Consider the following medical report that includes the patient's historical health records. Use it to predict the disease that the patient is high likely exposed to. 

 Medical Report: allergies: no known allergies / adverse drug reactions attending: chief complaint: nstemi ad left neglect major surgical or invasive procedure: none history of present illness: 80yo f w/ pmhx atrial septal aneursym and patent foramen ovale who has had a history of tia symptoms in the past not anticoagulated (previous notes suggest that the patient was anticoagulated with asa, unclear though) who initially presented to for tia symptoms and then transferred to for management of nstemi after being started on a heparin gtt at the osh; upon presentation to , the patient was noted to have coffee ground emesis as well as left hemineglect. . her family describes that she has been having several days of generalized malaise and fatigue. she was brought to the ed by her family because she woke up with right sided headache and right finger numbness. her symptoms are similar to prior episodes of tias. she did have a recent mvc one week prior but without head trauma or mental status changes surrounding that incident. she denies visual changes but has been more confused of late. she is currently asymptomatic. . during history patient also endorsed intermittent nausea and reflux symptoms for the past couple weeks. she feels "heartburn" which is worse when laying flat in bed or after a large meal. ed worked up these symptoms, and she was found to have a troponin of .107 and a ck-mb wnl, ekg at that time with non-significant st depressions ~1mm in v2 and v4-v6. she was chest pain free without chest pressure, sob, doe, orthopnea, lightheadedness, dizziness or diaphoresis. second ekg showed no change from prior. she was treated with full-dose aspirin, heparin bolus and started on heparin drip. in discussion with dr. it was decided to transfer her to for evaluation and treatment of nstemi with neurology consult as an inpatient for evaluation of tia. she was transferred hemodynamically stable and chest pain free. . upon admission physical exam by the admitting floor team, the patient was noted to have left hemineglect. neurology was consulted as well, confirming the patient's left hemineglect. in the process of being transferred to the radiology department for head mri/mra, the patient was noted to have coffee ground emesis. ngt was placed, and she was lavaged with 1l of ns. coffee-ground material was aspirated back and the material was not completely cleared. heaprin drip was stopped. . on arrival to the micu, vital signs, afebrile, bp 177/83 hr 87 o2 sat 100% ra. the patient is currently complaining of nausea. had an episode of dry heaves on presentation. . . neurology note: 80 year-old left handed woman who was transferred directly yo cardiology from this afternoon after she was noticed by her son to be confused today. he states that he had called her house around 10:30 am this morning and she reported that she had been dry-heaving. she sounded confused to him and he became concerned and went over to her house. when he arrived at her house he noticed that she did not seem right. she was inattentive to the left side and was not using her left hand at all despite being a lefty. he also felt that when she was trying to remember phone numbers she was having significant difficulty. her language was normal and he did not notice any word substitutions, or difficulty with comprehension. there was no report of dysarthria. he did not think she was having any difficulty with ambulation and she was able to make it up and down a set of stairs. she did describe a headache to her son. she has a history of migraines but does not think she'd had one in some time. she said it was a dull squeezing type headache. this morning she had been dry-heaving but did not report any discoloration or bright emesis. she was brought over to this afternoon where she described sensory problems on the left side. she was then thought to have her symptoms resolve in the ed. she had a noncontrast ct performed that was reported to be normal. she had a troponin elevation and was transferred directly to cardiology at . 