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Electrolyte Disturbances Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia.

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Presentation on theme: "Electrolyte Disturbances Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia."— Presentation transcript:

1 Electrolyte Disturbances Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia

2 Hypercalcemia

3 Etiology Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone. Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone. Sources of calcium are most commonly the bone or the gastrointestinal tract Sources of calcium are most commonly the bone or the gastrointestinal tract

4 Etiology Hypercalcemia is a relatively common clinical problem. Hypercalcemia is a relatively common clinical problem. Elevation in the physiologically important ionized (or free) calcium concentration. Elevation in the physiologically important ionized (or free) calcium concentration. However, 40 to 45 percent of the calcium in serum is bound to protein, principally albumin;, increased protein binding causes elevation in the serum total calcium. However, 40 to 45 percent of the calcium in serum is bound to protein, principally albumin;, increased protein binding causes elevation in the serum total calcium.

5 Increased bone resorption Primary and secondary hyperparathyroidism Primary and secondary hyperparathyroidism Malignancy Malignancy Hyperthyroidism Hyperthyroidism Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid

6 Increased intestinal calcium absorption Increased calcium intake Increased calcium intake Renal failure (often with vitamin D supplementation) Renal failure (often with vitamin D supplementation) Milk-alkali syndrome Milk-alkali syndrome Hypervitaminosis D Hypervitaminosis D Enhanced intake of vitamin D or metabolites Enhanced intake of vitamin D or metabolites Chronic granulomatous diseases (eg, sarcoidosis) Chronic granulomatous diseases (eg, sarcoidosis) Malignant lymphoma Malignant lymphoma Acromegaly Acromegaly

7 Etiology Hyperalbuminemia Hyperalbuminemia 1) severe dehydration 1) severe dehydration 2) multiple myeloma who have a calcium- binding paraprotein. 2) multiple myeloma who have a calcium- binding paraprotein. This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia) This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia)

8 Other causes Chronic lithium intake Chronic lithium intake Thiazide diuretics Thiazide diuretics Pheochromocytoma Pheochromocytoma Adrenal insufficiency Adrenal insufficiency Rhabdomyolysis and acute renal failure Rhabdomyolysis and acute renal failure Theophylline toxicity Theophylline toxicity Familial hypocalciuric hypercalcemia Familial hypocalciuric hypercalcemia Immobilization Immobilization Total parenteral nutrition Total parenteral nutrition

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10 Primary hyperparathyroidism Activation of osteoclasts leading to increased bone resorption in primary hyperparathyroidism (also cancer). Activation of osteoclasts leading to increased bone resorption in primary hyperparathyroidism (also cancer). Adenoma (80%) Adenoma (80%) Hyperplasia (15-20%) Hyperplasia (15-20%) Carcinoma (<1%) Carcinoma (<1%)

11 Secondary hyperparathyroidism Due to increased PTH in response to decreased calcium Due to increased PTH in response to decreased calcium ESRD ESRD

12 Tertiary hyperparathyroidism An autonomous nodule develops after longstanding secondary hyperparathyroidism An autonomous nodule develops after longstanding secondary hyperparathyroidism

13 Familial hypocalciuric hypercalcemia (FHH) Mutation in the Ca-sensing receptor in parathyroid and kidney which increases the Ca set point Mutation in the Ca-sensing receptor in parathyroid and kidney which increases the Ca set point May also increase the PTH ( parathyroid isn’t sensing Calcium) May also increase the PTH ( parathyroid isn’t sensing Calcium)

14 Malignancy PTHrP- PTH related peptide (squamous cell lung cancer, renal, breast, bladder) PTHrP- PTH related peptide (squamous cell lung cancer, renal, breast, bladder) Cytokines (TNF, INTERLEUKIN-1) Cytokines (TNF, INTERLEUKIN-1) OAF: Local osteolysis (breast cancer, multiple myeloma) OAF: Local osteolysis (breast cancer, multiple myeloma) Tumoral effect (Hogkins / NHL) Tumoral effect (Hogkins / NHL)

15 Vitamin D Excess Granulomas (sarcoid, TB, histo) Granulomas (sarcoid, TB, histo) Vitamin D Intoxication Vitamin D Intoxication

16 Increased bone turnover Hyperthyroidism Hyperthyroidism Immobilization Immobilization Paget’s disease Paget’s disease Vitamin A Vitamin A

