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Welcome to Seminar
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A 5 years old child admitted with loose motion for 2 days and abdominal distension for 6 hours. The Child was severely dehydrated, floppy, lethargic. How to Diagnose and manage the child?
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Common Problem ???
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Management of Dyselectrolytemia at our situation.
Presented by Dr. Abdullah Al Mamun Dr. Azizur Rahman Dr. Shahana ferdous
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Sodium Dominant cation of ECF.
Principal determinant of extracellular osmolality. >40% total body Na+ is in Bone. Remainders in interstitial & intravascular space. Daily requirement 2-3 mEq/Kg Normal serum value mEq/L.
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Function: Principal determinant of extracellular osmolality.
Maintain neuromuscular conductivity. Maintain cardiac rhythmicity & contractility. Forms Alkali reserve of the body.
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Absorption Throughout the gut mostly by diffusion. Mineralocorticoid increase absorption. Glucose enhance by Na-Glucose co-transport.
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Excretion Multifactorial & is the determinant of Na balance.
Excreted through Kidney, stool & sweat. Regulated by effective plasma volume which determines the Na+ in Urine. 99% filtered Na reabsorbed in kidney. Increase sweat Na+ in cystic fibrosis, aldosterone defc., pseudo aldosteronism.
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Hyponatremia Very common electrolyte abnormality in Hospitalized patient. Serum Na+ conc. <135 mEq/L Ratio of H2O to Na increases.
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Causes Pseudohyponatremia Hyperosmolality Hyperglycemia Mannitol
Water moves from ICF to ECF
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Hypovolemic Hypohyponatremia
Extrarenal losses: GIT Skin
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2. Renal losses: Loop diuretics Osmotic diuresis
Postobstructive diuresis Polyuric phase of ATN AR PCKD Tubulointerstitial nephritis Obstructive uropathy Cerebral salt wasting RTA ( Type 2 ) Lack of Aldosterone
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3. Euvolemic Hyponatremia
SIADH Desmopressin Acetate Glucocorticoid defc. Hypothyroidism. Water intoxication
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4. Hypervolemic Hyponatremia:
CCF Cirrhosis NS RF Sepsis Hypoalbuminemia due to GIT disease.
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Clinical Manifestations
Chronic hyponatremia even with Na+ 110 mEq/L may be asymptomatic. Acute hyponatremia in serum conc. From 140 to 125 mEq/L may cause seizure. Muscle cramp & weakness. More manifestation of dehydration.
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Clinical Manifestations (con…)
Symptoms occur due to brain cell swelling Anorexia, vomiting, nausea, diminish reflexes agitation, lethargy, confusion headache seizure coma. Acute severe hyponatremia may cause brainstem herniation & Apnea.
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Diagnosis History & physical examination Investigations:
Find out causes Degree of dehydration. Investigations: Serum Electrolytes Osmolality Urinary Na+ Non Renal <10 mEq/L Renal >20 mEq/L
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Correction of Hyponatremia
Treatment depends on : - Etiology and types of hyponatremia. - Clinical condition. - Serum Na+ level. - Ongoing loss.
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Level of Hyponatremia Usually correction not needed at 135-140 mmol/L
Mild : < mmol/L Moderate : < mmol/L Severe : < 115 mmol/L ( Ref: Harrison)
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Formula of correction mmol Na+ needed to correct the deficit = 0.6 X Wt X [ Des-Mes] ( Ref: Nelson )
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Flow Chart of management of hyponatremia
Hypovolumia Yes No Shock No Shock Correction of the cause then correction of Na+. Follow Steps of Protocol 3 Follow steps of protocol 1 Follow steps of protocol 2 ( Ref: Nelson )
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Steps of Protocol 1: Correction of Hypovolumic hyponatremia.
