CHIEF COMPLAINT: Weakness, altered mental status

PRESENT ILLNESS: 39 yo m w/ hx EtOH abuse, no other significant PMH, presents
with extreme weakness of his legs and arms.  Pt reports being in
usoh until [**1-10**] when he began to notice right leg swelling and
weakness.  This has slowly progressed to involve bilateral leg
weakness and mild discomfort, as well as arm weakness, that he
cannot describe further.  He was seen at [**Hospital1 778**] where he was
told
that his liver enzymes were elevated, and was started on
"vitamin supplementation" although he is unsure exactly what
kind.  He does report N/V 2 days ago, brought up iced tea that
he had recently drank.  No dark or bloody BMs; one BM per day.
No abd pain, fevers.  Does admit to "swelling" multiple
extremities.  Pt with long hx of EtOH use; drank 8-9 beers/day
for many years.
Over last 2 years 4 vodkas per night.  Last drink 4 days ago per
his report.  Denies hx of withdrawal.  No recent tylenol use,
herbal meds, or other medications.  He adamantly denies other
ingestions.

MEDICAL HISTORY: Alcohol abuse
Ankle Fracture

MEDICATION ON ADMISSION: none

ALLERGIES: Keppra

PHYSICAL EXAM: ICU Admission Exam:
Vitals: T: BP: P: R: 18 O2:
General: Alert, oriented, no acute distress
HEENT: Sclera anicteric, MMM, oropharynx clear
Neck: supple, JVP not elevated, no LAD
Lungs: Clear to auscultation bilaterally, no wheezes, rales,
ronchi
CV: Regular rate and rhythm, normal S1 + S2, no murmurs, rubs,
gallops
Abdomen:  soft, non-tender, non-distended, bowel sounds present,
no rebound tenderness or guarding, no organomegaly
Ext: Warm, well perfused, 2+ pulses, no clubbing, cyanosis or
edema

FAMILY HISTORY: Noncontributory

SOCIAL HISTORY: On disability, previously worked in finance. MSM lives with
partner, Denies tobacco/IVDU. Drinks 5 vodka drinks/day. Tattoo
from [**2178**].
Beriberi,Acute respiratory failure,Acidosis,Pneumonitis due to inhalation of food or vomitus,Alcohol withdrawal,Nutritional marasmus,Quadriplegia, unspecified,Nutritional and metabolic cardiomyopathy,Acute pancreatitis,Other disorders of neurohypophysis,Hemorrhage of gastrointestinal tract, unspecified,Subdural hemorrhage,Other convulsions,Other demyelinating diseases of central nervous system,Other and unspecified coagulation defects,Encephalopathy, unspecified,Polyneuropathy in other diseases classified elsewhere,Dermatitis due to drugs and medicines taken internally,Other and unspecified anticonvulsants causing adverse effects in therapeutic use,Other and unspecified agents primarily affecting the cardiovascular system causing adverse effects in therapeutic use,Acute alcoholic hepatitis
Beriberi,Acute respiratry failure,Acidosis,Food/vomit pneumonitis,Alcohol withdrawal,Nutritional marasmus,Quadriplegia, unspecifd,Metabolic cardiomyopathy,Acute pancreatitis,Neurohypophysis dis NEC,Gastrointest hemorr NOS,Subdural hemorrhage,Convulsions NEC,Cns demyelination NEC,Coagulat defect NEC/NOS,Encephalopathy NOS,Neuropathy in other dis,Drug dermatitis NOS,Adv eff antconvl NEC/NOS,Adv eff cardiovasc NEC,Ac alcoholic hepatitis
Admission Date:  [**2191-3-18**]              Discharge Date:   [**2191-4-16**]

Date of Birth:  [**2151-5-7**]             Sex:   M

Service: MEDICINE

Allergies:
Keppra

Attending:[**First Name3 (LF) 2297**]
Chief Complaint:
Weakness, altered mental status

Major Surgical or Invasive Procedure:
Endotracheal intubation
Lumbar puncture
Central venous line insertion
Atrial line insertion
Thoracentesis x2
Tracheostomy
Dobhoff feeding tube
Percutaneous endoscopic gastrostomy tube

History of Present Illness:
39 yo m w/ hx EtOH abuse, no other significant PMH, presents
with extreme weakness of his legs and arms.  Pt reports being in
usoh until [**1-10**] when he began to notice right leg swelling and
weakness.  This has slowly progressed to involve bilateral leg
weakness and mild discomfort, as well as arm weakness, that he
cannot describe further.  He was seen at [**Hospital1 778**] where he was
told
that his liver enzymes were elevated, and was started on
"vitamin supplementation" although he is unsure exactly what
kind.  He does report N/V 2 days ago, brought up iced tea that
he had recently drank.  No dark or bloody BMs; one BM per day.
No abd pain, fevers.  Does admit to "swelling" multiple
extremities.  Pt with long hx of EtOH use; drank 8-9 beers/day
for many years.
Over last 2 years 4 vodkas per night.  Last drink 4 days ago per
his report.  Denies hx of withdrawal.  No recent tylenol use,
herbal meds, or other medications.  He adamantly denies other
ingestions.

