CHIEF COMPLAINT: Tip of basilar clot: phenomenologically manifested as flailing
arms, confusion followed by stupor

PRESENT ILLNESS: Time Code Stroke called: 12:02
Time Neurology at bedside for evaluation: 11:30
Time (and date) the patient was last known well: 8:30
NIH Stroke Scale Score: 21
t-[**MD Number(3) 6360**]: Yes
Time t-PA was given 12:40
I was present during the CT scanning and reviewed the images
instantly within 20 minutes of their completion.

MEDICAL HISTORY: - Atrial fibrillation, not on Coumadin
- Dyslipemia
- Osteoporosis

MEDICATION ON ADMISSION: - Atenolol 12.5mg
- Aspirin 81mg
- Simvastatin 40mg
- Alendronate 70mg weekly
- MVI
- Calcium

ALLERGIES: No Known Allergies / Adverse Drug Reactions

PHYSICAL EXAM: At Admission:

FAMILY HISTORY: Unknown.

SOCIAL HISTORY: Lives in [**Location 14663**] with her husband. Is her husband's carer.
Previously independent in all ADL.
Cerebral embolism with cerebral infarction,Occlusion and stenosis of basilar artery with cerebral infarction,Anomalies of cerebrovascular system,Acute respiratory failure,Atrial fibrillation,Unspecified essential hypertension,Other and unspecified hyperlipidemia,Osteoporosis, unspecified,Thrombocytopenia, unspecified
Crbl emblsm w infrct,Ocl bslr art w infrct,Cerebrovascular anomaly,Acute respiratry failure,Atrial fibrillation,Hypertension NOS,Hyperlipidemia NEC/NOS,Osteoporosis NOS,Thrombocytopenia NOS
Admission Date:  [**2187-5-15**]              Discharge Date:   [**2187-5-25**]

Date of Birth:  [**2106-12-25**]             Sex:   F

Service: NEUROLOGY

Allergies:
No Known Allergies / Adverse Drug Reactions

Attending:[**First Name3 (LF) 618**]
Chief Complaint:
Tip of basilar clot: phenomenologically manifested as flailing
arms, confusion followed by stupor

Major Surgical or Invasive Procedure:
Intravenous t-PA
Cerebral angiogram with clot retrieval
Endotracheal intubation x 2
Transesophageal echocardiography
Central venous line placement
Arterial line placement

History of Present Illness:
Time Code Stroke called: 12:02
Time Neurology at bedside for evaluation: 11:30
Time (and date) the patient was last known well: 8:30
NIH Stroke Scale Score: 21
t-[**MD Number(3) 6360**]: Yes
Time t-PA was given 12:40
I was present during the CT scanning and reviewed the images
instantly within 20 minutes of their completion.

NIH Stroke Scale score was: 21
1a. Level of Consciousness: 3
1b. LOC Question: 2
1c. LOC Commands: 1
2. Best gaze: 0
3. Visual fields: 0
4. Facial palsy: 0
5a. Motor arm, left: 2
5b. Motor arm, right: 3
6a. Motor leg, left: 2
6b. Motor leg, right: 3
7. Limb Ataxia: 0
8. Sensory: 0
9. Language: 3
10. Dysarthria: UN
11. Extinction and Neglect: 2

HPI: The pt is a 80 year-old right-handed woman with a history
of Afib and HTN who presents with loss of consciousness.

Per discussion with her husband, the patient was sitting at the
table eating breakfast with him this morning, when she asked him
to take some things into the other room so they wouldn't be on
the table.  He walked into the other room briefly, and when he
got back into the room she was sitting a the table, arms flexed
towards her face, shaking.  He reports that she looked as though
she wanted to tell him something, and that something was wrong,
but wasn't actually speaking.  He called EMS, who reportedly
were concerned that she might be seizing, and gave her Ativan
and Narcan.  She was taken to [**Hospital3 10310**] hospital, where
she was reported to be obtunded and was intubated because she
was not protecting her airway.  She underwent a NCHCT which
showed a 4mm R frontal hyperdensity that was possibly a
hemorrhage, and was then transferred to [**Hospital1 18**] for further
evaluation.  Reportedly on arrival she was actively fighting the
ventilator, and was observed to be making purposeful movements
towards the ventilator with both hands.  Neurology was then
consulted to examine the patient before she was given sedation.