Step 1: If associated with Shock Replace intravascular volume with NS 20ml/Kg over 20 min. May Repeat if needed. Step 2: Rapid volume repletion with NS 20ml/Kg over 2 hr. Step 3: Calculate 24 hr fluid needs: Maintenance + Deficit
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cont... Step 4: Subtract Isotonic fluid already administered from 24 hr fluid need. Step 5: Administer remaining fluid over 24 hr using D1/2 NS + 20 meq/L KCl Step 6 : Replace ongoing loss as they occur. ( Ref: Nelson )
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Protocol 2: for correction of Hyponatremia.
Step 1: Calculate the deficit using formula. Step 2: Assess the level of deficit ( Mild/Moderate/Severe) Step 3 : Calculate the maintenance and ongoing loss. Step 4 : Choose the Drug Step 5 : Choose the route Step 6 : Check for co-morbidity and conditions. ( Ref: Nelson )
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Steps of Protocol 3: Isovolumic Hyponatremia: - Water restriction.
- Diuretics - May need to follow Protocol 2. - Treatment of the specific cause. - Conivaptan (newer drug, V 2 receptor antagonist in renal tubule) may be used in SIADH. ( Ref: Nelson )
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Cont... Hypervolumic Hyponatremia. - Water and Na+ restriction.
- Diuretics may help. - Treatment of the cause. ( Ref: Nelson )
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Correction Of going loss
Steps: - Calculate the volume loss of stool or emesis matter. - Volume X Na+ content of the fluid lost. - Add this amount with the deficit value and maintenance value. Total = Deficit + Maintenance + On going loss.
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Mild Hyponatremia Usually asymptomatic.
Oral correction with Table salt or ORS solution should be used. - 1 tsf table salt = 5 gm = 85 mmol - 1 gm = 17 mmol - 1 tsf ORS solution = 0.3 mmol - Give correction over 24 hours.
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Example: A 6 year old boy weighing 20 kg , S. Na+ is 128 mmol/L
Example: A 6 year old boy weighing 20 kg , S. Na+ is 128 mmol/L. How to correct? Deficit = 0.6 X 20 X [ ] = 14.4 mmol. Maintenance = 3 X 20 = 60 mmol Total = 74.4 mmol + Ongoing loss if present. So, 248 tsf = 1240 ml ORS Solution should be given over 24 hrs + Ongoing loss.
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Moderate Hyponatremia
Usually symptomatic Correction not more than 0.5mmol/L/hr = 12 mmol/L/24 hr So calculate the total duration. Use Na+ containing fluid with 20 meq/L KCl. Usually < 10 kg child should get D1/4 NS and > 10 Kg child should get D ½ NS. ( Ref: Nelson )
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Example: A 5 year old boy weighing 16 kg ,S. Na+ is 116 mmol/L
Example: A 5 year old boy weighing 16 kg ,S. Na+ is 116 mmol/L. How to correct? Correction time 48 hrs. Deficit = 0.6 X 16 X [ ] = mmol Maintenance = 3 X 16 = 48 mmol/ 24 hrs Total = mmol IV fluid maintenance = 1300ml/24hrs = 2600ml/48hrs. So, 5% DNS 1000ml = 133 mmol 5% D1/2 NS 1000ml = 77 mmol 5% DA ml = 0 mmol with 1 amp KCl/L Fluid 55 μdrops/min over 48 hrs will correct the condition.
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Severe Hyponatremia Usually neurological signs present.
Slow correction is the choice in chronic cases. Acute hyponatremia can be corrected rapidly. Rapid correction may cause Central Pontine Myelinolysis ( CPM ) So, calculate the total duration of correction. Acute neurological signs such as seizure can be corrected by using IV 3% NaCl 4 ml/Kg over 4 hrs. ( Ref: Nelson )
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CPM Hypernatremia causes generation of Idiogenic Osmole production in neuron. So when hypotonic fluid is present in ECF cerebral edema and myelin breakdown occurs which is called Central Pontine Myelinolysis. It is a grave condition and mortality is high. C/F: - Confusion - Agitation. - Flaccid or spastic quadriplegia and death. Treatment : Rapid IV 3% NaCl 4 ml/Kg over 4 hrs.