20 minutes after arrival on the floor cardiology team called neurology regarding a left sided neglect. family felt that this problem had been there all day and had never resolved. during the examination she vomited several times with dark coffee-ground emesis. on neuro ros, the pt had a headache, reported no loss of vision, blurred vision, diplopia, dysarthria, dysphagia, lightheadedness, vertigo, tinnitus or hearing difficulty. denies difficulties producing or comprehending speech. denies focal weakness. she did heave numbness on the left side, no parasthesiaes. no bowel or bladder incontinence or retention. denies difficulty with gait. on general review of systems, the pt denies recent fever or chills. no night sweats or recent weight loss or gain. denies cough, shortness of breath. denies chest pain or tightness, palpitations. she was nauseaous and vomiting this morning, no diarrhea, constipation or abdominal pain. no recent change in bowel or bladder habits. no dysuria. denies arthralgias or myalgias. denies rash. past medical history: migraines tia (reported in chart from 15 years ago) - no history from family or patient as to what symptoms she had atrial septal aneurysm pfo hypothyroidism iron deficiency anemia social history: lives alone in , ma recnetly widowed in . she worked in an office for years and retired. no smoking. no etoh. no illicits. family history: mother - healthy throat cancer, heavy smoker 3 sons - healthy physical exam: admission exam: vitals: t: 97.4 bp: 172/83 p: 94 r: 19 o2: 99% ra general: a&o times 3 to person, place, and time. in nad heent: perrl. eomi. sclera anicteric. mmm. tongue midline. op clear neck: supple, no lad cv: regular rate and rhythm, normal s1 + s2, no murmurs, rubs, gallops lungs: kyphotic. clear to auscultation bilaterally, no wheezes, rales, ronchi abdomen: soft, non-tender throughout the abdomen, non-distended, bowel sounds present, no organomegaly gu: foley in place ext: wwp. 2+ pulses dps bilaterally. no clubbing, cyanosis. trace to 1+ pitting edema bilaterally. neuro: perrl. tongue midline. sensory deficit to light touch through all branches of v. scm and trapezius bilaterally. strength: le: plantar flexion of ankles bilaterally; dorsiflexion of the ankles bilaterally. ue: grip strength on the right. unable to grip with left hand, though patient able to make some movements with left hand. sensation: le: to light touch intact through the le bilaterally. ue: to light touch intact through dermatomes of the rue, though patient reports unable to sense light touch on the lue through all dermatomes. gait deferred. . . admission neurology exam: considerably improved and previous errors in visuospatial testing were greatly improved but continued to have significant cognitive impairment but attentional issues had improved, able to back in 12 seconds, skipping one.. she was fully oriented and left hemiparesis hd essentially resolved in addition to left neglect, with no reproducible extinction to double simultaneous stimulation. physical examination: vitals: temp: 96.9 hr:72 regular bp: 99/49 resp:16 o2sat: 96% ra general: awake, cooperative, nad. heent: nc/at neck: supple, no carotid bruits appreciated. no nuchal rigidity pulmonary: slight decreased breath sounds right base cardiac: rrr, hs1+2+0 no mrg jvp not elevated or depressed abdomen: soft, nontender, nondistended extremities: no edema, distal pulses palpable calves snt skin: no rashes or lesions noted. neurologic: -mental status: a+)x3. she had no deficits of language in naming, comnprehension, repetition, or fluency. some left/right confusion. patiennt is quite anosagnosic to her deficits although thi seems to be much improved from initial consult.she had no motor apraxia. soem difficulty with backwards but able to do his forwards. left visual and sensory inattention to the left but seems better and less consistent. she -cranial nerves: i: olfaction not tested. ii: perrl 3 to 2mm and brisk. vff seems improved with no deficit seen on improvement in neglect. iii, iv, vi: eomi without nystagmus. normal saccades. v: facial sensation now seems symmetriccal to light touch per patient vii: ?l nasolabial fold flattening viii: hearing intact to finger-rub bilaterally. ix, x: palate elevates symmetrically. : 5/5 strength in trapezii and scm bilaterally. xii: tongue protrudes in midline. -motor: normal bulk and generally noraml tone altthough slightly increased in legs. no clear parietal drift. no pronator drift. no adventitious movements, such as tremor, noted. no asterixis noted. power: delt bic tri wre ffl fe ip quad ham ta edb l 4+ 4+ 4+ 4+ 5 4 4+ 5 4 5 5 5 5 r 4+ 5 5 4+ 5 5 4+ 5 5 5 5 5 5 -sensory: intact light touch and vbration throughout. -dtrs: tri pat ach l 2 2 2 2 1 r 2 2 2 2 1 bilateral flexor plantar reflexes. -coordination: no intention tremor, no dysdiadochokinesia noted. misses nose at time swith fnf on right adn now sems inatct on left. -gait: deferred . . discharge examination: pertinent results: admission labs: 09:39pm blood wbc-11.7* rbc-4.07* hgb-10.5* hct-33.0* mcv-81* mch-25.7* mchc-31.7 