Transcript document

Alan Chan
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Chief Complaint: LOC
HPI: 57-year-old WM, presents to the ED via MAST
with a chief complaint of new-onset LOC. he got up
to urinate at the bedside commode and had
witnessed shaking. Last memory is going to
bathroom and then to the floor, per report a couple
minutes max duration. no trauma. No new
medications. There were no pre-aura symptoms.
He denies having any postictal symptoms.
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Medications
Allergies
• PCN - hives
Lisinopril
Verapamil
Prozac
spironolactone
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PMH:Hep C, HTN, depression, EtOH abuse
PSH: hernia repair
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SH: 1-2 pt a day of hard liquor – vodka; 20+
py tob, occ MJ
FH: HTN
ROS: fatigue, nausea, HA (intermittent, and
no hx of migrane), malaise --- all for a long
time
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Sig findings….
VS: Temp 98.3, Resp 18, BP 99/65, Pulse 88
General: NAD, thin, fragile appearance
Skin: a few old scars
HEENT: poor dentition
Neck:
Chest: dec air mvt, otherwise clear
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Significant findings…
CVS: rrr
Abd: mildly protuberant abdomen, nl BS. Mild
hepatomegaly. No splenomegaly
Ext: unsteady gait initially in ED, but nl on later days
Neuro: CN, sensory, motor, cerebellar, DTR
actually tested and no deficits
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Differential Diagnosis
CC: 57 yo with “LOC”
HPI: witnessed LOC of a
couple minutes; no
prodrome
PMH: hepC, EtOH abuse,
HTN, depression
PE Findings
Nothing specific
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Laboratory Data
CBC
BMP
Urinalysis
Cardiac Enzymes
Liver Function Tests
Coagulation
Endocrinology
Serology
Immunologic Studies
Other Serology
Body Fluid Analysis
Cytology
Pathology
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Microbiology
CXR
EKG
Ultrasound
CT Scan
MRI
2-D Echo
Other Studies
Other Imaging
Clinical Course
Differential Diagnosis
Discussion
Please Press to Return
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CBC
10.3
204
3.8
29.5
Normal diff
MCV 93 (80-99)
RDW 14.2 (<14.5)
ESR 20
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BMP
127
4.7
95
22
11
1.1
AG 7 (3-15)
Ca 9.7 (8.8-10.5)
Mg 1.7 (1.8-2.5)
PO4 3.6 (2.4-4.7)
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76
Urine Analysis
color
sp gr
pH
Hgb
ketone
glu
prot
LE
nitrite
urobil
bili
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X
X
X
X
X
X
X
X
X
X
X
Microscopic
UA wnl c micro
FeNa > 2 on two
measurements
Cardiac Enzymes
CK
CK-MB
Troponin
Neg x 3 sets
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XX (30-225)
X (0-6.0)
X (0-1.9)
Liver Function Tests
AST
ALT
Alk Phos
Albumin
T Bilirubin
Protein
NH3 < 16
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127 (15-41)
85 (7-35)
56 (32-91)
4 (3.5-4.8)
.9 (0.3-1.2)
7.7 nl
Coagulation
PTT
PT
INR
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27 (21-33)
9.8 (10.3-13.0)
0.98
Endocrinology
TSH
2.1 (0.34-5.6)
Baseline AM cortisol 15 (5-25)
Cortisol stim test nl
24hr Urine Cr 600 (800-1200)
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Serology
• Urine Na 96
• Urine Osm 461
• P osm 260
• Uric acid 5.3
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Immunologic Studies
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Cytology
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Other Serology
• Results
• Chol 188, TG 103, HDL 85, LDL 82
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Fe 106
%sat 48
TIBC 248
Trans 177 all values normal
Body Fluid Analysis
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EtOH 265
UDS MJ
Folate > 20
Vit B12 wnl
Pathology
• none
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Microbiology
• Blood Cx 2 set neg
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CXR
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EKG
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Ultrasound
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LIVER: The liver is mildly prominent, measuring 17.4 cm in length. It demonstrates normal
shape, configuration, and echotexture. No discrete intraparenchymal masses or fluid
collections are identified. The portal vein is patent and demonstrates hepatopedal flow.
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BILIARY SYSTEM: No intrahepatic nor extra hepatic biliary ductal dilatation is present. The
common bile duct measures 5 mm. The gallbladder is normal in appearance, and
demonstrates no evidence of echogenic calculi.
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PANCREAS: The pancreas demonstrates heterogeneous echotexture without evidence of
abnormality.
