Dyselectrolytemia by Dr Sheikh Tufail

ELECTROLYTE ELECTROLYTE DISORDERSDISORDERS

+ +2+

2+4- -

ELECTROLYTE ELECTROLYTE DISORDERSDISORDERS Moderator:Prof Showket H Moderator:Prof Showket H

NengrooNengroo Speaker:Dr Tufail AhmadSpeaker:Dr Tufail Ahmad


Total fluid volume 42 litersECF 33% --- 1) Plasma 7% 2) Interstitial Fluid 26% 3) Lymph <1%ICF 67% mEqui per liter

Cations Plasma ISF Cell

Na+ 142.0 145.1 12K+ 4.3 4.4 150

Ca2+ 5 2.4 4Mg2+ 3 1.5 34Total 154 153.0 200

Anions Plasma ISF Cell

Cl- 104 117.4 4HCO3

- 24 27.1 12Phosphates 2 2.3 40

Proteins 14 0.0 54Other 5.9 6.2 90Total 149.9 153.0 200

Body Fluid Composition


Fluid Compartments

Basic conceptsBasic concepts Osmotic Activity Osmotic Activity The solute activity in a solution is also called the The solute activity in a solution is also called the osmotic osmotic

activity and is expressed in osmoles (osm). The total activity and is expressed in osmoles (osm). The total osmotic osmotic activity in a solution is the sum of the individual activity in a solution is the sum of the individual osmotic activities of all the solute particles in the solution.osmotic activities of all the solute particles in the solution.

OsmolarityOsmolarity is the osmotic activity per volume of solution is the osmotic activity per volume of solution (solutes plus water) and is expressed as mOsm/L(solutes plus water) and is expressed as mOsm/L

OsmolalityOsmolality is the osmotic activity per volume of water is the osmotic activity per volume of water and is expressed as mOsm/kg H2O.and is expressed as mOsm/kg H2O.

The osmotic activity of body fluids usually is expressed in The osmotic activity of body fluids usually is expressed in relation to the volume of water (i.e., osmolality). However, relation to the volume of water (i.e., osmolality). However, the volume of water in body fluids is far greater than the the volume of water in body fluids is far greater than the volume of solutes, so there is little difference between the volume of solutes, so there is little difference between the osmolality and osmolarity of body fluids.osmolality and osmolarity of body fluids.

TonicityTonicity When two solutions are separated by a membrane When two solutions are separated by a membrane

that allows the passage of water but not solutes, the that allows the passage of water but not solutes, the water passes from the solution with the lower water passes from the solution with the lower osmotic activity to the solution with the higher osmotic activity to the solution with the higher osmotic activity. The osmotic activity. The relative osmotic activity in the relative osmotic activity in the two solutions two solutions is called the is called the effective osmolality, or effective osmolality, or tonicitytonicity.. The solution with the higher osmolality is The solution with the higher osmolality is described as hypertonic, and the solution with the described as hypertonic, and the solution with the lower osmolality is described as hypotoniclower osmolality is described as hypotonic..

Plasma osmolality=(2×plasma Plasma osmolality=(2×plasma Na)+glu/18+BUN/2.8Na)+glu/18+BUN/2.8

Plasma tonicity= =(2×plasma Na)+glu/18Plasma tonicity= =(2×plasma Na)+glu/18

Osmolar gapOsmolar gap Plasma osmolality normally varies between 280 and Plasma osmolality normally varies between 280 and

290 mOsm/L. Plasma sodium concentration 290 mOsm/L. Plasma sodium concentration decreases approximately 1 mEq/L for every 62 mg/dL decreases approximately 1 mEq/L for every 62 mg/dL increase in glucose concentration. increase in glucose concentration.

A discrepancy between the measured and calculated A discrepancy between the measured and calculated osmolality is referred to as an osmolality is referred to as an osmolal gap osmolal gap . . SignifiSignificant osmolal gaps indicate a high cant osmolal gaps indicate a high concentration of an abnormal osmotically active concentration of an abnormal osmotically active molecule in plasma such as ethanol, mannitol, molecule in plasma such as ethanol, mannitol, methanol, ethylene glycol, or isopropyl alcoholmethanol, ethylene glycol, or isopropyl alcohol..

Osmolar gapOsmolar gap

Osmolal gaps may also be seen in patients with Osmolal gaps may also be seen in patients with chronic kidney failure (attributed to retention of chronic kidney failure (attributed to retention of small solutes), patients with ketoacidosis (as a small solutes), patients with ketoacidosis (as a result of a high concentration of ketone bodies), result of a high concentration of ketone bodies), and those receiving large amounts of glycine (as and those receiving large amounts of glycine (as during transurethral resection of the prostate). during transurethral resection of the prostate).

Osmolal gaps may also be present in patients Osmolal gaps may also be present in patients with marked hyperlipidemia or hyperproteinemia. with marked hyperlipidemia or hyperproteinemia.


Major extracellular cation- sodium Normal range of sodium

– 135 to 145 meq/L Serum Na+ < 135 meq/L

– Primary water gain or Na+ loss > water loss– Sx at Na+ < 120 meq/L– Seizures likely at Na+ < 113– Mild to moderate hyponatremia[Na]>125

mEq/L) are frequently asymptomatic

Hyponatremia


Pathophysiology: Pathophysiology: CNSCNS– Water shifts into brain cellsWater shifts into brain cells

– ApathyApathy –– Altered Consciousness Altered Consciousness– AgitationAgitation –– Seizures Seizures– HeadacheHeadache –– Coma Coma

Musculoskeletal SystemMusculoskeletal System– Muscle cramps & weakness with exerciseMuscle cramps & weakness with exercise– Sx if sweat losses replaced with waterSx if sweat losses replaced with water

Renal SystemRenal System Production of dilute urineProduction of dilute urine

– Impacted by amount of ADH presentImpacted by amount of ADH present– Urine NaUrine Na++ < 10 renal handling of NA intact < 10 renal handling of NA intact– Urine NaUrine Na++ > 20 intrinsic renal tubular damage > 20 intrinsic renal tubular damage