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Example: A 5 year old boy with convulsion weighing 16 kg , S
Example: A 5 year old boy with convulsion weighing 16 kg , S. Na+ is 108 mmol/L. How to correct? Duration : = 27/10 = 2.7 days. Acute correction: 4ml/Kg IV 3% NaCl over 4 hrs = 64 ml . It corrects = 4 mmol Usually 1ml/Kg 3%NaCl corrects serum Na+ 1 mmol/L Daily correction 10 mmol/L Rest 6 mmol correction needed = 0.6X16X6 = 57.6 mmol Na+ Daily maintenance = 3X16=48 mmol
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Cont… Total = 105.6 mmol 1 ml 3% NaCl= 0.514 mmol
So 3% NaCl needed=205.4 ml So 1st Day = Inf 3% NaCl 16 μdrops/min for 4 hours then 10 μdrops/min over next 20 hours. Then 11 μdrops/min continue for next 36 hrs. Correction may be done with NS or ORS solution from 2nd day.
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Hypernatremia Serum Na+ conc. > 145 mEq/L (>150 mEq/L).
Mild hypernatremia fairly common in children. Hypernatremia in hospitalized pt. may be iatrogenic.
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Causes of Hypernatremia
1. Excessive Sodium: Improperly mixed formula Excess NaHCO3 Ingestion of sea water IV hypertonic Saline Hyperaldosteronism
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Causes of Hypernatremia (con….)
2. Water deficit Diabetes Insipidus Increased insensible loss Inadequate intake 3. Water & sodium deficit GIT loss Diarrhea Emesis/NG suction Lactulose
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Causes of Hypernatremia (con….)
Cutaneous losses Burn Excess sweating. Renal losses Osmotic Diuretics DM Chr. Kidney disease Polyuric phase of ATN Post obstructive Diuresis.
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Clinical Manifestations
Dehydration is common Pts are irritable, thirsty, weak & lethargic. High pitched cry, fever. Skin is doughy. Seizure & coma due to brain Hmrg. Thrombotic complications.
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Diagnosis History. Physical Examination. Investigations
S. Electrolytes Blood & Urine Osmolality H2O Deprivation test Urinary Na+
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Correction of Hypernatremia
Acute hypernatremia can be corrected rapidly Chronic hypernatremia should be corrected slowly. Not lowering serum Na+ level > 12 mmol/L/24 hrs that is not >0.5mmol/L/hr. (Ref: Nelson)
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Principles of correction
Rehydrate slowly ( Over hrs) Oral Rehydration is preferable to IV Serum Na+ should not drop by more than mmol/L/24 hrs Treat other co-morbidities Continue breast feeding if age < 2 yrs. (Ref: icddr’b)
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Some Notes If severe dehydration : NS 20 ml/Kg over 20 mins should be given. May be repeated. Do not use hypotonic fluid to correct hyponatremic dehydration. Time Frame for correction of dehydration: meq/L hrs meq/L hrs meq/L hrs meq/L hrs Typical fluid for correction is D1/2 NS or D ¼ NS with 20 meq KCl /L. Typical rate times of maintenance.
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Cont... 2 IV line with D1/2 NS in one channel and D1/4 NS in another channel helps better adjustment. Close F/U of Serum Na+ value. - If Na+ is decreasing slowly: Conc. of Na+ or rate of IV fluid. - If Na+ is decreasing rapidly: Conc. of Na+ or rate of IV fluid. ORS solution over hrs can be used to correct hyponatremic dehydration. (Ref: Nelson)
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Diagnostic Criteria of SIADH
1. Absence of Renal, adrenal, thyroid insufficiency. CCF, NS, Cirrhosis. Dehydration. Diuretic ingestion. 2. Urine Osmolality > 100 ( > Plasma ) 3. Serum osmolality <280 4. Serum Na+ < 135 5. Urine Na+ > 25
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Potassium The principal Intra Cellular Cation
About 30 times higher in ICF Majority in Muscle <1% in Plasma Plasma conc. Does not reflex total body K+ content Normal value in serum mEq/L Daily requirement 1-2 mEq/Kg/day
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Functions Main intracellular cation
Maintain membrane potential of all irritable cells Influence the activity of cardiac muscles Essential in conducting nerve impulse.
