5. ELECTROLYTES
Na+ is critical for maintaining (ECF) volume
K+ is vital for maintaining cellular electrophysiology
Water regulation is primarily influenced by changes in serum
osmolality and volume status.
The kidney is the primary site for regulation of Na+, K+, and
water
6. SODIUM (Na+)
Dominant cation of ECF
Principal determinant of extracellular osmolality
Necessary for maintenance of intravascular volume
<3% of sodium is intracellular
>40% of total body sodium is in bone
Remainder in interstitial and intravascular spaces
7. SODIUM INTAKE
Diet determines the amount of sodium ingested
Readily absorbed throughout the GIT
Mineralocorticoids increase sodium transport into body (limited clinical significance)
Presence of glucose enhances sodium absorption
8. SODIUM EXCRETION
Kidney , stool, sweat
Kidney
Regulate sodium balance
Principal site of sodium excretion
Stool
Some sodium loss in stool
Minimal unless diarrhea is present
Sweat
Increased in CF, Aldosterone deficiency
9. SODIUM REGULATION
Sodium is unique among electrolytes because
Water balance , not sodium balance, usually determines its concentration
Serum sodium 135-145 meq/L
Osmolality 285-295 osm/kg
Hypothalamic osmoregulators : regulate thirst and appropriate release of ADH
ADH regulates excretion of free water from kidney
10. SODIUM REGULATION
Effect of rise in Na+ concentration :
Higher plasma osmolality
Increased thirst
Increased ADH secretion --- which leads to renal conservation
of water
Both of these mechanisms increase water content of body
Sodium concentration returns to normal
During hyponatremia
Decrease in plasma osmolality
Stops ADH secretion
Renal water excretion leads to an increase in the sodium
concentration
11. SODIUM REGULATION
Volume depletion does not stimulate
thirst
Volume depletion stimulates ADH
secretion even if hyponatremia
Volume depletion takes precedence over
osmolality
In contrast to the small increases in
osmolality that stimulate AVP(ADH)
release, relatively large decreases in
blood pressure (effective ECF volume)
are required to mount an AVP response.
14. CASE 1
1yr old male child admitted for respiratory failure with community acquired pneumonia
develops next day seizure with Na+ 114 mmol/L, serum osmolality - 238mosm /kg, urine
osmolality – 510mosm/kg.
What is the underlying dyselectrolytemia and its treatment plan?
15. HYPONATREMIA
• Serum sodium level <135 meq/L
• Very common electrolyte abnormality in critically ill
children(20-45%)
• Associated with increased morbidity and mortality
16. ETIOLOGY
Based on Volume status
Hypovolemic
Euvolemic
Hypervolemic
Based on the osmolality, hyponatraemia is classified into:
Pseudohyponatraemia (normal plasma osmolality)
– Hyperlipidaemia, hyperproteinaemia
– True hyponatraemia, but high urea or ethanol
Translocational hyponatraemia (hyperosmolality)
– Hyperglycaemia
– Mannitol administration
Based on the onset of occurrence of hyponatraemia, it is
classified into:
Acute hyponatraemia < 48-hour duration
Chronic hyponatraemia > 48-hour duration
17. HYPOVOLEMIC HYPONATREMIA
Renal Losses
Thiazide/Loop Diuretics
Osmotic diuresis
Polyuric phase of ATN
Tubular Dysfubction( Juvenile
nephronophthisis,intersitial
nephrutus,ARPKD)
Lack of aldosterone effect (High potassium)
CAH
Pseudohypoaldostreronism
Addison disease
UTI
Extra Renal Losses
GI losses( vomiting, diarrhea)
Skin(burns)
Third space losses( bowel obstruction,
peritonitis, sepsis)
18. EUVOLEMIC
HYPONATREMIA
SIADH
Glucocorticoid deficiency, Hypothyroidism
Drugs- Vincristine, Cyclophosphamide, SSRIs
Water intoxication ( Iatrogenic, water to infants, diluted
formula, psychogenic, child abuse)
19. EXCESS WATER INGESTION
Normally increased water intake > Hyponatremia> ADH suppression > free water secretion
In Infants low GFR and limited ability to secrete free water