17 Miscellaneous Thiazides (increase resorption in kidney) Thiazides (increase resorption in kidney) Ca-based antacids (Milk-Alkali Syndrome) Ca-based antacids (Milk-Alkali Syndrome) Adrenal insufficiency Adrenal insufficiency

18 Clinical Manifestations Bones Bones stones stones abdominal groans abdominal groans psychic moans psychic moans

19 Bones Osteopenia Osteopenia Osteitis fibrosa cystica (seen in severe hyperparathyroidism only) Osteitis fibrosa cystica (seen in severe hyperparathyroidism only)

20 Osteitis Fibrosa Cystica Cysts, fibrous nodules, salt and pepper appearance on X-ray

21 Stones Nephrolithiasis Nephrolithiasis Nephrocalcinosis Nephrocalcinosis Nephrogenic Diabetes Insipidus Nephrogenic Diabetes Insipidus

22 Abdominal Groans Anorexia Anorexia Nausea Nausea Vomiting Vomiting Constipation Constipation Pancreatitis Pancreatitis Peptic ulcer disease Peptic ulcer disease

23 Psychic Moans Fatigue Fatigue Depression Depression Confusion Confusion

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25 Labs Free Calcium Measured or Free Calcium Measured or Calculated( Measured Ca+(0.8x(4.0-alb) or use med-math? Calculated( Measured Ca+(0.8x(4.0-alb) or use med-math? PTH (irma assay) PTH (irma assay) PTH rp PTH rp VIT D, VIT A VIT D, VIT A PO4 PO4 URINE CALCIUM- 24 HRS URINE CALCIUM- 24 HRS

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28 Treatment Normal Saline (4-6L per day) Normal Saline (4-6L per day) FILL THE TANK Furosemide-CALCIURESIS Furosemide-CALCIURESIS Start after patient is intravascularly repleted Bisphosphonates- Inhibits osteoclast activity(reducing bone resorption and turnover) malignancy and ?Immobilization Bisphosphonates- Inhibits osteoclast activity(reducing bone resorption and turnover) malignancy and ?Immobilization 28 hrs half-life( zolendronate, pamidronate) 28 hrs half-life( zolendronate, pamidronate)

29 Treatment SQ/IM( not nasal spray)Calcitonin 4 u/kg q12 hrs SQ/IM( not nasal spray)Calcitonin 4 u/kg q12 hrs increase to 8 units q 12 hrs increase to 8 units q 12 hrs Onset 6-8 hours,duration 2-3 days Steroids( targets OAF, 5-A Hydroxylase) Steroids( targets OAF, 5-A Hydroxylase) Onset hrs days

30 Primary Hyperparathyroid Surgery (JCEM 2009) Age <50 yrs, GFR <60ml/min, Cal 1 mg/dl above normal, DEXA <-2.5 Medical Bisphonates,Calcitonin,estrogen,serm Early DEXA scans

31 Hypercalcemia Quiz PTH Increased PTH Increased Cal Increased Cal Increased PO4 decreased PO4 decreased What do I have?

32 quiz PTH DECREASED PTH DECREASED CAL INCREASED CAL INCREASED PO4 DECREASED/ INCREASED- EITHER PO4 DECREASED/ INCREASED- EITHER WHAT IS IT?

33 QUIZ PTH DECREASED PTH DECREASED CAL INCREASED CAL INCREASED PO4 INCREASED PO4 INCREASED WHAT IS IT?

34 QUIZ PTH NORMAL PTH NORMAL CAL INCREASED CAL INCREASED PO4 DECREASED PO4 DECREASED

35 QUIZ PTH INCREASED PTH INCREASED CAL DECREASED CAL DECREASED PO4 INCREASED PO4 INCREASED

36 QUIZ PTH INCREASED PTH INCREASED CAL DECREASED CAL DECREASED PO4 DECREASED PO4 DECREASED

37 Hyponatremia Hyponatremia Santosh Reddy MD

38 DEFINITION Defined as Serum Sodium less than 136 meq/lt Defined as Serum Sodium less than 136 meq/lt 4 % of hospitalized patients 4 % of hospitalized patients NEJM 2000:342:1581-9( Adrogue,Madias) NEJM 2000:342:1581-9( Adrogue,Madias)

39 Hyponatremia Disorders of sodium are generally due to changes in total body water, not sodium Disorders of sodium are generally due to changes in total body water, not sodium Hyper- or Hypo- osmolality Hyper- or Hypo- osmolality watershifts watershifts changes in brain cell volume changes in brain cell volume changes in mental status, seizures changes in mental status, seizures

