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Electrolyte Disorders
Resident Rounds Aric Storck February 26, 2004
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Case 1 75 yo woman PMHx Meds orthostatic presyncope x 2 days
diarrhea x 1 week drinking 2-3 litres of tea a day PMHx HTN Meds HCTZ 25 mg po od
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O/E JVP ASA significant orthostatic drop in BP lab Na 128 K 3.1 Cr 125
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Hyponatremia Clinical SSx
Severity depends on absolute value AND rate of decrease Source: Yeates K, et al. CMAJ 2004;170(3):365-9
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Symptoms Delirium Coma Seizures < 120 Weakness Lethargy
Restlessness Confusion Thirst Anorexia, N + V Muscle cramps Decreased taste Symptoms Serum Na+ (mEq/L)
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Approach to hyponatremia
Hypo-osmolar Iso-osmolar Hyper-osmolar Normal ECF osmolality Increased serum solids, lipids (nephrotic syndrome) , protein (multiple myeloma) Vast majority Glucose / mannitol Draws H2O into ECF
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Hypo-osmolar hyponatremia
Hypovolemic Non-hypovolemic GI Losses Renal Losses Skin Losses Vommitting diarrhea bleeding obstruction Diuretics hypoaldo salt-wasting neph Burns GPP/ erythroderma SIADH Edematous States CNS Disease Pulmonary Drugs CHF nephrotic Synd cirrhosis Slide courtesy of Adam Oster
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Hypovolemic Hyponatremia
Loss Na > Loss H2O ADH released (low ECF) increases tubular reabsorption of H2O low urine volume Renin released (low renal perfusion) kidneys retain sodium urine sodium low (<20 mmol/L)
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What caused our patient’s hyponatremia?
GI losses HCTZ (impairs excretion of free water) as ECF decreases kidney exchanges K for Na to maintain volume - thus low K
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How will you treat our patient
d/c HCTZ oral rehydration salts IV NS + KCl until no further postural drop oral sodium and K recheck lytes in a few days
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Case 2 58 yo man No Meds O/E small cell lung cancer
confusion & lethargy x 2 days No Meds O/E JVP 3cm MMM no ascites / no edema no sign of hypothyroidism or hypoadrenalism
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lab Na 108 K 3.9 Cr 44 urine Na 44
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Euvolemic Hyponatremia DDx
SIADH hypothyroidism adrenal insufficiency psychogenic polydipsia
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SIADH Diagnosis clinically euvolemic normal renal function
normal thyroid (TSH) normal adrenal (cortisol stim test) no medications known to cause SIADH-like syndrome
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SIADH causes Source: Yeates K, et al. CMAJ 2004;170(3):365-9
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SIADH - Treatment acute chronic hypertonic saline fluid restriction
goal to increase Na by ~5 over 12 hours or until asymptomatic fluid restriction ml/d goal to increase Na by ~5 over 12 hours chronic Li (inhibits renal effects of ADH) demeclocycline 600 mg po od
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What happens if you use normal saline?
More water retained than Na worsening hyponatremia
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How do you calculate amount of fluid needed?
Source: Adrogue H, et al. NEJM 2000: 342(1)
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Sample calculation Change [Na] per litre 3% HTS =
( ) / (0.6x60 +1) =10.8 mmol thus 0.46 litres (5/10.8) over 12 hours =38ml/h x 12 hours
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Case 3 45 year old woman alcoholic, HCV, end stage hepatic disease
gross ascites and peripheral edema Na 125
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Hypervolemic hyponatremia
Increased ECF CHF cirrhosis / ascites nephrotic syndrome low effective circulating volume body retains Na and H20 low urine Na (<20) Treatment Na and free water restriction
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Source: Yeates K, et al. CMAJ 2004;170(3):365-9
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Pseudohyponatremia = falsely low Na+ due to:
high serum protein concentration high serum lipids was an issue w/ flame photometry but not w/ potentiometric measurment techniques Slide courtesy of Moritz Haager
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Redistributive Hyponatremia
= dilutional picture due to presence of excess osmotically active substances drawing water out of cells into extracellular space Hyperglycemia (e.g. DKA) Correction = ~3mmol Na+ decrease for every 10 mmol increase in glucose Mannitol Slide courtesy of Moritz Haager
