Electrolyte Imbalance

Stella Palar

Division of Nephrology and HypertensionDepartment of Internal Medicine Faculty of Medicine

Sam Ratulangi University

HYPOKALEMIA

Serum K level < 3.5 mmol/L (normal: 3.5 – 5.0 mmol/L)

True hypokalemia : decreased of serum K level

False (spurious) hypokalemia : − false in laboratory result − in extreme leucocytosis (in vitro), wbc uptake kalium

in the test tube

DIAGNOSTIC APPROACH OF HYPOKALEMIA

Hypokalemia

Kalium depletionTranscelular shift• insulin therapy• beta2 agonists• alkalosis

Urine K <20 meq/L• GI losses• decreased intake

Urine K>20 meq/L • renal losses

Viarable PH• post obstructive • ATN recovery• aminoglycoside

Metabolic acidosis • RTA • Diabetic ketoacidosis

CLINICAL MANIFESTATIONS

• Cardiac• ventricular irritability• abnormal ECG• predisposition of digitalis intoxication• coronary artery spasm

• Neuromuscular• muscle spasm, tetany, paralysis• gastrointestinal (constipation, ileus)

• Renal• polyuria• increased amoniogenesis

• Endocrene• carbohydrate intolerance

MANAGEMENT

Emergency or not emergenny ?• clinical manifestation• ECG• degree of hypo K

Estimated degree of decreases in total body kalium• decreased in average of 0,3 mmol/L for each 100 mmol of

kalium depletion

Serum K level Deficit

Mild 3.00 – 3.4 meq/L 150 – 200 meq/L

Moderate 2.00 – 3.0 meq/L 200 – 400 meq/L

Severe < 2 meq/L 500 – 1000 meq/L

Treat the underlying causes

In mild hypo K : oral K preparation 600 -1200 meq/day

- small risk of hyper K

MANAGEMENT

• Moderate and severe hypo K : intravenous administration

• do not give direct i.v injection : CRIME

• intravenous drips peripheral or central venous line

– 10 – 20 meq/hr : into peripheral vein

– > 40 meq/hr : into central vein with ECG monitor

• Monitoring K level carefully (every 4-6 hrs)

Definition :• Plasma potassium consentration > 5. meq/L

• (N. 3.5 -.5 meq/L)

----- excess concentration K ion in extracellular fluid

HYPERKALEMIA

Causes of Hyper K1. Extrarenal2. Renal

1. Extrarenal causes of hyper K

A. Increased intakeExogenous sources

potassium supplement

stored PRC

salt substitute

Endogenous sourcerhabdomyolysis

tumor lysis syndrome

catabolic state

B. Compartment shift a. inhibition of Na/K – ATPase

• insulin resistance/deficiency

• B2 adrenergic deficiency/resistance

• Familial hyperkalemic periodic paralysis

b. Altered transcellular electrochemical K gradient

• inorganic metabolic acidosis

• ECF hypertonicity/hyperosmolar state :

• (hyperglycemia, mannitol

2. Renal causes of hyper K• AKI• CKD• Hypoaldosteronism (secondary/primary)

Clinical feature • often asymptomatic• neuromuscular disturbance (K>6.5 meq/L)

• distal parasthesia• generalized muscle weakness• ascending flaccid paralysis• ventilatory failure

• sudden cardiac death (K>7-7.5 meq/L)

ECG changes• K+, 5-6 meq/L

• 50% no ECG changes• peaked T, shortened QT

• K+, 6-7 meq/L• Prolonged QR, AV dissociation • flattening and loss P• widening QRS complex

• K+ > 7 – 8 meq/L - VT

Pseudo Hyper K• Caused by released of K from damage cell in vitro ------ 1-2 meq/L artifactual release

• hemolysis• thrombocytosis • leukocytosis• familial psudohyper K

MANAGEMENTHyper K >6.5 meq/L : medical emergency

- therapy should begin immediately

1. Stabilization of cardiac membrane

- 10 ml Ca gluconas 10% over 2-3 min into large vein

- evident within minutes and lasts for 30 to 60 min

- represents a temporizing measure only

- plasma K concentration is unaltered

Management2. Transcellular redistribution a. insulin and dextrose --- activated insulin receptor stimulates N+/K+-ATPase driving cellular uptake of K - 1 iu insulin setiap 5 gr glukosa - each 10 iu insulin can expected to lower K by 0.5-1.5 meq/l within 15 min, lasting 2-4 hrs b. sodium bicarbonate - increasing the pH of ECF (100 mmol over 1-2 hrs) - when hyper K associated by severe inorganic acidosis c. Salbutamol - meter dose inhaler, nebulized, intravenous