rdw-16.6* plt ct-410 09:39pm blood neuts-87.3* lymphs-9.3* monos-2.8 eos-0.4 baso-0.2 10:56pm blood pt-11.7 ptt-33.7 inr(pt)-1.0 09:39pm blood glucose-132* urean-12 creat-0.7 na-131* k-4.3 cl-95* hco3-23 angap-17 09:39pm blood calcium-8.7 phos-2.5* mg-1.7 09:39pm blood alt-14 ast-22 ld(ldh)-202 alkphos-68 totbili-0.3 ce trend 09:39pm blood ck-mb-4 ctropnt-0.12* 03:10am blood ck-mb-5 ctropnt-0.13* 11:55pm blood ck-mb-5 ctropnt-0.10* 06:45am blood ck-mb-3 ctropnt-0.05* hyponatremia work up (see hospital course) 03:10am blood glucose-119* urean-10 creat-0.7 na-125* k-3.9 cl-91* hco3-25 angap-13 06:45am blood glucose-102* urean-13 creat-0.7 na-129* k-3.4 cl-94* hco3-24 angap-14 02:50pm blood glucose-94 urean-14 creat-0.8 na-133 k-4.6 cl-102 hco3-22 angap-14 06:45am blood osmolal-262* 05:31am urine osmolal-538 02:53pm urine osmolal-104 09:38pm urine hours-random urean-164 creat-17 na-212 k-27 cl-197 11:38am urine hours-random urean-528 creat-73 na-23 k-31 cl-35 uric ac-30.2 02:53pm urine hours-random urean-142 creat-16 na-<10 k-16 cl-17 uric ac-7.8 cad risk factors 03:10am blood triglyc-60 hdl-89 chol/hd-2.2 ldlcalc-97 ldlmeas-107 03:10am blood %hba1c-5.8 eag-120 anemia work up 06:45am blood caltibc-328 ferritn-18 trf-252 other pertinent labs: 06:49am blood esr-10 06:49am blood vitb12-1330* 06:45am blood osmolal-262* 06:49am blood tsh-4.7* 06:45am blood tsh-0.88 06:49am blood crp-9.5* antitpo-less than . hb trend: 09:39pm blood wbc-11.7* rbc-4.07* hgb-10.5* hct-33.0* mcv-81* mch-25.7* mchc-31.7 rdw-16.6* plt ct-410 03:10am blood wbc-13.1* rbc-4.06* hgb-10.5* hct-32.7* mcv-81* mch-26.0* mchc-32.2 rdw-16.5* plt ct-419 08:16am blood hct-31.4* 04:32pm blood hct-32.5* 09:45pm blood hct-32.7* 02:22am blood hct-30.3* 06:45am blood wbc-8.2 rbc-3.81* hgb-10.0* hct-30.5* mcv-80* mch-26.1* mchc-32.6 rdw-17.2* plt ct-342 06:49am blood wbc-5.3 rbc-3.67* hgb-9.6* hct-30.1* mcv-82 mch-26.2* mchc-31.9 rdw-16.9* plt ct-315 05:05am blood wbc-6.2 rbc-3.51* hgb-9.3* hct-28.9* mcv-82 mch-26.4* mchc-32.1 rdw-16.9* plt ct-316 04:20am blood wbc-6.6 rbc-3.30* hgb-8.8* hct-27.5* mcv-83 mch-26.6* mchc-31.9 rdw-17.4* plt ct-291 04:30am blood wbc-6.1 rbc-3.25* hgb-8.6* hct-27.0* mcv-83 mch-26.5* mchc-31.9 rdw-17.3* plt ct-315 . discharge labs: 04:30am blood wbc-6.1 rbc-3.25* hgb-8.6* hct-27.0* mcv-83 mch-26.5* mchc-31.9 rdw-17.3* plt ct-315 04:27pm blood pt-12.6 ptt-58.4* inr(pt)-1.1 04:30am blood glucose-100 urean-14 creat-0.8 na-139 k-3.8 cl-106 hco3-25 angap-12 04:30am blood alt-19 ast-26 alkphos-63 totbili-0.2 04:30am blood albumin-3.6 calcium-8.8 phos-3.7 mg-1.9 . . urine: 09:38pm urine color-straw appear-clear sp -1.008 09:38pm urine blood-neg nitrite-neg protein-neg glucose-70 ketone-10 bilirub-neg urobiln-neg ph-7.5 leuks-neg 11:38am urine color-straw appear-clear sp -1.009 11:38am urine blood-sm nitrite-neg protein-neg glucose-neg ketone-40 bilirub-neg urobiln-neg ph-5.0 leuks-neg 11:38am urine rbc-13* wbc-3 bacteri-few yeast-none epi-0 transe-<1 02:53pm urine color-straw appear-clear sp -1.002 02:53pm urine rbc-4* wbc-1 bacteri-few yeast-none epi-<1 09:38pm urine hours-random urean-164 creat-17 na-212 k-27 cl-197 05:31am urine hours-random 05:31am urine hours-random urean-192 creat-22 na-199 k-30 cl-184 11:38am urine hours-random urean-528 creat-73 na-23 k-31 cl-35 uric ac-30.2 02:53pm urine hours-random urean-142 creat-16 na-<10 k-16 cl-17 uric ac-7.8 05:31am urine osmolal-538 11:38am urine osmolal-361 02:53pm urine osmolal-104 . . microbiology: 9:38 pm urine source: cvs. **final report ** urine culture (final ): mixed bacterial flora ( >= 3 colony types), consistent with skin and/or genital contamination. time taken not noted log-in date/time: 9:27 am serology/blood chem # 62864c. **final report ** rapid plasma reagin test (final ): nonreactive. reference range: non-reactive. 5:05 am serology/blood chem # 63387c 5:05am. **final report ** helicobacter pylori antibody test (final ): negative by eia. (reference range-negative). . . cardiology: ecg study date of 9:32:10 pm normal sinus rhythm. early transition. st-t wave changes in leads v3-v6. these changes are consistent with acute anterior wall ischemia. no previous tracing available for comparison. read by: , m. intervals axes rate pr qrs qt/qtc p qrs t 92 128 98 402/458 72 -10 50 . ecg study date of 9:02:30 pm sinus rhythm. left axis deviation. st-t wave changes in leads v3-v6 noted on are improving, likely representing anterolateral ischemia. read by: ,elad intervals axes rate pr qrs qt/qtc p qrs t 97 118 104 392/456 72 -26 56 . portable tte (complete) done at 10:06:49 am conclusions the left atrium is normal