Normal serum osmolarity 275 to 295 mosm/l. Osmolarity: conc. of solution expressed as total # of solute particles per liter

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1 Fluid Homeostasis IV Crystalloid Solutions Normal serum osmolarity 275 to 295 mosm/l ml H2O/day maintain fluid balance Insensible loses ( mL) -Respiratory tract mL -Skin mL -Feces 100mL Accelerated with fever (500mL/1C), sweating (1500mL), GI losses Urinary loss ( mL) Osmolarity: conc. of solution expressed as total # of solute particles per liter Osmolality: conc. of particles found in fluid part of blood (can also be measured in urine) -Low = decreased solutes, more dilute fluid -High = increased solutes, more concentrated fluid Sodium (Na+) Hyponatremia (Serum Na+ <135 meq/l, increase in volume) 98% extracellular fluid Normal range = meq/l normal range Hypernatremia >150 meq/l Hyponatremia <135 meq/l 2% intracellular fluid, conc. <10-12 meq/l Na+ passively moves into cells along concentration gradient Actively extruded via Na-K pump, ATP dependent Primary H2O gain Alteration in distribution of body H2O Aberrant lab value Generally d/t changes in TBW not Na <120 meq/l more likely assoc. w/sx s regardless of change Types of HypoNa+ Hypertonic: osmolality >295, H2O from ICF to ECF Isotonic: osmolality , no movement between ICF and ECF, pseudohyponatremia true Na+/Osm normal Hypotonic: osmolality <275, H2O from ECF to ICF Mild ( meq/l): n/v, HA, anorexia, lethargy Moderate ( meq/l): vomiting, irritability, muscle cramps, muscular weakness, confusion, ataxia Severe <125 meq/l: drowsiness, diminished reflexes, convulsions <115 meq/l = coma/death

2 SIADH (syndrome of inappropriate antidiuretic hormone) Hypotonic HypoNa+ (osmotic pressure <275) Inappropriately elevated urine osmolality >200mOsm/kg Clinically euvolemic normal adrenal, renal, cardiac, hepatic, thyroid fxn Multiple causes (CNS, pulmonary, carcinoma) Dx of exclusion Tx: H2O restriction Labs: serum Na+ (via BMP or CMP), clinical evaluation of ECF volume status (any adrenal, renal, cardiac, hepatic, thyroid signs), serum osmolality Evaluation of basic labs true hypona+ plasma osmolality reduced vs. factitious hypona+ osmolality normal or increased Other labs (based on underlying cause): urine Na+, urine osmolality, UA, TSH, BNP, lipase, LFT, CBC, tox screen Imaging: CXR (malignancy), CT (AMS) General tx Tx options -Fluid resuscitation: hypertonic/hypotonic hypovolemic -Hypertonic fluids: severe/symptomatic -Fluid restriction: euvolemic (not organic sx s), SIADH -Diuretics: hypotonic hypervolemic -Observe: isotonic Emergency tx Indicated if <115 meq/l or symptomatic (hypovolemic/ams/coma), try to confirm w/urine electrolytes first Symptomatic/hypovolemic -Replace volume w/normal saline until tissue perfusion restored -Calculate Na+ deficient: (desired Na+ - actual Na+) X TBW Severe + seizure/coma -Hypertonic saline cc/hr -Careful titration and close monitoring -Looking for rise 1-2mEq/L/hr until sx s stop and/or Na+ at least 120mEq/L -May need to add diuretics Complications of tx Central pontine myelinolysis: destruction of myelin layer; occurs when Na+ replaced to quickly; exact mechanism unknown but assoc. w/rapid change in osmolality surrounding neurons in pontine region

