache (8 out of 10) that was much improved since she had been in the hospital.The patient's vital signs were a temperature of 98, pulse of 85, respirations of 16, and blood pressure of 107/55.A ct scan of the head showed no acute intracranial pathology.Chronic microvascular ischemic changes and generalized atrophy.Ct angiogram of the brain and back were negative.The impressions were noted as dysarthria, left facial droop, and left hemiparesis that was much improved in the emergency room (er); nih stroke scale of 2, suspect a subcortical stoke syndrome of the right hemisphere, and thyroid carcinoma with subsequent hypothyroidism.Recommendations included they would initiate plavix since the patient w as allergic to aspirin, continue statin medication, a repeat ct scan of the head at 24 hours, echocardiogram, and physical therapy evaluation.On (b)(6) 2017 the patient reported feeling better.The headache had resolved but her left side was still somewhat painful.She noted she had some fleeting intermittent cp no worse than usual.It was noted she was having some increase in dyspnea.The patient had left leg tenderness and was fatigued.Laboratory results revealed low values for co2 level, calcium, total protein, and hdl.They also indicated high glucose poc bedside and tsh, and critical potassium levels.The plan was to obtain a limited echo with bubble study to evaluate pfo.The pump was refilled per protocol and was uneventful.The patient was to resume pah medications letairis and adcirca.It was recommended reducing the dose of crestor as the patient had had lft abnormality on statins previously.If the echo bubble study was unremarkable, the patient was okay for discharge from the hcp's standpoint.It was the third tia on the patient and there was concern that the antiplatelet therapy may not be enough to stop the tias and the concern that it may be a forebearer to a large cva in the future.In the setting of pulmonary hypertension, dilated atrial chambers, she was set up for occult afib to be cause for those events.They would recommend a looprecorder implant.If on follow-up there was any evidence of afib, they would strongly recommend that she be then considered for antiacoagulation therapy.The plan for then was to continue with aspirin therapy.It was further reported the patient continued to have left lower extremity weakness, return of a previous headache, and neck pain.Home health physical therapy (pt) versus outpatient pt was recommended.A chest x-ray on 2017-apr-11 revealed new left basilar airspace disease and small left effusion correlate for pneumonia/aspiration, right subclavian central line with the tip terminating in the upper svc - no pneumothorax, and pulmonary hypertension with enlarged pulmonary arteries.On (b)(6) 2017 the patient's neck pain improved.The ct head scan did not show any signs of stroke.The ct c-spine showed multiple spondylitheses.Tte bubble study ordered by ph team despite normal bubble study in (b)(6) 2016.The possible diagnoses on (b)(6) 2017 included cva, tia, complex migrane, and spinal cord impingement less likely - persistent, minimally improved.The plan was to continue plavix, reduce crestor for history of elevated liver enzymes on statin, follow-up tte with bubble study, monitor neuro status, regular diet, and place loop recorder for possible cryptogenic stroke.There was left lower lobe airspace disease with effusion, concerning for pna, afebrile no elevated wbc.The loop recorder was placed on the night of (b)(6) 2017 and minimal pain was noted.The patient was tolerating their diet, and had improved weakness.The patient was discharged on (b)(6) 2017 and had a follow-up appointment on (b)(6) 2017 at 9 am.The patient was negative for ct evidence of large territorial acute infarction, acute intracranial hemorrhage or mass effect.The visualized portions of the brain demonstrated no significant perfusion deficit to suggest infarction or ischemic penumbra.Laboratory results on (b)(6) 2017 indicated low abg ph, abg hco3 (bicarb), abg co2, mch, mchc, lymphocytes, abs lymphocyte cnt, co2 level, gfr non afr amer by mdrd, calcium, total protein, ven lactacte poc istat, vbg pco2, vbg o2 sat, vbg hco3 (bicarb), bun poc istat, creatinine poc istat, and ionized ca poc istat.Laboratory results also indicated high abg po2, wbc (white blood