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Absorption About 90% of ingested K+ is absorbed mostly in small intestine Small amount secreted from Colon.
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Excretion Mostly excreted by Kidneys
About 10-15% filtered K+ is excreted 90% reabsorption in PT In DCT & CT secretion in exchange of Na+ (Aldosterone mediated)
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Hyperkalemia Serum K+ >5.5 mEq/L.
Most alarming electrolytes abnormality. Potential for lethal arrythmia.
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Causes of Hyperkalemia
Spurious lab value: Haemolysis Tissue ischaemia Thrombocytosis Leukocytosis Increased intake: Oral/IV BT
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Causes of Hyperkalemia (con…)
Transcellular shift Acidosis Rhabdomyolosis Tumour lysis syndrome Haemolysis/GI bleeding Exercise Insulin defc. β-adrenergic blocker Hyperkalemic periodic paralysis
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Causes of Hyperkalemia (con…)
Decreased excretion: Renal failure Primary Adrenal disease RTA Medications ACE inhibitors K+ sparing diuretics
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Clinical Manifestations
Cardiac arrythmia may occur without other symptoms. Skeletal muscle-weakness, tingling, paraesthesia,fasciculation, paralysis.
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Diagnosis History & physical exam. Investigations:
S. Electrolytes ECG Blood gas analysis TTKG (normal 5-15) <8 indicates defect in renal excretion. transtubular potassium gradient (TTKG)
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ECG Change Serum K+ ECG Change 6-7.5 mEq/L Tall peak T wave 8.0 mEq/L
Prolonged PR Wide QRS 9.0 mEq/L ST depression Further widening QRS 10.0 mEq/L Bradycardia Sine wave Ventricular arrythmia Asystole
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Hypokalemia Serum K+ <3.5 mEq/L
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Causes of Hypokalemia Spurious: Trascellular shift: Decreased uptake:
High WBC count (if stored in room temp.) Trascellular shift: Alkalemia Insulin β-adrenergic agonist Hypokalemic periodic paralysis. Decreased uptake: PEM
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Causes of Hypokalemia (con…)
Renal loss RTA (Type 1 & 2) DKA with metabolic alkalosis Emesis/NG suction Chloride loosing diarrhoea Cystic fibrosis Loop & Thiazide diuretics Adrenal adenoma/hyperplasia Cushing syndrome Glucocorticoid Renovascular disease
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Clinical Manifestations
Heart & skeletal muscle most vulnerable Heart-Ectopic beats, atrial & ventricular tachycardia/Arrest. SK. Muscle-Weakness, cramp, paralysis, resp. paralysis. Smooth muscle-paralytic ileus, urinary retention Kidney (if chronic)- Polyuria Polydipsia Decrease conc. Ability Stimulates renal NH3 production may worsen hepatic encephalopathy.
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Diagnosis History & physical exam. Investigations: S. Electrolytes
Blood pH Acidosis (RTA, Diarrhoea) Alkalosis (Emesis, Diuretics, Aldosterone)
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Diagnosis (con…) ECG Changes occur usually if < 2.5 mEq/L.
Flattened T wave ST depression Appearance of U wave Ventricular fibrillation.