Management3. Removal of excess

- loop diuretic

- cation exchange resin (kayexilate)

- hemodialysis or CRRT

- laxantia (MgS04)

Plasma sondium (Na+) concentration : the ratio between sodium and water in the plasma

Normal : 135 – 145 mmol/LHyponatremia : < 135 mmol/LIs, Na+ loss or water gain

HYPONATREMIA

Types and Causes of Hyponatremia

PseudohyponatremiaA rare measurement artefact caused by reduced plasma water, as a result of excess lipids (triglycerides) or abnormal proteins (e.g. IgM)

Hyperosmolar (iso-osmolar and other) hyponatremia• Hyperglycaemia (and other impairment solutes, but not urea)• Surgical (e.g. transurethral prostatectomy) irrigation fluids (mannitol,

sorbitol, glycine)• Subarachnoid haemorrhage

True (hypo-osmolar) hyponatremia ECF ( TBNa+) – reduced effective arterial volume (Na+ loss) ECF ( TBNa+) – reduced effective arterial volume (oedema) ECF ( TBNa+) – normal effective arterial volume (no oedema),

SIADH, drugs, stress, cortisol, thyroxine)

The formula of osmolality

Posm = 2[Na+] + [glucose]/18 + [BUN]/2.8

Hiponatremia

Translocational

• hyperglycemia• irrigation fluids

(mannitol, sorbitol)• surgical

(transurethral prostatectomy)

Normal or high osmotic Low osmotic(true hyponatremia)

Pseudohyponatremia

• protein• lipid

Urinary osmolality *)> 100 mosm/kg

Urinary osmolality<100 mosm/kg

Water intake exceeding urine dilutionLow solute intakeCorrection phase of hyponatremia

Diagnostic approach for the patient with hyponatremiaChoncol M, Hyponatremia, 2005

A Clinical Approach to Hyponatremia

Hypo-osmotic hyponatremia

Urinary sodium concentration

Urinary osmolality

Treatment Normal saline Water restriction Treat + restrict water

Hypovolaemia Euvolaemia Hypervolaemia

Renal loss• Diuretic• Na+ loss

Extra Renal loss• Gastrointestinal

tract• Skin

Heart failureLiver failureNephrotic syndrome

Syndrome of inappropriate antidiuretic

PsychogenicHypothyroidDrugs

(Robert U, NEPHROLOGY Medical Progress December 2003)

SALT LOSING NEPHRITIS

• Nephritis with an excessive urinary loss of Na• hypovolemic hyponatremia• urinary Na+ >20 mmol/L• mostly without hypertension

• medullary cystic disease• chronic interstitial nephritis• polycystic kidney disease• analgetic nephropathy• partial urinary tract obstruction• chronic glomerulonephritis (rarely)

Diagnosis criteria for SIADH(Syndrome of inappropriate ADH secretion

Essential• ECF effective osmolality below 270 mosmol/kg water• Inappropriate urinary concentration (> 100 mosmol/kg)• Clinical euvolemia• Increased urinary [Na+] while on a normal salt and water intake• Absence of adrenal, thyroid, pituitary or renal insufficiency or

diuretic use

Supplemental• Abnormal water load test (inability to excrete at least 90% of 20

mL/kg water load in 4 h and/or failure to dilute urinary osmolality to below 100 mosmol/kg)

• Plasma ADH level inappropriately raised relative to plasma osmolality

• No significant correction of plasma [Na+] with volume expansion but improvement after fluid restriction

THE LANCET, Vol 352, July 18, 1998)

CLINICAL MANIFESTATION:

Symtoms of hyponatremia due to the consequences of plasma hypoosmolality

HypoosmolalityMove of water from extra to intracellular

intracellular edema

Particularly in CNS

Symptoms:

- Lethargy- confusion - nausea-vometing

- muscle cramps - seizures- coma

Note: • Permanent neurologic damage may be occur in premenopausal women

- the cause is not well understood- so: hyponatremic women must be watched carefully

Lauriat, SM. J. Am Soc Nephrol. 8 : 1997

• postoperative menstrual women• elderly women in thiazide diuretics• children• psychiatric polydipsic patients• hypoxemic patients

PATIENTS AT RISK FOR PERMANENT NEUROLOGIC COMPLICATION

Important questions must be answered :

1. Is the patients symptomatic ? Symptomatic patients have to treat aggressively but promptly

2. is the hyponatremia - acute (before 48 hrs) ? - chronic (after 48 hrs) ?

