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Electrolyte Disturbances. Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia . Hypercalcemia. Etiology. Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone.

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electrolyte disturbances

Electrolyte Disturbances

Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia

etiology
Etiology
  • 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
etiology1
Etiology
  • Hypercalcemia is a relatively common clinical problem.
  • 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.
increased bone resorption
Increased bone resorption
  • Primary and secondary hyperparathyroidism
  • Malignancy
  • Hyperthyroidism
  • Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid
increased intestinal calcium absorption
Increased intestinal calcium absorption
  • Increased calcium intake
  • Renal failure (often with vitamin D supplementation)
  • Milk-alkali syndrome
  • Hypervitaminosis D
  • Enhanced intake of vitamin D or metabolites
  • Chronic granulomatous diseases (eg, sarcoidosis)
  • Malignant lymphoma
  • Acromegaly
etiology2
Etiology
  • Hyperalbuminemia
  • 1) severe dehydration

2) multiple myeloma who have a calcium-binding paraprotein.

  • This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia)
other causes
Other causes
  • Chronic lithium intake
  • Thiazide diuretics
  • Pheochromocytoma
  • Adrenal insufficiency
  • Rhabdomyolysis and acute renal failure
  • Theophylline toxicity
  • Familial hypocalciuric hypercalcemia
  • Immobilization
  • Total parenteral nutrition
primary hyperparathyroidism
Primary hyperparathyroidism
  • Activation of osteoclasts leading to increased bone resorption in primary hyperparathyroidism (also cancer).
  • Adenoma (80%)
  • Hyperplasia (15-20%)
  • Carcinoma (<1%)
secondary hyperparathyroidism
Secondary hyperparathyroidism
  • Due to increased PTH in response to decreased calcium
  • ESRD
tertiary hyperparathyroidism
Tertiary hyperparathyroidism
  • An autonomous nodule develops after longstanding secondary hyperparathyroidism
familial hypocalciuric hypercalcemia fhh
Familial hypocalciuric hypercalcemia (FHH)
  • 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)
malignancy
Malignancy
  • PTHrP- PTH related peptide (squamous cell lung cancer, renal, breast, bladder)
  • Cytokines (TNF, INTERLEUKIN-1)
  • OAF: Local osteolysis (breast cancer, multiple myeloma)
  • Tumoral effect (Hogkins / NHL)
vitamin d excess
Vitamin D Excess
  • Granulomas (sarcoid, TB, histo)
  • Vitamin D Intoxication
increased bone turnover
Increased bone turnover
  • Hyperthyroidism
  • Immobilization
  • Paget’s disease
  • Vitamin A
miscellaneous
Miscellaneous
  • Thiazides (increase resorption in kidney)
  • Ca-based antacids (Milk-Alkali Syndrome)
  • Adrenal insufficiency
clinical manifestations
Clinical Manifestations
  • Bones
  • stones
  • abdominal groans
  • psychic moans
bones
Bones
  • Osteopenia
  • Osteitis fibrosa cystica (seen in severe hyperparathyroidism only)
slide20

Osteitis Fibrosa Cystica

Cysts, fibrous nodules, salt and pepper appearance on X-ray

stones
Stones
  • Nephrolithiasis
  • Nephrocalcinosis
  • Nephrogenic Diabetes Insipidus
abdominal groans
Abdominal Groans
  • Anorexia
  • Nausea
  • Vomiting
  • Constipation
  • Pancreatitis
  • Peptic ulcer disease
psychic moans
Psychic Moans
  • Fatigue
  • Depression
  • Confusion
slide25
Labs
  • Free Calcium Measured or

Calculated( Measured Ca+(0.8x(4.0-alb) or use med-math?

  • PTH (irma assay)
  • PTH rp
  • VIT D , VIT A
  • PO4
  • URINE CALCIUM- 24 HRS
treatment
Treatment
  • Normal Saline (4-6L per day)

FILL THE TANK

  • Furosemide-CALCIURESIS

Start after patient is intravascularly repleted

  • Bisphosphonates- Inhibits osteoclast activity(reducing bone resorption and turnover) malignancy and ?Immobilization

28 hrs half-life( zolendronate, pamidronate)

treatment1
Treatment
  • SQ/IM( not nasal spray)Calcitonin 4 u/kg q12 hrs

increase to 8 units q 12 hrs

Onset 6-8 hours,duration 2-3 days

  • Steroids( targets OAF, 5-A Hydroxylase)

Onset 24-48 hrs days

primary hyperparathyroid
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

hypercalcemia quiz
Hypercalcemia Quiz
  • PTH Increased
  • Cal Increased
  • PO4 decreased

What do I have?

slide32
quiz
  • PTH DECREASED
  • CAL INCREASED
  • PO4 DECREASED/ INCREASED- EITHER

WHAT IS IT?