Hyponatremia


DiagnosisDiagnosis

Hyponatremia

Plasma Osmolality

Normal (275-295)Isotonichyponatremia

Low (< 275)Hypotonichyponatremia

High (> 295)Hypertonichyponatremia

Hypovolemic Hypervolemic Euvolemic


HypertonicHypertonic Hyponatremia (P Hyponatremia (Posmosm > 295)> 295)– Large quantities of solute in ECFLarge quantities of solute in ECF– Water moves from ICF to ECFWater moves from ICF to ECF– Hyperglycemia most common causeHyperglycemia most common cause

Each 100 mg/dl plasma glucose will Each 100 mg/dl plasma glucose will serum Naserum Na++ by 1.6 meq/L by 1.6 meq/L

– TreatmentTreatment Volume replacementVolume replacement

Hyponatremia


IsotonicIsotonic Hyponatremia (P Hyponatremia (Posmosm 275-295) 275-295)– ““Pseudohyponatremia”Pseudohyponatremia”– Artifact in serum NaArtifact in serum Na++ measurement measurement

Hyponatremia with a normal plasma osmolalityHyponatremia with a normal plasma osmolality AsymptomaticAsymptomatic Marked hyperlipidemiaMarked hyperlipidemia Marked hyperproteinemiaMarked hyperproteinemia SymptomaticSymptomatic Marked glycine absorption during transurethral surgeryMarked glycine absorption during transurethral surgery Hyponatremia with an elevated plasma osmolalityHyponatremia with an elevated plasma osmolality HyperglycemiaHyperglycemia Administration of mannitolAdministration of mannitol

Hyponatremia


HypotonicHypotonic Hyponatremia Hyponatremia (P(Posmosm<275)<275)

Hyponatremia

Plasma Osmolality

Normal (275-295)Isotonichyponatremia

Low (< 275)Hypotonichyponatremia

High (> 295)Hypertonichyponatremia

Hypovolemic Hypervolemic Euvolemic


HypovolemicHypovolemic Hyponatremia Hyponatremia– Loss of NaLoss of Na++ and water and water– Replacement with hypotonic fluidsReplacement with hypotonic fluids– Sodium loss “renal” vs “extrarenal”Sodium loss “renal” vs “extrarenal”

Hyponatremia


HypovolemicHypovolemic Hyponatremia Hyponatremia– Renal NaRenal Na++ loss loss

Urine NaUrine Na++ > 20 meq/L > 20 meq/L Etiology:Etiology:

– Diuretic use(Thiazides)Diuretic use(Thiazides)– Salt-wasting nephropathy (renal tubular Salt-wasting nephropathy (renal tubular

acidosis, chronic renal failure, interstitial acidosis, chronic renal failure, interstitial nephritis)nephritis)

– Osmotic diuresis (glucose, urea, mannitol, Osmotic diuresis (glucose, urea, mannitol, hyperproteinemiahyperproteinemia

– Mineralocorticoid (aldosterone) deficiencyMineralocorticoid (aldosterone) deficiency

Hyponatremia


HypovolemicHypovolemic Hyponatremia Hyponatremia– Extrarenal NaExtrarenal Na++ loss loss

Urine NaUrine Na++ < 20 meq/L exception vomitting (Na < 20 meq/L exception vomitting (Na >20meq)>20meq)

Etiology:Etiology:– Volume replacement with hypotonic fluidsVolume replacement with hypotonic fluids– GI loss (vomiting, diarrhea, fistula, tube suction)GI loss (vomiting, diarrhea, fistula, tube suction)– Third-space loss (burns, hemorrhagic Third-space loss (burns, hemorrhagic

pancreatitis, peritonitis)pancreatitis, peritonitis)– Sweating (cystic fibrosis)Sweating (cystic fibrosis)

Hyponatremia


HypovolemicHypovolemic Hyponatremia Hyponatremia– TreatmentTreatment

Re-expansion of ECF with isotonic saline in Re-expansion of ECF with isotonic saline in asymptomatic patients and hypertonic asymptomatic patients and hypertonic saline(3%) in symptomatic patients.saline(3%) in symptomatic patients.

Correction of underlying disorderCorrection of underlying disorder

Hyponatremia


EuvolemicEuvolemic Hyponatremia Hyponatremia– Normal volume status and Normal volume status and

hyponatremiahyponatremia– Sx usually 2Sx usually 2° t0 CNS hypotonicity° t0 CNS hypotonicity– SIADH most notable causeSIADH most notable cause

Hyponatremia


EuvolemicEuvolemic Hyponatremia Hyponatremia– SIADHSIADH

Hypotonic hyponatremia Inappropriately elevated urine osmolality (usually > 100

mosm/kg) Elevated urine Na+ (> 20 meq/L) Clinical euvolemia Normal adrenal, renal, cardiac, hepatic, and thyroid

function Correctable with water restriction

Various malignant tumors, pulmonary diseases, and central nervous system disorders are commonly associated with SIADH.

Hyponatremia


EuvolemicEuvolemic Hyponatremia Hyponatremia– Etiology:Etiology:

HypothyroidismHypothyroidism Pain, stress, nausea, psychosis (stimulates Pain, stress, nausea, psychosis (stimulates

ADH)ADH) Drugs: Cyclophosphamide and Drugs: Cyclophosphamide and

chlorpropamidechlorpropamide Water intoxication (psychogenic polydipsia)Water intoxication (psychogenic polydipsia) Glucocorticoid deficiencyGlucocorticoid deficiency PorphyriaPorphyria

Hyponatremia


EuvolemicEuvolemic Hyponatremia Hyponatremia– TreatmentTreatment

Fluid restrictionFluid restriction Work-up and management of underlying Work-up and management of underlying

disorderdisorder Combine furosemide diuresis with infusion of Combine furosemide diuresis with infusion of

hypertonic saline in symptomatic patients or hypertonic saline in symptomatic patients or isotonic saline in asymptomatic patients.isotonic saline in asymptomatic patients.

