WORKSHOP CASE FOR FLUID AND ELECTROLYTE DISORDERS Subsection d3 Facilitator: dra. Comes-natividad Rivere. Robosa. Rodas. Rodriguez. Rogelio. Roque. Ruanto. Sabalvaro. Salac. Salazar, j. Salazar, r. salcedo
Salient Features • 51 year old, female • Vomiting • Fever, dysuria, urgency • Headache, body malaise, nausea • Vomiting: 50cc/episode • Known hypertensive • Telmisartan (40 mg) • Hydrochlorthiazide (12.5 daily) • Weak looking, wheelchair-borne • BP: 120/80 (supine), 90/60 (sitting), 130/80 (usual) • HR: 90/min (supine), 105/min (sitting) • Lost weight, poor skin turgor, dry mouth, tongue and axillae • Normal JVP
2. What factors contributed to the development of hyponatremia in the patient?
Factors in the Development of Hyponatremia • Vomited 3x (50 cc/episode) • Primary Sodium Loss (Secondary water gain): GastointestinaI Losses • Due to vomitingpredisposes the patient to hyponatremiasince there is a corresponding sodium loss associated with water loss
Factors in the Development of Hyponatremia • Intake of hydrochlorothiazide • Primary Sodium Loss (Secondary water gain): Renal Losses • It is important to note that diuretic-induced hyponatremia is almost always due to thiazide diuretics lead to Na+ and K+ depletion and AVP-mediated water retention. • Inhibits reabsorption of sodium and chloride in the distal convoluted tubule promoting water loss.
Factors in the Development of Hyponatremia • Intake of telmisartan • ARB • Inhibits tubular Na and Clreabsorption, K excretion, water retention promotes water loss.
3. Compute for the plasma osmolality and the effective plasma osmolality. What is the importance of computing for such?
Plasma Osmolality and Effective Plasma Osmolality • Osmolality (calc) = 2 x Na + glucose + urea **if all measurements in mmol/L • Osmolality (calc) = 2 x Na + glucose/18 + urea/2.8 **if measurements are in mg/dL • Given: • Plasma Na = 123 mEq/L • Glucose = 98 mg/dL • Urea = 22 mg/dL • Osmolality = 2(123) + (98/18) + (22/2.8) • Osmolality = 259. 301 N = 275 – 295 milli-osmoles per kilogram Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.
Plasma Osmolality and Effective Plasma Osmolality • Effective Osmolality (calc) = 2 x Na + glucose **if all measurements in mmol/L • Osmolality (calc) = 2 x Na + glucose/18 **if measurements are in mg/dL • Given: • Plasma Na = 123 mEq/L • Glucose = 98 mg/dL • Urea = 22 mg/dL • Osmolality = 2(123) + (98/18) • Osmolality = 251.44 < 275 = Hyponatremia Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.
Importance of computing for the plasma osmolality and the effective plasma osmolality ECF tonicity is determined primarily by the Na+ concentration and patients who have hyponatremia have a decreased plasma osmolality. Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.
4. What are the significance of urine osmolality (Uosm) and urine sodium (Una)?
Urine Osmolality (Uosm) • A more exact measurement of urine concentration than specific gravity • Patient with Uosm below 100 mOsm/kg are able to appropriately suppress ADH release, leading to a maximally dilute urine • Patients with a higher urine osmolality have an impairment in water excretion due to the presence of ADH • Indicated to evaluate the concentrating and diluting ability of the kidney • Accurate test for decreased kidney function • Monitor course of renal disease/ electrolyte therapy Reference: RennkeH., Denker, B. 2007. Renal Pathophysiology: The Essentials
Urine Sodium (UNa) • Helps distinguish renal from non- renal causes of hyponatremia • Urine sodium exceeding 20 mEq/L is consistent with renal salt wasting. • Diuretics, ACE inhibitors, mineralocorticoid deficiency, salt losing nephropathy • Urine sodium less than 10 mEq/L implies avid sodium retention by the kidney. • Compensation for extra-renal fluid loss (vomiting, diarrhea, sweating or third space wasting) Reference: RennkeH., Denker, B. 2007. Renal Pathophysiology: The Essentials
Urine Sodium (UNa) • Effective circulating volume depletion and SIADH are the two major causes of true hyponatremia (with an inappropriately high urine osmolality) and these disordes can be distinguished by measuring the Una. • Patients with hypovolemia are sodium avid in an attempt to limit further losses. • Urine sodium is generally below 25 mEq/L. • In comparison, patients with SIADH are normovolemic and sodium excretion is in a steady state equal to intake. • Urine sodium concentration is typically above 40 mEq/L. Reference: RennkeH., Denker, B. 2007. Renal Pathophysiology: The Essentials
Na deficit Sodium Deficit = Total Body Water * Normal Wt in kg * (Pt's Na - Desired Na) (TBW = 0.6 if male and 0.5 if female)
Na deficit Sodium Deficit = (0.5)* (53kg)* (135mEq/L-123mEq/L) Sodium Deficit= 318mmol/L
Principles of Therapy Raise plasma sodium concentration by restricting water intake and promoting water loss. Correct underlying disorder.