Intubated, unable to answer ROS

Past Medical History:
- Atrial fibrillation, not on Coumadin
- Dyslipemia
- Osteoporosis

Social History:
Lives in [**Location 14663**] with her husband. Is her husband's carer.
Previously independent in all ADL.

Family History:
Unknown.

Physical Exam:
At Admission:

Vitals: P: 49 R: 16  BP: 99/50 SaO2: 100% intubated

General: Intubated, sedated
HEENT: NC/AT, no scleral icterus noted, MMM, no lesions noted in
oropharynx
Neck: Supple, no carotid bruits appreciated. No nuchal rigidity
Pulmonary: Lungs CTA bilaterally without R/R/W
Cardiac: irregular, bradycardic
Abdomen: soft, NT/ND, normoactive bowel sounds, no masses or
organomegaly noted.
Extremities: No C/C/E bilaterally, 2+ radial, DP pulses
bilaterally.
Skin: no rashes or lesions noted.

Neurologic:
-Mental Status: Intubated, makes slight attempts to open eyes in
response to sternal rub and calling her name, but otherwise is
not able to follow commands.

-Cranial Nerves: 2.5mm->2mm bilaterally.  Eyes midline, intact
oculocephalics.  Intact corneals.  Intact gag

-Motor/Sensory: Normal bulk, tone throughout.  Purposeful slight
anti-gravity movements with left arm and leg.  Extensor
posturing
in right arm, triple flexion in right leg in response to painful
stimuli.

-DTRs:
  [**Name2 (NI) **] Tri [**Last Name (un) 1035**] Pat Ach
L  2  2    2    2   1
R  2  2    2    2   1
Plantar response was extensor bilaterally.