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Principles of management
Treatment of the cause Correction of deficit/Excess Ensure maintenance Correction of ongoing loss/Excess (Ref: Nelson)
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Principles of Assessment of the patient
How severe the clinical condition is? Level of consciousness. Oral intake possible or not? Is he getting any fluid? Associated morbidity. Current Serum electrolyte level. How severe is the deficit/Excess? (Ref: Nelson)
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Correction of HypoKalemia
Treatment depends on: - Serum K+ level - Clinical symptoms - Renal function - Ongoing loss - Ability to tolerate oral potassium (Ref: Nelson)
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Formula for correction of K+
Required K+ mmol = 0.3 X Wt X [ Des-Mes] Des = Desired level Mes = Measured level
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Protocol of correction
Mild Hypokalemia = ( k mmol/L) Moderate Hypokalemia = (K mmol/L) Severe Hypokalemia = ( k+ <2 mmol/L) (Ref: Nelson)
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Cont... Oral correction: - Asymptomatic patient - Can take orally
- Mild or Moderate Hypokalemia (Ref: Harrison)
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Cont... Indication of IV correction: - Symptomatic patient
- Can not take orally - Severe Hypokalemia (Ref: Harrison)
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Steps of Correction Step: 1 = Calculate the deficit
Step: 2 = Calculate the maintenance Step : 3= Choose the route of administration of drug Step : 4 = Choose the Drug Step : 5 = Choose the Fluid if needed. Step: 6 = Consider other morbidity.
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Example: A 3 year old unconscious child weighing 10 kg have severe dehydration and Serum K+ is 2.1mmol/L. How to correct? Step 1 : Deficit= 0.3X10X[4-2.1]=5.7mmol Step 2: Maintenance= 2X10=20 mmol/L K+ and 1000 ml fluid Step 3: Route= IV Step 4: Drug= KCl IV Solution Step 5: Fluid getting=Cholera saline ( 13 mmol/L ) Step 6: Correction of severe dehydration over 3 hours (1000 ml fluid needed).
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Cont... Total KCl needed = 25.7 mmol Cholera saline gives = 13 mmol
Rest = = mmol 1 ml KCl = 2 mmol, so 6.35 ml KCl is needed. Total Fluid = = 2000ml
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Cont... Correction of severe dehydration corrects almost 50% of K+ & water deficit in this patient over 3 hours. So, 6.35 ml KCl in 1000ml D1/4NS after correction of Severe dehydration is the choice. That is, Inj KCl 6.35 ml in Infusion D1/4NS μdrops/min over 21 hours. 1st hour correction = 5.72 mmol (0.5 mmol/Kg)
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Easy Process (Ref:icddr’b)
Serum K + Level KCl needed Serum K + >3 mmol/L Inj KCl 1 ml in each 100 ml fluid Serum K+ >2-3mmol/L Inj KCl 1.5 ml in each 100 ml Fluid. Serum K+ <2 mmol/L Inj KCl 2 ml in each 100 ml Fluid.
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Some important notes: 1 mmol/L change of serum K+ indicates change of mmol of Total body K+.(Ref:Harrison) Total Body K+ = 55mmol/Kg ( Ref:Journal ) So, Oral correction should be continued for 5-7 days after acute phase management.(Ref:CPDT) Rate of correction: 0.5 mmol/Kg for 1st hour then 0.25 mmol/Kg/hr for next hours.(Ref: CPDT) Not > 40 mmol/L of fluid in IV and > 60 mmol/L in CV line. (Ref: Nelson) IV correction should be avoided unless strictly needed. Hypokalemia + Metabolic Acidosis = Correction by KHCO3/ K+acetate/K+citrate
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Cont... Hypokalemia + Metabolic Alkalosis = Correction by KCl
Hypokalemia+Metabolic Alkalosis / Hypovolumia usually responds to volume correction. (Ref: Harrison) IV KCl should be given only after being ensured that urine output is normal. Lack of response to KCl therapy suggest associated Hypomagnesemia and should measure S. Mg level and correct by Inj 50% MgSO4 0.1ml/Kg IM daily for 3-7 days. (Ref: R N Srivastava.)
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Cont… K+ rich food: Banana, Citrus fruit, milk, chocolate.
< 3.5 mmol/L serum K+ is usually symptomatic and < 2 mmol/L causes Paralytic Ileus. Inj KCl should be given in Glucose-free fluid as glucose causes rapid entry of K+ and therefore delays serum K+ correction. (Ref: Harrison) If glucose free fluid have to give over long time , IV bolus doses of 5 ml/Kg 10% DA should be given intermittently to maintain blood glucose level. ECG monitoring and hourly (Daily at our situation) electrolyte measurement is needed. K+ rich food: Banana, Citrus fruit, milk, chocolate.
