Hyponatremia. Mis-named talk? Basic Pathophysiology
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1 Hyponatremia Great Lakes Hospital Medicine Symposium by Brian Wolfe, MD Assistant Professor of Internal Medicine University of Colorado Denver Mis-named talk? Why do we care about Hyponatremia? concentration key driver of water movement to and from intracellular space Neurologic dysfunction caused by changes in the amount total brain water Basic Pathophysiology Brain Cell Extracellular space
2 Basic Pathophysiology Brain Cell Extracellular space Basic Pathophysiology Brain Cell Extracellular space Principles 1. Focus on preventing/treating cerebral edema as opposed to sodium values 2. Hyponatremia generally indicates excess free water retention 3. Symptom assessment is critical to determining a treatment plan
3 Physiology Total Body Water = 60% of lean body mass 80kg man with 48 L of TBW Physiology 60% Intracellular 28.8 L 140meq/L + 40% Extracellular 19.2 L 140meq/L + 80kg man with 48 L of TBW Physiology 2L H L 30L 19.2 L 20L meq/L meq/L + 80kg man with 48 L of TBW
4 Physiology 280meq L L meq/L meq/L + 80kg man with 48 L of TBW Physiology 2L NSS 28.8 L L 140meq/L + 140meq/L + 80kg man with 48 L of TBW Summary of /H20 association 2 Liters of water added to ECF, then both compartments added volume and concentration went down Pure solute was added to ECF, then volume shifted from ICF to ECF and concentration went up 2 Liters of saline added to ECF, then ECF only added volume and concentration was unchanged
5 Regulation of and Volume oregulation Plasma osmolality Hypothalamus ADH, thirst Leads to changes in water excretion/thirst Volume regulation Effective Circulating Vol Carotid sinus, Atrial stretch, others ADH, norepinephrine Renin-angiotensin-aldo Leads to changes in excretion Antidiuretic hormone (ADH) Physiologically stimulated by both changes in osmolality and volume Non-physiologically by drugs, infections, pain and many other factors Increases permeability of collecting duct to water Leads to free water retention and decrease in plasma osmolality (decrease in concentration) Suppression of ADH leads to free water excretion Renin-angiotensin-aldosterone Physiologically stimulated by decreased delivery of volume to kidney and sympathetic outflow Decreased by an increase in volume delivery Combined effects of system leads to retention (and subsequently volume) In absence, leads to net excretion
6 Conflicting Signals? > 1% change in olality will lead to changes in ADH release 10% change in Volume will lead to changes in ADH release When conflicting, Volume depletion more powerful signal (etio of hypovol hypo) Symptoms of hyponatremia Dependent on risk factors, cause, acuity >125mEq/L usually asymptomatic or very minimally symptomatic If acute, most symptomatic <120 lethargy, HA, confusion < more severely symptomatic seizures, coma, death Needed for Diagnosis History GI symptoms Weight change Meds/changes (especially diuretics) Alcohol History of liver, heart, kidney disease BMP Plasma osmolality (measured)
7 Needed for Diagnosis Exam Jugular venous press, Hepatojugular reflux Peripheral edema, ascites, pulm edema Mucus membranes (not very helpful) Needed for Diagnosis Labs Basic metabolic panel, glucose Plasma osmolality Urine and osmolality Fractional excretion of (FE) usually unhelpful and can be misleading Diagnosis Two questions: 1. What is the osmolality of serum? elevated/normal or decreased = true hyponatremia 2. What is the volume status? hypovolemic, euvolemic, hypervolemic
8 Elevated or Normal Plasma osmolality Pseudohyponatremia Severe hyperlipidemia Severe hyperproteinemia status post TURP Mannitol, IVIG, other extra osmols True Hyponatremia Hypervolemia The -Osis s Cirrhosis Cardiosis - CHF Nephrosis - Advanced renal failure True Hyponatremia Hypovolemia Sources of Volume loss Gastrointestinal Renal Skin
9 True Hyponatremia Euvolemia Cortisol Deficiency Hypothyroidism (rare) Polydipsia Decreased solute intake (potomania) Syndrome of inappropriate ADH How to differentiate? Hypervolemia Hypervolemic causes usually obvious as hypo only occurs in late disease states Usually asymptomatic from hypo Increased associated risk of M&M low U /U s (exception: renal failure) treatment focused on primary disease process How to differentiate? Hypovolemia Hypovolemia usually clinically obvious Hypovolemic etiologies: renal or non-renal Renal loss - U > 20 Diuretics, Hypoaldo, cerebral salt wasting Non-renal loss - U < 10 GI losses, Burns, sweating
10 How to differentiate? Euvolemia Sometimes can be difficult to differentiate from hypovolemia (sometimes can coexist) adrenal insufficiency - low cortisol hypothyroidism - high TSH/low T4 SIADH - high urine osms (usually >300), U > 40, lower BUN/Uric acid Treatment: Considerations Remember that primary concern is cerebral edema... not hyponatremia! concentration is not the only regulator of brain fluid otic adaptation that prevents neuronal damage in hyponatremic states needs consideration when correcting hypo Acute hyponatremia Brain Cell Extracellular space
11 otic adaptation s prevent cerebral edema Brain Cell Extracellular space otic adaptation If corrected too quickly Brain Cell Extracellular space Treatment: Volume states Hypervolemic patients Rarely symptomatic from hyponatremia Treatment focuses on underlying disease Administration of or Fluids will only worsen clinical condition
12 Treatment: Volume states Hypovolemic patients w/o severe symptoms Treatment is usually volume repletion with normal saline will initially rise slowly Once volume replaced, frequent monitoring needed as ADH will be suppressed, will rise quickly Treatment: Volume states Euvolemic patients w/o severe symptoms Fluid restriction mainstay of therapy (Depending on Urine output/s often needs to be <800cc/day) Cl tabs (usually 9gm/d) effective in patients with poor solute intake Furosemide occasionally helpful in patients unresponsive to above therapies Treatment: Vasopressin Receptor Antagonists Vaptans - block vasopressin receptors Clinical trials show sustainable small increases in plasma sodiums without severe side effects (thirst, overcorrection) Show improvements in psychomotor function in testing - significance unclear Currently very expensive Conivaptan (IV) and Tolvaptan (PO) approved in US for mild-moderate hypona (not severe)
13 Treatment: Severe symptoms Hypertonic saline should be given mL of 3% saline frequent monitoring of symptoms/ Treatment: Goals of therapy No more than 12meq/L rise in 24 h No more than 18meq/L rise in 48 h Occasionally need to given ddavp to prevent too rapid correction Principles 1. Focus on preventing/treating cerebral edema as opposed to sodium values 2. Hyponatremia generally indicates excess free water retention 3. Symptom assessment is critical to determining a treatment plan
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