in size. the interatrial septum is aneurysmal. no definite atrial septal defect or patent foramen ovale is seen by 2d, color doppler or saline contrast with maneuvers (however, the technically suboptimal nature of this study precludes definitive exclusion of shunt). left ventricular wall thickness, cavity size, and global systolic function are normal (lvef 65%). due to suboptimal technical quality, a focal wall motion abnormality cannot be fully excluded. right ventricular chamber size and free wall motion are normal. the aortic valve leaflets (3) are mildly thickened but aortic stenosis is not present. no aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. there is mild bileaflet mitral valve prolapse. an eccentric, posteriorly directed jet of mild to moderate (+) mitral regurgitation is seen. due to the eccentric nature of the regurgitant jet, its severity may be significantly underestimated (coanda effect). the left ventricular inflow pattern suggests impaired relaxation. the pulmonary artery systolic pressure could not be determined. there is no pericardial effusion. . stress study date of interpretation: this was an 80 year old woman with pvd who was referred to the lab from the inpatient floor for an evaluation after a pre-syncopal episode. she received 0.142mg/kg/min of iv persantine infused over 4 minutes. she denied any chest, arm, neck or back discomfort throughout the study. there were no changes in st segments or t waves noted during the infusion or in recovery. the rhythm was sinus with one single apb seen in recovery. the heart rate and blood pressure responded appropriately to the persantine infusion. at 2.5 minutes post infusion, 125mg iv aminophylline was given to reverse any potential persantine side effects. impression: no ischemic ecg changes. no anginal type symptoms. appropriate hemodynamic response. nuclear report sent separately. . cardiac perfusion persantine study date of interpretation: left ventricular cavity size is within normal limits; edv = 55 ml. rest and stress perfusion images reveal uniform tracer uptake throughout the left ventricular myocardium. gated images reveal normal wall motion. the calculated left ventricular ejection fraction is 74%. impression: normal cardiac perfusion study. . . radiology: chest (portable ap) study date of 11:05 pm findings: nasogastric tube extends to the distal esophagus then curls upon itself. it is lying within a large hiatal hernia. the lungs are essentially clear. . cta head and neck w&w/oc & recons study date of 12:54 am findings: ct head: the cerebral sulci, ventricles and extra-axial csf-containing spaces are age appropriate. there is no shift of the midline structures. the -white matter differentiation is preserved. there are extensive periventricular white matter hypodensities that likely reflect sequela of longstanding small vessel ischemic disease. a more focal and more marked hypodensity in the left frontal periventricular white matter involving the tail of the caudate nucleus likely represents an old infarct. there is no ct evidence of acute territorial infarction, intracranial hemorrhage or space-occupying lesion. the visualized paranasal sinuses and mastoid air cells are clear. no fractures are identified. cta of head: focal, likely atherosclerotic narrowings are seen along the left m1 and p2 segments, each with unremarkable peripheral run-off. othersie, the intracranial internal carotid, vertebrobasilar and anterior, middle and posterior cerebral arteries are patent with normal contrast enhancement and branching pattern. the anterior and posterior communicating arteries are visualized. there is no evidence of further stenosis, occlusion, aneurysm, or arteriovenous malformation. incidential note is made of a small, 4 mm lipoma anterior to the tip of the basilar artery. cta of the neck: the origins of the common carotid and vertebral arteries are patent without significant stenosis. there is bilateral calcified plaque, involving the common carotid artery bifurcation. however, the lumen of the branching internal carotid arteries is not significantly compromised. the cervical portions of the vertebral arteries demonstrate normal contrast opacification. impression: 1. extensive sequela of small vessel ischemic disease with a more focal hypodensity in the left frontal periventricular white matter that likely represents an old infarct. 2. no evidence of hemorrhage or acute infarct. 3. atherosclerotic disease involving the common carotid artery bifurcations, but no hemodynamically significant stenosis. 