Demeclocycline for SIADH---Antagonises ADH Demeclocycline for SIADH---Antagonises ADH at renal tubulesat renal tubules

Hyponatremia


HypervolemicHypervolemic Hyponatremia Hyponatremia– Total body water in great excessTotal body water in great excess– Sx of volume overloadSx of volume overload

Peripheral/pulmonary edemaPeripheral/pulmonary edema– Impaired water excretionImpaired water excretion– Water retention in excess of NaWater retention in excess of Na++

retentionretention

Hyponatremia


HypervolemicHypervolemic Hyponatremia Hyponatremia– Without advanced renal insufficiencyWithout advanced renal insufficiency

Urine NaUrine Na++ < 20 meq/L < 20 meq/L Cirrhosis, CHF, Nephrotic syndromeCirrhosis, CHF, Nephrotic syndrome

– Advanced acute or chronic renal Advanced acute or chronic renal insufficiencyinsufficiency Urine NaUrine Na++ > 20 meq/L > 20 meq/L Renal failure (inability to excrete free water)Renal failure (inability to excrete free water)

Hyponatremia


HypervolemicHypervolemic Hyponatremia Hyponatremia– TreatmentTreatment

Optimize treatment for underlying disorderOptimize treatment for underlying disorder Judicious salt and water restrictionJudicious salt and water restriction ++ Diuretics Diuretics ++ Dialysis Dialysis

Hyponatremia


Treatment of Severe Treatment of Severe HyponatremiaHyponatremia– Indications:Indications:

Serum Na+ < 120 meq/L Rapid development ( Na+ > 0.5 meq/L/hr) Patient in extremis (coma, seizures)

– 3% Saline Solution (513 meq/L) @ 25 - 100 ml/hr Sodium deficit=Normal TBW×(Desired sodium-

Current NA). Correction rates : for mild symptoms, 0.5 mEq/L/h or less; for

moderate symptoms, 1 mEq/L/h or less; and for severe symptoms, 1.5 mEq/L/h or less.

Hyponatremia


Complications of TherapyComplications of Therapy– Central Pontine Myelinolysis (CPM)Central Pontine Myelinolysis (CPM)

22° excessively rapid correction of ° excessively rapid correction of hyponatremiahyponatremia

Fluctuating level of consciousnessFluctuating level of consciousness Behavioral disturbancesBehavioral disturbances DysarthriaDysarthria DysphagiaDysphagia ConvulsionsConvulsions Pseudobulbar palsyPseudobulbar palsy QuadriparesisQuadriparesis

Hyponatremia

HyponatremiaHyponatremia


Serum NaSerum Na++ > 150 meq/L > 150 meq/L– Result of loss of hypotonic fluidsResult of loss of hypotonic fluids– Net loss of free waterNet loss of free water– Gain of hypertonic fluidsGain of hypertonic fluids– Rapid hypertonicity or short durationRapid hypertonicity or short duration

Loss of 10% of body wt 2° dehydrationLoss of 10% of body wt 2° dehydration– Dec Skin turgor, “doughy” skinDec Skin turgor, “doughy” skin

CNS cellular dehydrationCNS cellular dehydration– HemorrhageHemorrhage– Tearing of cerebral blood vessels 2° brain Tearing of cerebral blood vessels 2° brain

shrinkageshrinkage

Hypernatremia

HypernatremiaHypernatremia Even when renal concentrating ability is impaired, Even when renal concentrating ability is impaired,

thirst is normally highly effective in preventing thirst is normally highly effective in preventing hypernatremia. hypernatremia.

Hypernatremia is therefore most commonly seen in Hypernatremia is therefore most commonly seen in debilitated patients who are unable to drink, the very debilitated patients who are unable to drink, the very aged, the very young, and patients with altered aged, the very young, and patients with altered consciousness.consciousness.

ETIOLOGYETIOLOGY Impaired thirstImpaired thirst ComaComa Essential hypernatremiaEssential hypernatremia Solute diuresisSolute diuresis Osmotic diuresis: diabetic ketoacidosis, nonketotic Osmotic diuresis: diabetic ketoacidosis, nonketotic

hyperosmolar coma, mannitol administrationhyperosmolar coma, mannitol administration


Excessive water lossesExcessive water losses RenalRenal Neurogenic diabetes insipidusNeurogenic diabetes insipidus Nephrogenic diabetes insipidusNephrogenic diabetes insipidus ExtrarenalExtrarenal SweatingSweating DiarrhoeaDiarrhoea

Combined disordersCombined disorders Coma plus hypertonic nasogastric feedingComa plus hypertonic nasogastric feeding

Hypernatremia

HypernatremiaHypernatremia Hypernatremia & low total body sodium contentHypernatremia & low total body sodium content Water loss > sodium lossWater loss > sodium loss Renal (osmotic diuresis) or extrarenal (diarrhea or sweat).Renal (osmotic diuresis) or extrarenal (diarrhea or sweat). Urinary sodium concentration is generally greater than 20 Urinary sodium concentration is generally greater than 20

mEq/L with renal losses and less than 10 mEq/L with mEq/L with renal losses and less than 10 mEq/L with extrarenal losses.extrarenal losses.

Hypernatremia & normal total body sodium contentHypernatremia & normal total body sodium content Water loss without overt hypovolemia unless water loss is Water loss without overt hypovolemia unless water loss is

massive. Total body sodium content is generally normal.massive. Total body sodium content is generally normal. Exercise, seizures, or rhabdomyolysis.Exercise, seizures, or rhabdomyolysis. DI-----central or nephrogenicDI-----central or nephrogenic Hypernatremia & increased total body sodium contentHypernatremia & increased total body sodium content Administration of large quantities of hypertonic saline Administration of large quantities of hypertonic saline

solutions (3% NaCl or 7.5% NaHCO 3 ).solutions (3% NaCl or 7.5% NaHCO 3 ). primary hyperaldosteronism and Cushing’s syndromeprimary hyperaldosteronism and Cushing’s syndrome


Clinical Features:Clinical Features:– Acute sx at NaAcute sx at Na++ > 158 meq/L > 158 meq/L

OsmolOsmol– Restless, irritabilityRestless, irritability 350-375350-375– Tremulousness, ataxiaTremulousness, ataxia 375-400375-400– Hyperreflexia, twitching, spasticityHyperreflexia, twitching, spasticity

400-430400-430– Seizures and deathSeizures and death > 430> 430

Hypernatremia


TreatmentTreatment Water deficits should generally be corrected over 48 h with a Water deficits should generally be corrected over 48 h with a

hypotonic solution such as 5% dextrose in water.hypotonic solution such as 5% dextrose in water. Hypernatremic patients with decreased total body sodium Hypernatremic patients with decreased total body sodium

should be given isotonic fluids(0.9% saline) to restore plasma should be given isotonic fluids(0.9% saline) to restore plasma volume to normal prior to treatment with a hypotonic solution volume to normal prior to treatment with a hypotonic solution to reduce risk of cerebral odemato reduce risk of cerebral odema

Hypernatremic patients with increased total body sodium Hypernatremic patients with increased total body sodium should be treated with a loop diuretic along with intravenous should be treated with a loop diuretic along with intravenous 5% dextrose in water.5% dextrose in water.