Do not give water to drink to infants- better to give breastmilk/formula
21. SIADH
Absence of :
Adrenal , renal or thyroid isufficiency
CCF, nephrotic syndrome or cirrhosis
Diuretic ingestion
Dehydration
Urine osmolality > 100 mosm/ L
Urine sodium > 30 meq/ L
Serum osmolality < 280 mosm/L
Reversal of sodium wasting and correction of hyponatremia with water restriction
22. Feature SIADH CSWS
S.Urea Normal - low Normal - High
S.Uric acid low Normal - High
Urine volume Normal - low High
Urine sodium > 20 meq/L >>20 meq/L
BP Normal Normal – orthostatic
hypertension
23. DIAGNOSIS
History usually points to a cause: diarrhea/ diuretic use/polyuria
Step 1: Determination of plasma osmolality and urine osmolality
Step 2: Evaluate volume status of patient
Step 3: Urine sodium
24. URINE SODIUM
Hypovolemia hyponatremia- Renal causes Na>20, non-renal <10
Hypervolemia hyponatremia – Na <10 other than in renal failure
Renal causes are more difficult to diagnose- association with hyperkalemia points to a decreased or
ineffectiveness of aldosterone
28. Symptomatic hyponatremia
Bolus of 3% saline @ 2-5ml/kg
Followed by 0.5meq/l/hr( 10-12 meq/l over 24hr)
Each ml/kg of 3% increases Na+ by 1meq/l
29. TREATMENT BASED ON UNDERLYING ETIOLOGY
Hypovolemic Hyponatremia- Correct sodium and water deficit, intravascular volume repletion
Hypervolemic hyponatremia- fluid restriction, diuretics, vaptans, albumin, dialysis
SIADH- Fluid restriction , Difficult cases- furosemide, NaCl supplementation, Vaptans
30. COMPLICATION
Brain shrinkage triggers demyelination of
pontine and extrapontine neurons
Can cause neurologic dysfunction
(quadriplegia, pseudobulbar palsy,
seizures, coma, and even death)
31. CASE 2
4months old male child , developmentally normal brought with c/o- multiple episodes of loose stool X 02
days, vomiting 5-6 episode x o1 day with lethargy , irritability and poor oral intake
O/E : Dry oral mucosa, Skin turgor delayed, Doughy feel to skin
Airway : open & stable
Breathing : RR-56/min, increased effort , air entry normal, spo2 -95%
Circulation :HR: 158/min, CFT 2 seconds, BP: 66/40mmHg Central pulse- good, Peripheral pulse- good,
INV: Na- 176 , K- 3.2, Cl- 154
ABG: pH 7.18, pO2/pCO2 60.5/22.6 , HCO3/Lac - 11.9/1.3
32. HYPERNATREMIA
Hypernatremia is defined as sodium concentration > 145 mEq/L
Results from net loss of body water relative to sodium
Can occur with or without a loss or even a gain in body sodium content
34. CLINICAL
MANIFESTATIONS
Better preservation of intra vascular volume because of shift of water from intra cellular space
to extra cellular space
This intra cellular water loss leads to a doughy feel of the skin
35. CLINICAL
MANIFESTATIONS
CNS manifestations depend on large or rapid increases in serum Na+ concentration
Infants: hyperpnea, high pitched cry, restlessness, Muscle weakness, lethargy, coma
Older children: increased thirst, occasionally nausea
Complications:
ICH-- subdural , subarachnoid or parenchymal hemorrhage
Thrombotic complications like Stroke , Sinus thrombosis can also occur
36. TREATMENT
Likely cause of elevated serum sodium is due to water deficit rather than to salt excess (likely secondary
to diarrhea and vomiting)
1st Priority : RESTORATION OF INTRAVASCULAR VOLUME
NS bolus
How to correct further ? Water deficit ???
37. TREATMENT
Correcting the prevailing hypertonicity:
rate of correction depends on duration of hypernatremia to avoid cerebral edema
Addressing the underlying cause:
Stopping GI loss
Controlling pyrexia, hyperglycemia,
Correcting hypercalcemia or
Start feed
38. PRINCIPLES OF CORRECTION OF ACUTE HYPERNATREMIA
Hypernatremia that developed over a period of hours (e.g. accidental sodium loading)
Rapid correction improves prognosis without cerebral edema
Accumulated electrolytes in brain rapidly extruded
Reducing Na+ by 1 mmol/L/hr appropriate
39.
