Electrolyte Disorder - Muhammad Sobri Maulana

Hyponatremia
Definition: plasma natrium <135 mmol/L.

– Acute: rapid onset < 48 hours
– Chronic: late onset > 48 hours
Clinical manifestations:
– Headache, lethargy, nausea
– Reversible ataxia, psychosis, seizures, coma
– Signs of cerebral edema
– Osmotic demyelination
Johnson RJ, Feehally J, Floege J, et al. Comprehensive clinical nephrology. 5th ed. Philadephia:Elsevire Saunders;2015.
Clinical approach of hyponatremia
HYPONATREMIA
Assess volume status
Hypovolemia Euvolemia (no edema) Hipervolemia

Total body fluid↓↓ Total body fluid ↓ Total body fluid ↑
Total body Na+ ↓ No change of Na+ Total body Na+ ↑↑
Urine Na+ >20 Urine Na+ <20 Urine Na+ >20 Urine Na+ <20
mmol/l mmol/l mmol/l mmol/l
Renal Extrarenal Glucocorticoid Acute or chronic Nephrotoxic syndrome

Diuresis osmosis Vomiting deficiency kidney injury Cirrhosis
or loop diuretic Diarrhea Hypothyroidism Cardiac failure
Mineralocorticoid Third space of Stress
deficiency fluids in Drugs
Ketonuria pancreatitis, burn Syndrome of
Cerebral salt injuries Inappropriate ADH
wasting secretion (SIADH)
Management of hyponatremia
Acute Hyponatremia Chronic Hyponatremia
Rapid Na correction with Gradual Na correction:

hypertonic natrium fluid • 0,5 meq/L every hour,
intravena
• Max: 10 meq/L in 24 hours
1. Increase plasma Na+ 5
meq/L from baseline in 1
hours
2. Increase plasma Na+ 1
meq/L every 1 hour until
reach 130 meq/L
Setiati S, Alwi I, Sudoyo AW, et al. Buku Ajar Ilmu Penyakit Dalam. Edisi 6. Jakarta: Interna Publishing
Hypernatremia
• Definition: plasma natrium >145 mmol/L
• Dehydration (hypovolemia hypernatremia) VS
volume depletion (hypovolemia normonatremia)
• Clinical manifestations:
– CNS symptoms: altered mental status, lethargy,
irritability, restlessness, seizures (usually in children),
muscle twitching, hyperreflexia, and spasticity
– Fever, nausea or vomiting, labored breathing, and
intense thirst
Clinical approach of
hypernatremia HYPERNATREMIA
Assess volume status
Hypovolemia Euvolemia (no edema) Hipervolemia

Total body fluid↓↓ Total body fluid ↓ Total body fluid ↑
Total body Na+ ↓ No change of Na+ Total body Na+ ↑↑
Urine Na+ >20 Urine Na+ <20 Variabel Urine Na+ Urine Na+ >20
mmol/l mmol/l <20 mmol/l mmol/l
Renal Extrarenal Renal Losses Extrarenal lossess Sodium gains

Osmotic or loop Excess sweating Diabetes Insipidus Insensible losses: Primary
diuretics Burns Hypodipsia respiratory, dermal hyperaldosteronism
Post obstruction Diarrhea Cushing’s syndrome
Intrinsic Renal Fistulas Hypertonic dialysis
Disease Hypertonic NaHCO3
NaCl tablets
Management of hypernatremia
Hypokalemia
Definition: plasma K+ < 3,5 meq/L
Etiologies of hypokalemia:
1. Decrease intake
2. Shifting of potassium into the cell: extracell alkalosis, insulin,
use of β2-agonis, hypokalemic periodic paralysis,
hypothermia
3. Excessive potassium excretion: through GI (vomitting,
diarrhea), renal (diuretics, primary hyperaldosteronism,
hypomagnesemia, polyuria, excessive sweating, etc.
Clinical manifestation of hypokalemia
Organ system Clinical Manifestation

Cardiovascular Increases blood pressure
Ventricular arrhythmias especially with dygoxin
Hormonal Impaired insulin release and induces insulin
resistance
Muscle Impaired muscle contraction
Reduced skeletal muscle blood flow
Renal Decreased renal blood flow, eGFR
Nephrogenic diabetes insipidus
Increased amoniagenesis (hepatic encephalopathy)
Alkalosis metabolic/chloride wasting
Cyst formation
Nefritis interstitial
ECG results: U wave, prolonged QT interval, ST depression, arrythmia

Management of hypokalemia
Indication of K+ correction:
• Absolute: rapid correction severe hypokalemia
(K<2 meq/L), on digitalis treatment, ketoacidosis
• Strong: myocardial ischemia, encephalopathy
hepatic
• Mild: if K+ 3-3,5 meq/L
Agents: oral and IV KCl
Hyperkalemia
Definition: plasma K+ > 5 meq/L
Etiologies of hypokalemia:
Impaired excretion
• Renal failure
• mineralocorticoid deficiency
• Pseudohypoaldosteronism
• drugs (potassium sparing diuretics, ACE-
inhibitors NSAID, cyclosporin)
Shifts of K out of cells
• Tissue breakdown
• Acidosis
• insulin deficiency
Clinical Manifestations
• Generally increased cell