cell), rdw, neutrophils, abs neutrophil cnt, abs monocyte cnt, glucose level, bun level, alk phos, alt, ast, procalcitonin level, sodium poc istat, random glucose, calculated osmolality, and chloride poc istat.It was further reported the patient was taking plavix 75 mg daily and levofloxacin 500 mg daily as of (b)(6) 2017.A review of symptoms was unobtainable due to the patient's medical condition (respiratory distress) on (b)(6) 2017.It was noted the patient appeared anxious.The patient's last vital signs were temperature of 98.8 f, pulse of 99, respiratory rate of 24h, blood pressure of 96/55 l, and pulse oximetry of 95.The patient had not been hospitalized within 30 days.It was further reported the patient complained of shortness of breath for the last two weeks associated with worsening cough productive of yellowish sputum, no wheezing.The patient had noted she was evaluated by her pulmonologist and was started on levaquin on (b)(6) 2017 when no improvement in symptoms.She was evaluated by her primary care physician on wednesday of the previous week and found to be extremely hypoxic on 6l of 86 percent.The patient took 6l of oxygen at baseline.She went to the emergency room due to her worsening shortness of breath and hypoxemia and was sent to the hospital for further care.At the time of the hcp's evaluation she was able to speak in full sentences and she would be transitioned to high flow nasal cannula.She seemed not to be in any respiratory distress but she was still having significant cough.The assessment and plan was acute on chronic hypoxic respiratory failure rule out cap/seemed not to be volume overloaded on exam/rule out respiratory viral infection, pulmonary hypertension on multiple drugs, paroxysmal a fib, pre renal azotemia received 3 liters of iv fluids, and neurofibromatosis.They were to continue levaquin to complete 7 days tomorrow ((b)(6) 2017) that the patient started on (b)(6) 2017, pulmonary hypertension team following and the patient was to continue remodulin, ambrisentan and tiladafil, requested the records from the patient's pulonologist to check pft's, hrct, started on eliquis, sotolol per pulm hypertension team, check procalcitonin, repsiratory pcr suspected a viral infection, and hfnc wean as able.Respiratory examination revealed breath sounds were equal, symmetrical chest wall expansion, barrel shaped thorax, inspiratory crackles at the right base, and no wheezing.It was noted the patient was admitted in early (b)(6) 2017 with a small bowel obstruction (partial) and was following now with the doctor.She had also been admitted twice with stroke like symptoms including hemiparesis and some slurring of speech, which eventually resovled.The echo, bubble study, ct head and telemetry monitoring were unremarkable.The patient did tend to have a tendency to hypoventilate when she had chest pain, causing a significant drop in her oxygen saturations which resolved with deeper breathing.She had chronically increased interstitial markings of unclear etiology.She had prior workup for nosocomial infections which were negative.Consideration was given to hypersensitivity pneumonitis (she had many birds in and around her home) and she had responded to steriods in the past.The chronic non-cardiac chest pain was musculoskeletal in etiology.The doctor was called for code blue at 22:29 pm on (b)(6) 2017.The patient was noted to have vfib and shock, then pea and asystole multiple rounds of acls, epinephrine, bicarb, calcium, potassium for hypokalemia on istat.Vbg showed ph 6.6/31/37.She was not able to regain a pulse, remained asystole, and the time of death was 2300 pm.She had no pupillary response, corneal response, did not withdraw to pain or have spontaneous breaths, and no gag reflex.According to the arrhythmia episode list summarizing the patient's arrhythmias between (b)(6) 2017 at 15:47:01 and (b)(6) 2017 at 05:33:31, the patient had 57 total arrhythmias as follows: 29 pause events from (b)(6) 2017 to (b)(6) 2017 ranging from 3 seconds to 10 minutes 55 seconds, 9 tachy events from (b)(6) 2017 to (b)(6) 2017 ranging from 5 seconds to 45 minutes 38 seconds, 14 af events from (b)(6) 2017 to (b)(6) 2017 ranging from 2 minutes to 46 minutes, and 5 symptoms events from (b)(6) 2017 to (b)(6) 2017.
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