4. focal, likely atherosclerotic narrowings of left m1 and p2 segments, each with unremarkable peripheral run-off. . mr head w/o contrast study date of 5:36 pm findings: there is no acute infarct seen. there is no mass effect or midline shift seen. extensive periventricular and subcortical changes of small vessel disease identified. moderate ventriculomegaly and mild prominence of temporal horns seen indicating atrophy. moderate cortical atrophy is also noted. there is no evidence of chronic or acute blood products. . mr head w & w/o contrast study date of 5:30 pm preliminary report !! pfi !! 1. no acute intracranial abnormality or space-occupying lesion. 2. generalized cerebral atrophy with extensive changes of chronic small vessel ischemic disease. 3. bilateral hippocampi are small with left hipppocampus smaller than the right. . . neurophysiology: eeg study date of mpression: this bedside monitoring did not capture any pushbuttons for overt seizures; however, three electrographic seizures were recorded each showing clinical signs. the eeg prior to the seizures, however, shows a marked suppression of electrical activity broadly present over the right hemisphere but maximum in the central parietal and mid to lateral temporal regions. relative preservation of activity is seen in the frontal and occipital polar regions. there were three electrographic seizures, all arising from what appears to be the left posterior frontal temporal region associated with clinical rhythmic movement of the right hand and one seizure lasting seconds, on the other two lasting about 25 seconds. . eeg study date of impression: there were no pushbutton events. the striking asymmetry present during the first 24-hour recording seems to be gradually resolving with some more normal frequencies being seen in the right central region and the alpha rhythm is now bilateral and relatively symmetrical with only some voltage asymmetry noted. there continues to be interictal epileptiform activity from the left posterior frontal and anterior temporal and left frontal central region, some of these associated with brief jerking in the right hand forearm region. . eeg study date of impression: there were no pushbuttons for seizures during this session. the recording continues to show voltage suppression over the right hemisphere maximum centrally although it appears less prominent. there continues to be multifocal leftsided epileptic activity and, late in the recording, the spike detection and seizure detection algorithm picked up fairly significant interictal discharges from the right parietal occipital area. . eeg study date of impression: this eeg continues to show multifocal potential epileptiform areas manifest by interictal epileptic activity. these include the left dorsal lateral prefrontal and anterior temporal regions and the right posterior parietal occipital region. there continues to be suppression of activity over the right central parietal region; however, it appears to be gradually improving. . . gi: egd findings: esophagus: lumen: a medium size hiatal hernia was seen. additional findings include erythema and linear erosion. mucosa: localized a linear erosion of the mucosa with no bleeding was noted in the gastroesophageal junction. these findings are compatible with reflux esophagitis. stomach: mucosa: patchy erosion and erythema of the mucosa with no bleeding were noted in the antrum. these findings are compatible with gastritis. duodenum: normal duodenum. impression: a linear erosion in the gastroesophageal junction compatible with reflux esophagitis erosion and erythema in the antrum compatible with gastritis medium hiatal hernia otherwise normal egd to third part of the duodenum brief hospital course: 80yo f w/ history of tia symptoms in the past not anticoagulated who initially presented to for left neglect and found to have ecg changes and tnt elevation to 0.13 and transferred to for management of nstemi after being started on a heparin iv infusion at the osh. upon presentation to , the patient was noted to have coffee ground emesis as well as left hemi-neglect with left parietal drift and mid left hemiparesis and stroke work-up was initially sought and returned negative for an acute infarct. given this, concern was for seizures and patient was presumptively treated with keppra with marked improvement in symptoms. eeg showed multifocal epileptiform activity in addition to clinical seizures with rue shaking and patient was commenced on keppra with improvement of her eeg. patient had further visual phenomena in her left visual field concerning for seizures and keppra dose was increased. egd showed gastric and esophageal erosions with gastritis/esophagitis and