Pertinent Results:
[**2187-5-24**] 05:58AM BLOOD WBC-6.2 RBC-3.30* Hgb-10.2* Hct-30.2*
MCV-92 MCH-31.0 MCHC-33.8 RDW-14.3 Plt Ct-235
[**2187-5-23**] 06:00AM BLOOD WBC-8.8 RBC-3.59* Hgb-11.1* Hct-32.7*
MCV-91 MCH-30.9 MCHC-33.9 RDW-14.2 Plt Ct-202
[**2187-5-17**] 07:44PM BLOOD WBC-3.9* RBC-3.35* Hgb-10.5* Hct-30.6*
MCV-91 MCH-31.2 MCHC-34.1 RDW-13.9 Plt Ct-87*
[**2187-5-15**] 10:56AM BLOOD WBC-5.4 RBC-3.71* Hgb-11.8* Hct-34.6*
MCV-93 MCH-31.8 MCHC-34.1 RDW-13.6 Plt Ct-134*
[**2187-5-23**] 06:00AM BLOOD Neuts-85* Bands-0 Lymphs-7* Monos-3 Eos-3
Baso-1 Atyps-0 Metas-1* Myelos-0
[**2187-5-24**] 05:58AM BLOOD PT-17.9* PTT-30.2 INR(PT)-1.6*
[**2187-5-23**] 06:00AM BLOOD PT-16.4* PTT-27.5 INR(PT)-1.4*
[**2187-5-22**] 02:08AM BLOOD PT-13.7* PTT-19.6* INR(PT)-1.2*
[**2187-5-17**] 03:46PM BLOOD Fibrino-818*
[**2187-5-24**] 05:58AM BLOOD Glucose-106* UreaN-22* Creat-0.7 Na-138
K-4.4 Cl-101 HCO3-30 AnGap-11
[**2187-5-23**] 06:00AM BLOOD Glucose-107* UreaN-14 Creat-0.6 Na-139
K-4.0 Cl-101 HCO3-28 AnGap-14
[**2187-5-22**] 03:14AM BLOOD Glucose-140* UreaN-12 Creat-0.5 Na-136
K-3.4 Cl-99 HCO3-26 AnGap-14
[**2187-5-15**] 10:56AM BLOOD Glucose-123* UreaN-18 Creat-0.7 Na-142
K-4.4 Cl-112* HCO3-24 AnGap-10
[**2187-5-17**] 07:44PM BLOOD ALT-12 AST-35 LD(LDH)-165 AlkPhos-55
TotBili-0.7
[**2187-5-17**] 10:20AM BLOOD ALT-10 AST-29 LD(LDH)-132 AlkPhos-38
TotBili-0.5
[**2187-5-16**] 04:49PM BLOOD CK(CPK)-100
[**2187-5-16**] 12:35AM BLOOD CK(CPK)-62
[**2187-5-18**] 02:58AM BLOOD proBNP-2898*
[**2187-5-16**] 04:49PM BLOOD CK-MB-2 cTropnT-<0.01
[**2187-5-16**] 12:35AM BLOOD CK-MB-2 cTropnT-<0.01
[**2187-5-15**] 10:56AM BLOOD cTropnT-<0.01
[**2187-5-23**] 06:00AM BLOOD Calcium-8.3* Phos-4.3# Mg-1.9
[**2187-5-20**] 05:48PM BLOOD Calcium-8.1* Phos-1.8* Mg-2.1
[**2187-5-16**] 04:49PM BLOOD Calcium-7.6* Mg-1.8
[**2187-5-15**] 10:56AM BLOOD Calcium-7.6* Phos-1.9* Mg-1.5*
[**2187-5-16**] 12:35AM BLOOD %HbA1c-6.1* eAG-128*
[**2187-5-16**] 12:35AM BLOOD Triglyc-54 HDL-50 CHOL/HD-2.2 LDLcalc-48
[**2187-5-21**] 06:44AM BLOOD Vanco-22.5*
[**2187-5-17**] 10:30AM URINE Color-Yellow Appear-Hazy Sp [**Last Name (un) **]-1.022
[**2187-5-17**] 10:30AM URINE Blood-TR Nitrite-NEG Protein-30
Glucose-NEG Ketone-NEG Bilirub-NEG Urobiln-NEG pH-5.0 Leuks-NEG
[**2187-5-17**] 10:30AM URINE RBC-1 WBC-3 Bacteri-FEW Yeast-NONE Epi-<1
[**2187-5-17**] 10:30AM URINE CastHy-9*
[**2187-5-15**] 11:05AM URINE Color-Yellow Appear-Clear Sp [**Last Name (un) **]-1.009
[**2187-5-15**] 11:05AM URINE Blood-NEG Nitrite-NEG Protein-TR
Glucose-NEG Ketone-NEG Bilirub-NEG Urobiln-NEG pH-7.0 Leuks-NEG
[**2187-5-15**] 11:05AM URINE RBC-<1 WBC-1 Bacteri-FEW Yeast-NONE
Epi-<1
[**2187-5-15**] 11:05AM URINE CastHy-8*
[**2187-5-15**] 11:05AM URINE bnzodzp-NEG barbitr-NEG opiates-NEG
cocaine-NEG amphetm-NEG mthdone-NEG

Blood Culture [**2187-5-16**], Routine (Final [**2187-5-20**]):
      STAPHYLOCOCCUS, COAGULASE NEGATIVE.    FINAL
SENSITIVITIES.
         Staphylococcus species may develop resistance during
prolonged
         therapy with quinolones.   Therefore, isolates that are
initially
         susceptible may become resistant within three to four
days after
         initiation of therapy.  Testing of repeat isolates may
be
         warranted.
      VIRIDANS STREPTOCOCCI.    FIRST MORPHOLOGY.
         IDENTIFICATION AND SENSITIVITIES PERFORMED ON CULTURE #
[**Numeric Identifier 88786**]
         FROM [**2187-5-16**].
      VIRIDANS STREPTOCOCCI.    SECOND MORPHOLOGY.
         IDENTIFICATION AND SENSITIVITIES PERFORMED ON CULTURE #
[**Numeric Identifier 88786**]
         FROM [**2187-5-16**].

                              SENSITIVITIES: MIC expressed in
MCG/ML

_________________________________________________________
                             STAPHYLOCOCCUS, COAGULASE NEGATIVE
                             |
CLINDAMYCIN-----------<=0.25 S
ERYTHROMYCIN----------<=0.25 S
GENTAMICIN------------ <=0.5 S
LEVOFLOXACIN----------<=0.12 S
OXACILLIN-------------<=0.25 S
TETRACYCLINE----------   <=1 S
VANCOMYCIN------------     2 S

   Aerobic Bottle Gram Stain (Final [**2187-5-17**]):
      GRAM POSITIVE COCCI IN PAIRS, CHAINS, AND CLUSTERS.
      Reported to and read back by [**First Name8 (NamePattern2) **] [**Last Name (NamePattern1) 88787**] AT 0200
[**2187-5-17**].