Severe solute losses and hemodynamic compromise-colloids(5% albumin or 6% hetastarch) preferred.

Decreases in plasma sodium concentration should not proceed Decreases in plasma sodium concentration should not proceed at a rate faster than 0.5 mEq/L/h.at a rate faster than 0.5 mEq/L/h.

Hypernatremia


Complications of therapyComplications of therapy– Excessively rapid correction

Cerebral edema Seizures Permanent neuro sequelae Death

Hypernatremia

Free water Free water replacementreplacement

Current TBW ×Current P Na=Normal TBW ×Normal P NaCurrent TBW ×Current P Na=Normal TBW ×Normal P Na

TBW deficit(l)=Normal TBW—Current TBWTBW deficit(l)=Normal TBW—Current TBW

Replacement Volume(l)=TBW deficit ×(1/1—X)Replacement Volume(l)=TBW deficit ×(1/1—X)

X=sod conc in resuscitation fluid/sod conc in isotonic X=sod conc in resuscitation fluid/sod conc in isotonic saline(154meq/l)saline(154meq/l)

HypernatremiaHypernatremia

Anesthetic Anesthetic implicationsimplications Disorders of sodium balance present either Disorders of sodium balance present either as as

hypovolemia (sodium deficit) or hypervolemiahypovolemia (sodium deficit) or hypervolemia(sodium (sodium excess)excess)..

Hypovolemic patients are sensitive to the vasodilating and Hypovolemic patients are sensitive to the vasodilating and negative inotropic effects of vapor anesthetics, propofol, negative inotropic effects of vapor anesthetics, propofol, and agents associated with histamine release (morphine, and agents associated with histamine release (morphine, meperidine). meperidine).

Dosage requirements for other drugs must also be Dosage requirements for other drugs must also be reduced to compensate for decreases in their volume of reduced to compensate for decreases in their volume of distribution.distribution.

Hypovolemic patients are particularly sensitive to Hypovolemic patients are particularly sensitive to sympathetic blockade from spinal or epidural anesthesia.sympathetic blockade from spinal or epidural anesthesia.

Major hazard of hypervolemia is impaired gas exchange Major hazard of hypervolemia is impaired gas exchange due to pulmonary interstitial edema, alveolar edema.due to pulmonary interstitial edema, alveolar edema.


Major intracellular cationMajor intracellular cation Normal rangeNormal range

– 3.5 to 5.5 meq/L3.5 to 5.5 meq/L Serum level does not reflect total body KSerum level does not reflect total body K++

Plasma potassium concentration changes Plasma potassium concentration changes approximately 0.6 mEq/L per 0.1 unit change in approximately 0.6 mEq/L per 0.1 unit change in arterial pHarterial pH

Urinary [K +] l<20 mEq/L indicative of increased Urinary [K +] l<20 mEq/L indicative of increased extrarenal losses, whereas concentrations >20 extrarenal losses, whereas concentrations >20 mEq/L suggest renal wasting of K + .mEq/L suggest renal wasting of K + .

Potassium

ELECTROLYTE ELECTROLYTE DISORDERSDISORDERS Serum KSerum K++ < 3.5 < 3.5

meq/Lmeq/L PathophysiologyPathophysiology ECF → ICF shiftsECF → ICF shifts Acute alkalosisAcute alkalosis Hypokalemic Hypokalemic

periodic paralysisperiodic paralysis Barium ingestionBarium ingestion Insulin therapyInsulin therapy Vitamin B 12 Vitamin B 12

therapytherapy HypothermiaHypothermia

Excess renal lossExcess renal loss Mineralocorticoid excess(MC)Mineralocorticoid excess(MC) Primary hyperaldosteronism Primary hyperaldosteronism

(Conn’s syndrome)(Conn’s syndrome) Glucocorticoid-remediable Glucocorticoid-remediable

hyperaldosteronismhyperaldosteronism Renin excessRenin excess Renovascular hypertensionRenovascular hypertension Bartter’s Bartter’s

syndrome(hypochloremia,metabolic syndrome(hypochloremia,metabolic alkalosis,hyperrenemia wth normal alkalosis,hyperrenemia wth normal bp)bp)

Liddle’s syndrome(metabolic Liddle’s syndrome(metabolic alkalosis,high bp,low renin activity)alkalosis,high bp,low renin activity)

Diuresis(MC)Diuresis(MC)

Hypokalemia

HypoklaemiaHypoklaemia

Chronic metabolic Chronic metabolic alkalosisalkalosis

AntibioticsAntibiotics CarbenicillinCarbenicillin GentamicinGentamicin Amphotericin BAmphotericin B Renal tubular acidosisRenal tubular acidosis Distal, gradient-limitedDistal, gradient-limited ProximalProximal UreterosigmoidostomyUreterosigmoidostomy HypomagnesemiaHypomagnesemia DKADKA

Gastrointestinal lossesGastrointestinal losses VomitingVomiting Diarrhea, particularly Diarrhea, particularly

secretory diarrheassecretory diarrheas Nasogastric suctioningNasogastric suctioning fistulae,fistulae, laxative abuselaxative abuse villous adenomas, and villous adenomas, and

pancreaticpancreatic Tumors secreting Tumors secreting

vasoactive intestinal vasoactive intestinal peptide.peptide.

