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The Different Faces of Hyponatremia: Multifaceted Patients and Multidisciplined Providers Alpesh N. Amin, MD, MBA Professor of Medicine Chair, Department.

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Presentation on theme: "The Different Faces of Hyponatremia: Multifaceted Patients and Multidisciplined Providers Alpesh N. Amin, MD, MBA Professor of Medicine Chair, Department."— Presentation transcript:

1 The Different Faces of Hyponatremia: Multifaceted Patients and Multidisciplined Providers Alpesh N. Amin, MD, MBA Professor of Medicine Chair, Department of Medicine Executive Director, Hospitalist Program University of California, Irvine School of Medicine Arthur Greenberg, MD Professor of Medicine Division of Nephrology Department of Medicine Duke University School of Medicine Durham, North Carolina Paul J. Hauptman, MD Professor of Internal Medicine Division of Cardiology Assistant Dean, Clinical and Translational Research St. Louis University School of Medicine St. Louis, Missouri Steven l. Zacks, MD, MPH, FRCPC Associate Professor of Medicine Division of Gastroenterology and Hepatology The University of North Carolina at Chapel Hill School of Medicine

2 Most common disorder of electrolytes, affecting 15% to 30% of acutely and chronically hospitalized patients a Approximately 1 million hospitalizations per year are due to hyponatremia as a primary or secondary diagnosis Direct cost of managing hyponatremia is estimated to range from $1.6 to $3.6 billion per year in the United States b Prevalence and Epidemiology of Hyponatremia a. From Schrier R. [1] b. From Boscoe A, et al. [2]

3 Primarily caused by inappropriately elevated plasma AVP, which is secreted in response to increased plasma osmolality or decreased volume/pressure (hypovolemia) and results in water reabsorption Etiology varies with classification –Hypovolemia (gastrointestinal/dermal/third-space loss, diuretics) –Euvolemia (SIADH, drugs [diuretics, SSRIs, carbamazepine, TCAs, phenothiazines, etc]) –Hypervolemia (heart failure, cirrhosis, renal failure) Clinical manifestation of underlying medical conditions and hyponatremia may provide important diagnostic and prognostic information Patients At Risk for Hyponatremia

4 Acute, severe hyponatremia can cause substantial morbidity and mortality Mortality is higher in patients with a wide range of underlying diseases Overly rapid correction can cause severe neurologic deficits and death Treatment Challenges

5 Definition of Hyponatremia Severity of Hyponatremia b SeverityNeurologic Manifestations*Sodium Mild Asymptomatic or associated with subtle changes in mental and physical function mEq/L ModerateNonspecific symptoms (nausea and malaise) mEq/L Severe Progressive neurologic symptoms ranging from confusion to coma < 125 mEq/L *Neurologic manifestations are also influenced by the speed of onset of hyponatremia Hyponatremia: serum sodium ≤ 135 mEq/L a a. From Adrogué HJ, Madias NE et al. [3] b. From Thompson. [4]

6 Clinical Symptoms in Hyponatremia From Adrogué HJ, et al. [3] Seizures Coma Permanent brain damage Respiratory arrest Brainstem herniation Death Headache Nausea Vomiting Muscle cramps Lethargy Restlessness Depressed reflexes Disorientation More likely to occur with serum sodium < 125 mEq/L Potential complications Potential complications are associated with: Severe, rapidly evolving hyponatremia Excessive water retention in euvolemia Menstruation Common symptoms

7 Case Presentation Neurosurgical Hyponatremia 30-year-old man with a known third ventricle tumor of 8 years’ duration Intractable headaches, seizure disorder Medications: oxycodone, levetiracetam Admitted for tumor resection BP 123/86, no JVD, clear chest, no edema, normal neurological exam Sodium 139 mmol/L, BUN 12 mg/dL, creatinine 1.0 mg/dL, glucose 147 mg/dL

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9 Case Presentation Neurosurgical Hyponatremia (cont) Brought to the operating room –Craniectomy, bone flap, excision of tumor from left lateral and third ventricles –Pathology: central neurocytoma, WHO grade III Returned to neurosurgical ICU Initially awake, but deteriorated neurologically CT of brain showed interval development of hydrocephalus Returned to operating room for placement of ventriculoperitoneal shunt Returned to neurosurgical ICU