   Anaerobic Bottle Gram Stain (Final [**2187-5-17**]):
      GRAM POSITIVE COCCI IN PAIRS , CHAINS AND CLUSTERS.

Sputum Culture [**2187-5-18**]:

GRAM STAIN (Final [**2187-5-18**]):
      >25 PMNs and <10 epithelial cells/100X field.
      4+   (>10 per 1000X FIELD):   GRAM NEGATIVE ROD(S).

   RESPIRATORY CULTURE (Final [**2187-5-23**]):
      SPARSE GROWTH Commensal Respiratory Flora.
      HAEMOPHILUS INFLUENZAE, BETA-LACTAMASE NEGATIVE.    HEAVY
GROWTH.
         Beta-lactamse negative: presumptively sensitive to
ampicillin.
         Confirmation should be requested in cases of treatment
failure in
         life-threatening infections..
      GRAM NEGATIVE ROD(S).    RARE GROWTH.

Mini-BAL [**2187-5-18**]:
GRAM STAIN (Final [**2187-5-18**]):
      2+   (1-5 per 1000X FIELD):   POLYMORPHONUCLEAR
LEUKOCYTES.
      2+   (1-5 per 1000X FIELD):   GRAM NEGATIVE ROD(S).

   RESPIRATORY CULTURE (Final [**2187-5-23**]):
      10,000-100,000 ORGANISMS/ML. Commensal Respiratory Flora.
      HAEMOPHILUS INFLUENZAE, BETA-LACTAMASE NEGATIVE.
         >100,000 ORGANISMS/ML..
         Beta-lactamse negative: presumptively sensitive to
ampicillin.
         Confirmation should be requested in cases of treatment
failure in
         life-threatening infections..

CT/CTA head and neck/CT Perfusion [**2187-5-15**]:
FINDINGS:

NON-CONTRAST HEAD CT: There is hyperdense material within the
basilar artery,
likely thrombus. No evidence of an acute large infarction is
seen, though CT
has limited sensitivity for brainstem infarction. The ventricles
are normal
in size. There is a 3-mm hyperdense focus in the deep white
matter of the
right frontal lobe (image 2:19), without evidence of surrounding
edema. This
most likely represents a cavernous malformation with
calcifications. Absence
of surrounding edema suggests that a recent hemorrhage within
this
malformation is unlikely, though the possibility of a recent
microhemorrhage
cannot be completely excluded. No acute hemorrhage is seen
elsewhere in the
brain or extra-axial compartments.

There is a small amount of fluid in the maxillary and sphenoid
sinuses, and in
the ethmoid air cells bilaterally. Fluid in the nasopharynx and
posterior
nasal cavity. These findings may be related to endotracheal
intubation.

NECK CTA: There is a three-vessel aortic arch. The cervical
common carotid
and internal carotid arteries are patent without evidence of
significant
atherosclerosis or hemodynamically significant stenosis. The
distal cervical
internal carotid arteries measure 3.9 mm in diameter on the
right and 3.7 mm
in diameter on the left. The left vertebral artery is dominant
and patent
throughout its cervical course. The non-dominant right vertebral
artery is
diminutive throughout its cervical course.

There are mild degenerative changes in the imaged cervical and
upper thoracic
spine. There is extensive pleural/parenchymal scarring at the
imaged lung
apices.

HEAD CTA: The non-dominant right vertebral artery has a markedly
hypoplastic
intracranial segment, most likely due to normal anatomic
variation. The
intracranial left vertebral artery is patent. Left posterior
inferior and
anterior inferior cerebellar arteries are patent. There is a
right anterior
inferior cerebellar artery/posterior inferior cerebellar artery
complex, which
appears patent. The distal 1 cm of the basilar artery is
occluded, with
thrombus reaching but not completely occluding the basilar tip.
The right
superior cerebellar and posterior cerebral arteries are patent.
There is a
small right posterior communicating artery, which is patent. The
proximal
left superior cerebellar artery appears occluded, with distal
reconstitution.
There is a small but patent P1 segment of the left posterior
cerebral artery,
with a large left posterior communicating artery. There is a
duplicated P2
segment of the left posterior cerebral artery, with a focal
communication
between the two segments at the level of the posterior
communicating artery
(series 7, image 258, and series 855, image 20).