In [**Name (NI) **], pt noted to be jaundiced.  Head CT negative.  Abd CT with
thickened esophagus, fatty, enlarged liver, and large appendix,
but othewise negative.  Labs extremely abn with Na 119, HCO3 8,
glucose 31, AG 32, Cr 0.7, AST 169, ALT 31, ALK 105, TB 6.3, CK
NL, Lactate 12, NH3 13, Serum Osms 280, urine/serum tox screen
negative except for EtOH level of 110.  ABG 7.45/14/141.  Urine
urobililogen 8, + ketones.  UNa < 10.  Hct 24 to 20 with IVFs.
Guaiac negative per report.  Vitals with BPs 90's systolic, HR
120's.  Pt started empirically on vanc/zosyn, given a banana
bag, and 6 L NS.


Past Medical History:
Alcohol abuse
Ankle Fracture

Social History:
On disability, previously worked in finance. MSM lives with
partner, Denies tobacco/IVDU. Drinks 5 vodka drinks/day. Tattoo
from [**2178**].

Family History:
Noncontributory

Physical Exam:
ICU Admission Exam:
Vitals: T: BP: P: R: 18 O2:
General: Alert, oriented, no acute distress
HEENT: Sclera anicteric, MMM, oropharynx clear
Neck: supple, JVP not elevated, no LAD
Lungs: Clear to auscultation bilaterally, no wheezes, rales,
ronchi
CV: Regular rate and rhythm, normal S1 + S2, no murmurs, rubs,
gallops
Abdomen:  soft, non-tender, non-distended, bowel sounds present,
no rebound tenderness or guarding, no organomegaly
Ext: Warm, well perfused, 2+ pulses, no clubbing, cyanosis or
edema

Pertinent Results:
Head CT [**2191-3-17**]: No acute intracranial process.
.
CXR [**2191-3-17**]: No acute intrathoracic process.
.
CT abdomen [**2191-3-17**]: Diffuse esophageal wall thickening
consistent with esophagitis. Appendix measures up to 8mm and
appears indistinct- any evidence for acute appendicitis?
Hypoattenuating liver may represent fatty infiltration A few
small hypoattenuating hepatic lesions are of unclear etiology.
Trace free fluid.
.
TTE [**2191-3-18**]: Mildly dilated left ventricular cavity with
vigorous global systolic function and high cardiac output. No
significant valvular disease or pulmonary hypertension.
.
CXR [**2191-3-20**]: The NG tube is coiled in the stomach with the tip
in the mid
stomach. There are new bilateral infiltrates in the left lower
lobe and in
the right lower lobe with the left lower lobe infiltrate being
more densely opacified on the right.
.
MRI Spine [**3-21**]: 3. At L4/5, there is a left lateral disc
protrusion which contacts the left [**Name (NI) 5774**] nerve root in the
moderately narrowed left neural foramen
.
MRI Brain [**3-21**]: Minimal T2 hyperintensity in the periventricular
white matter abutting the lateral ventricles, which is a non
specific finding. While sometimes seen in asymptomatic patients,
it also may seen in demyelinating disease, Lyme disease,
sarcoidosis or other infectious/postinfectious states.
.
EMG [**3-22**]: Limited, abnormal study. There is electrophysiologic
evidence for a moderate- to-severe generalized sensorimotor
polyneuropathy with axonal features. Based on the limited data
available, there is no electrophysiologic evidence for a
demyelinating polyneuropathy, as in Guillain-[**Location (un) **] syndrome
.
CXR [**3-24**]: Left lower lobe opacity may represent pneumonia with
parapneumonic effusion given history.
.
CT chest [**3-24**]: 1. Mild pulmonary edema and moderate bilateral
pleural effusions. 2. Solitary focus of infection or small
infarction right upper lobe. Followup with routine chest
radiographs recommended.
3. Bibasilar consolidation is more likely atelectasis than
pneumonia.
.
Bilateral LENIs [**3-25**]: No evidence of DVT in either lower
extremity.
.
EEG [**3-25**]: Largely normal EEG for wakefulness and drowsiness.
There
was plentiful movement artifact, obscuring large portions of the

background. There were no areas of persistent focal slowing, and
there were no epileptiform features.
.
CTA chest [**3-25**]: 1. No PE to the segmental level.
2. Moderate bilateral effusions with associated compression
atelectasis are unchanged since yesterday.
3. Right apical lung lesion may represent infection or infarct
but should be followed after therapy to ensure resolution or
stability.
.
CT head [**3-25**]: While the study is very limited by motion, a new
small isodense left frontoparietal subdural collection could
represent subacute hemorrhage.
.
CXR [**3-26**]: The ET tube is 5.9 cm above the carina. The NG tube is
in the stomach. There is a moderate left effusion and left
retrocardiac
opacification consistent with volume loss/infiltrate. Compared
to the prior study, the left effusion is increased in size.
.
RUQ US [**3-26**]:
1. Mild splenomegaly. Slightly increased liver echogenicity.
2. Ascites.
3. Right pleural effusion.
4. Mildly distended gallbladder, containing thick bile/sludge,
which can be seen in the prolonged fasting state.
.
CXR [**3-27**]: Moderate bilateral pleural effusion, stable on the
left, increased on the right since [**3-26**]. Upper lungs
clear. Heart size normal. ET tube and nasogastric tube in
standard placements. No radiopaque central venous catheter is
noted. Right apical lung lesion seen on recent chest CT and CTA
scans is not clearly visible on conventional bedside radiographs
suggesting it is not enlarging rapidly, but followup is
indicated.
.
Left UE US [**3-28**]: No evidence of left upper extremity deep venous
thrombosis.
.
CXR [**3-29**]: In comparison with the study of [**3-27**], the nasogastric
tube has
been removed and replaced with a Dobbhoff tube that extends to
the mid body of the stomach. Endotracheal tube has been removed.
The bilateral hazy opacification consistent with pleural fluid
is seen at both bases. It appears to be less prominent, though
some of this could reflect the upright rather than supine
position.
.
CXR [**3-30**]: Left lower lobe consolidation has been present since
it developed between [**3-18**] and [**3-20**] could be
persistent pneumonia, or alternatively atelectasis. Moderate
right and small left pleural effusion have increased since
[**3-29**], though heart size is normal and unchanged. No
pneumothorax. Feeding tube ends in the stomach.
.
Echo [**4-4**]:
The left atrium is mildly dilated. Left ventricular wall
thicknesses are normal. The left ventricular cavity size is
normal. Regional left ventricular wall motion is normal. Overall
left ventricular systolic function is normal (LVEF>55%). The
estimated cardiac index is high (>4.0L/min/m2). Right
ventricular chamber size and free wall motion are normal. The
diameters of aorta at the sinus, ascending and arch levels are
normal. The aortic valve leaflets (3) appear structurally normal
with good leaflet excursion and no aortic regurgitation. There
is no valvular aortic stenosis. The increased transaortic
velocity is likely related to high cardiac output. The mitral
valve appears structurally normal with trivial mitral
regurgitation. The pulmonary artery systolic pressure could not
be determined. There is a trivial/physiologic pericardial
effusion.
IMPRESSION: Normal biventricular systolic function, with high
cardiac output c/w a high output state (hyperthyroidism, shunt,
anemia, etc).
Compared with the prior study (images reviewed) of [**2191-3-18**],
trivial pericardial effusion is new. Other findings are similar.