40.
41. PRINCIPLES OF CORRECTION OF CHRONIC HYPERNATREMIA
Hypernatremia of prolonged or unknown duration
A slow pace of correction prudent
Full dissipation of brain solutes occurs over several days
Maximum rate 0.5 mmol/L/hr to prevent cerebral edema
A targeted fall in Na+ of 10 mmol/L/24 hr
42. GOALS OF TREATMENT
In patients with seizures/encephalopathy, prompt airway and neurological stabilization
Reduce serum sodium concentration gradually to 145 mmol/L
Make allowance for ongoing obligatory or incidental losses of hypotonic fluids that will
aggravate the hypernatremia
43. POTASSIUM(K+)
Principal intracellular cation (98% body potassium)
Resting membrane potential
Propensity to cause fatal arrhythmia
Regulated by kidney: aldosterone is the primary regulator
44. CASE SCENARIO 3
A 2yr old boy was brought to hospital with h/o -- loose motions and vomiting since x 3days
He has not passed urine since 24 hrs
Urea- 160mg/dl, creat – 3.6 mg/dl
Na+ - 136, K+ - 7.5 meq/L
45. HYPERKALEMIA
Hyperkalemia is defined as the serum potassium (K) > 5.5
mEq/L
Even though hyperkalemia is less common than hypokalemia,
it is more likely to cause serious complications, mainly cardiac
arrhythmias, in critically ill patients.
The measured value of serum K may be high due to in vitro
haemolysis of the blood sample
True hyperkalemia vs pseudohyperkalemia
- Pseudohyperkalemia has no associated ECG changes
46. PATHOPHYSIOLOGY
The mechanisms that can, either in isolation or in combination, cause hyperkalaemia include:
Increased potassium load
Decreased excretion of potassium
Increased transcellular shift (with or without a solute drag)
49. TREATMENT
Life threatening emergency
Primary goal is to prevent complication
Treatment modalities:
1. Cardiac cell stabilization
2. Shifts K+ into cell
3. Remove K+ from body
51. CASE 4
A 3yr old boy with VSD on syp Lasix 3mg/kg/day since past 6month. He had 8 episode of diarrhea since
today morning for which he was taken to ER.
O/E: some dehydration, abdominal distension with sluggish bowel movement
Electolytes : Na+ - 142, K+ - 2.0
ECG : showing U wave
What is underlying dyselectroltemia ?
TBW(Total body water) as the percentage of body weight :75% in term infants which decreases to 60 % in a child
Females more fat with less water content hence less TBW
Major cation in ECF – Na, in ICF – Potassium, maintained by Na-K pump
For intracellular cations/anions serum concentration does not reflect Total body content
Electroneutrality i
ORS co transporters
Pseudohyponatremia is asymptomatic : lab artefact
Child has lost sodium from body, water balance can be positive or negative but sodium loss is more than free water loss
Diarrheal fluid- normally Na-50 , formula feeds Na -10 (Hyponatremia)
Third space losses are generally isotonic leading to hypovolemia and ADH secretion hence hyponatremia
Osmotic diuresis will cause both sodium and water loss , hyponatremia when replacement is hypotonic
Typically have excess of TBW with slight decrease in TB sodium
Clinically normal or subtle signs of FO
SIADH ADH not inhibited by either low osmolarity or expanded IV volume hence kidneys are not able to excrete free water
Problem : Decreased effective blood volume –kidneys try to preserve sodium and water
Csw is a hypovolemic state and SIADH is euto hypervolemic
Children with hypernatremic dehydration have preserved IV volume so present late
Neurological : paraesthesias, weakness, ascending paralysis
ECG- Peaked T waves, prolonged PR, Loss of P wave QRS widening, sine waves,vfib, aystole
ST depression, wide P wave, flat t wave, U waves, prominent U waves Qt prolongation
Paralysis <2.4 , ileus,urinary retention