Electrolyte imbalance

• TBW• Physiology• Daily requirements• Electrolyte imbalance sodium potassium calcium magnesium

TOTAL BODY WATER(TBW)

Age group Total body water in %

FETUS 90%PREMATURE BABIES

80%

TERM INFANTS 70%YOUNG CHILDRENS

65%

ADOLESCENTS 60%ADULT MALE 60%ADULT FEMALE 50%

TBW in diff age groups

TBW• 60% of body weight in a young adult male.• 50% in young adult female• 80%in neonates.

20% 40%

75% 25%

Normal water balance

Sensible water loss Insensible water loss

kidneys GIT skin Respiratory tract

Factors affecting IWL in neonates

• Increased IWL

• Decreased IWL

conditions Percentage change

Radiant warmer 50-100Hyperventilation

20-30

Increased activity

5-25

hyperthermia 12conditions % change

Humidefied air 15-30sedation 5-25Decreased activity 5-25hypothermia 5-15

Daily requirementsrequirements By body weight

WaterUpto 10 kg 100 ml/kg11-20 kg 1000+50ml/kg for extra

weight above 10 kg> 20 kg 1500ml+20ml/kg for

extra weight above 20 kg

sodium 3-4 mEq/kgPotassium 2-3mEq/kg

chloride 3-4 mEq/kg

plasma Interstitial fluid Intracellular fluid

ELECTROLYTES

Normal valuesELECTROLYTES ICF ECFNa+ 20 135-145K+ 150 3-5cl_- 98-110Hco3- 10 20-25Ca 8.8-10.8

4.2-5.5(mg/dl)ion calcium

Protein 75 10Phosphates 110-115 5

SODIUM(Na)• PHYSIOLOGICAL BASIS• Normal =135-145mEq/L• Dominant cation of ECF• Major determinant of serum osmolality.

– Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)– Normal: 285-295

• Daily requirement 3-4mEq/kg

IVF NS/DNS Iso E RL Iso P 3%NaClmEq/L 154 140 130 25 513

Deficiency of sodium

hypovolemia

Angiotensin 2

Response to Na deficit

Potent vasoconstrictor

Na and H2O reabsorption at

PCT

Release of aldosterone from zona glomerulosa

Sodium and water reabsorption

Increases ECF volume

Response to Na excess

Decreased release of AT2 and aldosterone Release of ANP

Decreased renal reabsorption of

sodium

Natriuresisdiuresis

Hypernatremia

• Sodium (Na+) concentration of greater than 145 mEq/L

• Produces a state of hyperosmolality

hypernatremia

Hypotonic fluid losses(hypovolemic

hypernatremia)Water deficit Sodium excess

(euvolemic hypernatremia)

Extra renal losses Renal losses

• Vomiting• Diarrhoea• Sweating• Osmotic

cataratics(lactulose)

• osmotic diuretics

• Diuretic phase of ATN

• CKD

• Diabetes insipidus(nephrogenic/central)

• Increased insensible loss

• Improperly mixed formula

• Iatrogenic• Hyperaldosteronism

<10mEq/L

>20mEq/L

Clinical features• Shock occurs late as ECF hyperosmolality causes water

to shift from ICF to ECF and plasma volume is maintained till dehydration is >10%.

• Doughy consistency of skin >10%dehydration.• CNS effects-symptoms seen >160mEq/l causes cellular

dehydration-brain shrinkage and tearing of bridging blood vessels.

• Intracerebral hemorrhage • Thrombosis(dehydration and probable

hypercoagulability)

• Lethargy/irritatbility,fever.hyper reflexia.• Seizure more common during correction .• Chronic hyper natremia leads to brain cell

production of organic osmolytes/idiogenic osmoles which cause flux of fluid into brain cells returning normal brain volume.