slide33
QUIZ
  • PTH DECREASED
  • CAL INCREASED
  • PO4 INCREASED

WHAT IS IT?

slide34
QUIZ
  • PTH NORMAL
  • CAL INCREASED
  • PO4 DECREASED
slide35
QUIZ
  • PTH INCREASED
  • CAL DECREASED
  • PO4 INCREASED
slide36
QUIZ
  • PTH INCREASED
  • CAL DECREASED
  • PO4 DECREASED
hyponatremia

Hyponatremia

Santosh Reddy MD

definition
DEFINITION
  • Defined as Serum Sodium less than 136 meq/lt
  • 4 % of hospitalized patients
  • NEJM 2000:342:1581-9( Adrogue,Madias)
hyponatremia1
Hyponatremia
  • Disorders of sodium are generally due to changes in total body water, not sodium
  • Hyper- or Hypo- osmolality
  • watershifts
  • changes in brain cell volume
  • changes in mental status, seizures
hyponatremia pathophysiology
Hyponatremia: pathophysiology
  • 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.
  • Inappropriate (e.g. SIADH)
workup
Workup
  • Measure plasma osmolality to determine if hypo, hyper, or isotonic hyponatremia
  • Urine Osmolality
  • Serum NA
  • Urine NA
hypertonic hyponatremia
Hypertonic Hyponatremia
  • 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
isotonic hyponatremia
Isotonic Hyponatremia
  • Lab artifact from
  • hyperlipidemia
  • or hyperproteinemia
hypotonic hyponatremia
Hypotonic Hyponatremia
  • Most common scenario
  • True excess of water compared to Na
hypotonic hyponatremia hypovolemic euvolemic hypervolemic
Hypotonic Hyponatremiahypovolemic euvolemic hypervolemic

UNa<10 UNa>20

FeNa<1% FeNa>1%

UNa>20 UNa<10

FeNa>1% FeNa<1%

CHF, cirrhosis, nephrosis

Renal failure

Renal losses

Extrarenal losses

Pt’s clinical history

Uosm>100 Uosm<100 Uosm var.

SIADH,

adrenal insuff,

hypothyroidism

Primary polydipsia,

low solute

Reset osmostat

hypovolemic hypotonic hyponatremia
Hypovolemic Hypotonic Hyponatremia
  • Renal losses: Thiazides or other diuretics, salt-wasting nephropathy, adrenal insufficiency
  • Extra-renal losses: GI losses (diarrhea), third-spacing (pancreatitis), inadequate intake, insensible losses
euvolemic hypotonic hyponatremia
Euvolemic Hypotonic Hyponatremia
  • 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)
  • Reset osmostat ( exercise, seizures)
low solute
Low solute
  • “tea & toast”, “beer potomania” – increased free water intake with greatly decreased solute load
  • Maximum rate of water excretion on a normal diet is 10-12 L per day – more than this you overwhelm the excretory capacity of the kidney
hypervolemic hypotonic hyponatremia
Hypervolemic Hypotonic Hyponatremia
  • CHF: low effective arterial volume (EAV)  ADH
  • Cirrhosis: ascites causes low EAV ADH
  • Nephrotic syndrome: hypoalbuminemia causes low EAV  ADH
  • Advanced renal failure
methods to increase na
Methods to increase Na
  • Restrict free water range 800-1.2 lt per day
  • Remove stimulus for ADH (volume replete, increase EAV, treat pulmonary pathology, etc)
  • Demeclocycline (ADH antagonist) 300MG BID TO QID
  • Normal saline after NA deficit is calculated
treatment2
Treatment
  • NA deficit: HYPOTONIC EUVOLEMIA

TBW ( 60 % MEN : 50% WOMEN) x

(DESIRED NA----MEASURED NA )

  • Ex: 100 kg Man, MEASURED NA 120

TBW 60 MEQ x 12( D--- M sodium)

720 MEQ PER 24 HOURS

treatment3
Treatment
  • 0.9 % : 154 meq/ LT
  • 3% : 514 meq / LT

GIVE : 4. 6 LT OF 0.9 % NACL

1.4 LT OF 3 % NACL

treatment of euvolemic hyponatremia
Treatment of Euvolemic Hyponatremia
  • Asymptomatic: correct at rate of < 0.5 mEq/L/hr
  • 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)
  • NEPHROLOGY 1994;4:1522-30
treatment4
Treatment
  • Conivaptan( vaprisol): Aquaresis:blocks the activity of AVP ,free water excretion,without losses of NA/K
  • EVEREST trial for CHF
  • Tolvaptan( Salt 1 and 2 trials) V2 receptor antagonist( hypervolemic or Euvolemic)
hypernatremia