patient was commenced on high dose ppi and will be followed by gi. myocardial perfusion scan was negative and tnt elevation was considered more likely a consequence of her seizures. she has neurology follow-up and was discharged with services on . . # multifocal seizures: patient initially presented as transfer from after she was noticed by her son to be confused with nausea and vomiting on . at that time, patient was noted by her son to be ignoring the left hand side. there were also memory issues regarding remembering phone numbers. there was no apparent language disorder or aphasia or dysarthria or report of weakness. when the patient was more able, she described having brief episodes where she felt distant and disconnected and not herself lasting <1 minute on the day of presentation. of particular mention, she had a low velocity motor vehicle collision on when she was exiting a supermarket and a car hit her from the left hand side. she had no head injury or loss of consciousness although had worsening of a right sided headache after this. the headache was still present at the time of discharge. ct-head showed extensive periventricular small vessel disease and multiple areas of hypodensities in the centrum semioval region (on both sides, left more than right). on arrival to , neurology were consulted regarding left neglect. she had been commenced on iv heparin at osh given previous atrial septal aneurysm and (at that time) likely nstemi given tnt elevation to 0.12 and shortly thereafter developed coffee-ground emesis on neurological review, patient had a mild left hemiparesis and severe left neglect with left parietal drift and no language disturbance. as there was obvious concern regarding possible stroke and new gi bleeding, she was briefly transferred to the micu for monitoring. she was transferred out of the icu to the floor and proceeded to mri-head which showed no acute infarct but extensive small vessel disease and heparin was stopped. in the absence of other cause and given transient symptoms, patient was monitored on eeg ltm and was presumptively treated with keppra 500mg iv x1 for likely seizures. after this, the patient had a dramatic improvement in symptoms with almost complete resolution of her neglect although also seemed to have some variable right sided neglect in addition which latterly resolved. she was then continued on po keppra 500mg . of note, she was mostly amnestic of the events of the day of admission. eeg showed initially marked suppression of electrical activity broadly present over the right hemisphere felt to be post-ictal in nature in addition to electrographic and clinical seizures in the left posterior frontal temporal region associated with clinical correlate with rhythmic movement of the right hand and one seizure lasting 10-15 seconds, on the other two lasting about 25 seconds with post-octal right parietal depression in addition to inter-ictal right parietal discharges. further eegs showed the striking left-right voltage asymmetry improved and there was inter-ictal epileptiform activity from the left posterior frontal and anterior temporal and left frontal central region and some of these were associated with brief jerking in the right ue and latterly multifocal left-sided epileptic activity with fairly significant inter-ictal discharges from the right parietal occipital area which gradually improved. she was taken off ltm on . she had repeated mri and w/o contrast which showed no significant contrast enhancement. she improved clinically with left neglect but began to notice intermittent odd sensory symptoms with seeing balloons and a lace pattern in her left visual field concerning for seizures. we increased keppra to 750mg sensory symptoms seemed to resolve. on discharge, she had considerably improved and previous errors in visuospatial testing were greatly improved but continued to have significant cognitive impairment but attentional issues had improved, able to back in 12 seconds, skipping one.. she was fully oriented and left hemiparesis had essentially resolved in addition to left neglect, with no reproducible extinction to double simultaneous stimulation. the etiology of her seizures was ut down to her large burden of small vessel disease. she was discharged on to home with services. she has neurology follow-up. # upper gi bleed: coffee ground emesis on the floor while on heparin drip for nstemi and for presumed stroke, but none after transfer to micu. hct remained stable initially at around 34 but slowly downtrended. iv pantoprazole started for ugib, hematemesis resolved and had no melena. aspirin and nadolol were