.
CTA Chest, CT abdomen and pelvis with contrast [**2191-4-4**]:
1. No evidence of pulmonary embolus. Slightly limited study,
particularly in the upper lobes.
2. Large bilateral nonhemorrhagic pleural effusions are
increased. There is no CT evidence to suggest empyema (no thick
or enhancing pleura).
3. Worsened consolidation in the left upper lobe, suggestive of
worsening
pneumonia. A nodular opacity in the right upper lobe is
decreased in size,
but follow up to complete resolution is recommended. Followup
may be obtained when treatment concludes and the patient's
clinical condition improves.
4. Possible tracheomalacia, though this is not a dedicated study
to evaluate for this.
5. Collection of fluid posterior to the pancreatic body as
described, new
from the prior study of [**3-17**], most likely a locule of
ascites fluid
rather than a discrete collection. There is a clear fat plane
between this
fluid and the pancreas. The pancreas is unremarkable in
appearance with
homogeneous enhancement.
5. Splenomegaly, with the spleen increased in size comparing to
[**3-17**] (15 cm today versus 11.5 cm previously).
Prominent/enlarged liver.
6. New small amount of ascites fluid.
7. Increased gallbladder distention. There is concern for
gallbladder
pathology, consider dedicated son[**Name (NI) 867**].
.
CT Head [**2191-4-4**]
IMPRESSION: Normal CT of the sinuses. No evidence of sinusitis.
.
MRI brain [**2191-4-5**]
1. Small subdural collection along the left convexity has
decreased in size, but increased in complexity and viscosity.
Evaluation for associated contrast enhancement is technically
limited.
2. New nonspecific signal abnormality in the central pons, which
may
represent a subacute infarction or central pontine myelinolysis.
Infectious and inflammatory causes should also be considered.
The location of this lesion does not correspond to typical or
atypical manifestations of Wernicke encephalopathy.
.
MRA brain [**2191-4-6**]
Apparent short-segment stenosis in the distal right vertebral
artery, immediately proximal to the basilar artery origin, which
may be
artifactual. The basilar artery and other major intracranial
arteries appear patent.
.
CT chest [**4-7**]
Worsening bilateral symmetrical mostly perihilar consolidation
in both
upper lobes and right middle lobe, likely due to pulmonary
edema. Extensive consolidation within both lower lobes could
potentially reflect developing ARDS. Multifocal rapidly
progressing multifocal pneumonia and pulmonary hemorrhage are
also in the differential. Improvement of bilateral
nonhemorrhagic pleural effusions, now moderate. Possible anemia.
Ascites.
.
CXR [**4-12**]
In comparison with the study of [**4-11**], there is little overall
change
in the bilateral ground-glass densities compatible with
congestive failure. Bilateral pleural effusions persist. The
left subclavian catheter has been removed. Tracheostomy tube and
Dobbhoff tube remain in place.
.
MRI head [**4-12**]:
1. Unchanged small left subdural collection. Evaluation for
contrast
enhancement is again technically limited by patient motion
artifact.
2. Slightly increased prominence of the geographic focal
T2-signal
abnormality in the central pons, which may relate to further
evolution and/or technical factors; the appearance remains in
keeping with central pontine myelinolysis, as suggested
previously, which could be correlated with volume/serum
osmolality shifts at time of its development. There is no
evidence of extra-pontine myelinolysis.
3. No new intracranial process.
.
CXR [**4-14**]:
Tracheostomy tube tip terminates 2.5 cm above carina and feeding

tube remains within the proximal stomach. Cardiac silhouette is
enlarged but unchanged in size, and there is persistent vascular
engorgement accompanied by bilateral confluent perihilar
opacities likely representing widespread, but slightly improving
pulmonary edema. Layering bilateral moderate pleural effusions
are present, right greater than left.