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About KCl Oral Syrup 5 ml = 6.7 mmol Inj 1 ml = 2 mmol, 1 amp = 10ml
Trade name : KT, Electro K Adverse effect of Oral KCl: - GIT irritation - Esophageal and small intestinal erosion and stricture.
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Correction of Hyperkalemia
Hyperkalemia is more dangerous than Hypokalemia Hyperkalemia with ECG changes is a medical emergency. (Ref: Harrison)
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Treatment of Hyperkalemia
Treatment depends on - Serum K+ level - Clinical symptoms - Renal function - Other morbidity.
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Principles of management
Mild to Moderate: K+ 6-7 mmol/L - Goal is to enhance excretion of K+ - Place on Cardiac monitor - Eliminate K+ from diet / IV fluid. (Ref: Harrison)
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Cont… Severe : K+ >7 mmol/L - Goal is to protect the heart.
- Decrease serum K+ level at once. - Elimination of K+ from body. - Consider Dialysis if S. K+ > 8 mmol/L. (Ref: Harrison)
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Drug treatment of Hyperkalemia (Ref: R N Srivastava)
SL Drug Dose Onset of action Duration Mechanism of action 1 10% Cal-gluconate 0.5 ml/Kg IV slowly 1-3 min 30 min Cardio protective. Threshold for depolarization of cardiac muscle 2 NaHCO3 1-2 meq/Kg IV 10-30 min 2 hour Cellular uptake of K+ 3 Insulin + glucose U/Kg ê gm/Kg glucose IV 20-30 min 2-4 hour Do
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Excretetion of K+ from gut in exchange of Na+
Cont… SL Drug Dose Onset of action Duration Mechanism of action 4 Salbutamol 5-10 mg Nebulization 30 min 4-6 hour Cellular uptake of K+ 5 Kayexalate 1gm/Kg/dose oral/ enema 4 hours 6-8 hour Excretetion of K+ from gut in exchange of Na+ 6 Dialysis
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Some Notes Mild to Moderate Hyperkalemia: - K+ restriction
+ - Kayexalate is sufficient. Severe Hyperkalemia >7.5 mmol/L should be managed by using - Inj 10% Cal-gluconate + - Insulin with glucose (1st Choice) / Salbutamol (2nd Choice)) / Inj NaHCO3 (3rd Choice) Kayexalate. (Ref: Harrison)
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Cont… There is no cut off level of starting or stopping the drug.
Drug of choice differ from patient to patient. - Hyperkalemia + Metabolic Acidosis = May use Inj NaHCO3 - Hyperkalemia + Hyperglycemia = May Use Inj Insulin. NB: 1 ml Inj SODIBICARB ~ 1 meq NaHCO3. (Ref: Harrison)
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Cont… How to use Kayexalate :
-- 1 gm/Kg mixed with 100ml 20% Sorbitol orally – 6 hourly. 1 gm binds 1 mmol of K+ and generally reduces Serum K mmol/L within 1-2 hr. -- Enema: 1 gm/Kg mixed with 50 ml of 70% Sorbitol ml of tape water– per ractally. (Ref: Harrison)
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Calcium Calcium is an important cation in plasma.
99% Body Ca+ is in Bone. The normal range 2.2 to 2.6 mmol/L. Appox. 40% of plasma ca++ is bound to plasma proteins, primarily albumin.
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Functions Controls physiological process – Blood coagulation
Muscular contraction Nerve conduction Cardiac contraction
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Absorption
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Excretion
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Hypocalcemia The ionized Ca concentration is low in true Hypocalcemia.
May give rise to severe symptoms, so needs to be identified & treated expeditiously.