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SPLEEN: Spleen demonstrates a normal echotexture and size.
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RENAL: The right kidney measures 10.8 cm, and the left kidney measures 11.1 centimeters.
Both kidneys demonstrate normal cortical thickness, echotexture, and preserved
corticomedullary differentiation. There is no evidence of hydronephrosis/obstruction.
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OTHER: No abnormal intraperitoneal or retroperitoneal masses nor fluid collections were
identified. The aorta and IVC both appear normal. Diameter of the aorta is 1.9 cm.
Impression:
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Mildly prominent liver.
CT Scan
Generalized atrophy. No extra-axial fluid collections. The
Gray-white matter interface is well-maintained. No sulcal
effacement. Pneumatized left interclinoid. The sinuses are well
aerated. No hydrocephalus. No midline shift.
Impression:
1. No CT evidence of acute intracranial abnormalities detected.
Generalized atrophy.
2. Full evaluation of seizures requires MRI with and without
contrast.
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MRI
FINDINGS:
No focus of water diffusion restriction is identified. No intracranial hemorrhage,
hydrocephalus or brain herniation is seen. No abnormal enhancement is noted.
Minimal left frontal encephalomalacia is identified. Scattered foci of hyperintense signal are
identified on axial T2 FLAIR imaging involving the periventricular white matter and centrum
semiovale. Normal gray-white matter interface is maintained. Normal vascular flow voids
are preserved. Cerebral, cerebellar and corpus callosal atrophy are identified.
The visualized portions of the orbits, paranasal sinuses, and mastoid air cells are normal.
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IMPRESSION
No acute intracranial abnormality.
Findings suggestive of minimal left frontal encephalomalacia and chronic small vessel
ischemic disease.
Cerebral, cerebellar and corpus callosal atrophy. These findings can be seen with
alcoholism.
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2-D Echocardiogram
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Other Imaging – CT chest/abd/pelvis – Man scan
IMPRESSION
1. No acute osseous injury or formation of hematoma.
2. Osseous changes within both femoral heads demonstrating cystic
lesions and flattening of the superior articular surface, right greater
than left. This formation is worrisome and is questionable for
avascular necrosis.
3. Old, healed, displaced rib defects compatible with remote fractures
of the right ribs 4-8.
4. Lumbar facet arthrosis and generalized osseous degenerative
changes.
5. Dependent atelectasis in the right base.
6. Prostatic enlargement with central zone calcifications.
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Other Studies
• Truman special
• Cbc, BMP, CT head, CE x1, LFTs, UDS, UA, EKG
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Clinical Course
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Pt admitted to tele. Had MI r/o with neg CE x3
Normal CT head; MRI/A later showed changes r/t EtOH
Placed on EtOH precautions, but no s/s of withdrawl
Noted low Na despite a couple liters IVF hydration with NS
over the next couple days.
• Old records showed some consistently low Na, generally <
130
• Pt worked with PT/OT and made gradual improvement, but
still c/o some malaise and fatigue
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Clinical course
• Neuro – improved, no seizures noted
• CV - Still some HTN and had to adjust meds; no
events on tele
• Hep c – no signs of cirrhosis on imaging or exam
• Will f/u in clinic for hypoNa (chronic) and HTN
• Dx with SIADH
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Hyponatremia, dx and workup
• Suppresed Antidiuretic Hormone
- can’t dilute urine in advanced CRF
- 1° polydipsia – in excessive water drinking
- beer drinker’s potomania – water rich, salt poor,
excess loss salt
• Pseudohyponatremia – nl or inc Posm
- inc P osm – mannitol or hyperglycemia
- nl P osm – HL or hyper protein state
- also renal failure
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MCC is non-osmotic release – inc ADH
• Vol depletion
– True, CHF, cirrhosis, diuretics, thiazide diuretics
• Hormonal
– Adrenal insuff
– Hypothyroidism
– Pregnancy
• SIADH @!!!!!!!!!!!!!
