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Morning Report Alan Chan
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
Medications Lisinopril Verapamil Prozac spironolactone Allergies PCN - hives
PMH:Hep C, HTN, depression, EtOH abuse PSH: hernia repair
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
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
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
CC: 57 yo with “LOC” HPI: witnessed LOC of a couple minutes; no prodrome PMH: hepC, EtOH abuse, HTN, depression PE Findings Nothing specific Differential Diagnosis
CBC BMP Urinalysis Cardiac Enzymes Liver Function Tests Coagulation Endocrinology Serology Immunologic Studies Other Serology Body Fluid Analysis Cytology Pathology Microbiology CXR EKG Ultrasound CT Scan MRI 2-D Echo Other Studies Other Imaging Clinical Course Differential Diagnosis Discussion Laboratory Data
CBC 10.3 204 3.8 29.5 Normal diff MCV 93 (80-99) RDW 14.2 (<14.5) ESR 20
BMP 127 95 11 76 22 1.1 4.7 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)
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 Urine Analysis
CK XX (30-225) CK-MB X (0-6.0) Troponin X (0-1.9) Neg x 3 sets Cardiac Enzymes
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 Liver Function Tests
PTT 27 (21-33) PT 9.8 (10.3-13.0) INR 0.98 Coagulation
TSH 2.1 (0.34-5.6) Baseline AM cortisol 15 (5-25) Cortisol stim test nl 24hr Urine Cr 600 (800-1200) Endocrinology
Serology • Urine Na 96 • Urine Osm 461 • P osm 260 • Uric acid 5.3
Other Serology • Results • Chol 188, TG 103, HDL 85, LDL 82 • Fe 106 • %sat 48 • TIBC 248 • Trans 177 all values normal
Body Fluid Analysis • EtOH 265 • UDS MJ • Folate > 20 • Vit B12 wnl
Pathology • none
Microbiology • Blood Cx 2 set neg
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.
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.
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.
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.
Other Studies • Truman special • Cbc, BMP, CT head, CE x1, LFTs, UDS, UA, EKG
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
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 Clinical course
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 Hyponatremia, dx and workup
Vol depletion True, CHF, cirrhosis, diuretics, thiazide diuretics Hormonal Adrenal insuff Hypothyroidism Pregnancy SIADH @!!!!!!!!!!!!! MCC is non-osmotic release – inc ADH
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 SIADH dx criteria
Uric acid < 4 BUN < 10 FeNa > 1; Fe urea > 55 Still hypoNa after NS Corrects in fluid restriction Other things that help
multifactorial Causes of SIADH
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) Discussion
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. Time for a question… MKSAP14
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) Laboratory Studies
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 54 yo, s/p pleurodesis, SCLC w/ mets, here for f/u
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. Hypertonic saline is not indicated for asymptomatic hyponatremia.