Inadequate intakeInadequate intake


Clinical FeaturesClinical Features– Sx onset at serum KSx onset at serum K++ << 2.5 meq/L 2.5 meq/L– Cardiovascular

Orthostatic hypotensionOrthostatic hypotension DysrhythmiasDysrhythmias EKG abnormalitiesEKG abnormalities Flattening and inversion of T waves Prominent U waves(>1 mm in height)

ST segment depression, increased P-wave amplitude, and prolongation of the P–R interval

Hypokalemia

ECG ChangesECG Changes

ECG ChangesECG Changes

Flattening of T Flattening of T waveswaves


Clinical Clinical Features (Cont):Features (Cont):– Neuromuscular

Skeletal muscle Skeletal muscle weaknessweakness

TetanyTetany RhabdomyolysisRhabdomyolysis Ileus Ileus Renal Polyuria (nephrogenic Polyuria (nephrogenic

diabetes insipidus)diabetes insipidus) Increased ammonia Increased ammonia

productionproduction Increased bicarbonate Increased bicarbonate

reabsorptionreabsorption

HormonalHormonal Decreased insulin Decreased insulin

secretionsecretion Decreased aldosterone Decreased aldosterone

secretionsecretion MetabolicMetabolic Negative nitrogen Negative nitrogen

balancebalance Encephalopathy in Encephalopathy in

patients with liver patients with liver diseasedisease

Hypokalemia


TreatmentTreatment– Replace K+

OralOral Intravenous as kcl (2 meq/ml)or pot phosphate(4.5 Intravenous as kcl (2 meq/ml)or pot phosphate(4.5

meq/ml pot and 3mM phosphate/ml)meq/ml pot and 3mM phosphate/ml) Kcl has osmolality of 4000 mosm/l .Must be dilutedKcl has osmolality of 4000 mosm/l .Must be diluted Potassium phosphate preferred for pot replacement in Potassium phosphate preferred for pot replacement in

DKA DKA – Not > 40 meq in 1 hourNot > 40 meq in 1 hour– peripheral intravenous replacement should not

exceed 8 mEq/h..– Concentrations > 20 meq/L require a central line.Concentrations > 20 meq/L require a central line.– Intravenous replacement should generally not exceed

240 mEq/d. Refractory hypokalemia check serum magnesium levelsRefractory hypokalemia check serum magnesium levels

– Cardiac monitor during replacement therapyCardiac monitor during replacement therapy

Hypokalemia

Anesthetic Anesthetic ConsiderationsConsiderations The intraoperative management of hypokalemia The intraoperative management of hypokalemia

requires vigilant ECG monitoring. requires vigilant ECG monitoring. Intravenous potassium should be given if atrial Intravenous potassium should be given if atrial

or ventricular arrhythmias develop. or ventricular arrhythmias develop. Glucose-free intravenous solutions should be Glucose-free intravenous solutions should be

used and hyperventilation avoided to prevent used and hyperventilation avoided to prevent further decreases in plasma [K+].further decreases in plasma [K+].

Increased sensitivity to neuromuscular blockers Increased sensitivity to neuromuscular blockers (NMBs) may be seen; therefore dosages of NMBs (NMBs) may be seen; therefore dosages of NMBs should be reduced 25–50%.should be reduced 25–50%.


Serum KSerum K++ > 5.5 meq/L > 5.5 meq/L Pseudohyperkalemia Red cell hemolysis Marked

leukocytosis/thrombocytosis Intercompartmental

shifts Acidosis Hypertonicity Rhabdomyolysis Excessive exercise Periodic paralysis Succinylcholine Digitalis

overdose,Beta2blockers

Decreased renal Decreased renal potassium excretionpotassium excretion

Renal failure Decreased mineralocorticoid

activity and impaired Na reabsorption

Acquired immunodeficiency syndrome(CMV infection)

Potassium-sparing diuretics ACE inhibitors Nonsteroidal anti

inflammatory drugs Pentamidine Trimethoprim

Hyperkalemia

HyperkalemiaHyperkalemia Enhanced Cl − reabsorptionEnhanced Cl − reabsorption Gordon’s syndrome Cyclosporine Increased potassium intakeIncreased potassium intake Salt substitutes transfusion of stored whole blood.


Clinical FeaturesClinical Features– CardiovascularCardiovascular

EKG abnormalities>6meq/l– Tall, peaked T-waves, short QT (6.5-7.5meq/l)– QRS widening, prolongation of the P–R interval

flattening of P-wave (7.5 to 8.0 meq/L)– loss of R-wave amplitude →ST-segment depression

(occasionally elevation) → an ECG that resembles a sine wave, before progression to ventricular fibrillation and asystole (10 to 12 meq/L)

– Neuromuscular(>8meq/l)Neuromuscular(>8meq/l) Weakness, paresthesiasWeakness, paresthesias Areflexia, ascending paralysisAreflexia, ascending paralysis

Hyperkalemia


EKGEKG

Hyperkalemia


TreatmentTreatment Cardiac irritability or KCardiac irritability or K++ > 7.5 meq/L > 7.5 meq/L 10 ml of 10% Calcium Gluconate over 3 10 ml of 10% Calcium Gluconate over 3

mins.Response lasts 20-30 mins.mins.Response lasts 20-30 mins. ECG changes and circulatory collapse---Calcium ECG changes and circulatory collapse---Calcium

chloride(10%) 10 ml IV over 3 mins.chloride(10%) 10 ml IV over 3 mins. AV block refractory to calcium treatment.AV block refractory to calcium treatment. Glucose/Insulin (bolus, infusion)10 U of R insulin in Glucose/Insulin (bolus, infusion)10 U of R insulin in

500 ml of 20% dextrose infused over 1h.Acts by 500 ml of 20% dextrose infused over 1h.Acts by transcellular shift of potassium.transcellular shift of potassium.

NaHCONaHCO33 - 50 to 100 meq IV over 2 - 50 to 100 meq IV over 2 min(Onset 5 to 10 min, duration 1 to 2 hrs)

B-Agonists (Albuterol neb)B-Agonists (Albuterol neb)

Hyperkalemia


TreatmentTreatment– Remove KRemove K++ from the body from the body

DiureticsDiuretics– Lasix 40 mg IVLasix 40 mg IV

Kaexalate PO/PR(Exchange Resins)Kaexalate PO/PR(Exchange Resins)– Each gram eliminates 1 meq KEach gram eliminates 1 meq K++

DialysisDialysis Digitalis CardiotoxicityDigitalis Cardiotoxicity• Mgso4 2g as IV bolusMgso4 2g as IV bolus• Digitalis specific antibodiesDigitalis specific antibodies

Hyperkalemia

Anesthetic Anesthetic ConsiderationsConsiderations The ECG should be carefully monitored. Succinylcholine is contraindicated, as is the use of

potassium containing intravenous solutions such as lactated Ringer’s injection.

The avoidance of metabolic or respiratory acidosis is critical to prevent further increases in plasma [K+].