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Case 4 Your med student saw the pt and w/o discussing with you ordered a 1 L bolus of NS X 2 and then 200 cc/h The pts Na+ corrects to 138 by next AM Pt is sent home asymptomatic 36 hrs after admission Comes back 3 days later unable to stand, confused, with slurred speech What’s going on? Slide courtesy of Moritz Haager
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CPM central pontine myelinolysis
Pathophysiology Acute non-inflammatory demyelination in basis pontis and other CNS sites (in ~10%) Mechanism unknown; felt to occur due to rapid changes in cell volume Actual incidence is unknown Risk factors Na+ <120 mEq/L for > 48 hrs Aggressive IV resuscitation w/ hypertonic saline Most cases occurred with rates of correction > 12 mmol/L /24 hrs Hypernatremia during treatment Slide courtesy of Moritz Haager
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CPM central pontine myelinolysis
Clinical Features Usually neurologic deterioration hrs after rapid Na+ correction Confusion, horizontal gaze paralysis, spastic quadriplegia, pseudobulbar palsy, encephalopathy – coma, locked-in syndrome Dx MRI Tx supportive Slide courtesy of Moritz Haager
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Treatment summary Hypovolemic hyponatremia Euvolemic hyponatremia:
Correct with NS (0.9%) which is mildly hypertonic compared to pts serum Euvolemic hyponatremia: Restrict free water intake Identify underlying cause SIADH: Giving normal saline will worsen condition due to free water retention Can Tx with lithium and demeclocycline inhibit action of ADH Hypervolemic hyponatremia: +/- diuretics may worsen due to further Na+ loss dialysis if large amount of fluid needs to be taken off Slide courtesy of M Haager
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“Dry” Normovolemic (excess total body water but no edema) Hyponatremia
Fluid overloaded (excess water > excess Na+) “Dry” Normovolemic (excess total body water but no edema) Source of Sodium loss? SIADH Drugs Glucocorticoid deficiency Hypothyroidism Pain / emotion Nephrotic Syndrome Cirrhosis CHF Acute / Chronic Renal Failure Renal: -Diuretics -Adrenal insufficiency -Salt-wasting nephritis -Bicarbonate loss -RTA -metabolic alkalosis -ketonuria -Osmotic diuresis -glucose -mannitol Extra-renal losses -GI losses -Third spacing Urine Na+ >20 mmol/L Urine Na+ <10 mmol/L Urine Na+ >20 mmol/L Urine Na+ <10 mmol/L Urine Na+ >20 mmol/L Normal Saline Water restriction Slide courtesy of M Haager
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Case 5 93 year old man from nursing home demented not eating well
less perky than usual - in ER to be “checked out” O/E JVP down, dry mouth /53 99% 37.3 Na = 157
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Hypernatremia Signs Symptoms lethargy anorexia stupor N/V coma fatigue
muscle twitching hyperreflexia spasticity tremor ataxia focal neurological signs Symptoms anorexia N/V fatigue irritable
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Causes of Hypernatremia
Gain in Na exogenous Na intake NaCl NaHCO3 hypertonic NS salt water drowning increased Na reabsorption hyperaldosteronism cushing’s disease exogenous corticosteroids congenital adrenal hyperplasia Reduced H2O intake disorders of thirst can’t get H20 Increased H2O loss GI V&D NG 3rd spacing renal DI osmotic diuresis post-obstructive diuresis dermal burns perspiration
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Causes of DI Nephrogenic Central drugs Systemic diseases
congenital renal disorders obstructive uropathy polycystic disease drugs amphotericin B phenytoin Li aminoglycosides methoxyflurane Central idiopathic head trauma cerebral hemorrhage suprasellar infection granulomatous disorders Systemic diseases sickle cell sarcoidosis amyloidosis
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Management of hypernatremia
Hypovolemic goal: restore volume deficits 0.9% NS Euvolemic DI oral fluids hypotonic saline (0.45%) vasopressin Hypervolemic increase renal sodium excretion > H20 diuretics +/- hypotonic saline may need dialysis
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Calculation of water deficit
Weight (kg) x ( Normal [Na] / Measured [Na] - 1 )
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Case 6 53 year old man O/E What would you like to order?
DM 1, chronic renal failure presents via EMS from home Wife tells you that he has had N/V/D for the last 4 days with decreased po intake. O/E 140, 89/59, 26, 94%, 37.3 JVP down, dry MM Slightly tender abdomen What would you like to order?