3 Hypernatremia (Serum Na+ >150 meq/l, decrease in volume) Decrease in TBW: main defense = thirst mechanism (stimulated by 2% increase in osmolality), may have AMS (psychiatric/elderly) Not commonly d/t increase in Na+ Often see w/severe volume loss in ED Types of HyperNa+ Hypovolemic hyperna+ volume loss, hemoconcentrated -Severe volume loss, inadequate water intake, extra-renal losses (GI diarrhea, vomiting, fistulas, significant burns), renal losses (osmotic diuretics, post-obstructive diuresis, intrinsic renal dz) Hypervolemic hyperna+ serum sodium increases and water follows -Hypertonic saline, sodium bicarbonate, accidental salt ingestion/seawater drowning (error in prep of infant formula), mineralcorticoid excess (Cushing syndrome) Euvolemic hyperna+ no clinical sx or organic sx s seen -Extra-renal losses (increased insensible loss), renal loses (central/nephrogenic DI) Diabetes Insipidus Central: failure to secrete ADH -Neoplasm, pituitary surgery, trauma, granulomas, idiopathic Nephrogenic: kidneys unresponsive to ADH -Familial, hypercalcemia, hypokalemia, renal dz, drug induced, hematologic disorders, malnutrition Result = water dumping excessive loss of hypotonic urine (not a lot of Na+ in ECF) Eventually leads to volume loss and increased Na+ W/u: serum osmolality, urine osmolality, and Na+, vasopressin challenge (if kidneys respond = central, if kidneys don t respond = nephrogenic) Clinical Manifestations Symptomatic: Na+ >158 meq/l (rate of change important as well) Nonspecific sx s -Anorexia, restlessness, n/v occur early -Followed by AMS, lethargy, irritability -Eventually leads to stupor or coma -MSK sx s may include twitching, stiffness, tremor General: irritability Volume status: dry mucous membranes, skin turgor, orthostatic VS, flat neck veins NMSK: lethargy, AMS, increased tone/ataxia/tremor, hyperreflexia, seizure, coma Plasma osmolality >350mOsm/kg = M&M >50% Vitals: orthostatics Labs: BMP/CMP, Mg, Ph, CBC (serum osmolality), UA (urine electrolytes, osmolality), water deprivation, ADH stimulation EKG CT/MRI brain Consult renal Volume repletion via normal saline or lactate ringer Once adequate tissue perfusion achieved change to 0.45 NS or D5W to correct fluid deficit -Goal: Na+ reduction should be less <10-15 meq/l/day (want to prevent cerebral edema) -Free water deficit = body weight (kg) X %TBW X [(serum Na+/140) 1] -Each L of H20 = 3-5mEq/L drop in Na+ (change in Na (measured Na+ - Na+ infused)/tbw +1) Complications of tx Cerebral edema: occurs w/rapid rehydration and decrease in ECF concentrations of Na+; cells become hypotonic to environment and water flows into them; brain cells swell

4 Potassium (K+) Hypokalemia (Serum K+ <3.5 meq/l) Major intracellular cation maintains resting membrane potential, ICG and ECG facilitates propagation of electrical pulses in heart Intracellular conc. = mEq/L Extracellular conc mEq/L Shifts in conc. occurring during severe injury, acid-base disturbance, catabolic states, increase in extracellular osmolality, insulin deficiency MC d/t intracellular shifts and increased loss Intracellular shifts: K+ shifts into cells as ECF ph increases in exchange for H+ (increase of 0.1 in ph = decrease 0.5mEq/L in K+), insulin causes K+ to shift into cells GI and renal losses: dehydration, vomiting, gastric suction, excessive diuretic use (thiazide and loop diuretics), magnesium depletion Clinical Presentation Clinical manifestations begin K+ <2.5mEq/L Weakness/malaise/fatigue Muscle cramps, weakness Paresthesia, paralysis Dizziness (orthostatic hypotension) N/V, ileus, constipation, abd cramping Polyuria, nocturia, polydipsia Palpitations Depression, hallucinations GI: ileus CV: hypotension, premature atrial/ventricular beats, bradycardia or tachycardia, ventricular arrhythmias, cardiac arrest Pulm: hypoventiliation, respiratory distress/failure NMSK: lethargy, AMS, decreased muscle strength, fasciculations, tetany, decreased tendon reflexes Vitals: orthostatics Labs: BMP/CMP, Mg, Ph, CBC, UA, urine electrolytes, drug levels, dig level, AB EKG: Flat T, QRS widens, ST depression, U wave, T and U waves fuse (late finding) (caution about DKA) K+ replenishment -Mild to moderate ( mEq/L): PO (20-40mEq K+ q30-60min) -Severe/symptomatic: IV (10mEq q30-60min 40mEq in 1L NS infused 2-4hr, need to monitor pt) -10mEq = increase 0.1mEq/L K+ May want to add Mg replenishment