10 Neurosurgical Hyponatremia Postoperative Days 4 and 5 Maintained on antibiotics, IV fluids, levetiracetam, IV fentanyl, high-dose dexamethasone Vital signs stable with pulse averaging 70 bpm range and BP in the range of 110 to 130/60 to 75 Physical examination revealed waxing and waning mental status, clear chest, no edema Intake and output roughly balanced with 2-3 L/d 0.9% saline or 0.45% saline in, 2-3 L/d urine out Decrease in serum sodium level from 140 to 127 mmol/L

11 Diagnostic Approach to Hyponatremia Genuinely hyponatremic? Pseudohyponatremia N Genuinely hypotonic? Hyperglycemia Radiocontrast Mannitol N Diluting defect? Primary polydipsia Beer potomania N Assess extracellular volume GI fluid Loss Adrenal insufficiency Diuretics Cerebral salt wasting Burns and third space fluid loss Marathon runners SIADH Glucocorticoid deficiency Hypothyroidism (Reset osmostat) NSAID Edema-forming states Heart failure Cirrhosis Nephrosis High Low Normal Not AVP Mediated

12 Case Presentation Neurosurgical Hyponatremia (cont) Serum cortisol 0.8 μg/dL (normal, μg/dL ) Free thyroxine 0.68 ng/dL (normal, ng/dL) Thyroid stimulating hormone 0.23 mIU/L (normal, mIU/L) Follicle-stimulating hormone 1.0 mIU/mL (normal, ) Luteinizing hormone 0.3 mIU/mL (normal, mIU/mL) Sodium 127 mEq/L Plasma osmolality 272 mOsm/kg Urine osmolality 875 mOsm/kg Urine sodium 245 mmol/L Uric acid 3.6 mg/dL (normal, mg/dL)

13 Postoperative Day Sodium, mmol/L Tumor Resection 3% NaCl Dexamethasone or Hydrocortisone U Osm 708 Neurosurgical SIADH I

14 Postoperative Day Sodium, mmol/L Tumor Resection 3% NaCl Dexamethasone or Hydrocortisone U Osm 708 Neurosurgical SIADH II

15 Postoperative Day Sodium, mmol/L Tumor Resection 3% NaCl Dexamethasone or Hydrocortisone U Osm 708 Tolvaptan, 15 mg Neurosurgical SIADH III

16 Postoperative Day Sodium, mmol/L Tumor Resection 3% NaCl Dexamethasone or Hydrocortisone U Osm 708 Tolvaptan, 15 mg U Osm 650 Neurosurgical SIADH IV

17 Postoperative Day Sodium, mmol/L Tumor Resection 3% NaCl Dexamethasone or Hydrocortisone U Osm 708 Tolvaptan, 15 mg Tolvaptan, 30 mg U Osm 650 U Osm 280 Neurosurgical SIADH V

18 Hyponatremia in Heart Failure Increased sodium reabsorption in the kidney Angiotensin IIVasopressinAldosterone

19 Complicating Factors Associated With Prolonged Length of Stay in Heart Failure Hyponatremia Volume overload Worsening renal failure Advanced age Comorbidities Marked antecedent weight gain Lack of (early) resolution of weight gain Hypotension Organ hypoperfusion

20 Predicted probability of freedom from death and death or HF rehospitalization across levels of sodium after adjusting for important covariates From Gheorghiade M, et al. [5] ESCAPE Relationship between clinical events and patients with persistent hyponatremia, corrected hyponatremia, or normonatremia Plots are for the “average” patient using the mean values of all covariates. Lighter line pairs represent 95% CI. To convert sodium to mmol/L, multiply by 1.0 Error brackets indicate exact binomial 95% CI intervals IMAGES NO LONGER AVAILABLE

21 EFFECT Multivariable Predictors of Mortality Age Systolic blood pressure Respiratory rate Serum sodium Hemoglobin Blood urea nitrogen From Lee DS, et al. [8]

22 Hyponatremia in Patients With Cirrhosis Diuretics cause contraction of central blood volume resulting in nonosmotic release of AVP Patients with cirrhosis have increased renin- angiotensin-mediated free water reabsorption while diuretics block sodium reabsorption Hyponatremia is significant because: –The MELD score combined with the serum sodium concentration was a better predictor of death than the MELD score alone a –It is associated with the development of hepatic encephalopathy b –Hyponatremia is a more sensitive marker of renal dysfunction than creatinine in patients with cirrhosis c a. From Kim WR, et al. [11] b. From Häussinger D, Schliess F. [12] c. From Ruf AE, et al. [13]

23 From Kim WR, et al. [11] Serum Sodium Concentration and Relative Risk of Death After Adjustment for MELD Score

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