LABS:

[**2191-4-1**] 07:15AM BLOOD WBC-7.3 RBC-2.50* Hgb-8.5* Hct-25.0*
MCV-100* MCH-33.9* MCHC-34.0 RDW-17.7* Plt Ct-259
[**2191-3-17**] 08:05PM BLOOD WBC-12.4* RBC-2.38* Hgb-8.7* Hct-24.3*
MCV-102* MCH-36.4* MCHC-35.7* RDW-13.7 Plt Ct-246
[**2191-3-24**] 06:00AM BLOOD Neuts-91* Bands-0 Lymphs-1* Monos-7 Eos-0
Baso-1 Atyps-0 Metas-0 Myelos-0
[**2191-3-25**] 06:05AM BLOOD Hypochr-OCCASIONAL Anisocy-1+ Poiklo-1+
Macrocy-NORMAL Microcy-1+ Polychr-1+ Target-OCCASIONAL
Schisto-OCCASIONAL Burr-1+ Stipple-OCCASIONAL
[**2191-3-30**] 12:50PM BLOOD PT-19.1* PTT-63.9* INR(PT)-1.8*
[**2191-3-26**] 04:01AM BLOOD Fibrino-194 D-Dimer-As of [**1-4**]
[**2191-3-18**] 03:12AM BLOOD FDP-10-40*
[**2191-4-1**] 07:15AM BLOOD Glucose-118* UreaN-10 Creat-0.5 Na-139
K-3.5 Cl-109* HCO3-24 AnGap-10
[**2191-3-17**] 08:05PM BLOOD Glucose-31* UreaN-14 Creat-0.7 Na-119*
K-4.9 Cl-82* HCO3-10* AnGap-32*
[**2191-3-30**] 12:50PM BLOOD ALT-67* AST-139* AlkPhos-115 TotBili-2.6*
[**2191-3-17**] 08:05PM BLOOD ALT-31 AST-169* LD(LDH)-245 CK(CPK)-125
AlkPhos-105 TotBili-6.3*
[**2191-3-17**] 10:50PM BLOOD TotBili-6.5* DirBili-3.8* IndBili-2.7
[**2191-3-21**] 03:26AM BLOOD Lipase-808*
[**2191-3-30**] 12:50PM BLOOD Lipase-216*
[**2191-3-17**] 08:05PM BLOOD cTropnT-0.01
[**2191-3-17**] 08:05PM BLOOD CK-MB-6
[**2191-3-31**] 07:20AM BLOOD Calcium-8.2* Phos-3.5 Mg-1.7
[**2191-3-17**] 10:50PM BLOOD Albumin-2.2*
[**2191-3-30**] 12:50PM BLOOD VitB12-1711* Folate-13.5
[**2191-3-26**] 04:01AM BLOOD D-Dimer-5623*
[**2191-3-18**] 12:22PM BLOOD Hapto-29*
[**2191-3-18**] 12:22PM BLOOD Triglyc-78 HDL-12 CHOL/HD-5.9 LDLcalc-43
LDLmeas-<50
[**2191-3-17**] 10:50PM BLOOD Osmolal-280
[**2191-3-17**] 08:05PM BLOOD Ammonia-39
[**2191-3-22**] 04:45AM BLOOD TSH-6.7*
[**2191-3-25**] 06:05AM BLOOD Free T4-1.0
[**2191-3-17**] 08:05PM BLOOD HBsAg-NEGATIVE HBsAb-POSITIVE
HBcAb-POSITIVE
[**2191-3-18**] 03:12AM BLOOD Smooth-NEGATIVE
[**2191-3-18**] 03:12AM BLOOD [**Doctor First Name **]-NEGATIVE
[**2191-3-18**] 02:20AM BLOOD [**Doctor First Name **]-NEGATIVE dsDNA-NEGATIVE
[**2191-3-19**] 01:12PM BLOOD HIV Ab-NEGATIVE
[**2191-3-17**] 08:05PM BLOOD ASA-NEG Ethanol-110* Acetmnp-NEG
Bnzodzp-NEG Barbitr-NEG Tricycl-NEG
[**2191-3-17**] 08:05PM BLOOD HCV Ab-NEGATIVE
[**2191-3-17**] 08:28PM BLOOD Lactate-13.4*
[**2191-3-26**] 01:56AM BLOOD Lactate-0.7 K-3.9
[**2191-3-18**] 03:12AM BLOOD HERPES SIMPLEX VIRUS 1 AND 2 ANTIBODY
IGM-Test Name
[**2191-3-18**] 03:12AM BLOOD BETA-HYDROXYBUTYRATE-Test
[**2191-3-18**] 02:20AM BLOOD HERPES SIMPLEX (HSV) 2, IGG-Test Name
[**2191-3-18**] 02:20AM BLOOD HERPES SIMPLEX (HSV) 1, IGG-Test
[**2191-3-18**] 02:20AM BLOOD CERULOPLASMIN-Test
[**2191-3-24**] 04:03PM CEREBROSPINAL FLUID (CSF) WBC-2 RBC-366*
Polys-91 Lymphs-9 Monos-0
[**2191-3-24**] 04:03PM CEREBROSPINAL FLUID (CSF) WBC-2 RBC-153*
Polys-78 Lymphs-22 Monos-0
[**2191-3-24**] 04:03PM CEREBROSPINAL FLUID (CSF) TotProt-28 Glucose-63
LD(LDH)-40
[**2191-3-24**] 04:03PM CEREBROSPINAL FLUID (CSF) HERPES SIMPLEX VIRUS
PCR-Test Name
[**2191-3-30**] 11:51AM URINE Color-Yellow Appear-Clear Sp [**Last Name (un) **]-1.037*
[**2191-3-30**] 11:51AM URINE Blood-NEG Nitrite-NEG Protein-TR
Glucose-NEG Ketone-TR Bilirub-NEG Urobiln-NEG pH-6.0 Leuks-NEG
[**2191-3-30**] 11:51AM URINE RBC-5* WBC-6* Bacteri-NONE Yeast-NONE
Epi-0