Hypernatremia

Santosh Reddy

definition1
Definition
  • Increase in the serum sodium concentration greater than 145 meq /L
hypernatremia1
Hypernatremia
  • 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)
hypernatremia2
Hypernatremia
  • By definition, all pts are hypertonic
  • Can be Hypovolemic
  • Hypervolemic
  • Euvolemic
workup hypernatremia
Workup: Hypernatremia
  • Check volume status (vitals, orthostatics, JVP, skin turgor, mucous membranes, BUN, Cr)
  • If hypovolemic, check Uosm and UNa to determine whether free water loss is renal or extra-renal
  • If euvolemic, check Uosm to evaluate for complete or partial DI
hypernatremia hypovolemic euvolemic hypervolemic
Hypernatremiahypovolemic euvolemic hypervolemic

UOsm300-600 UOsm>600

UNa>20 UNa<20

Exogenous hypertonic saline, Mineralocorticoid excess

Renal losses

Extrarenal losses

Uosm<300 Uosm 300-600 Uosm >600

Complete DI

Partial DI, reset osmostat

Intracellular osmole generation

hypovolemic hypernatremia
Hypovolemic Hypernatremia
  • Renal water losses: osmotic diuresis from glucose/mannitol
  • Extra-renal water losses: diarrhea, insensible (fever, exercise)
euvolemic hypernatremia
Euvolemic Hypernatremia
  • Diabetes Insipidus: central or nephrogenic
  • Seizures, exercise: intracellular osmole generation  water shifts  transient increase in Na
  • Reset osmostat( I,I,I)
hypervolemic hypernatremia
Hypervolemic hypernatremia
  • Hypertonic saline administration
  • Mineralocorticoid excess: causes ADH suppression
treatment5
Treatment
  • Replete free water deficit

Free water deficit = TBW x (SerumNa-140)

140

  • D5 W replacement
  • Restore access to water
  • Correct volume status
treatment6
Treatment
  • Must replete free water deficit via IVF or enteral feeds
  • Correct at rate < 0.5 mEq/L/hr to avoid cerebral edema
  • Must consume > 1L H2O/day
treatment7
Treatment
  • For hypovolemia hypernatremia
    • Correct with ¼ or ½ NS
  • For Hypervolemic hypernatremia
    • Correct with D5W and a loop diuretic
treatment8
Treatment
  • DI: Central: desmopressin

Nephrogenic : Salt restriction + Thiazides Amiloride, Nsaids.

  • V 1 A AND V2 receptor blockage trials
hyperkalemia1
Hyperkalemia
  • Transcellular shifts
  • Decreased excretion by kidneys
  • Normal GFR

a)Normal aldosterone (CHF,Cirrhosis)

b)Hypoaldosterone(Diabetes etc)

hyperkalemia transcellular shifts
Hyperkalemia: Transcellular shifts
  • Acidosis,
  • Beta-blockers
  • insulin deficiency
  • dig intoxication
  • massive cellular necrosis
  • hyperkalemic periodic paralysis
hyperkalemia decreased excretion
Hyperkalemia: decreased excretion
  • Decreased GFR (AKI)
  • Hypoaldosteronism with a normal GFR (due to low renin, low aldosterone, or decreased response to aldosterone)
hyperkalemia symptoms
Hyperkalemia: symptoms
  • Weakness
  • Paresthesias
  • Palpitations
  • 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
workup1
Workup
  • Rule out pseudohyperkalemia (IVF + KCl, hemolysis due to venipuncture, increased plt or WBC)
  • Rule out transcellular shift
  • Assess GFR
  • If normal GFR, calculate TTKG
ttkg trans tubular potassium gradient
TTKG: Trans-Tubular Potassium Gradient
  • (UrineK/PlasmaK)/(UrineOsm/PlasmaOsm)
  • TTKG tells you how well aldosterone is working
  • TTKG<7  decreased effective aldosterone function
  • TTKG>7  normal aldosterone function
treatment9
Treatment
  • Calcium Gluconate/Calcium Chloride: stabilizes cell membranes

1-2 amps I.V

1-3 mins onset lasts 20-30mins

  • Insulin:drives K into cells

regular Insulin 10 units IV with 1-2 amps of D50

  • Beta-2 agonists: drives K into cells;

Albuterol 10-20mcg inh or IV 0.5mg

Onset 30-60 mins

treatment10
Treatment
  • Bicarbonate: drives K into cells in exchange for H

1-3 amps

Onset 15-30 mins last 60 mins

  • Kayexalate: exchanges Na for K in gut

30-90 mg PO/PR

Onset 1-2 hrs

  • Diuretics;decreases total body K; IV lasix
  • hemodialysis: decreases total body K