initially held and restarted later in her hospital stay. heparin drip was initially continued for possible stroke but after mri did not show evidence of this, this was discontinued. ugie on showed showed evidence of erosions in the stomach with gastritis and g-e junction erosion compatible with reflux esophagitis and h pylori ab testing was negative. she was transitioned from iv ppi to po omeprazole 40mg which she will continue for 2 weeks and then change to 40mg qd thereafter. hb slowly decreased and was hb 8.6 hct 27 on discharge. this should be monitored by her pcp . she has gi follow-up. # possible nstemi: patient with elevated troponin at osh with negative mb. patient with ecg changes at osh: st depressions ~1mm in v2 and v4-v6. troponin at at 0.12 with negative mb fraction and tnt max was 0.13. st segment depressions were more pronounced in leads v3-v6 when compared with ecg at and were suggestive of antero-lateral ischemia. troponin and ecgs were trended. heparin drip continued but then discontinued as above. given high risk of ugib with anticoagulation it was decided to treat medically since she was >48 hours outside event. tnt downtrended and ck-mb remained flat. echo showed no clear focal wall motion abnormality although this could not be ruled out given technical quality however, lv wall thickness, cavity size, and global systolic function were normal (lvef 65%). patient had a persantine pharmacologic stress on which was negative and therefore it is unclear as to the cause of her tnt elevation and ecg changes but may have been secondary to seizures as opposed to cardiac ischemia. # atrial septal aneurysm and patent foramen ovale: last echo at in showing atrial septal aneurysm present with right to left shunting with valsalva. echo with bubble study performed during this admission to evaluate for presence of thrombi and pfo/atrial septal aneurysm did not show pfo but tte was limited and no focal wall motion abnormalities. given evidence of pfo found on tte in the past there was felt no need for a tee. asa 325mg daily for primary prevention of stroke given pfo was started and given gi bleeding was discharged on 81mg home dose. no need for repair of pfo. #hyponatremia: na downtrending 131 on admission -> 125. uosm 538 and sosm 262 and una of 212 on admission. after 500cc bolus her una improved to 23 and serum na increased to 129. after further boluses, her na remained stable and discharge na was 139. #depression: continued home citalopram 30mg, nortriptyline 25mg, buspirone 10mg transitional issues: - no need for closure of pfo - consider iron supplementation as an outpatient and consider further work up of anemia - repeat labs on to monitor for worsening anemia medications on admission: - aspirin 81mg - nadolol 20 mg once a day - alendronate 70mg - citalopram 30mg - nortriptyline 25mg - buspirone 10mg - meloxicam 15mg - vitamin b12 1000mcg discharge medications: 1. alendronate 70 mg tablet sig: one (1) tablet po once a week: please take at your normal dose time. 2. vitamin b-12 1,000 mcg tablet sig: one (1) tablet po once a day. 3. citalopram 20 mg tablet sig: 1.5 tablets po daily (daily). 4. nadolol 20 mg tablet sig: one (1) tablet po once a day. 5. nortriptyline 25 mg capsule sig: one (1) capsule po hs (at bedtime). 6. buspirone 10 mg tablet sig: one (1) tablet po daily (daily). 7. atorvastatin 40 mg tablet sig: one (1) tablet po at bedtime. disp:*30 tablet(s)* refills:*2* 8. omeprazole 40 mg capsule, delayed release(e.c.) sig: one (1) capsule, delayed release(e.c.) po twice a day: continue at 40mg twice daily for 2 weeks and decrease to 40mg daily thereafter. disp:*60 capsule, delayed release(e.c.)(s)* refills:*2* 9. levetiracetam 250 mg tablet sig: three (3) tablet po bid (2 times a day). disp:*180 tablet(s)* refills:*2* 10. outpatient lab work please check cbc and chem 7 on 11. aspirin 81 mg tablet, chewable sig: one (1) tablet, chewable po once a day. discharge disposition: home with service facility: homecare discharge diagnosis: 1) multifocal seizures presenting with episodes of confusion and left sided neglect (secondary to microvascular disease) . 2) abnormal ecg and elevated troponins of unclear etiology and possibly secondary to seizures given negative myocardial perfusion scan . 