Ventilation should be controlled under general anesthesia, and mild hyperventilation may be desirable.

Neuromuscular function should be monitored closely, as hyperkalemia can accentuate the effects of NMBs.


Normal rangeNormal range– 8.5 to 10.5 mg/dL(2.1-2.6 mmol/l)– Ionized fraction is physiologically active– Most abundant mineral in body

Approximately 50% is in the free ionized form, 40% is protein bound (mainly to albumin), and 10% is complexed with anions such as citrate and amino acids

for each increase or decrease of 1 g/dL in albumin, the total plasma calcium concentration increases or decreases approximately 0.8–1.0 mg/dL respectively.

Ionized calcium increases approximately 0.16 mg/dL for each decrease of 0.1 unit in plasma pH and vice versa

Calcium


Serum CaSerum Ca2+2+< 8.5 mg/dL< 8.5 mg/dLIonized level< 2.0 meq/lIonized level< 2.0 meq/l

EtiologyEtiology HypoparathyroidismHypoparathyroidism PseudohypoparathyroidiPseudohypoparathyroidi

smsm Vitamin D deficiencyVitamin D deficiency NutritionalNutritional MalabsorptionMalabsorption Postsurgical (gastrectomy, Postsurgical (gastrectomy,

short bowel)short bowel) Inflammatory bowel Inflammatory bowel

diseasedisease

HyperphosphatemiaHyperphosphatemia Precipitation of Precipitation of

calciumcalcium PancreatitisPancreatitis RhabdomyolysisRhabdomyolysis Fat embolismFat embolism Chelation of calciumChelation of calcium Multiple rapid red blood Multiple rapid red blood

transfusions or rapid transfusions or rapid infusion of large infusion of large amounts of albuminamounts of albumin

HypomagnesemiaHypomagnesemia SepsisSepsis

Hypocalcemia


Clinical FeaturesClinical Features– NeurologicalNeurological

Circumoral & digital paresthesias Tetany,laryngospasm Chvostek sign(Twitch at corner of mouth when

tapped over facial nerve just in front of ear). Trousseau signTrousseau sign((– – Carpal spasm produced when BP cuff

to upper arm maintains a pressure above systolic for 3 min.Fingers spastically extend at the IP joints and flex at the MCP joints. Wrist flexed, forearm pronated.

Impaired memory, confusion,seizures.

Hypocalcemia


Clinical Features (Cont)Clinical Features (Cont)– MuscularMuscular

Biliary colic and bronchospasmBiliary colic and bronchospasm– CardiovascularCardiovascular

Heart failureHeart failure HypotensionHypotension EKG abnormalitiesEKG abnormalities

– Prolonged QTProlonged QT

Hypocalcemia

CHOVSTEK’S SIGN

TROUSSEAU’S SIGNTROUSSEAU’S SIGN

ECG CHANGESECG CHANGES


TreatmentTreatment– AsymptomaticAsymptomatic

Oral replacementOral replacement– Symptomatic or SevereSymptomatic or Severe

10% Calcium Gluconate(9mg/ml) IV10% Calcium Gluconate(9mg/ml) IV 10% Calcium Chloride(27mg/ml) IV10% Calcium Chloride(27mg/ml) IV Infuse calcium into a large central vein if possible.If a Infuse calcium into a large central vein if possible.If a

peripheral vein is used ca gluconate should be used.peripheral vein is used ca gluconate should be used. Give bolus dose of 200 mg elemental calcium(8 ml of Give bolus dose of 200 mg elemental calcium(8 ml of

10% ca chloride or 22 ml of 10% calcium gluconate)in 10% ca chloride or 22 ml of 10% calcium gluconate)in 100 ml of isotonic saline over 10 minutes.100 ml of isotonic saline over 10 minutes.

Follow with continuous infusion of 1-2 mg elemental Follow with continuous infusion of 1-2 mg elemental calcium /kg/h for 6-12 hours.calcium /kg/h for 6-12 hours.

Hypocalcemia

Anesthetic Anesthetic ConsiderationsConsiderations Alkalosis should be avoided to prevent further Alkalosis should be avoided to prevent further

decreases in [Ca]. decreases in [Ca]. Intravenous calcium may be necessary following Intravenous calcium may be necessary following

rapid transfusions of citrated blood products or rapid transfusions of citrated blood products or large volumes of albumin solutions. large volumes of albumin solutions.

Potentiation of the negative inotropic effects of Potentiation of the negative inotropic effects of barbiturates and volatile anesthetics should be barbiturates and volatile anesthetics should be expected.expected.

Responses to NMBs are inconsistent and Responses to NMBs are inconsistent and require close monitoring with a nerve stimulatorrequire close monitoring with a nerve stimulator


Total CaTotal Ca2+2+ > 10.5 mg/dL > 10.5 mg/dL Ionized CaIonized Ca2+2+ > 2.7 meq/L > 2.7 meq/L

Hypercalcemia


EtiologyEtiology Hyperparathyroidism Malignancy Excessive vitamin D intake Paget’s disease of bone Granulomatous disorders (sarcoidosis, tuberculosis) Chronic immobilization Milk-alkali syndrome Adrenal insufficiency Drug-induced Thiazide diuretics Lithium

Hypercalcemia


Clinical FeaturesClinical Features– GeneralGeneral

Malaise, weakness, dehydration, polydipsiaMalaise, weakness, dehydration, polydipsia– NeurologicNeurologic

Confusion, apathy, decreased memory, irritabilityConfusion, apathy, decreased memory, irritability Hallucinations, headache, ataxiaHallucinations, headache, ataxia Hyporeflexia, hypotoniaHyporeflexia, hypotonia

– CardiovascularCardiovascular Hypotension,hypovolemia, dysrhythmiasHypotension,hypovolemia, dysrhythmias EKG abnormalitiesEKG abnormalities

– Short QT & ST, Wide T-waveShort QT & ST, Wide T-wave

Hypercalcemia


Clinical Features (Cont)Clinical Features (Cont)– GastrointestinalGastrointestinal

N/V, anorexiaN/V, anorexia Constipation, abdominal painConstipation, abdominal pain PUD, PancreatitisPUD, Pancreatitis

– SkeletalSkeletal Fractures, bone pain, deformitiesFractures, bone pain, deformities