• Rapid correction of chronic hypernatremia can worsen neuronal swelling and increase neurologic sequalae.

managementRestore intravascular volume. NS 20 ml/kg over 20 min Determine time for correction based on initial [Na]:

[Na] 145-157 mEq/L : 24 hr[Na] 158-170 mEq/L: 48 hr[Na] 171-183 mEq/L: 72 hr[Na] 184-196 mEq/L: 84 hr

Administer fluid at a constant rate over the time for correctionTypical fluids: D5¼ NS or D5 ½ NS (with 20mEq/L KCl unless contraindicated)

Typical rate: 1.25-1.5 times the maintainance

HYPERNATREMIC DEHYDRATION• Resusticate shock with isotonic solution• Calculate free water deficit A)0.6x BW[(pt Na/140)-1]• Replace free water deficit and correct dehydration over

48-72hrs• suggested max rate of Na fall 10mEq/L/day in order to

prevent CNS complication

• Monitor Sr Na (at least Q2-4hr)• During therapy if Na falls too rapidly and/or neurological

symptoms occur,or imminent ,consider short infusion of 3%NaCl over 1-2hrs

TREATMENT OF HYPERNATREMIA WITH EUVOLEMIA• Slow correction of Na levels with minimum sodium input• Drinking water by enteral route or D5w intravenously will

result in excretion of excess sodium in urine• Diuretic administration (thiazide) may be necessary

and ,in extreme cases,dialysis will be required

Hyponatremia• Sodium less than <135mEq/L.• Low Sr Na+ leads to decreased Sr osmolality;so true

hypo Na+ is characterised by hypoosmolality.

Hypo Na+

Pseudo hypo Na+ Hypo osmolar Hypo Na+

Normal osmolality

Increased osmolality

Hyperlipidemiahyperproteinemia

Hyperglycemiamannitol

Hypo osmolar Hypo Na+

Hypo Na+ with ECF voldepletion

Hypo Na+ with hypervolemia

Hypo Na+ with normal ECF

Extral renal loss Renal loss Urine Na+

<20mEq/LUrine Na+

>20mEq/L

VomitingDiarrhoeaperitonitis

DiureticsCSWDKA

CHFCirrhosisnephrotic

Renal failure

SIADHHypothyroid

Glucocorticoid defPsy polydipsia

<20 >20

Clinical features of hypoNa+ • Depends on rapid fall of Na+ and also the magnitude

and etiology of Na+ .• Clinically related to cerebral edemamovt of water from

hypoosmolar plasma to brain cells.• Mild hypoNa+ (120-130)headache,vomiting• Rapid fall of Na+ (<120mEq/L)coma,seizure,brain herniation.• To defend neuronal swellingneuronal adaptation with

extrusion of osmoles/idiogenic osmoles

Contd…• Chronic hypoNa+ (>48hrs)-minimal or no symptoms• Rapid fall of Na+ over 12-24hrs(acute hypo Na+ ) may

produceneurological symptoms• So rapid correction in a asyptomatic patient with chronic

hypoNa+ osmotic disquilibrium syndrome and central pontine myelinolysispermanent neurological damage.

Approach to hypoNa+ • History and physical evalutation

Initial evaluation in hypoNa+

Plasma osmolality Urinary osmolality Urine sodium concentration

low normal <100mOsm/kg

>100mOsm/kg

<15mEq/L >20mEq/L

True hypo Na+ • Pseudo

hypoNa+ • RF

Polydipsia with normal

water excretion

Diarrhoeavomiting

SIADHRSW

– Hyponatremic seizures» Poorly responsive to anti-convulsants» Hypertonic saline(quickly reduce cerebral edema).1ml

of 3% Nacl increases the serum Na+ by approx 1 mEq/l.child with active symptoms often improves with 4-6 ml/kg of 3%nacl

» Goal is to increase ECF osmolality so that water moves from ICS to ECS

» Need to bring Na to above seizure threshold» Hypoxia worsens cerebral edema

• Acute symptomatic hyponatremia• Seizures• Impaired level of consciuosnes• Serum sodium < 120

• Treated with 3% nacl, 4-6 ml/kg b wt to correct the sodium deficit of 5 meq/l

• Rest of the correction should be achieved slowly by saline o.9% or 0.45%

• Deficit can be calculated by • Sodium deficit= 0.6xB wtX( 140-observed serum Na+)• Correction rate not greater than 0.5 meq/l or 10-12

meq/l/day

Hypervolemic Hyponatremia management:• Disorder with excess of both sodiun and water• Administration of sodium leads to worsening of vol

overload and edema• Pt is retaining water and sodium because of

ineffective intravascular vol and renal insufficiency• Goal of therapy is restriction of fluids• Diuretics may be helpful causing excretion of both

sodium and water• Vasopressin antagonist(tolvaptan) by blocking the

action of ADH causes water diuresis, particularly effective in hypervolumic hyponatremia due to heart failure and cirrhosis