.
[**2191-4-13**] 03:01AM BLOOD WBC-9.7 RBC-2.55* Hgb-8.4* Hct-24.9*
MCV-98 MCH-33.1* MCHC-33.7 RDW-17.6* Plt Ct-198
[**2191-4-11**] 02:51AM BLOOD Neuts-74.6* Lymphs-14.2* Monos-7.1
Eos-3.6 Baso-0.5
[**2191-4-13**] 03:01AM BLOOD Plt Ct-198
[**2191-4-13**] 03:01AM BLOOD PT-18.6* PTT-51.3* INR(PT)-1.7*
[**2191-4-13**] 03:01AM BLOOD Glucose-105 UreaN-17 Creat-0.4* Na-143
K-3.9 Cl-114* HCO3-23 AnGap-10
[**2191-4-12**] 03:37AM BLOOD ALT-69* AST-114* LD(LDH)-214 AlkPhos-167*
TotBili-1.1
[**2191-4-13**] 03:01AM BLOOD Calcium-8.4 Phos-4.0 Mg-1.8
[**2191-4-13**] 03:01AM BLOOD ANCA-NEGATIVE B
[**2191-3-19**] 01:12PM BLOOD HIV Ab-NEGATIVE
[**2191-3-18**] 03:12AM BLOOD [**Doctor First Name **]-NEGATIVE
[**2191-3-18**] 02:20AM BLOOD [**Doctor First Name **]-NEGATIVE dsDNA-NEGATIVE
[**2191-3-18**] 03:12AM BLOOD Smooth-NEGATIVE
[**2191-3-17**] 08:05PM BLOOD HCV Ab-NEGATIVE
[**2191-4-12**] 01:03PM BLOOD Type-ART Temp-39.0 Rates-/24 FiO2-50
pO2-166* pCO2-34* pH-7.50* calTCO2-27 Base XS-4 \NOT INTUBATED
[**2191-4-12**] 04:13AM BLOOD Lactate-0.8
.
[**2191-4-7**] 05:44PM PLEURAL FLUID WBC-450* RBC-4050* Polys-74*
Lymphs-18* Monos-5* Macro-3*
[**2191-4-5**] 12:41PM PLEURAL TotProt-1.9 Glucose-128 LD(LDH)-89
Amylase-25 Albumin-<1.0
[**2191-4-5**] 05:54PM PLEURAL TotProt-1.3 Glucose-120 LD(LDH)-66
Amylase-20 Albumin-<1.0
[**2191-4-5**] 12:41PM PLEURAL WBC-433* RBC-1889* Polys-1* Lymphs-8*
Monos-2* Meso-10* Macro-79*
[**2191-4-5**] 05:54PM PLEURAL WBC-783* RBC-1783* Polys-1* Lymphs-3*
Monos-2* Meso-68* Macro-26*
.
Blood cultures: neg on [**2195-3-17**], 17, 19, 20, 25, 27, 28, [**4-3**], 2, 3, 4, 5
Urine cultures: neg on [**2195-3-17**], 25, 27, [**4-3**], 2, 3. Minimal
Staphylococcus on [**3-24**], pos for yeast [**4-11**]
Spinal fluid culture: neg
CMV, EBV, HCV neg
BAL: neg, no PCP, [**Name10 (NameIs) **] fungus, no Legionella
C Diff neg x 7
Sputum cx pos for yeast


Brief Hospital Course:
Hospital course summary:
Mr. [**Known lastname **] is a 39 year old male with ETOH abuse who presented on
[**3-18**] with lactic acidosis, profound weakness and found to be
severely thiamine deficient consistent with a diagnosis of Beri
Beri. He had components of both wet and dry: high output heart
failure, edema and severe weakness.  The patient was repleted
aggressively with Thiamine, a multivitamin, and had an NG placed
for nutrition. He developed refeeding syndrome requiring
agressive electrolyte repletion. He developed ETOH withdrawal
and mental status changes approximately 24-48hr after admission.
He was treated with small doses of benzos and mental status
improved somewhat before he was called out to the general
medicine team on [**3-21**]. Initially, the patient was working with
PT/OT and was evaluated by speech & swallow. On [**3-23**], he was
advanced a dysphagia diet and the following day, he spiked a
fever to 101.8. Initial infectious work up revealed negative UA,
neg Blood Cx, negative Cdiff and possible infiltrate on CXR.
Chest CT revealed bilateral pleural effusions and atelectasis.
Lumbar puncture showed 2 WBCs, RBC 366, glucose 62 and protein
28. The patient was started on Vanc, Zosyn, and Cipro for
possible HAP/Asp PNA. He triggered on [**2191-3-24**] for tachypnea,
tachycardia, and hypoxia. His hypoxia resolved, and CTA was
subsequently negative for PE. Mental status further deteriorated
after fevers began and there was concern for intermittent
seizures due to bilateral upper extremity tremors and periodic
eye deviation. 2mg Ativan was given without significant
improvement. The patient was loaded with Keppra 1gram, started
on empiric Acyclovir 700mg IV TID and Keppra 1500mg [**Hospital1 **]. The
neurology attending recommended transfer to MICU where he had
continuous EEG monitoring.