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lab CBC Lytes Hb 146 WBC 35 Platelets 223 Na 133 K 7.4 HCO3 4 Cl 97
neutrophils 30 0.3 bands Platelets 223 Lytes Na 133 K 7.4 HCO3 4 Cl 97 Cr 223 glucose 43
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Case 6 ECG
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Hyperkalemia Clinical Features
Cardiac 2/3 degree heart block wide complex tachycardias VF asystole ECG progression peaked T waves loss of P waves prolonged PR interval widening of QRS sine wave pattern ventricular fibrillation asystole
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Hyperkalemia Neurological SSx
Non-specific muscle cramps weakness paralysis paresthesias tetany focal neurological deficits
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Potassium a precisely controlled cation
Mostly intracellular Precise transcellular gradients required for neuronal transmission and cardiac conduction Also important in acid-base balance and buffering. K+/H+ pump Extracellular K controlled by serum pH change in pH of 0.1 0.6mEq change in K+ aldosterone insulin catecholamines
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Hyperkalemia Mechanisms
CELLULAR INJURY INCREASED INTAKE TRANSCELLULAR SHIFT IMPAIRED EXCRETION RENAL FAILURE NON RENAL FAILURE Slide courtesy of A. Oster
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Hyperkalemia - etiology
Transcellular shifts acidosis insulin deficient drugs B-Blockers sux digitalis cellular injury rhabdomyolysis tumour lysis syndrome crush/burn pseudohyperkalemia hemolysis increased intake impaired renal excretion renal failure hypoaldosteronism K-sparing diuretics
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Management Principles
Cardiac monitoring stabilize myocardium shift K into cells decrease GI absorption treat underlying cause
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Immediate Management Calcium
mechanism antagonises K and stabilizes myocardium indications dysrhythmia hypotension ECG changes onset 0-5 minutes duration 20-40 minutes dose 5-30ml 10% calcium gluconate IV Slide courtesy of A. Oster
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Immediate Management Ventolin
Mechanism shifts K into cells onset 15 minutes duration 2-4 hours dose 5-10mg neb repeat prn Slide courtesy of A. Oster
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Immediate Management Glucose and Insulin
mechanism shifts K into cells onset 15 minutes duration 4-6 hours dose 10-20 units of R 1 amp D50W (no D50W if hyperglycemic)
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Immediate Management bicarbonate
mechanism shifts K into cells only works if acidotic onset 15 minutes duration 2 hours dose 1 amp (44 meq) IV push over 5 minutes beware if hypertonic hypernatremic alkalotic
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Delayed Therapy Exchange Resins
kayelalate (polystyrene sulfonate) mechanism ion exchange resin removes K from body onset 1 hour duration 1-3 hours dose 1g binds 1mEq of K oral or rectal 20g in 70% sorbitol po (Rosen) 30g pr retained for 30 minutes
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Delayed Therapy hemodialysis
Mechanism removes K from blood can remove meq Indications renal failure unstable patient unresponsive to other treatment
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Case 6 K+ 7.4 Slide courtesy of A. Oster
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Case 6 K+6.2 Slide courtesy of A. Oster
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Case 6 K+ 5.5 Slide courtesy of A. Oster
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Case 7 General surgery rotation
03:30 - you are awakened from a sound sleep by a nurse who tells you that Mr. X’s potassium is only 3.0. Do you care? Why do you care? What are you going to do about it?
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Hypokalemia Spectrum of Symptoms
Asymptomatic K 3-3.5 Neuromuscular K usually < 2.5 lethargy confusion fasciculations weakness decreased DTRs paralysis (K<2) Cardiovascular usually no symptoms in patients without heart disease palpitations ectopy dysrhythmias 1 - 2 degree HB atrial fibrillation ventricular fibrillation
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GI Renal impairs intestinal smooth muscle N/V paralytic ileus polyuria
polydipsia
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Approach TRANSCELLULAR SHIFT INCREASED LOSSES RENAL GI DECREASED
INTAKE TRANSCELLULAR SHIFT INCREASED LOSSES RENAL GI Slide courtesy A. Oster
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Hypokalemia Decreased Intake Transcellular Shifts Increased Loss
decreased dietary intake decreased absorption Transcellular Shifts alkalosis insulin B2 agonists eg: ventolin - lowers K ~ 0.4 mmol/L x 4 hours coffee Increased Loss renal hyperaldosteronism renal tubular defects mineralocorticoids glucocorticoids (alter GFR) +++diuretics drugs GI N/V/D Skin burns perspiration
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His ECG... Slide courtesy A. Oster
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Hypokalemia ECG findings small or absent T waves prominent U waves
ST segment depression Slide courtesy A. Oster
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How will you treat him? Potassium is an intracellular ion
1 mEq/L decrease in serum K may equal up to 370 mEq total body deficit ~50% of administered K excreted in urine - therefore several days to correct deficit
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Oral IV S/E’s K-Dur (20mmol/tab) KCl elixir(20mmol/15ml)
