Electrolyte imbalance anupam
-
Upload
anuupam -
Category
Health & Medicine
-
view
283 -
download
1
Transcript of Electrolyte imbalance anupam
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