– UrologicUrologic Polyuria, polydipsiaPolyuria, polydipsia Renal insufficiencyRenal insufficiency NephrolithiasisNephrolithiasis

Hypercalcemia


Memory AidMemory Aid– StonesStones ---- ---- Renal CalculiRenal Calculi– BonesBones ---- ---- OsteolysisOsteolysis– MoansMoans ---- ---- Psychiatric disordersPsychiatric disorders– GroansGroans ---- ---- Abdominal (PUD, Abdominal (PUD,

Pancreatitis)Pancreatitis)

Hypercalcemia


TreatmentTreatment– Treat dehydrationTreat dehydration

IV NS until ECF volume restoredIV NS until ECF volume restored Lasix 40 to 100 mg IV q 2-4 hrsLasix 40 to 100 mg IV q 2-4 hrs

– Decrease bone absorptionDecrease bone absorption CalcitoninCalcitonin(4U/kg IM or SC every 12 h)(4U/kg IM or SC every 12 h) MithramycinMithramycin(25µg/kg IV over 4 h)(25µg/kg IV over 4 h) HydrocortisoneHydrocortisone(200 mg daily in 2-3 divided doses)(200 mg daily in 2-3 divided doses) BisphosphonatesBisphosphonates PamidronatePamidronate-90 mg IV over 2 h-90 mg IV over 2 h ZolendronateZolendronate-4 mgIV over 15 minutes-4 mgIV over 15 minutes

– Monitor for hypokalemia, hypomagnesemiaMonitor for hypokalemia, hypomagnesemia

Hypercalcemia

Anesthetic Anesthetic ConsiderationsConsiderations Ionized calcium levels should be monitored

closely. Saline diuresis should be continued

intraoperatively with care to avoid hypovolemia.

Serial measurements of [K] and [Mg] are helpful in detecting iatrogenic hypokalemia and hypomagnesemia.

Responses to anesthetic agents are not predictable.

Acidosis should be avoided so as to not worsen the elevated plasma [Ca ].


Intracellular cation Normal range

– 1.5 to 2.5 meq/L Only 1–2% of total body magnesium stores is

present in the ECF compartment; 67% is contained in bone, and the remaining 31% is intracellular

Magnesium has been reported to decrease anesthetic requirements, attenuate nociception, blunt the cardiovascular response to laryngoscopy and intubation, and potentiate NMBs.

Magnesium


Serum MgSerum Mg2+2+ < 1.5 meq/L < 1.5 meq/L Coexistent disorders

– Hypokalemia(renal loss)Hypokalemia(renal loss)– Hypocalcemia(dec PTH)Hypocalcemia(dec PTH)– Etiology

Inadequate intake Reduced gastrointestinal

absorption Malabsorption syndromes Small bowel or biliary

fistulas Prolonged nasogastric

suctioning Severe vomiting or diarrhea

Increased renal losses Diuresis Diabetic ketoacidosis Hyperparathyroidism Hyperaldosteronism Hypophosphatemia Nephrotoxic drugs Postobstructive diuresis MultifactorialMultifactorial Chronic alcoholism Hyperthyroidism Pancreatitis Burns

Hypomagnesemia


Clinical FeaturesClinical Features– NeuromuscularNeuromuscular

TetanyTetany Cerebellar (ataxia, nystagmus, vertigo)Cerebellar (ataxia, nystagmus, vertigo) Confusion, obtundation, comaConfusion, obtundation, coma SeizureSeizure TremorsTremors HyperreflexiaHyperreflexia

– CardiovascularCardiovascular Heart failureHeart failure Dysrhythmias(Torsades de pointes,Atrial fib)Dysrhythmias(Torsades de pointes,Atrial fib) HypotenstionHypotenstion EKG----------Prolonged PR and QTEKG----------Prolonged PR and QT

Hypomagnesemia


Renal Magnesium Retention TestRenal Magnesium Retention Test Indications:Indications:1. For suspected magnesium deficiency when the 1. For suspected magnesium deficiency when the

serum magnesium concentration is normal.serum magnesium concentration is normal.2. Can be useful for determining the end-point of 2. Can be useful for determining the end-point of

magnesium replacement therapy.magnesium replacement therapy. 3. Is 3. Is not reliable in the setting of renal magnesium not reliable in the setting of renal magnesium

wasting or when renal wasting or when renal function is impairedfunction is impaired Contraindications:Contraindications:1. Cardiovascular instability or renal failure1. Cardiovascular instability or renal failure

Diagnosis

MethodologyMethodology

11. Add 24 mmol of magnesium (6 g of MgSO4) to . Add 24 mmol of magnesium (6 g of MgSO4) to 250 mL of isotonic saline and infuse over 1 hour.250 mL of isotonic saline and infuse over 1 hour.

2. Collect urine for 24 hours, beginning at the onset 2. Collect urine for 24 hours, beginning at the onset of the magnesium infusion.of the magnesium infusion.

3. A urinary magnesium excretion of less than 12 3. A urinary magnesium excretion of less than 12 mmol (24 mEq) in 24 hours (i.e., less than 50% of mmol (24 mEq) in 24 hours (i.e., less than 50% of the infused magnesium) is evidence of total the infused magnesium) is evidence of total body magnesium depletionbody magnesium depletion


TreatmentTreatmentOral(Magnesium sulfate 50%,12.5%)Oral(Magnesium sulfate 50%,12.5%) IV replacement(Mgso4)IV replacement(Mgso4) 1g contains 8 meq(4mmol) of elemental magnesium1g contains 8 meq(4mmol) of elemental magnesiumMild asymptomatic hypomagnesemiaMild asymptomatic hypomagnesemia Replace 1 meq/kg for 24 hours 0.5meq/kg for 3-5 Replace 1 meq/kg for 24 hours 0.5meq/kg for 3-5

days.days.Moderate hypomagnesemiaModerate hypomagnesemia(<1meq/l)(<1meq/l) 6g of Mgso4 in 250/500 ml of isotonic saline and infuse 6g of Mgso4 in 250/500 ml of isotonic saline and infuse

over 3h 5g of Mgso4 in same vol over next 6h over 3h 5g of Mgso4 in same vol over next 6h Continue with 5g Mgso4 every 12 hours for next 5 days.Continue with 5g Mgso4 every 12 hours for next 5 days.