6. What are the basic principles in the treatment of hyponatremia?
Principles of Therapy • Asymptomatic hyponatremia • Sodium repletion (isotonic saline) • Restoration of euvolemia removes the hemodynamic stimulus for AVP release. • Restriction of sodium and water intake, correction of hypokalemia, and promotion of water loss in excess of sodium. • Dietary water restriction should be less than urine output.
Principles of Therapy • Asymptomatic Hyponatremia • Sodium concentration should be raised by no more than 0.5 – 1.0mmol/L over the first 24 hours. • Acute or severe Hyponatremia • Plasma sodium conc: < 110-115mmol/L • Rapid correction • Severe symptomatic • Hypertonic saline • 1-2 mmol/l per hour for the first 3-4 hours • Raised by no more than 12mmol/L during the first 24 hours
Complication of Rapid Correction of Hyponatremia • Rate of correction: depends on the absence or presence of neurologic dysfunction • Related to the rapidity of onset and magnitude of fall in plasma Na+ concentration • Rapid correction of hyponatremia leads to osmotic demyelination syndrome (ODS).
Osmotic Demyelination Syndrome Neurologic disorder characterized by flaccid paralysis, dysarthria and dysphagia Mechanism: Patients with chronic hyponatremia (brain cell volume has returned to near normal) Malnutrition secondary to alcoholism Prior cerebral anoxic injury Hypokalemia Administration of hypertonic saline • Sudden osmotic shrinkage of brain cells References: Vellaichamy M. Hyponatremia. 2009. http://emedicine.medscape.com/article/907841-followup. Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.
References: Vellaichamy M. Hyponatremia. 2009. http://emedicine.medscape.com/article/907841-followup. Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed. Schwartz’s Principles of Surgery, 8th ed.
Central Pontine Myelinolysis Predilection for pons: During hyponatremia, these cells can adapt only by losing ions instead of swelling. This limitation makes them prone to damage when Na is replaced. Reference: Vellaichamy M. Hyponatremia. 2009. <http://emedicine.medscape.com/article/907841-followup>
T2 weighted magnetic resonance scan image showing bilaterally symmetrical hyperintensities in caudate nucleus (small, thin arrow), putamen (long arrow), with sparing of globuspallidus (broad arrow), suggestive of extrapontinemyelinolysis. Central pontinemyelinolysis, MRI FLAIR
Intravenous fluid to use and rate of infusion 3% saline infused at a rate of ≤ 0.05 mL/kg body weight per minute. Effect should be monitored continuously by STAT measurements of serum sodium at least once every 2 hours. Reference: Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.
Intravenous fluid to use and rate of infusion • Infusion should be stopped as soon as serum sodium increases by 12 mmol/L or to 130 mmol/L, whichever comes first. • Urine output should be monitored continuously. • SIAD can remit spontaneously at any time, resulting in an acute water diuresis that greatly accelerates the rate of rise in serum sodium produced by fluid restriction and 3% saline. Reference: Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.
A 62 y/o M diabetic with chronic kidney disease and a creatinine of 3.5 mg/dl and an estimated GFR of 15 ml/min consults due to the inability to lift himself from a chair. He had been eating fruits with each meal for the past two weeks. On PE there is marked proximal weakness and decreased skin turgor. The ECG revealed peaked T waves and widening of the P wave and QRS complex.
Salient Features 62, M CKD Diabetic CC: inability to lift himself from a chair Creatinine of 3.5 mg/dl GFR of 15 ml/min – Low Decreased skin turgor and marked proximal weakness ECG: Peaked T waves and widening of P wave and QRS complex
1. What are the most likely factors responsible for the elevation of the plasma potassium?
Most likely causes of Hyperkalemia in the patient 1. ) The patient has chronic kidney disease and is in renal failure – GFR 15 ml/min • Compensatory mechanism for increasing distal flow rate and K secretion per nephron is decreased because there is decreased renal mass in chronic renal insufficiency 2.) The patient has diabetes - Insulin deficiency and hypertonicity promote K shift from the ICF to the ECF.
3. Intake of fruits does not necessarily cause hyperkalemia. - Huge amount of parenteral K can elicit hyperkalemia. 4. Acidosis causes shift of potassium from intracellular space into extracellular space.
PSEUDOHYPERKALEMIA Artificially elevated plasma K+ concentration due to K + movement out of cells immediately prior to or following venipuncture Contributing factors: prolonged use of tourniquet with or without repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis marked leukocytosis or thrombocytosis results in an elevated serum K + concentration due to release of intracellular K + following clot formation References: Harrison’s Principles of Internal Medicine 17th ed. OnyekachiIfudu, Mariana S. Markell, Eli A. Friedman. Unrecognized Pseudohyperkalemia as a Cause of Elevated Potassium in Patients with Renal Disease.
PSEUDOHYPERKALEMIA • Serum to plasma potassium difference of more than 0.4 mmol/l • Occurs when platelets, leukocytes or erythrocytes release intracellular potassium in vitrofalsely elevated serum values. • Observed in: • Myeloproliferative disorders including leukemia • Infectious mononucleosis • Rheumatoid arthritis
2. Is this pseudohyperkalemia? Why or why not? NO… this is not pseudohyperkalemia since there are no enough evidence of blood count differentials as well as no history predisposing the patient to develop such. Also, the presence of ECG abnormalities which require emergency therapy is not a common indication in pseudohyperkalemia.