3) gi bleed and egd showing erosions in the gastroesophageal junction compatible with reflux esophagitis and gastritis discharge condition: mental status: clear and coherent. level of consciousness: alert and interactive. activity status: ambulatory - requires assistance or aid (walker or cane). neurological: fully oriented. able to name months of the year backeards. left neglect essentially resolved; no reproduceible extinction to double simultaneous stimulation. visual fields full to confrontation. no left parietal drift. discharge instructions: it was a pleasure taking care of you during your time at the . you presented with episodes of confusion (and a disconnected feeling) and you were found to be paying less attention to your left hand side. . given your neurological symptoms, there was initial concern for a stroke. however mri and ct scans showed no evidence of stroke. the studies do show lots of changes related to small vessel disease (which is quite common with ageing.) because there was no clear structural explanation for the symptoms on imaging, a brain wave test called an eeg was done. over several days of monitoring, the tracings revealed that you were having seizures originating from both sides of the brain. a medicine called keppra (levitaracetam) was started to help prevent further seizures. within 24 hours of starting the medicine, you paid attention to the left side of your body and the left visual space. you became much more like yourself. because you started to have episodes in which you saw lace (also thought to represent seizure), the inital keppra dose of 500 mg twice daily was increased to 750 mg twice daily. . to ensure there was no detectable covert infection or other lesion causing the seizures, you had a second mri scan with contrast. it was unchanged from the first mri of the head. the seizures are thought to be related to brain tissue changes from hardening of small blood vessels. to help reduce stroke risk, please continue aspirin and a cholesterol lowering medication started during the hospitalization. . upon your arrival, initial investigatory tests showed ecg (heart tracing) changes and elevations in blood tests which can suggest a heart attack. for this reason a blood thinner called heparin was transeintly given. you had a cardiac stress test which was negative indicating that your heart arteries are working well and that this was likely not a heart attack and instead secondary to seizures. . you also had vomiting after starting the blood thinner suggestive of a bleed in your stomach. you were started on potent antacid medication and endoscopy revealed inflammation and erosions for which you should continue the acid suppressing medication. the stomach doctors on would to see you again on . . because your blood count dropped, it was carefully monitored. although it has remained stable, the labs (complete blood count)should be checked again on friday and reviewed by your pcp. . you were deemed safe to go home with home physical and occupational therapists in addition to visiting nurses. you were discharged on . . please note that it is very important you avoid driving until you have been seizure-free for a period of at least six months. it will also be important to avoid potentially dangerous activities such as swimming independently. please continue to take the keppra as prescribed. . medication changes: we started keppra 750mg twice daily (this is an anti-seizure medication) we started atorvastatin 40mg daily at night (cholesterol lowering medication) we started omeprazole 40mg twice daily which should be continued for 2 weeks followed by 40mg daily thereafter we stopped meloxicam given gi bleeding please continue your other medications as prescribed followup instructions: please see your pcp on and have repeat labs taken at this time. . we have organised gastroenterology follow-up on as below: department: gastroenterology when: thursday at 2:00 pm with: , md building: (, ma) campus: off campus best parking: parking on site . we have organised neurology follow-up as below: department: neurology when: thursday at 4:30 pm with: drs. / building: sc clinical ctr campus: east best parking: garage procedure: other endoscopy of small intestine diagnoses: hyposmolality and/or hyponatremia unspecified acquired hypothyroidism other convulsions depressive disorder, not elsewhere classified diaphragmatic hernia without mention of obstruction or gangrene ostium secundum type atrial septal defect iron deficiency anemia, unspecified migraine, unspecified, without mention of intractable migraine without mention of status migrainosus unspecified gastritis and gastroduodenitis, without mention of hemorrhage leukocytosis, unspecified hemiplegia, unspecified, affecting unspecified side other nonspecific abnormal serum enzyme levels cerebral atherosclerosis nonspecific abnormal electrocardiogram [ecg] [ekg] aneurysm of heart (wall) reflux esophagitis 

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