After Keppra loading the patient became more somnolent and
acidotic and required intubation for airway protection. CT
revealed a small 4mm subdural hematoma but follow up MRI showed
resolution. ABGs improved quickly on the vent and the patient
was easily awakened and extubated on [**3-27**]. He continued to be
dysarthric, have low grade fevers and tachycardia to 90s-110s.
He was continued on Vanc/Zosyn for presumed aspiration pneumonia
but no positive cultures.  The 24hr EEG monitoring was been
discontinued, NGT was removed and the patient was taking some
meds crushed in apple sauce and was advanced to dysphagia diet.

Upon return to the medicine floor, the patient continued to have
fluctuating mental status, occasional tachycardia and
temperatures, presumed to be related to repeated aspiration
pneumonitis. All cultures continued to be negative.  The patient
had a dobhoff tube placed for primary nutrition with tube feeds
and eventually was restarted on pureed oral feeding only when
alert and awake. The patient was again transferred to the ICU
for tachycardia and tachypnea that did not resolve with
non-rebreather treatment, and with fevers to 102F.

## Weakness: On initial presentation the patient was
quadraplegic. With thiamine repletion he improved to extremity
strength of [**4-6**]/5 and plateaued at this strength. He was seen by
PT and OT while in house and discharged to [**Hospital 98**] rehab for
aggressive rehabilitation.

## AMS: When initially hospitalized, pt had been completely
alert and oriented. His mental status then deteriorated and
fluctuated, consistent with delirium. Possibile etiologies are
broad and ultimately much of his mental status changes were
attributed to infection and central pontine myelinolysis. The
considered possibilities included:
1) Aspiration PNA - despite CT chest showing no consolidation
(does show bilateral pleural effusions), the patient completed a
course of Vancomycin and Zosyn. There was concern for repeated
aspiration pneumonitis to explain occasional fevers, tachycardia
and fluctuating mental status.
2) Seizures: The patient was noted to have involuntary upper
extremity shaking and eye deviation to the left. He had multiple
risk factors for seizures (ie cerebellar atrophy) but has had
repeated EEGs without findings consistent with seizure. He was
loaded and maintained on Keppra for several weeks. However,
ultimately keppra was found to be a cause of drug rash and
fevers, and neurology was not highly suspicious of seizure
activity in this patient. Thus keppra was discontinued.
3) Meningitis/encephalitis: In the setting of fever and AMS but
no meningeal signs, the patient had a lumbar puncture which was
inconsistent with bacterial infection or HSV.  Empiric treatment
with broad antibiotics and acyclovir were stopped after
confirmed LP findings.
4) Intracranial bleed or infarct: CT head with 4mm frontal SDH,
but follow up MRI had no sign of bleed. This was thought to be
either artifact or transient SDH secondary to LP in setting of
elevated INR. A repeat MRI did show ongoing small subdural
collection, but per neurology, this was unlikely to be
contributing to the patient's poor mental status. A neurosurgery
consult was obtained, and they did not recommend drainage of
this collection.
5) Withdrawal: The patient was initially treated for withdrawal
but mental status deteriorated after he stopped [**Doctor Last Name **] on the
CIWA scale. Once about 7 days after his last etoh ingestion,
benzos were stopped out of concern for delirium.
6) Wernickes: Deemed unlikely given his initial presention with
normal MS. Also no findings on MRI of mammilary body
abnormality.
7) Hepatic encephalopathy: Given pt's alcohol hepatitis, he was
treated with lactulose and rifaximin for possible contribution
of encephalopathy to altered mental status. Once LFTs returned
to near normal, these meds were stopped, but waxing and [**Doctor Last Name 688**]
mental status persisted.
8) Pellagra: Per case reports, Niacin deficiency in setting of
thiamine repletion has been known to cause altered mental status
and shaking. Pt received niacin repletion via his tube feeds,
which contained 220% of daily niacin requirement.
9) Central Pontine Myelinolysis: Lesion was found on MRI [**2191-4-5**]
in the setting of ongoing altered mental status. An MRA was
obtained to definitively rule out stroke as cause of this
lesion, and MRA was normal. Per neurology, he likely has CPM due
to rapid correction of hyponatremia earler in his hospital
course. CPM is an irreversible process, and neurology consult
attributed his mental status to CPM; however the patient was
quite alert and oriented on the days immediately prior to
discharge, which indicates that he has not suffered an
irreversible insult.

## Respiratory Failure: Upon second transfer to the ICU, the
patient was tachycardic and tachypneic. LENIs were negative for
DVT and suspicion for pulmonary embolus was low. An ECHO was
obtained which showed hyperdynamic systolic function with a
small pericardial effusion and large bilateral pleural
effusions, likely related to his wet Beri-Beri. He was started
on vancomycin/zosyn/ciprofloxacin for presumed  aspiration
pneumonia. He was diuresed with IV lasix boluses and he
underwent needle thoracentesis bilaterally on [**2191-4-5**]. Pleural
fluid was transudative and cultures were negative. The patient
was intubated for tachypnea and fatigue on [**2191-4-7**], likely in the
setting of extreme weakness due to BeriBeri and underwent
bronchoscopy that same day. His airways showed normal anatomy
and mucosa. He had RML and RUL bronchoalveolar lavage, which
returned mildly bloody fluid. This BAL fluid was negative for
infection and hemosiderin-laden macrophages. Ultimately the
patient's antibiotics were discontinued on [**2188-4-5**] because
infectious workup for pneumonia was negative, and these
medications were thought to be contributing to his fevers. He
had a repeat mini-bronchoalveolar lavage on [**4-11**], and again BAL
fluid was negative for infection. The patient underwent
tracheostomy on [**2191-4-11**] and was able to be weaned to trach mask
ventilation on [**2191-4-13**]. He had a Passy-Muir valve placed on [**4-13**]
to enable better speech.