In the anterior circulation, there is minimal calcified plaque
in the
supraclinoid internal carotid arteries, without a
hemodynamically significant
stenosis.

There is no evidence of an intracranial aneurysm. No abnormal
arteries are
seen in the region of the right frontal hyperdense lesion to
suggest an
arteriovenous malformation. This arterial phase study has
limited sensitivity
for developmental venous anomalies.

CT PERFUSION: There is no evidence of asymmetries in the mean
transit time or
cerebral blood volume to suggest acute ischemia or acute
infarction in a major
vascular arterial territory. Please note that CT perfusion has
limited
sensitivity for acute infarctions related to occlusion of
pontine perforator
arteries or left superior cerebellar artery.

IMPRESSION:
1. Occlusion of the distal 1 cm of the basilar artery, which may
be related
to thrombosis or embolism, given the patient's history of atrial
fibrillation.
The proximal left superior cerebellar artery is occluded, with
distal
reconstitution. The right and left posterior cerebral arteries,
and the right
superior cerebellar artery, are patent.

2. No evidence of an acute major vascular territory infarction
on
conventional imaging or CT perfusion. Please note that MRI would
be more
sensitive for an acute infarction involving the brainstem or
cerebellum.

3. 3-mm hyperdensity in the right frontal deep white matter,
which most
likely represents a cavernous malformation. Absence of
surrounding edema
indicates that a recent hemorrhage within this malformation is
unlikely,
though the possibility of a recent microhemorrhage cannot be
completely
excluded.

4. The non-dominant right vertebral artery is diminutive
throughout its
cervical and intracranial course, likely indicating normal
anatomic variation.

5. Duplicated P2 segment of the left posterior cerebral artery,
with a
communication at level of the posterior communicating artery.
The left P1
segment is small, and the left posterior communicating artery is
large,
indicating fetal-type anatomy.

TTE [**2187-5-16**]:
The left atrium is normal in size. Left ventricular wall
thickness, cavity size, and global systolic function are normal
(LVEF>55%). Due to suboptimal technical quality, a focal wall
motion abnormality cannot be fully excluded. The right
ventricular cavity is dilated with depressed free wall
contractility. The number of aortic valve leaflets cannot be
determined. The mitral valve leaflets are mildly thickened.
There is no mitral valve prolapse. Mild (1+) mitral
regurgitation is seen. The tricuspid valve leaflets are mildly
thickened. There is moderate pulmonary artery systolic
hypertension. There is no pericardial effusion. There is an
anterior space which most likely represents a prominent fat pad.


IMPRESSION: Suboptimal image quality. Left ventricular systolic
function is probably normal, a focal wall motion abnormality
cannot be excluded. The right ventricle appears dilated and
hypokinetic - the RV apex is relatively spared. Mild mitral
regurgitation. Moderately elevated pulmonary artery systolic
pressures.

CT head [**2187-5-16**]:
FINDINGS:

There is no evidence of hemorrhage, mass effect, or shift of
normally midline
structures. The hyperdense appearance of basilar artery seen on
[**2187-5-15**]
exam is not visualized on current study. There is no cerebral
edema or loss
of [**Doctor Last Name 352**]-white matter differentiation to suggest an acute
ischemic event. The
basal cisterns are preserved. The sulci and ventricles are
normal in size and
configuration. A focal hyperdensity of the right frontal lobe
(2:19) appears
unchanged from prior exams and is most compatible with
cavernoma. There is no
significant surrounding edema, which argues against acute bleed.


There are air-fluid levels in bilateral sphenoid sinuses. There
is moderate
mucosal thickening of ethmoid air cells. The remainder of
paranasal sinuses
and mastoid air cells appear well aerated. Visualized soft
tissues and
osseous structures are intact. There is no acute fracture.