K-Phos(4.4mmol/ml) useful if hypophosphatemic K-Citrate (0.9mmol/ml) useful in RTA IV KCl (10/20/40mmol/100cc) 10-20mEq/h >20mEq/h requires central line and cardiac monitor S/E’s transient hyperkalemia burning at IV site
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Hypomagnesemia Magnesium required in Na-K ATP-ase
hypomag often co-exists with hypokalemia Mg must be corrected along with K Cofactor in PTH metabolism often coexists with low Ca
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Hypomagnesemia Diuretic use EtOH abuse Renal losses GI losses
thiazide and loop diuretics decrease Mg ~25-50% EtOH abuse 30-80% Renal losses GI losses V/D short bowel pancreatitis Endocrine disorders DM hyperaldosteronism hyperthyroidism Pregnancy Drugs aminoglycosides, B-agonists, cyclosporine, pentamidine, theophylline Congenital disorders
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Hypomagnesemia clinical features
Non-specific Neuromuscular weakness tremor hyperreflexia Chvostek/Trousseau seizures coma Cardiac supraventricular dysrhythmias ventricular dysrhythmias ECG non-specific long PR/QRS/QT ST-T abnormalities flattened T Uwave
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Hypomagnesemia Management
Treat if Magnesium < 1.2 mg/dl or, symptomatic IV Magnesium sulfate 1g = 8.3mEq magnesium Oral Magnesium Rougier multiple others cause diarrhea
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Hypermagnesemia Very rare …. especially in ER
kidneys can excrete >6g / day generally iatrogenic renally insufficient
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Hypermagnesemia Clinical Features
>3 mg/dl N/V weakness >4mg/dl hyporeflexia loss of DTR’s >5-6mg/dl hypotension ECG changes QRS widenine QT/PR prolongation conduction abnormalities >9mg/dl repiratory depression coma complete heart block
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Hypermagnesemia Treatment
Mild symptoms & normal renal function Observe Moderate symptoms IV normal saline & furosemide watch K Severe symptoms IV Calcium antagonizes membrane effects of Mg reverses respiratory depression/dysrhytmias, etc Dialysis refractory symptoms renal failure
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Case 8 55 woman with metastatic breast cancer Vitals O/E
Increasing weakness and confusion x 24 hours Ataxic this morning Headache Thirsty Vitals /80 92% 37.0 O/E alert but disoriented and confused, GCS 15 otherwise unremarkable
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Case 8 Labs How do you correct [Ca] for albumin? CBC
normal electrolytes Calcium 4.5 Albumin 30 How do you correct [Ca] for albumin? Add 0.2 for every 10 units albumin is below 40 ie: 47
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Characteristic changes
Case 8 ECG Characteristic changes Short QT prolongation or PR QRS widening Occasionally see sinus bradycardia BBB AV block cardiac arrest
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Calcium Metabolism 1200g Ca in body parathyroid hormone calcitonin
99% in bone 1% in serum 60% protein bound 40% free parathyroid hormone bone resorption renal Ca reabsorption renal conversion vitamin D to 1,25DHCC) renal phosphate excretion calcitonin decreases osteoclastic activity and enhances skeletal deposition
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Hypercalcemia Etiology
Most (~90%) Primary hyperparathyroidism Malignancies Others medications thiazides Li Vitamin D toxicity Ca ingestion granulomatous disease other endocrine disorders
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Hypercalcemia Clinical Features
Neurologic fatigue, weakness confusion, lethargy ataxia coma hypotonia CV hypertension sinus bradycardia AV block ECG abnormalities (short QT, BBB) Renal polyuria, polydipsia pre-renal azotemia nephrolithiasis nephrocalcinosis GI N/V pancreatitis constipation ileus
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Hypercalcemia Treatment Principles
restore intravascular volume Serum calcium will decrease with hydration increase renal calcium elimination hydration fursosemide 40-80mg iv q6-8h AVOID thiazides reduction of osteoclastic activity Etidronate/Pamidronate Plicamycin calcitonin 4U/kg sc q12h treatment of primary disorder parathyroidectomy treat malignancy withdrawal of meds
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Case 9 52 year old woman HTN diarrhea x 1 week
B-Blocker, thiazide diarrhea x 1 week tingling around mouth and in fingers cramps in arms and legs
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When taking her blood pressure
Source: Meininger et al. NEJM 2000:343 (25): 1855
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Case 9 ECG
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Hypocalcemia Etiology
PTH PTH insufficiency primary secondary neck surgery Mg disorders pancreatitis drugs PTH Vitamin D insufficiency malnutrition malabsorption hepatic/renal disease Calcium chelation hyperphosphatemia citrate alkalosis fluoride poisoning
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Hypocalcemia Clinical Features
Neuromuscular confusion/anxiety paresthesias weakness spasms tetany Chvostek/Trousseau hyperreflexia seizures CV bradycardia decreased contractility hypotension CHF ECG QT prolongation
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Hypocalcemia Management recommended initial adult dose is 100-300mg
IV calcium chloride 10ml amps of 10% 360mg elemental Ca IV calcium gluconate 93mg elemental Ca recommended initial adult dose is mg pediatric dose is mg/kg of Ca gluconate lasts 2hours consider an infusion S/E’s HTN N/V bradycardia/HB tissue necrosis if interstitial
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