## Fevers: Upon second transfer to ICU, the patient was febrile
and his fevers persisted despite antibiotic therapy and an
extensive infectious work-up. Ultimately, per ID consult, fever
was attributed to medications, and the patient deffervesced when
all antibiotics and keppra were discontinued.  He subsequently
developed low grade fevers several days later which have
continued.  A repeat infectious work-up was negative and his
mental status slowly cleared.  His recurrent fevers are likely
related to his underlying CNS injury and may still have a
medication component.  If the patient develops a fever at rehab,
this is likely due to the above, rather than a new infection,
and should not automatically precipitate transfer back to the
hospital.

## Drug Rash: The patient developed a wide-spread, erythematous,
confluent macular rash on [**4-12**]. A dermatology consult was
obtained, and the rash was attributed to a drug reaction. Keppra
and captopril were thought to be most the likely causes of the
rash, and both were discontinued.  The rash had largely resolved
by the time of discharge, and the patient should be considered
allergic to keppra.

## Coagulopathy: The patient had an elevated PTT and INR thought
to be due to liver dysfunction and severe nutritional
deficiency.  He had no evidence of DIC or active bleeding. He
received Vit K and FFP while in the ICU for possibility of
subdural hematoma and prior to invasive procedures.  He also
received a total of 6 units of pRBCs for Hct <21.

## Volume status: The patient was consistently extravascularly
fluid overloaded, due to hypoalbuminemia from malnutrition,
beriberi related capillary leak, and initial aggressive fluid
resuscitation for tachycardia of unknown source. He was diuresed
with occasional IV lasix until he appeared euvolemic.

## Anemia: The patient was found to have a macrocytic anemia due
to malnutrition and alcohol effects. He was treated with B12 and
folate repletion. His hct has remained stable around 25. He was
also found to have guaiac positive stools. He was maintained on
a PPI and was transfused keep hct >21%.

## Tachycardia: Patient was tachycardic in 110s-120s for much of
his hospital course, likely due to his high-output cardiac
failure from wet BeriBeri and persistent fevers. Ultimately he
was placed on metoprolol with great improvement in his heart
rate to the 90s. Metoprolol 25mg TID should be continued as long
as he remains tachycardic, unless he becomes hypotensive to
SBP<100.

## Hyponatremia: The patient was hyponatremic throughout much of
his hospital stay. Hypothyroidism and adrenal insufficiency were
ruled out as possible etiologies. This was likely due to SIADH
in the setting of multiple pulmonary processes, and his sodium
had corrected by [**2191-4-7**] and has since remained stable.

## LFT abnormalities: On presentation the patient had LFT
abnormalities consistent with alcoholic hepatitis and
pancreatitis. Both improved throughout the admission.

## Nutrition: The patient was given tube feeds via gastric
dobhoff. On the day prior to discharge he had a PEG placed at
the bedside. This PEG can be used for tube feeds starting in the
afternoon of [**4-16**]. This PEG should not be removed until after
[**2191-5-16**].


Medications on Admission:
none

Discharge Medications:
1. Folic Acid 1 mg Tablet [**Month/Day/Year **]: One (1) Tablet PO DAILY (Daily).

2. Therapeutic Multivitamin     Liquid [**Month/Day/Year **]: One (1) Tablet PO
DAILY (Daily).
3. B-Complex with Vitamin C     Tablet [**Month/Day/Year **]: One (1) Tablet PO
TID (3 times a day).
4. Thiamine HCl 100 mg Tablet [**Month/Day/Year **]: Two (2) Tablet PO DAILY
(Daily).
5. Acetaminophen 325 mg Tablet [**Month/Day/Year **]: 1-2 Tablets PO Q6H (every 6
hours) as needed.
6. Lansoprazole 30 mg Tablet,Rapid Dissolve, DR [**Last Name (STitle) **]: One (1)
Tablet,Rapid Dissolve, DR [**Last Name (STitle) **] DAILY (Daily).
7. Metoprolol Tartrate 25 mg Tablet [**Last Name (STitle) **]: One (1) Tablet PO TID
(3 times a day).
8. Ipratropium Bromide 0.02 % Solution [**Last Name (STitle) **]: One (1)  Inhalation
Q6H (every 6 hours) as needed for wheezing.
9. Acetaminophen 325 mg Tablet [**Last Name (STitle) **]: Two (2) Tablet PO Q6H (every
6 hours) as needed for fever.
10. Olanzapine 2.5 mg Tablet [**Last Name (STitle) **]: One (1) Tablet PO BID (2 times
a day) as needed for agitation.
11. Pyridoxine 50 mg Tablet [**Last Name (STitle) **]: Two (2) Tablet PO DAILY
(Daily).
12. Heparin (Porcine) 5,000 unit/mL Solution [**Last Name (STitle) **]: One (1)
Injection TID (3 times a day).
13. Dextromethorphan-Guaifenesin 10-100 mg/5 mL Syrup [**Last Name (STitle) **]: Five
(5) ML PO Q6H (every 6 hours) as needed for cough.
14. Levalbuterol HCl 0.63 mg/3 mL Solution for Nebulization [**Last Name (STitle) **]:
One (1)  Inhalation Q4H (every 4 hours) as needed for wheezing.