40 Hyponatremia: pathophysiology Excess water compared to sodium, almost always due to increased ADH Excess water compared to sodium, almost always due to increased ADH The increased ADH may be: Appropriate (e.g. hypovolemia or hypervolemia with too little effective arterial volume)EAV. Appropriate (e.g. hypovolemia or hypervolemia with too little effective arterial volume)EAV. Inappropriate (e.g. SIADH) Inappropriate (e.g. SIADH)

41 Workup Measure plasma osmolality to determine if hypo, hyper, or isotonic hyponatremia Measure plasma osmolality to determine if hypo, hyper, or isotonic hyponatremia Urine Osmolality Urine Osmolality Serum NA Serum NA Urine NA Urine NA

42 Hypertonic Hyponatremia Excess of another effective osmoles, such as mannitol, glucose Excess of another effective osmoles, such as mannitol, glucose Each 100mg/dL of glucose above 100 causes a decrease in Na by 1.8 mEq/L Each 100mg/dL of glucose above 100 causes a decrease in Na by 1.8 mEq/L

43 Isotonic Hyponatremia Lab artifact from Lab artifact from hyperlipidemia hyperlipidemia or hyperproteinemia or hyperproteinemia

44 Hypotonic Hyponatremia Most common scenario Most common scenario True excess of water compared to Na True excess of water compared to Na

45 Hypotonic Hyponatremia hypovolemiceuvolemichypervolemic UNa>20 UNa<10 FeNa>1% FeNa<1% Pt’s clinical history Uosm>100 Uosm<100 Uosm var. UNa 20 FeNa 1% SIADH, adrenal insuff, hypothyroidism Primary polydipsia, low solute Reset osmostat Renal losses Extrarenal losses CHF, cirrhosis, nephrosis Renal failure

46 Hypovolemic Hypotonic Hyponatremia Renal losses: Thiazides or other diuretics, salt-wasting nephropathy, adrenal insufficiency Renal losses: Thiazides or other diuretics, salt-wasting nephropathy, adrenal insufficiency Extra-renal losses: GI losses (diarrhea), third-spacing (pancreatitis), inadequate intake, insensible losses Extra-renal losses: GI losses (diarrhea), third-spacing (pancreatitis), inadequate intake, insensible losses

47 Euvolemic Hypotonic Hyponatremia SIADH SIADH pulmonary-pneumonia, asthma, COPD, PTX, +pressure ventilation, small cell lung cancer intracranial-trauma, stroke, hemorrhage, tumors, infection, hydrocephalus drugs-antipsychotics, antidepressants, thaizides misc-pain, nausea, post-op state Endocrinopathies (adrenal insuff, hypothyroidism) Endocrinopathies (adrenal insuff, hypothyroidism) Reset osmostat ( exercise, seizures) Reset osmostat ( exercise, seizures)

48 Low solute “tea & toast”, “beer potomania” – increased free water intake with greatly decreased solute load “tea & toast”, “beer potomania” – increased free water intake with greatly decreased solute load Maximum rate of water excretion on a normal diet is L per day – more than this you overwhelm the excretory capacity of the kidney Maximum rate of water excretion on a normal diet is L per day – more than this you overwhelm the excretory capacity of the kidney

49 Hypervolemic Hypotonic Hyponatremia CHF: low effective arterial volume (EAV)  ADH CHF: low effective arterial volume (EAV)  ADH Cirrhosis: ascites causes low EAV  ADH Cirrhosis: ascites causes low EAV  ADH Nephrotic syndrome: hypoalbuminemia causes low EAV  ADH Nephrotic syndrome: hypoalbuminemia causes low EAV  ADH Advanced renal failure Advanced renal failure

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51 Methods to increase Na Restrict free water range lt per day Restrict free water range lt per day Remove stimulus for ADH (volume replete, increase EAV, treat pulmonary pathology, etc) Remove stimulus for ADH (volume replete, increase EAV, treat pulmonary pathology, etc) Demeclocycline (ADH antagonist) 300MG BID TO QID Demeclocycline (ADH antagonist) 300MG BID TO QID Normal saline after NA deficit is calculated Normal saline after NA deficit is calculated

52 Treatment NA deficit: HYPOTONIC EUVOLEMIA NA deficit: HYPOTONIC EUVOLEMIA TBW ( 60 % MEN : 50% WOMEN) x (DESIRED NA----MEASURED NA ) Ex: 100 kg Man, MEASURED NA 120 Ex: 100 kg Man, MEASURED NA 120 TBW 60 MEQ x 12( D--- M sodium) 720 MEQ PER 24 HOURS