membrane activation
threshold  impair
depolarization
• Impaired cardiac rhythm
• Paresthesias, weakness,
paralysis
• Acidosis
Management of hyperkalemia
1. Overcome hyperkalemia effect of cell
membrane:
– calcium gluconate IV
2. Return the K+ from extracellular to intracellular:
– insulin
– sodium bicarbonate
– α 2-agonist
3. Removal of excess K+:
– temporary loop diuretics
– hemodialysis (in acute setting)
Calcium-
phosphate
homeostasi
s
Jain S, Kennedy P, Srinivasan R, Chaudhry S. Calcium Homeostasis and osteoporosis. McMaster Pathophysiology Review
Distribution of calcium intra and
extracellular
• 45% bound to protein (mainly albumin)
• 15% bound to other anion such as phosphate
and citrate
• 40% free form or ionized  active form
Normal range:
• Plasma Ca= 8,5-10,5 mg/dl
• Ionized Ca= 4,65-5,25 mg/dl
In hypoalbumin patient:
Corrected Ca (mg/dl) = measured Ca (mg/dl) + [0.8 x (4 – albumin (g/dl))]
Hypocalcemia
Definition: serum
calcium <8,5 mg/dl
Clinical manifestation of
hypocalcemia
• fatigue and muscular weakness
• increased irritability
• a state of confusion
• paranoia, depression
• paresthesias of the lips and the Chvostek Sign (+)
extremities
• muscle cramps seizures
• cardiac: prolonged QT interval,
hypotension, arrythmia
Trousseau Sign (+)
Management of hypocalcemia
• Severe symptomatic (plasma Ca ≤7.5 mg/dl):
IV calcium gluconate
• Mild to moderate (plasma Ca >7.5 mg/dl) :
oral calcium
• Hypo parathyroid: vitamin D supplementation
(calcitriol, ergocalciferol or cholecalciferol)
• Vitamin D deficiency: oral vitamin D3 50,000
IU 1x/week for 6-8 weeks, and continued with
800-1000 IU vitamin D3/day.
Hypercalcemia
Definition: serum calcium >10,5 mg/dl
Clinical Manifestations
General increasing fatigue, muscle weakness, inability to concentrate,
nervousness, increased sleepiness
GI constipation, nausea and vomiting, and rarely peptic ulcer disease
or pancreatitis
Renal polyuria, urinary tract stone
Neuropsychiatric headache, loss of memory, somnolence, stupor
Ocular conjunctivitis from crystal deposition and rarely band keratopathy
Osteoarticular pain
Cardiac ECG shortening of the QT interval and coving of the ST wave
Increase cardiac contractility and amplify digitalis toxicity.
Etiology of Hypercalcemia
Management of hypercalcemia
Severe and symptomatic hypercalcemia:
– Rapid rehydration with isotonic saline to correct
volume depletion
– After euvolemia  loop diuretics to facilitate
urinary excretion of calcium
• Bisphosphonates
• Corticosteroids for hypervitaminosis D
Hyperphosphatemia
Definition: serum phosphate > 4.5 mg/dL
Clinical manifestation:
• Deposition of phosphate and calcium in soft
tissues
• Vascular calcification
• Block 25-hydroxyvitamin D to calcitriol induce
hypocalcemia and increase PTH
Treatment:
• In CKD  phosphate binder, restriction of
phosphate diet
Etiology of Hyperphosphatemia
Most common cause: AKI and CKD
Hypophosphatemia
Definition: serum
phosphate < 2.5 mg/dL
Hypophosphatemia
Clinical Manifestation
• metabolic encephalopathy, red and white
blood cell dysfunction, hemolysis, and
thrombocytopenia
• reduced muscle strength (e.g., diaphragmatic
strength) and decreased myocardial
contractility
Magnesium homeostasis
Hypermagnesemia
Definition: serum Mg2+ > 2.6 mg/dL (> 1.05
mmol/L)
Etiology:
Hypermagnesemia
Clinical Manifestation:
• up to 1.5 mmol/l (3.6 mg/dl) asymptomatic
• > 3 mmol/l (7.2 mg/dl  loss of deep tendon reflexes
• 5 mmol/l (12 mg/dl)  respiratory paralysis, hypotension,
abnormal cardiac conduction, and loss of consciousness
Management:
• Symptomatic hypermagnesemia: calcium gluconate
Hypomagnesemia
Definition: serum
Mg2+ < 1.8 mg/dL
(< 0.70 mmol/L)
Hypomagnesemia
Clinical manifestation:
• general weakness and neuromuscular
hyperexcitability with hyperreflexia
• carpopedal spasm, seizure, tremor, and rarely
tetany
• ECG: prolonged QT interval and ST depression
Treatment:
• Magnesium sulfate for parenteral therapy, 1500
to 3000 mg/day

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Hyponatremia

Definition: plasma natrium <135 mmol/L.

Assess volume status

Hypovolemia Euvolemia (no edema) Hipervolemia

Renal Extrarenal Glucocorticoid Acute or chronic Nephrotoxic syndrome

Rapid Na correction with Gradual Na correction:

Assess volume status

Hypovolemia Euvolemia (no edema) Hipervolemia

Renal Extrarenal Renal Losses Extrarenal lossess Sodium gains

Organ system Clinical Manifestation

ECG results: U wave, prolonged QT interval, ST depression, arrythmia

Agents: oral and IV KCl

• Generally increased cell

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