IMPRESSION:

1. No evidence infarction or hemorrhage.

2. Stable appearance of focal right frontal hyperdensity, most
compatible
with cavernoma.


CXR [**2187-5-16**]:
FINDINGS: As compared to the previous radiograph, the patient
has been
extubated, the patient also has received a nasogastric tube that
is coiled in
the upper parts of the esophagus. Moderate cardiomegaly with
extensive left
retrocardiac atelectasis and blunting of the costophrenic sinus
so that a
small pleural effusion cannot be excluded. Newly appeared right
basal and
perihilar opacity, making aspiration pneumonia a likely
diagnosis.

ABD U/S [**2187-5-18**]:
ABDOMINAL ULTRASOUND: This is a limited portable US exam. The
liver is
normal in echotexture without focal lesions. There are no stones
and no
intrahepatic or extrahepatic biliary ductal dilatation. The
normal CBD
measures 2 mm in diameter. There is normal hepatopetal portal
venous flow.
The spleen measures 8.6 cm. The visualized pancreas, aorta, and
IVC are
normal.

The right kidney measures 10.7 cm. The left kidney measures 9.8
cm. There is
no hydronephrosis, hydroureter, renal calculus or mass. No
ascites is noted.

Bilateral pleural effusions are incompletely evaluated, but
appear small.

IMPRESSION:
1. Normal abdominal ultrasound. No intra-abdominal free fluid or
fluid
collection to suggest intra-abdominal abscess.
2. Small bilateral pleural effusions.

MRI Brain [**2187-5-18**]:
FINDINGS: There is restricted diffusion seen to the left of
midline in the
pons indicative of an acute infarct. Additionally, there is
increased signal
diffusely identified within the pons extending to the right side
of the
midline which could be due to edema as this area does not
demonstrate
restricted diffusion. There is subtle enhancement in the left
paramedian
region at the infarct site indicative of mild enhancement of the
infarct.
There are no other areas of abnormal enhancement seen. There is
no
significant subcortical ischemic disease identified or midline
shift seen. A
small area of white matter hyperintensity in the right frontal
subcortical
region could be related to prior infarct. Fluid is seen in both
mastoid air
cells.

IMPRESSION:
1. Acute pontine infarct is identified to the left of midline,
with diffuse
increased signal within the pons, which could be due to
vasogenic edema.
Subtle enhancement of the infarct is seen.
2. No other enhancing brain lesions, mass effect or
hydrocephalus.
3. The basilar artery flow void, although narrowed is visualized
and no
abnormal signal seen within the basilar artery region on
T1-weighted images.

CXR [**2187-5-20**]:
One view. Comparison with the previous study done [**2187-5-18**].
Bilateral
interstitial infiltrates consistent with edema persist. Hazy
density at the
lung bases consistent with pleural fluid appears improved,
although this may
be due to more erect positioning. Increased density in the
retrocardiac area
consistent with atelectasis or consolidation is unchanged. The
cardiac
silhouette is prominent as before. An endotracheal tube and
nasogastric tube
remain in place.

IMPRESSION: Possible interval improvement in bilateral pleural
effusions. No other definite change.

CTA Chest and CT Abd/Pelvis [**2187-5-22**]:
TECHNIQUE: MDCT-acquired 2.5-mm axial images of the chest were
obtained prior
to and following the uneventful administration of 130 ml of
Optiray
intravenous contrast. Coronal, sagittal reformations were
performed at 5-mm
slice thickness. Additional right and left oblique
reconstructions were
obtained for further evaluation of the pulmonary vessels. MDCT
acquired 5-mm
axial images of the abdomen and pelvis were then obtained at the
delayed
phase, with 5-mm coronal and sagittal reformations.

CHEST: Bilateral lower lobe consolidations are present with
small bilateral
pleural effusions and adjacent atelectasis. Neighboring
ground-glass
opacities are scattered throughout both lungs. A small amount of
fluid is
present within the lower trachea (2:9). There is no
pneumothorax. The heart
size is top normal with an enlarged right atrium. A trace
pericardial
effusion is present. The great vessels are patent and normal in
caliber.
There is no dissection. No pulmonary embolus is detected to the
subsegmental
levels. Scattered axillary and mediastinal lymph nodes do not
meet CT
criteria for lymphadenopathy. The thyroid is normal.