SIADH

• Slightly increased or normal ECF Volume• Inappropriately high ADH levels• Antidiuresis leads to dilutional hyponatremia,

concentrated urine with elevated urinary sodium

Diagnostic criteria for SIADH• Hyponatremia <135mEq/L• S.osmolality < 280 mosm/kg• Clinically euvolemia• Inappropriate urinary concentration(urine osm >100)• High urinary sodium > 20 meq/l• NORMAL , renal, adrenal, pituitary and thyroid function

Etiology of SIADH• Pneumonia,pulm TB• CNS-trauma ,tumor,GBS, meningitis• Drugs- carbamazepine,cyclophosphamide• Pain induced increased ADH• Post operative hypotonic fluid• Malignancy-leukemia,GI malignancy

Treatment of SIADH• Fluid restriction in established asymptomatic SIADH –restrict fluid to 1/2-2/3 maintenance if hyponatremia is severe and refractory 0.9% saline may be combined with loop diuretics(frusemide)• 3%NaCl

Cerebral salt wasting syndrome• renal loss of sodium during acute intracranial disease

such as subarachnoid hemmorhage, infection,mass or post neurosurgical state

• Leading to hyponatremia and decrease ECF vol• Typically has hypovolumic hyponatremia due to urinary

loss of both sodium and water• Usually take few days after CNS insult• Attention to volume status is the key to diff b/n SIADH

and CSWS• Decrease in water balance and ECF vol is most

important feature of CSWS that diff b/n it and SIADH

• Lab features of CSWS are elevated hematocrit and serum protein conc in addition to hyponatremia

• Serum osmolality is normal or low but in SIADH its low• Urinary sodium is markedly elevated in CSWS, it is

variably elevated in SIADH.

Treatment of CSW• Asymptomatic pt –restoration of normal hydration is by

normal saline( 1.5 times the maintainance)• Symptomatic cases – 3%nacl• Persistance hyponatremia- fludrocortisone 0.05 mg/day• Side effects pulmonary edema, hypokalemia,

hypertension

SIADH CSWSSODIUM LOW LOWBODY WATER INCREASED DECREASEDSERUM OSMOLALITY <280 mosm/l DECREASEDURINE OSMOLALITY >100 mosm/l INCREASED

U/S OSMOLALILTY RATIO

<1 low >1 high

URINE OUT PUT low highURINARY Na CONCENTRATION

INCREASED INCREASED

potassium• Normal range: 3.5-4.5• Largely contained intra-cellular (150 mEq/l)• Principal regulator: kidneys• Daily requirement : 2 mEq/kg• Complete absorption in the upper GI tract

• Excretion Urine , GIT ,Sweat

IVF Iso-P Iso-M RL KCL 1amp(10ml)

K(mEq/l) 20 35 4 20

HYPOKALEMIA Defined as plasma concentration of K+ < 3.5 mEq/L

Mild Hypokalemia : 3.0 – 3.5 mEq/L : asymptomatic

Hypokalemia 2.5 to 3.0 mEq/L : Moderate, may be symptomatic

Hypokalemia < 2.5 mEq/L : Severe, may be symptomatic

etiology:(1). ↓K+ intake• Unable to eat, i.e. coma, digestive tract obstruction

• Fasting,(2). ↑K+ shift from ECF to ICF• Use of some drug, i.e. insulin, β-adrenergic agonist

• Toxin poisoning, i.e. barium

• Alkalosis

• Familial hypokalemic periodic paralysis

• (3). ↑K+ excretion• Via kidney-Use of certain diuretic agents, Primary and

secondary aldosteronism,Alkalosis, Renal tubular acidosis, Magnesium deficit

• Via gastrointestinal -Vomiting, diarrhea, gastric suction

• Via skin-Heavy sweat in hot environment

CLINICAL FEATURES• Occurs when serum potassium is less than

3mEq/L..manifestations of hypokalemia are mainly neuromuscular and cardiac

• Fatigue ,myalgia, and muscular weakness of lower extremity are commom complaints