Acute hyponatremic, carries a greater risk of permanent neurologic sequelae if the correction is not expeditiously

3. Whats the Na+ level ? Severe hypoNa+ is Na level<120 mmol/L target of treatment is Na level 130 mmol/L

4. Does the patients have Risk Factors for osmotic demyelination syndrome ?

- complication of too rapid Na+ replacement

MANAGEMENT

SEVERE HYPONATREMIA

(Na+ <120 mmol/L)

Acute

Symptomatic

Chronic

Asymptomatic Chronic

MANAGEMENT

HypoN+ present for <48 hrs• treatment should be promptly – risk of osmotic

demyelination • emergency correction with hypertonic saline (3%)

• infusion at the rate 1-2 mL perKg/hr• loop diuretic enhances solute free water excretion &

hastens the return to a normal serum Na• if severe neurologic symptoms (seizure, coma) are

present infusion rate may at 4-6 ml/kg/hr• until the symptoms resolved or Na+ level 130 mmol/L

• serum Na+ should be carefully monitored (every 4-6 hrs)

SEVERE ACUTE SYMPTOMATIC HYPONa+

HypoNa+ present for >48 hrs or the duration is unknown• increase the serum Na+ by 10% with hypertonic saline

infusion at rate 1,5 -2 ml/kg/hr (or in 4-6 hrs)• after the initial correction, do not exceed a correction

rate of 1-1,5 ml/kg/hr• coadministration of loop diuretic• until the symptoms resolved or Na+ level 130 mmol/L• do not increase the serum Na+ by more than 15 mmol/L

24 hrs• serum Na+ should be carefully monitored (every 4-6 hrs)

SEVERE CHRONIC SYMPTOMATIC HYPONa+

TreatmentTreatment MechanismMechanismFluid restrictionFluid restriction Decreases free waterDecreases free water

Pharmacological inhibition of ADHPharmacological inhibition of ADHLithiumLithium Inhibits renal response to ADHInhibits renal response to ADH

DemeclocyclineDemeclocycline Inhibits renal response to ADHInhibits renal response to ADH

VV22 receptor antagonist receptor antagonist Antagonises vasopressinAntagonises vasopressin

Increased solute intakeIncreased solute intakeFurosemideFurosemide Increases free water clearanceIncreases free water clearance

UreaUrea Osmotic diuresisOsmotic diuresisTHE LANCET, Vol 352, July 18, 1998)

CHRONIC ASYMPTOMATIC HYPONa+

• No immediate therapy is required and underlying disease can be sought

• No urgency to coorect the serum Na+

DefinitionSerum Na consentration > 145 meq/L

HYPERNATREMIA

Classification1. Decreased total body sodium

Extracelular water and sodium loss with excess water loss

Extra renal lossExtra renal loss - VomitingVomiting- DiarrheaDiarrhea- Excessive sweatingExcessive sweating- DialysisDialysis

Renal lossRenal loss - Osmotic diuretics (e.g., Osmotic diuretics (e.g., glucose, urea, mannitol)glucose, urea, mannitol)

Extra renal lossExtra renal loss - Unconscious stateUnconscious state- Thirst center dysfunctionThirst center dysfunction- Mechanical obstructionMechanical obstruction- Inappropriate intravenous Inappropriate intravenous

therapytherapy- No access to waterNo access to water

Renal lossRenal loss - Cranial diabetes insipidusCranial diabetes insipidus- Nephrogenic diabetes insipidusNephrogenic diabetes insipidus

2. Normal total body sodiumExtracellular water deficiency associated with

minimal sodium loss

3. Increased total body sodiumExtracellular water and sodium gain with

relatively excess sodium gain

High sodium intakeHigh sodium intake - Sea water ingestionSea water ingestion

- Accidental / intentional salt Accidental / intentional salt ingestioningestion

- Hypertonic salineHypertonic saline

- Sodium bicarbonate infusionSodium bicarbonate infusion

Low sodium outputLow sodium output - Mineralocorticoid excessMineralocorticoid excess

Clinical presentation• not seen until serum Na >155 meq/L• fever, restlessness, lethargy, confusion

Treatment• treat the underlying cause• fluid therapy with pure water or nasogastrically• intravenous therapy with dextrose 5% or pure water • through central vein

Note A rapid decreased of serum Na could be detrimental--- decrease of serum Na by 2 meq/L/hr

TAKE- HOME MESSAGE :

In diagnostic and treatment of water and electrolyte

dysbalance :• knowledge of basic renal physiology is useful for

understanding.• a promptly management and monitoring is needed