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Alan Chan

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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.

Chief Complaint: LOC

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Medications

Lisinopril

Verapamil

Prozac

spironolactone

Allergies• PCN - hives

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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 FindingsNothing specific

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Laboratory Data

CBCBMPUrinalysisCardiac EnzymesLiver Function Tests CoagulationEndocrinologySerology Immunologic StudiesOther SerologyBody Fluid AnalysisCytologyPathology

MicrobiologyCXREKGUltrasoundCT ScanMRI2-D EchoOther Studies Other Imaging

Clinical CourseDifferential DiagnosisDiscussion

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Please Press to Return

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CBC

3.810.3

29.5204

Normal diff

MCV 93 (80-99)RDW 14.2 (<14.5)ESR 20

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BMP

127

4.7

95

22

11

1.176

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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Urine Analysis

color X

sp gr X

pH X

Hgb X

ketone X

glu X

prot X

LE X

nitrite X

urobil X

bili X

Microscopic

UA wnl c micro

FeNa > 2 on two measurements

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Cardiac Enzymes

CK XX (30-225)

CK-MB X (0-6.0)

Troponin X (0-1.9)

Neg x 3 sets

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Liver Function Tests

AST 127 (15-41)

ALT 85 (7-35)

Alk Phos 56 (32-91)

Albumin 4 (3.5-4.8)

T Bilirubin .9 (0.3-1.2)

Protein 7.7 nl

NH3 < 16

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Coagulation

PTT 27 (21-33)

PT 9.8 (10.3-13.0)

INR 0.98

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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

• Fe 106

• %sat 48

• TIBC 248

• Trans 177 all values normal

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Body Fluid Analysis

• EtOH 265• UDS MJ• Folate > 20• Vit B12 wnl

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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

• 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.

• 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.

• PANCREAS: The pancreas demonstrates heterogeneous echotexture without evidence of abnormality.

• SPLEEN: Spleen demonstrates a normal echotexture and size.

• 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.

• 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:

• Mildly prominent liver.

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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.

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

• 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

• Uric acid < 4• BUN < 10• FeNa > 1; Fe urea > 55• Still hypoNa after NS• Corrects in fluid restriction

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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

• 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)

• Potassium 3.2 meq/L (3.2 mmol/L)

• Chloride 84 meq/L (84 mmol/L)

• Bicarbonate 21 meq/L (21 mmol/L)• Phosphorus 3.1 mg/dL (1 mmol/L)• Albumin 3.2 g/dL (32 g/L)

• Serum osmolality 243 mosm/kg H2O (243 mmol/kg)

• Urine sodium 20 meq/L (120 mmol/L)

• Urine potassium 24 meq/L (24 mmol/L)• Urine osmolality 42 mosm/kg H2O (542 mmol/kg)

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54 yo, s/p pleurodesis, SCLC w/ mets, here for f/u

• Which of the following is the most appropriate therapy at this time?

• 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

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Hypertonic saline is not indicated for asymptomatic hyponatremia.

• 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.

• 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.

• 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.

• 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.

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Discussion

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Discussion

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Discussion