• Smooth muscle involvement may result in constipation ,ileus or urinary retention

• More severe hypokalemia leads to progressive weakness ,hyporeflexia,hypoventilation and virtually complete paralysis

• Hypokalemia leads to increased risk of arrhythmia esp in patients on digitalis

• ECG changes early-flatenning or inversion of Twaves prominent Uwaves prolonged QT interval severe K+ depeletion prolonged PR interval decreaed voltage widening of QRS complex ventricular arrythmia

diagnosis• History-poor intake/GI losses/insulin intake/salbutamol

intake• Urinary K+

A)hypoK+ with low renal K+ excretion(<25mEq/L) poor intake,diarrhoea,excessive sweating,diuretics. B)high urinary K+ excretion besides normal K+ deficit 1) K+ wasting with metabolic acidosis with no HTN DKA,prox and distal RTA,ampho B

• 2) K+ wasting with metabolic alkalosis with no HTN a)low urinary Cl(<20mEq/L);vomiting b)high urinary Cl;diuretics,bartters• 3) K+ wasting with metabolic alkalosis with HTN primary and sec aldosteronism,cushings,liddle’s renovascular HTN.

Treatment of hypo K+

• When to treat ? 3.5-4mEq/Lno K+ supplement increased oral intake of K+ rich food 3-3.5mEq/Ltreatment in selected high risk pts (on digitalis/CHF) <3mEq/Lneeds definitive treatment• Potassium rich diet-beans, dark leafy greens, potatoes,

squash, yogurt, fish, avocados, mushrooms, and bananas. 

• In case of mild to moderate hypokalemia(2.5-3.5) and asymptomatic patient

oral potassium is preferred-less side effects,less dangerous

• Choose IV in patient who are NPO and severe hypokalemia

POTCHLOR STRENGTH: 20 ml=15 mEq KESOL 5 ml= 13 mEq

Dose : 2 mEq/kg PO q12hr

• IV K+ therapy• Reserved for severe symptomatic hypo K+ <2.5mEq/L or

patient who cannot ingest oral K+

• cardiac monitoring. Marked hypokalemia:Monitor serum K closely0.5-1 mEq/kg/dose given as an infusion of 0.5 mEq/kg/hr for

1-2 hour ,infusion rate should not exceed 1mEq/kg/hr and conc of K+ should not exceed 60mEq/L(peripheral line) and 80mEq/L(central line).

BOLUS OF KCL I.V. SHOULD NOT BE GIVEN

Hyperkalemia• Hyperkalemia exists when plasma [K +] exceeds 5.5

mEq/L.

• kidneys can excrete as much as 500 mEq of K +per day.

• So hyperkalemia rarely occurs in normal individuals

Causes:1)increased intake-IV fluid contaning K High K rich food 2)Tissue break down-Bleeding into soft tissue Hemolysis,rabdomyolysis Catabolc state3)Shift of K out of cell-tissue damage metabolic acidosis aldosterone def hyperkalemic periodic paralysis succinyl choline

4)impaired excretion-ARF/CRF K sparing diuretics,ACEI.NSAID Reduced tubular excretion5)Factitious hyperkalemia: hemolysis during blood drawing thrombocytosis,marked leukocytosis

ECG changes

Clinical features• Vague muscular weakness• Severe –hypo reflexia,paresthesia,ascending paralysis• Paralysis usually spares the muscles supplied by cranial

nerves and patient remains alert and apprehensive until cardiac arrest.

management• Primary goal: a) stablize myocardium b) shift k into cell c) increase k excretion

Stabilize myocardium IV Calcium Gluconate (10 %) 0.5 mL/kg IV over 5-10

min,monitor for bradycardia.May repeat.Has transient effect.

Indicated in all cases of severe hyperkalemia (ie, >7 mEq/L), especially when accompanied by ECG changes

Shift K into cell Regular insulin and glucose IV 2ml/kg 50% dextrose (1g/kg) and 0.1units/kg of regular

Insulin over 5-10 minutes (mixed in same syringe) ,can be repeated after 30 min.

Rapid action, Monitor sugar post insulin

Beta-adrenergic agents, such as salbutamol neb. 2.5-5 mg or Epinephrine (0.05 µg/kg per minute by intravenous infusion)

Increase K excretion Loop or thiazide diuretics work well if kidneys are

functioning normally.