53 Treatment 0.9 % : 154 meq/ LT 0.9 % : 154 meq/ LT 3% : 514 meq / LT 3% : 514 meq / LT GIVE : 4. 6 LT OF 0.9 % NACL 1.4 LT OF 3 % NACL 1.4 LT OF 3 % NACL

54 Treatment of Euvolemic Hyponatremia Asymptomatic: correct at rate of < 0.5 mEq/L/hr Asymptomatic: correct at rate of < 0.5 mEq/L/hr Symptomatic: initital rapid correction of Na (2 mEq/L/hr) until symptoms resolve Symptomatic: initital rapid correction of Na (2 mEq/L/hr) until symptoms resolve Rate of correction should NOT exceed 12mEq in a 24 hour period, or 18mEq in a 48 hour period to avoid Central pontine myelinosis (CNS demyelination  changes in mental status, paralysis, pseudobulbar palsy) Rate of correction should NOT exceed 12mEq in a 24 hour period, or 18mEq in a 48 hour period to avoid Central pontine myelinosis (CNS demyelination  changes in mental status, paralysis, pseudobulbar palsy) NEPHROLOGY 1994;4: NEPHROLOGY 1994;4:

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56 Treatment Conivaptan( vaprisol): Aquaresis:blocks the activity of AVP,free water excretion,without losses of NA/K Conivaptan( vaprisol): Aquaresis:blocks the activity of AVP,free water excretion,without losses of NA/K EVEREST trial for CHF EVEREST trial for CHF Tolvaptan( Salt 1 and 2 trials) V2 receptor antagonist( hypervolemic or Euvolemic) Tolvaptan( Salt 1 and 2 trials) V2 receptor antagonist( hypervolemic or Euvolemic)

57 Hypernatremia Hypernatremia Santosh Reddy

58 Definition Increase in the serum sodium concentration greater than 145 meq /L Increase in the serum sodium concentration greater than 145 meq /L

59 Hypernatremia Usually loss of hypotonic fluid, can also be infusion of too much hypertonic fluid Usually loss of hypotonic fluid, can also be infusion of too much hypertonic fluid Hypernatremia is a strong thirst stimulus, so usually only affects pts w/o access to water (intubated, altered mental status,insensible losses nursing home patient) Hypernatremia is a strong thirst stimulus, so usually only affects pts w/o access to water (intubated, altered mental status,insensible losses nursing home patient)

60 Hypernatremia By definition, all pts are hypertonic By definition, all pts are hypertonic Can be Hypovolemic Can be Hypovolemic Hypervolemic Hypervolemic Euvolemic Euvolemic

61 Workup: Hypernatremia Check volume status (vitals, orthostatics, JVP, skin turgor, mucous membranes, BUN, Cr) Check volume status (vitals, orthostatics, JVP, skin turgor, mucous membranes, BUN, Cr) If hypovolemic, check U osm and U Na to determine whether free water loss is renal or extra-renal If hypovolemic, check U osm and U Na to determine whether free water loss is renal or extra-renal If euvolemic, check U osm to evaluate for complete or partial DI If euvolemic, check U osm to evaluate for complete or partial DI

62 Hypernatremia hypovolemiceuvolemichypervolemic UOsm UOsm>600 UNa>20 UNa<20 Uosm 600 Complete DI Partial DI, reset osmostat Intracellular osmole generation Renal losses Extrarenal losses Exogenous hypertonic saline, Mineralocorticoid excess

63 Hypovolemic Hypernatremia Renal water losses: osmotic diuresis from glucose/mannitol Renal water losses: osmotic diuresis from glucose/mannitol Extra-renal water losses: diarrhea, insensible (fever, exercise) Extra-renal water losses: diarrhea, insensible (fever, exercise)

64 Euvolemic Hypernatremia Diabetes Insipidus: central or nephrogenic Diabetes Insipidus: central or nephrogenic Seizures, exercise: intracellular osmole generation  water shifts  transient increase in Na Seizures, exercise: intracellular osmole generation  water shifts  transient increase in Na Reset osmostat( I,I,I) Reset osmostat( I,I,I)

65 Hypervolemic hypernatremia Hypertonic saline administration Hypertonic saline administration Mineralocorticoid excess: causes ADH suppression Mineralocorticoid excess: causes ADH suppression