Discharge Disposition:
Extended Care

Facility:
[**Hospital3 7**] & Rehab Center - [**Hospital1 8**]

Discharge Diagnosis:
Primary:
Beri Beri (thiamine deficiency with profound weakness)
Pyridoxine deficiency
Cardiomyopathy
Alcohol Withdrawal
Aspiration Pneumonia
Mental status changes

Secondary:
Alcohol Dependence
Malnutrition


Discharge Condition:
HR 80s-110, SBP 110-150s, daily fevers, tolerating trach mask
ventilation well, general physical weakness.


Discharge Instructions:
You were admitted with profound weakness and found to have
severe thiamine and pyridoxine deficiency.  You were treated for
alcohol withdrawal and mental status changes likely due to
aspiration pneumonia.  You have been followed closely by
neurology and will need ongoing follow up with them.  You will
need to continue with aggressive physical therapy.

We have started you on nutritional supplements and anti-seizure
medications as shown below.

If you develop any chest pain, shortness of breath, mental
status changes, fevers or any other general worsening of
condition, please call your PCP or come directly to the ED.

Followup Instructions:
Please follow up with Dr. [**Last Name (STitle) **] in Neurology on the eighth
floor of the [**Hospital Ward Name 23**] Building, [**4-26**] at 9am.

Please call the Gastroenterology Department at [**Telephone/Fax (1) 463**] to
schedule a colonoscopy.

Please call the [**Hospital 778**] clinic to schedule a follow up
appointment prior to discharge from rehab.
{'Beriberi,Acute respiratory failure,Acidosis,Pneumonitis due to inhalation of food or vomitus,Alcohol withdrawal,Nutritional marasmus,Quadriplegia, unspecified,Nutritional and metabolic cardiomyopathy,Acute pancreatitis,Other disorders of neurohypophysis,Hemorrhage of gastrointestinal tract, unspecified,Subdural hemorrhage,Other convulsions,Other demyelinating diseases of central nervous system,Other and unspecified coagulation defects,Encephalopathy, unspecified,Polyneuropathy in other diseases classified elsewhere,Dermatitis due to drugs and medicines taken internally,Other and unspecified anticonvulsants causing adverse effects in therapeutic use,Other and unspecified agents primarily affecting the cardiovascular system causing adverse effects in therapeutic use,Acute alcoholic hepatitis'}


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: Weakness, altered mental status

PRESENT ILLNESS: 39 yo m w/ hx EtOH abuse, no other significant PMH, presents
with extreme weakness of his legs and arms.  Pt reports being in
usoh until [**1-10**] when he began to notice right leg swelling and
weakness.  This has slowly progressed to involve bilateral leg
weakness and mild discomfort, as well as arm weakness, that he
cannot describe further.  He was seen at [**Hospital1 778**] where he was
told
that his liver enzymes were elevated, and was started on
"vitamin supplementation" although he is unsure exactly what
kind.  He does report N/V 2 days ago, brought up iced tea that
he had recently drank.  No dark or bloody BMs; one BM per day.
No abd pain, fevers.  Does admit to "swelling" multiple
extremities.  Pt with long hx of EtOH use; drank 8-9 beers/day
for many years.
Over last 2 years 4 vodkas per night.  Last drink 4 days ago per
his report.  Denies hx of withdrawal.  No recent tylenol use,
herbal meds, or other medications.  He adamantly denies other
ingestions.

MEDICAL HISTORY: Alcohol abuse
Ankle Fracture

MEDICATION ON ADMISSION: none

ALLERGIES: Keppra

PHYSICAL EXAM: ICU Admission Exam:
Vitals: T: BP: P: R: 18 O2:
General: Alert, oriented, no acute distress
HEENT: Sclera anicteric, MMM, oropharynx clear
Neck: supple, JVP not elevated, no LAD
Lungs: Clear to auscultation bilaterally, no wheezes, rales,
ronchi
CV: Regular rate and rhythm, normal S1 + S2, no murmurs, rubs,
gallops
Abdomen:  soft, non-tender, non-distended, bowel sounds present,
no rebound tenderness or guarding, no organomegaly
Ext: Warm, well perfused, 2+ pulses, no clubbing, cyanosis or
edema

FAMILY HISTORY: Noncontributory

SOCIAL HISTORY: On disability, previously worked in finance. MSM lives with
partner, Denies tobacco/IVDU. Drinks 5 vodka drinks/day. Tattoo
from [**2178**]. 

### Response:
{'Beriberi,Acute respiratory failure,Acidosis,Pneumonitis due to inhalation of food or vomitus,Alcohol withdrawal,Nutritional marasmus,Quadriplegia, unspecified,Nutritional and metabolic cardiomyopathy,Acute pancreatitis,Other disorders of neurohypophysis,Hemorrhage of gastrointestinal tract, unspecified,Subdural hemorrhage,Other convulsions,Other demyelinating diseases of central nervous system,Other and unspecified coagulation defects,Encephalopathy, unspecified,Polyneuropathy in other diseases classified elsewhere,Dermatitis due to drugs and medicines taken internally,Other and unspecified anticonvulsants causing adverse effects in therapeutic use,Other and unspecified agents primarily affecting the cardiovascular system causing adverse effects in therapeutic use,Acute alcoholic hepatitis'}