Kayexalate(Cation Exchange Resin): exchanges Na for k.

Dose: 1gm/kg/dose every 6 to 8 hrly PO/PR.

• hemodialysis

calcium• normal, range is • Total calcium-8.8-10.8 mg/dl(2.2-2.7mmol/L)• Ionized calcium 4.2-5.5mg/dl(1-1.4mmol/L)• 45% in ionised form,45% bound to proteins,10% with

anions• Total calcium falls by 0.8 mg/dl per 1g/dl fall of albumin• Corrected cal = sr ca +0.8(4-sr albumin)

hypocalcemia• Calcium <8mg/dl,ionised <4.2mg/dl• Causes A)Chelation/depletion-transfusions,alkalosis,hyperphosphataemia,sepsis,rhabdomyolysis,hypocalcaemia B)Parathyroid hormone def 1)increased PTH-vit D def,CKD,pseudohypoPTH 2)decreased PTH-digeorge syndrome,autoimmune polyendocrinopathy,wilsons,hemosiderosis C)CaSR mutation-autosomal dominant hypocalcemia

D)tissue consumption of calcium acute pancreatitis osteoblastic bone metastasis hungry bone syd(post parathyroidectomy) hyperphosphatemia

Clinical features…. ACUTE-• Parasthesia of lips,extremities,tetany,seizures• Laryngeal stridor,• ECG-prolonged QT interval,peaked T

waves,arhythmias,heart blocks, CHRONIC• Subcapsular cataract,basal ganglia calcification,EPS,• Enamel hypoplasia• Features of rickets• Round facies,short neck with short metacarpals

Latent signs• Chvostek sign:tap the lateral cheek with

forefinger,0.5cm below zygomatic process and 2cm anterior to tragus.

positive sign-twitching of corner of mouth due to contraction of circumoral muscles• Trousseau sign:BP cuff is inflated above systolic

pressure for 3mins positive signs-flexion of wrist and MCP joints,extension of IP joints and adduction of fingers.

management• Asymptomatic Treated with oral 50mg/kg/day 3 -4 divided doses

• Symptomatic 0.5ml/kg 10% ca gluconate given over 10-15min under cardiac monitoring In equal dilution f/b 100-150mg/kg/24hrs(0.25-1mg/day with active vitamin d

hypercalcemia

• Total calcium >10.5

• Symptomatic >12-15mg/dl

causes1)Increased PTH parathyroid adenoma,CKD,2)Excessive vit D effect hypervitaminosis D,sarcoidosis,tuberculosis william syndrome hypophosphatasia3)Increased bone resorption malignancy,vit A overdose,prolonged immobilisation4)others-thiazide diuretics.

c/f• Cns depression,fatigue,seizures,coma• Cardiac arrhythmias,ventricular ectopy,myocardial

depression• GI-constipation,nausea,vomiting,peptic

ulcers,pancreatitis• Renal concentrating defects

Treatment:• Rehydration with saline to promote calcium excretion-3-

5ml/kg/hr• Cease intake of calcium• Diuretics frusemide• Haemodialysis in cardiac,renal failure• Other options-pamidronate,calcitonin,mithromycin.

hypomagnesemia• Normal Mg=1.7-2.2 mg/dl• Serum Mg <1.7mg/dl• Causes• GI losses• Renal losses• Pancreatitis,insulin• Hypokalemia/hypocalcaemia

c/f• Tetany,tremors,fasciculations,ataxia,nystagmus,seizures• Refractory hypocalcaemia• ECG-Shortened QT interval,ventricular dysrhythmias

such as ventricular tachycardia• Torsade pointes

treatment• Asymptomatic- oral supplementation of Mg(Mg gluconate/oxide) 100-200mg/kg/dose q 4-6hr• 0.2ml/kg of 50% MgSo4 may be given IM• Parenteral necessary symptomatic cases MgSO4 25-50kg/dose IM

hypermagnesemia• >2.2mg/dl• Causes• Renal• IatrogenicSymptoms• Muscle weakness,hypotonia,hyporeflexia• Cns depression,lethargy

• IV calcium gluconate 100mg/kg• hemodialysis

• Thank you