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SIADH dx criteria
• S osm < 275
• U osm > 100 during hypotonicity or when plasma
Osm is low
• Clinically euvolemic (no volume depletion or excess)
• U Na > 40
• Normal TSH and adrenal fxn
• Not on diuretics
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Other things that help
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Uric acid < 4
BUN < 10
FeNa > 1; Fe urea > 55
Still hypoNa after NS
Corrects in fluid restriction
Causes of SIADH
• multifactorial
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Discussion
• Malignancy
• Pulmonary d/o – inf’n, asthma, CF
• CNS d/o – inf’n, bleeding, other (DTs, GBS, MS)
• Drugs induced – SSRI, TCAs, nicotine, narcs,
antipsychotics, NSAIDs, vincristine, AVP analogues
(oxytocin, VP, desmopressin)
• Other – idiopathic/cyptogenic, transient (exercise,
anesthesia, nausea, stress)
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Discussion
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Time for a question… MKSAP14
• A 54-year-old woman comes for a follow-up examination. She was
discharged from the hospital 7 days ago after hospitalization for
severe shortness of breath. During her hospitalization, a large
pleural effusion was found and pleurodesis was performed. At
today's visit, she feels tired. She has not had nausea, headache,
or irritability and has not vomited. She was diagnosed with
metastatic small-cell lung carcinoma 13 months ago and was
treated with palliative chemotherapy with a good response.
Previous surgeries include two cesarean sections. She also has a
75-pack-year history of cigarette smoking.
• On physical examination, her temperature is 36.8 °C (98.2 °F),
pulse rate is 84/min, respiratory rate is 18/min, and blood pressure
is 126/84 mm Hg. She appears cachectic. Cardiac examination is
normal. On pulmonary examination, there are diminished breath
sounds in the right base and the left side is clear to auscultation.
There is no pedal edema.
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Laboratory Studies
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Glucose 114 mg/dL (6.33 mmol/L)
Blood urea nitrogen 10 mg/dL (3.57 mmol/L)
Creatinine 0.6 mg/dL (53.05 μmol/L)
• Sodium 112 meq/L (112 mmol/L)
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Potassium 3.2 meq/L (3.2 mmol/L)
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Chloride 84 meq/L (84 mmol/L)
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Bicarbonate 21 meq/L (21 mmol/L)
Phosphorus 3.1 mg/dL (1 mmol/L)
Albumin
3.2 g/dL (32 g/L)
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Serum osmolality 243 mosm/kg H2O (243 mmol/kg)
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Urine sodium 20 meq/L (120 mmol/L)
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Urine potassium
Urine osmolality
24 meq/L (24 mmol/L)
42 mosm/kg H2O (542 mmol/kg)
54 yo, s/p pleurodesis, SCLC w/ mets, here for f/u
• Which of the following is the most appropriate
therapy at this time?
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A 3% saline via infusion pump
B Demeclocycline
C Fluid restriction <1 L/d
D Sodium chloride tablets, 2 g three times daily
E Hydrochlorothiazide
•
Demeclocycline therapy is indicated to decrease this patient's urine osmolality. The most important
determination to make in dealing with hyponatremia is the presence or absence of symptoms of
hyponatremic encephalopathy, which include headache and nausea and correspond to cerebral edema.
Seizures are the next manifestation, followed by brainstem herniation and, ultimately, respiratory arrest
and death. This patient has a normal level of consciousness and does not manifest any of these signs.
Demeclocycline is known to decrease urinary concentration and is indicated in this patient to prevent her
water-retentive state from worsening. However, type 2 vasopressin receptor antagonists may soon
replace demeclocycline in treatment of chronic hyponatremia.
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Because she currently has no manifestations of hyponatremic encephalopathy, aggressive therapy is not
appropriate regardless of the degree of hyponatremia. Therefore, 3% saline infusion therapy to raise the
serum sodium level quickly is not warranted.
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Fluid restriction would be ineffective at increasing the serum sodium level. The excretion of electrolytes
(both sodium and potassium) is important for determining water balance, a fact that is formalized in the
concept of electrolyte-free water clearance. Water excretory capacity can be quickly estimated by
comparing the urine electrolytes (sodium + potassium) with the serum electrolytes (sodium + potassium).
In this case, the urine electrolyte concentration is 144 meq/L (120 + 24), which exceeds the serum
electrolyte concentration (111 + 3.6). Therefore, there is no electrolyte-free water clearance occurring. In
other words, the patient is not losing any water in the urine and, as such, any degree of fluid restriction will
not increase the serum sodium level.
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Sodium chloride tablets are not indicated for hyponatremia. Hyponatremia is a disorder of excess water
relative to the total solutes (total exchangeable sodium and potassium), but providing sodium alone does
not increase the serum sodium level. Moreover, oral saline contains very little sodium. Hydrochlorothiazide
impairs diluting capacity and therefore has no role in the treatment of hyponatremia.
Hypertonic saline is not indicated for asymptomatic
hyponatremia.
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Discussion
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Discussion
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Discussion
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