Hypomagnesemia

Replacement ProtocolReplacement Protocol Life threatning hypomagnesemia (serious cardiac

arrhythmias e.g torsades de pointes or generalised seizures).

Infuse 2g Mgso4 IV over 2-5 mins Follow with 5g in 250/500 ml isotonic saline over 6h Continue with 5g Mgso4 every 12 hours over next 5

days. Anesthetic ConsiderationsAnesthetic ConsiderationsElectrolyte disturbances such as Electrolyte disturbances such as

hypokalemia,hypophosphatemia, and hypocalcemia are hypokalemia,hypophosphatemia, and hypocalcemia are often present and should be corrected prior to surgery.often present and should be corrected prior to surgery.


Serum MgSerum Mg2+2+ > 2.5 meq/L > 2.5 meq/L EtiologyEtiology

– Renal failure (most common)Renal failure (most common)– Increased MgIncreased Mg2+2+ load load

Laxatives, antacids, enemasLaxatives, antacids, enemas Untreated DKAUntreated DKA Lithium intoxicationLithium intoxication HemolysisHemolysis

– Increased renal absorptionIncreased renal absorption HyperparathyroidismHyperparathyroidism HypothyroidismHypothyroidism Mineralocorticoid/adrenal insufficiencyMineralocorticoid/adrenal insufficiency

Hypermagnesemia


Clinical FeaturesClinical Features– NauseaNausea > 2.0 meq/L > 2.0 meq/L– SomnolenceSomnolence > 3.0 meq/L > 3.0 meq/L– Decreased/absent DTRsDecreased/absent DTRs > 4.0 meq/L > 4.0 meq/L– Resp compromise, apneaResp compromise, apnea > 8.0 meq/L > 8.0 meq/L– Hypotension, heart block Hypotension, heart block ≈ 15.0 ≈ 15.0

meq/Lmeq/L

– EKG abnormalitiesEKG abnormalities >> 5.0 meq/L 5.0 meq/L Prolonged PR & QTProlonged PR & QT Prolonged QRS durationProlonged QRS duration

Hypermagnesemia


TreatmentTreatment– D/C MgD/C Mg2+2+ administration administration– Dilution using IV NSDilution using IV NS– Lasix 40-80 mg IVLasix 40-80 mg IV– Dialysis(renal impairment)Dialysis(renal impairment)

In cases of relatively high [Mg ], and especially in the presence of clinical signs of magnesium toxicity, intravenous calcium can temporarily antagonise the toxic effects

Hypermagnesemia

Anesthetic Anesthetic ConsiderationsConsiderations Hypermagnesemia requires close monitoring ofHypermagnesemia requires close monitoring ofthe ECG, blood pressure, and neuromuscularthe ECG, blood pressure, and neuromuscularfunction.function. Potentiation of the vasodilatory andPotentiation of the vasodilatory andnegative inotropic properties of anesthetics negative inotropic properties of anesthetics

shouldshouldbe expected. be expected. Dosages of nondepolarizing NMBsDosages of nondepolarizing NMBsshould be reduced.should be reduced.


Intracellular anionIntracellular anion Normal rangeNormal range

– 2.5 to 4.5 mg/dL2.5 to 4.5 mg/dL– Only 0.1% of total body phosphorus is in ECF; Only 0.1% of total body phosphorus is in ECF;

85% is in bone and 15% is intracellular85% is in bone and 15% is intracellular– HypophosphatemiaHypophosphatemia

Serum POSerum PO44 < 2.5 mg/dL < 2.5 mg/dL Sx onset at POSx onset at PO44 < 1.0 mg/dL < 1.0 mg/dL

Phosphate


EtiologyEtiology– Decreased oral intakeDecreased oral intake

Malnutrition (Alcoholics)Malnutrition (Alcoholics)– Excessive lossExcessive loss– Shift from ECF ICFShift from ECF ICF

Respiratory/Metabolic AlkalosisRespiratory/Metabolic Alkalosis– HyperalimentationHyperalimentation– HyperparathyroidismHyperparathyroidism– DKADKA– Beta agonistsBeta agonists– SepsisSepsis– Phosphate binding agents-Aluminium containing Phosphate binding agents-Aluminium containing

compounds(Sucralfate,antacids)compounds(Sucralfate,antacids)

Hypophosphatemia


Clinical FeaturesClinical Features– Low cardiac outputLow cardiac output– Hemolytic anemiaHemolytic anemia– Impaired oxygen dissociation due to decreased Impaired oxygen dissociation due to decreased

2,3-DBG2,3-DBG– Impaired ATP productionImpaired ATP production

Hypophosphatemia


TreatmentTreatment Iv replacement-severe hypophosphatemia(serum

po4<1mg/dl) or evidence of cardiac dysfunction,respiratory failure,muscle weakness or impaired tissue oxygenation

Sodium phosphte or k phosphate is used(93 mg/ml or 3 mmol/ml phosphorus content).

Dosage Recommendations* For severe hypophosphatemia (PO4 <1 mg/dL) without

adverse effects:IV dose is 0.6 mg (0.02 mmol) / kg body weight /hour

For hypophosphatemia (PO4 <2 mg/dL) with adverse effects:

IV dose is 0.9 mg (0.03 mmol) / kg body weight /hour Monitor serum PO4 level every 6 hours.

Hypophosphatemia


Serum POSerum PO44 > 4.5 mg/dL > 4.5 mg/dL EtiologyEtiology

– Renal insufficiencyRenal insufficiency– Cell necrosis(Rhabdomyolysis or tumor lysis)Cell necrosis(Rhabdomyolysis or tumor lysis)– Increased Increased intake(abuse of phosphate laxatives)– HypoparathyroidismHypoparathyroidism

Clinical FeaturesClinical Features– Sx related to renal failureSx related to renal failure– Sx of hypocalcemiaSx of hypocalcemia– Sx of hypomagnesemiaSx of hypomagnesemia

Hyperphosphatemia


TreatmentTreatment– Treat underlying causeTreat underlying cause– Dilution using IV NSDilution using IV NS– Aluminum Carbonate/HydroxideAluminum Carbonate/Hydroxide

Absorbs phosphate secreted into gutAbsorbs phosphate secreted into gut– HemodialysisHemodialysis

Hyperphosphatemia

Health & Medicine

Dyselectrolytemia by Dr Sheikh Tufail