5 Hyperkalemia (Serum K+ >5.5 meq/l) Factitious mc cause (hemolysis in lab tube) Commonly seen in ED acidosis, insulin deficiency, rhabdomyolysis, decreased GFR, drugs (K-sparing diuretics), aldosterone deficiency Sx s d/t disorder membrane polarization in cells Weakness, general fatigue Nausea Paresthesia/paralysis Palpitations Can also be asx Diminished DTR s, decreased motor strength Muscular paralysis and hypoventilation (rare) Evidence of RF (edema, skin changes, dialysis sites) Signs of trauma (rhabdomyolysis) Initial: BMP/CMP, CBC Other: UA, urine electrolytes, VBG, Mg, Ph, dig level, drug levels, CK, cortisol, aldosterone EKG: peaked T waves, increased PR interval, decreased QT interval, followed by increased QRS and loss of P, sine wave and PEA/VF (late findings) -Repeat K+ if there are no EKG changes General tx No cardiac derangement, confirm elevated K+ w/redraw Stop any K+ supplementation Asx pts (K ): focus on treating underlying cause Symptomatic pts/ekg changes: focus on membrane stabilization, intracellular shifting, removal/excretion May need foley catheter Emergent tx Membrane stabilization: calcium chloride or calcium gluconate Intracellular: insulin and glucose, albuterol nebulizer, sodium bicarbonate only used in severe cases (increase M&M) Removal/excretion: Lasix, kayexalate, hemodialysis

6 Calcium (Ca++) Hypercalcemia (Serum Ca++ >10.5 mg/dl) Serum Ca mg/dl Hypocalcemia <8.5 mg/dl Hypercalcemia >10.5 mg/dl Maintained by parathyroid, Vit D metabolites and calcitonin Malignancy, primary hyperparathyroidism mc Other: sarcoidoses, thiazides, antacids, lithium toxicity Serum Ca++ >12.0 = symptomatic STONES, BONES, abd GROANS, psychic MOANS (renal calculi, osteolysis, peptic ulcer/pancreatitis/constipation, depression/ams) Weak, lethargic, confused Polyuria, polydipsia (d/t renal tubule dysfxn) Anorexia, n/v, dehydration Decreased DTR s Labs: CMC, CMP (albumin check corrected Ca++ w/albumin level), ionized Ca++, PTH, Mg, Ph, UA, TSH, HIV, LI level EKG: short QT +/- shortened ST, wide T, bradyarrhythmia, BBB, 2 nd or complete HB CXR (malignancy, granulomatous dz) CT heat US/MRI/nuclear study (primary hyperparathyroidism) Mild focus on supportive tx and treating underlying cause, typically can discharge w/outpatient f/u Severe -Adequate hydration (4-6L NS, may need dialysis if CHF or RF) -Increased urinary calcium excretion (loop diuretics (Lasix), thiazides CI increase Ca++) -Inhibit bone reabsorption (calcitonin) -Stop offending meds -Tx underlying cause Consults: renal, oncology, endocrinology, critical care, PCP Mild to moderate w/no sx s medial tx, can be evaluated outpatient after discussion w/pcp or specialist, f/u plan in place, underlying problem not serious or life-threatening Severe/requires IVF or dialysis admit to ICU

7 Hypocalcemia (Serum Ca++ <8.5 mg/dl) Typically secondary to another dz process or electrolyte abnormality -Hypoalbuminemia mc (cirrhosis, nephrosis), hypomagnesaemia (severe pancreatitis), PTH deficiency/resistance, Vit D deficiency/resistance (liver dz, RF, pancreatitis), hyperphosphatemia (rhabdo, tumor lysis) -Other: meds, blood transfusion NSMK and CV findings most prominent CV: syncope, CHF, angina NMSK: numbness and tingling sensations in perioral area/fingers/toes, muscle cramps progressing to tetany (carpopedal spasm) Neurologic: irritability, impaired intellectual capacity, depression, personality changes, fatigue, seizures Findings suggestive of decreased muscle contraction May have inspiratory or expiratory wheezes Bradycardia, tachycardia, S3, signs of HF Chvostek sign: twitching of facial muscles in response to tapping over facial nerve Trousseu sign: tetany caused by inflation of BP cuff above systolic pressure for 3min Labs: CBC, CMP (LFT, albumin), ionized Ca++, PT/INR, UA, BNP, Mg, Ph ABG, PTH, Vit D EKG: prolonged QT ventricular dysrhythmia CT head Plain films Mild PO (elemental) Ca++ and vitamin D Severe -IVFR (NS) -IV calcium chloride or calcium gluconate Calcium administration typically CI if pt on digoxin