66 Treatment Replete free water deficit Replete free water deficit Free water deficit = TBW x (Serum Na -140) D5 W replacement D5 W replacement Restore access to water Restore access to water Correct volume status Correct volume status

67 Treatment Must replete free water deficit via IVF or enteral feeds Must replete free water deficit via IVF or enteral feeds Correct at rate < 0.5 mEq/L/hr to avoid cerebral edema Correct at rate < 0.5 mEq/L/hr to avoid cerebral edema Must consume > 1L H 2 O/day Must consume > 1L H 2 O/day

68 Treatment For hypovolemia hypernatremia For hypovolemia hypernatremia –Correct with ¼ or ½ NS For Hypervolemic hypernatremia For Hypervolemic hypernatremia –Correct with D 5 W and a loop diuretic

69 Treatment DI: Central: desmopressin DI: Central: desmopressin Nephrogenic : Salt restriction + Thiazides Amiloride, Nsaids. Nephrogenic : Salt restriction + Thiazides Amiloride, Nsaids. V 1 A AND V2 receptor blockage trials V 1 A AND V2 receptor blockage trials

70 Hyperkalemia

71 Hyperkalemia Transcellular shifts Transcellular shifts Decreased excretion by kidneys Decreased excretion by kidneys Normal GFR Normal GFR a)Normal aldosterone (CHF,Cirrhosis) b)Hypoaldosterone(Diabetes etc)

72 Hyperkalemia: Transcellular shifts Acidosis, Acidosis, Beta-blockers Beta-blockers insulin deficiency insulin deficiency dig intoxication dig intoxication massive cellular necrosis massive cellular necrosis hyperkalemic periodic paralysis hyperkalemic periodic paralysis

73 Hyperkalemia: decreased excretion Decreased GFR (AKI) Decreased GFR (AKI) Hypoaldosteronism with a normal GFR (due to low renin, low aldosterone, or decreased response to aldosterone) Hypoaldosteronism with a normal GFR (due to low renin, low aldosterone, or decreased response to aldosterone)

74 Hyperkalemia: symptoms Weakness Weakness Paresthesias Paresthesias Palpitations Palpitations Peaked T waves on EKG (look like they might hurt to sit on) Peaked T waves on EKG (look like they might hurt to sit on) Other EKG findings: increased PR interval, widened QRS, sine wave pattern, PEA Other EKG findings: increased PR interval, widened QRS, sine wave pattern, PEA

75 Peaked T waves

76 Sine wave

77 Workup Rule out pseudohyperkalemia (IVF + KCl, hemolysis due to venipuncture, increased plt or WBC) Rule out pseudohyperkalemia (IVF + KCl, hemolysis due to venipuncture, increased plt or WBC) Rule out transcellular shift Rule out transcellular shift Assess GFR Assess GFR If normal GFR, calculate TTKG If normal GFR, calculate TTKG

78 TTKG: Trans-Tubular Potassium Gradient (Urine K /Plasma K )/(Urine Osm /Plasma Osm ) (Urine K /Plasma K )/(Urine Osm /Plasma Osm ) TTKG tells you how well aldosterone is working TTKG tells you how well aldosterone is working TTKG<7  decreased effective aldosterone function TTKG<7  decreased effective aldosterone function TTKG>7  normal aldosterone function TTKG>7  normal aldosterone function

79 Treatment Calcium Gluconate/Calcium Chloride: stabilizes cell membranes Calcium Gluconate/Calcium Chloride: stabilizes cell membranes 1-2 amps I.V 1-2 amps I.V 1-3 mins onset lasts 20-30mins 1-3 mins onset lasts 20-30mins Insulin:drives K into cells Insulin:drives K into cells regular Insulin 10 units IV with 1-2 amps of D50 regular Insulin 10 units IV with 1-2 amps of D50 Beta-2 agonists: drives K into cells; Beta-2 agonists: drives K into cells; Albuterol 10-20mcg inh or IV 0.5mg Onset mins

80 Treatment Bicarbonate: drives K into cells in exchange for H Bicarbonate: drives K into cells in exchange for H 1-3 amps Onset mins last 60 mins Kayexalate: exchanges Na for K in gut Kayexalate: exchanges Na for K in gut mg PO/PR Onset 1-2 hrs Diuretics;decreases total body K; IV lasix Diuretics;decreases total body K; IV lasix hemodialysis: decreases total body K hemodialysis: decreases total body K


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