ABDOMEN: The liver, gallbladder, spleen, adrenal glands,
kidneys, pancreas,
stomach, and intra-abdominal loops of small and large bowel are
normal. A
small left parapelvic renal cysts is present (3b:119). There is
no mesenteric
or retroperitoneal lymphadenopathy, and no free air or free
fluid. The
abdominal aorta, celiac trunk, SMA, and [**Female First Name (un) 899**] are patent and
normal in caliber.
There is no free air or free fluid.

PELVIS: A small amount of air is present within the bladder
(3B:161). The
rectum and uterus are normal. No adnexal masses are detected.
Colonic
diverticulosis is present, with no evidence of diverticulitis. A
trace amount
of intrapelvic fluid is seen. Mild stranding around the right
common femoral
artery is likely from recent vascular access.

OSSEOUS STRUCTURES: There is no acute fracture. No concerning
blastic or
lytic lesions are identified. Mild degenerative changes are
present within
the lumbar spine, including slight loss of the L5/S1 disc height
with
associated vacuum phenomenon and anterior and posterior
osteophytosis.

IMPRESSION:
1. Bilateral lower lobe pneumonia with small pleural and
pericardial
effusions.
2. No intra-abdominal or intrapelvic source of infection
identified.
3. No PE detected to the subsegmental levels.

TEE [**2187-5-24**]:
No spontaneous echo contrast or thrombus is seen in the body of
the left atrium/left atrial appendage or the body of the right
atrium/right atrial appendage. The right atrial appendage
ejection velocity is depressed (<0.2m/s). No atrial septal
defect is seen by 2D or color Doppler. Overall left ventricular
systolic function is normal (LVEF>55%). There are simple
atheroma in the aortic arch. There are complex, non-mobile
atheroma in the descending thoracic aorta. The aortic valve
leaflets (3) are mildly thickened. No masses or vegetations are
seen on the aortic valve. Trace aortic regurgitation is seen.
The mitral valve leaflets are mildly thickened. No mass or
vegetation is seen on the mitral valve. Mild to moderate ([**1-28**]+)
mitral regurgitation is seen. No vegetation/mass is seen on the
pulmonic valve. There is no pericardial effusion.

IMPRESSION: No intracardiac vegetation, abscess or thrombus.
Mild to moderate mitral regurgitation.


Brief Hospital Course:
Mrs. [**Known lastname 81211**] was intubated in the Emergency Room owing to
stupor progressing toward coma. Code stroke was actually not
called until the patient was seen by the Neurology Resident. The
history (including odd arm movements) and examination were more
consistent with top of the basilar ischemia than seizure.
Intravenous t-PA was given followed by clot retrieval. Over the
following hours her exam improved markedly. She was awake and
conversant with mild tetraparesis.

On the day following admission she developed a rapid onset high
fever of 102 F. Tylenol and then cooling blanket were employed.
She became less arousal, but this followed her fever curve and
resolved as fever remitted. This pattern of fever was classic
for central fever after stroke, which is associated with
disruption of pontine function (along with other central sites),
but her blood cultures were positive only a few hours later,
growing staphlococcus, streptococcus viridans and klebsiella
species. Broad specrum antiobiotics were started as soon as
cultures revealed growth (prior to the above organisms being
identified or speciated). Therfore vancomycin, cefepime and
metronidazole were given (tobramycin briefly before
metronidazole).

She was extubated and reintubated several hours later for
hypoxic episodes. This occurred in the context of likely
developing pulmonary infection (best appreciated by later CT
chest) and fluid overload. Diuresis restored respiratory
function but delayed TEE to evaluate for possible endocarditis
given the above organisms in blood.

Atrial fibrillation with rapid ventricular rate appeared on
several occasions in the context of fluid shifts, infection and
pneumonia, so rate control agents were up-titrated and digoxin
introduced.

When medically stable she was transferred to the floor. Her
course on the floor was complicated by continued intermittent
periods of oxygen desaturation and tachypnea. Out of concern for
a PE, she had a CTA of the chest, which was negative for PE, but
did show evidence for B/L pneumonias. She also had a CT of the
Abd/Pelvis to look for source of infection, but it was negative.
She was initially maintained on broad spectrum abx for her
bacteremia, but it was eventially speciated to include strep
viridans and klebsiella which were both broadly sensitive, and
her antiboitics were ultimately restricted to Ceftriaxone only,
which should continue daily through [**2187-6-1**].

