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
Urine Na+ >20
mmol/l
HYPONATREMIA
Assess volume status
Hypovolemia
Total body fluid↓↓
Total body Na+ ↓
Euvolemia (no edema)
Total body fluid ↓
No change of Na+
Hipervolemia
Total body fluid ↑
Total body Na+ ↑↑
Urine Na+ <20
mmol/l
Urine Na+ >20
mmol/l
Renal
Diuresis osmosis
or loop diuretic
Mineralocorticoid
deficiency
Ketonuria
Cerebral salt
wasting
Extrarenal
Vomiting
Diarrhea
Third space of
fluids in
pancreatitis, burn
injuries
Glucocorticoid
deficiency
Hypothyroidism
Stress
Drugs
Syndrome of
Inappropriate ADH
secretion (SIADH)
Acute or chronic
kidney injury
Nephrotoxic syndrome
Cirrhosis
Cardiac failure
Urine Na+ <20
mmol/l

Management of hyponatremia
Acute Hyponatremia Chronic Hyponatremia
Rapid Na correction with
hypertonic natrium fluid
intravena
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
Gradual Na correction:
• 0,5 meq/L every hour,
• Max: 10 meq/L in 24 hours
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
Urine Na+ >20
mmol/l
HYPERNATREMIA
Assess volume status
Hypovolemia
Total body fluid↓↓
Total body Na+ ↓
Euvolemia (no edema)
Total body fluid ↓
No change of Na+
Hipervolemia
Total body fluid ↑
Total body Na+ ↑↑
Urine Na+ <20
mmol/l
Urine Na+ >20
mmol/l
Renal
Osmotic or loop
diuretics
Post obstruction
Intrinsic Renal
Disease
Extrarenal
Excess sweating
Burns
Diarrhea
Fistulas
Renal Losses
Diabetes Insipidus
Hypodipsia
Extrarenal lossess
Insensible losses:
respiratory, dermal
Sodium gains
Primary
hyperaldosteronism
Cushing’s syndrome
Hypertonic dialysis
Hypertonic NaHCO3
NaCl tablets
Variabel Urine Na+
<20 mmol/l

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
extremities
• muscle cramps seizures
• cardiac: prolonged QT interval,
hypotension, arrythmia
Chvostek Sign (+)
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

Definition: serum
phosphate < 2.5 mg/dL
Hypophosphatemia

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

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

Electrolyte disorder muhammad sobri maulana

Electrolyte disorder muhammad sobri maulana

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