Stella Palar

Division of Nephrology and Hypertension Department 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

Transcelular shift insulin therapy beta2 agonists alkalosis Urine K <20 meq/L GI losses decreased intake

Kalium depletion

Urine K>20 meq/L renal losses

Metabolic acidosis RTA Diabetic ketoacidosis

Viarable PH post obstructive ATN recovery aminoglycoside

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 Mild Moderate Severe 3.00 3.4 meq/L 2.00 3.0 meq/L < 2 meq/L Deficit 150 200 meq/L 200 400 meq/L 500 1000 meq/L

MANAGEMENT
Treat the underlying causes In mild hypo K : oral K preparation 600 -1200 meq/day - small risk of hyper K

 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)

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

(N. 3.5 -.5 meq/L)

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

Causes of Hyper K
1. Extrarenal

2. Renal

1. Extrarenal causes of hyper K A. Increased intake

Exogenous sources
potassium supplement stored PRC salt substitute Endogenous source rhabdomyolysis 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

MANAGEMENT
Hyper 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

Management
2. 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

Management
3. Removal of excess - loop diuretic

- cation exchange resin (kayexilate)

- hemodialysis or CRRT - laxantia (MgS04)

HYPONATREMIA
Plasma sondium (Na+) concentration :

the ratio between sodium and water in the plasma

Normal : 135 145 mmol/L

Hyponatremia

: < 135 mmol/L

Is, Na+ loss or water gain

Types and Causes of Hyponatremia

Pseudohyponatremia
A 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

Normal or high osmotic

Low osmotic
(true hyponatremia)

Translocational

Pseudohyponatremia

protein hyperglycemia lipid irrigation fluids (mannitol, sorbitol) surgical (transurethral prostatectomy)

Urinary osmolality <100 mosm/kg

Water intake exceeding urine dilution Low solute intake Correction phase of hyponatremia

Urinary osmolality *) > 100 mosm/kg

Diagnostic approach for the patient with hyponatremia

Choncol M, Hyponatremia, 2005

A Clinical Approach to Hyponatremia

Hypo-osmotic hyponatremia
Hypovolaemia
Renal loss Diuretic Na+ loss Extra Renal loss Gastrointestinal tract Skin

Euvolaemia
Syndrome of inappropriate antidiuretic Psychogenic Hypothyroid Drugs

Hypervolaemia
Heart failure Liver failure Nephrotic syndrome

Urinary sodium concentration Urinary osmolality Treatment Normal saline Water restriction Treat + restrict water

(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
Hypoosmolality Move of water from extra to intracellular intracellular edema

Particularly in CNS Symptoms: - Lethargy - confusion - nausea-vometing

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

- muscle cramps - seizures- coma

PATIENTS AT RISK FOR PERMANENT NEUROLOGIC COMPLICATION

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

hypoxemic patients

MANAGEMENT
Important questions must be answered : 1. Is the patients symptomatic ? 2. is the hyponatremia - acute (before 48 hrs) ? - chronic (after 48 hrs) ? 3. Whats the Na+ level ? Symptomatic patients have to treat aggressively but promptly Acute hyponatremic, carries a greater risk of permanent neurologic sequelae if the correction is not expeditiously 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
Acute

Symptomatic

Chronic
SEVERE HYPONATREMIA (Na+ <120 mmol/L)

Asymptomatic

Chronic

SEVERE ACUTE SYMPTOMATIC HYPONa+

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 CHRONIC 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)

CHRONIC ASYMPTOMATIC HYPONa+

No immediate therapy is required and underlying disease can be sought No urgency to coorect the serum Na+
Treatment Mechanism
Decreases free water

Fluid restriction
Pharmacological inhibition of ADH
Lithium Demeclocycline V2 receptor antagonist

Inhibits renal response to ADH Inhibits renal response to ADH Antagonises vasopressin

Increased solute intake

Furosemide Increases free water clearance

Urea

Osmotic diuresis
THE LANCET, Vol 352, July 18, 1998)

HYPERNATREMIA

Definition Serum Na consentration > 145 meq/L

Classification
1. Decreased total body sodium Extracelular water and sodium loss with excess water loss Extra renal loss
-

Vomiting Diarrhea

Excessive sweating
Dialysis Osmotic diuretics (e.g.,

Renal loss

glucose, urea, mannitol)

2. Normal total body sodium Extracellular water deficiency associated with minimal sodium loss

Extra renal loss

Unconscious state
Thirst center dysfunction Mechanical obstruction

Inappropriate intravenous therapy

No access to water

Renal loss

Cranial diabetes insipidus

Nephrogenic diabetes insipidus

3. Increased total body sodium Extracellular water and sodium gain with relatively excess sodium gain
High sodium intake
-

Sea water ingestion

Accidental / intentional salt

ingestion

Hypertonic saline

Sodium bicarbonate infusion

Mineralocorticoid excess

Low sodium output

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