TEE was complted [**2187-5-24**] to look for possible endocarditis or
other valve vegetations, however this was negative.


With respect to bacteremia, it is possible that there is a
sequestrum with numerous colonies, the presence of which
increased coagulability. However, on balance, we feel that
cardioembolic stroke in the context of atrial fibrillation is
most likely. Thrombus is frequently not observe in the atrium
given that the whole of it might embolize. In this case, t-[**MD Number(3) 88788**] have also reduced the chance of thrombus being retained.
Given the AF with new stroke, she was started on coumadin with
goal INR of [**3-1**]. INR's should be checked daily until this
therapeutic range is reached. She was bridged with aspirin,
which can be discontinued once the INR is therapeutic.

Medications on Admission:
- Atenolol 12.5mg
- Aspirin 81mg
- Simvastatin 40mg
- Alendronate 70mg weekly
- MVI
- Calcium

Discharge Disposition:
Extended Care

Facility:
[**Hospital **] Hospital for Continuing Medical Care - [**Location (un) 1121**]
([**Hospital3 1122**] Center)

Discharge Diagnosis:
acute stroke


Discharge Condition:
Mental Status: Clear and coherent.
Level of Consciousness: Alert and interactive.
Activity Status: Out of Bed with assistance to chair or
wheelchair.


Discharge Instructions:
You were admitted with a stroke, which initially left you with
weakness and mental status changes, however, the clot was
retrieved and you were given medicines to break up the clot, and
ultimately, your weakness and mental status improved. The clot
was felt to have likely come from your heart, and you should
continue on the blood thinner coumadin. Your course was
complicated by a blood infection, for which you've been
maintained on antibiotics. You also developed a pneumonia in
both lungs, which caused you to experience some shortness of
breath, and this also is being treated with antibiotics.

                             [**Name6 (MD) **] [**Name8 (MD) **] MD, [**MD Number(3) 632**]

Completed by:[**2187-5-25**]
{'Cerebral embolism with cerebral infarction,Occlusion and stenosis of basilar artery with cerebral infarction,Anomalies of cerebrovascular system,Acute respiratory failure,Atrial fibrillation,Unspecified essential hypertension,Other and unspecified hyperlipidemia,Osteoporosis, unspecified,Thrombocytopenia, unspecified'}


You are an AI assistant analyzing clinical admission notes from the MIMIC III dataset. Your task is to map symptoms mentioned in the notes to a list of provided ICD-9 LONG_TEXT.



### Clinical text :
CHIEF COMPLAINT: Tip of basilar clot: phenomenologically manifested as flailing
arms, confusion followed by stupor

PRESENT ILLNESS: Time Code Stroke called: 12:02
Time Neurology at bedside for evaluation: 11:30
Time (and date) the patient was last known well: 8:30
NIH Stroke Scale Score: 21
t-[**MD Number(3) 6360**]: Yes
Time t-PA was given 12:40
I was present during the CT scanning and reviewed the images
instantly within 20 minutes of their completion.

MEDICAL HISTORY: - Atrial fibrillation, not on Coumadin
- Dyslipemia
- Osteoporosis

MEDICATION ON ADMISSION: - Atenolol 12.5mg
- Aspirin 81mg
- Simvastatin 40mg
- Alendronate 70mg weekly
- MVI
- Calcium

ALLERGIES: No Known Allergies / Adverse Drug Reactions

PHYSICAL EXAM: At Admission:

FAMILY HISTORY: Unknown.

SOCIAL HISTORY: Lives in [**Location 14663**] with her husband. Is her husband's carer.
Previously independent in all ADL. 

### Response:
{'Cerebral embolism with cerebral infarction,Occlusion and stenosis of basilar artery with cerebral infarction,Anomalies of cerebrovascular system,Acute respiratory failure,Atrial fibrillation,Unspecified essential hypertension,Other and unspecified hyperlipidemia,Osteoporosis, unspecified,Thrombocytopenia, unspecified'}