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Causes of Hypocalcemia
Specific causes in Neonates: Early Neonatal Hypocalcemia Late Neonatal Hypocalcemia Maternal Hypercalcemia 2. Hypoparathyroidism 3. Lack of response to PTH 4. Vitamin D deficiency.
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Causes of Hypocalcemia (con…)
5. Redistribution of Plasma Ca+: Hypophosphatemia Rhabdomyolosis Tumor lysis syndrome Blood transfusion Acute pancreatitis Osteopetrosis
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Causes of Hypocalcemia (con…)
6. Inadequate Ca intake 7. Unknown: Septic shock Critical illness
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Clinical Manifestations:
Mostly due to neuromuscular irritability Tetany is the classic manifestation. Symptoms may include carpopedal spasm, laryngospasm, seizure. Patients usually not loss consciousness between seizures. Consequence of long standing hypocalcemia depends on etiology. Chvostek & Trousseau’s signs may be elicited.
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Diagnosis History Physical examination Investigations:
Serum Ca, Phosphorus, alkaline phosphatase, Mg, PTH, BUN & Creatinine. Vitamin D level
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Correction of Hypocalcemia
Inj Cal-gluconate ml/Kg IV slowly over 30mins – 6-8 hourly. Orally : mg daily is equally effective . Tab CaCO mg = 10 mmol Vitamin D3 Supplementation may be needed. Ca++ rich diet such as milk, cheese, meat, fish/animal bones may play additive role. (Ref: Nelson + CPDT)
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Hypercalcemia Frequently discovered incidentally on a routine chemistry profile. Uncommon electrolyte imbalance.
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Causes of Hypercalcemia:
Excess parathyroid hormone Excess Vitamin D Excess Ca intake Excess renal reabsorption Release from bone: Thyrotoxicosis Hypervitaminosis A Malignancy Immobilization
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Clinical Manifestations
GIT Nausea & vomiting Poor feeding Failure to thrive Constipation Abdominal pain Pancreatitis Peptic Ulcer
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Clinical Manifestations (con…)
Cardiac Hypertension Decrease QT interval Arrythmias CNS: Lethargy Hypotonia Psychiatric disorder Coma
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Clinical Manifestations (con…)
Kidney: Polyuria & dehydration Hypernatremia Renal failure Nephrolithiasis
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Diagnosis History Investigations: Electrolytes BUN Creatinine
Phosphorus PTH Urinary Ca, P, Creatinine, Vitamin D level
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Correction of Hypercalcemia
Restrict Ca++ containing foods. Vigorous hydration with NS Force Ca++ diuresis by Frusemide 1 mg/Kg– 6 hourly. If inadequate response Glucocorticoides or Calcitonin may be helpful. (Ref: Nelson + CPDT)
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Magnesium Mg is the 4th most common cation of body 50-60% is in bone
Most intracellular Mg bound to protein Mostly present in muscle & liver.
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Functions Mg is necessary cofactor for hundreds of Enzymes
Important for membrane stabilization & Nerve conduction ATP & GTP need associated Mg when they are used by ATPases, cyclases & kinases.
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Absorption 30-50% dietary Mg absorbed in small intestine.
There is a passive absorption which is poorly understood Absorption diminished in the presence of substances that bind with Mg.
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Excretion Renal excretion is the principal regulator of Mg balance
PTH may increase tubular absorption 5-10% filtered Mg is resorbed in in distal tubule.
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Hypomagnesemia Relatively common in hospitalized pts.
Mg is not measured in most basic metabolic panels.
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Causes of Hypomagnesemia
Gastrointestinal Disorders: Diarrhoea NG suction/Emesis IBD Celiac disease Cystic fibrosis Pancreatitis Protein-calorie malnutrition
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Causes of Hypomagnesemia (con…)
2. Renal disorders: Medications ( amphotericin, cisplatin, cyclosporin, loop diuretics, mannitol, pentamidin, aminoglycosides, thiazide diuretics) Diabetes ATN (recovery phase) Postobstructive nephropathy Hypercalcemia Chronic kidney disease IV fluids Prim. aldosteronism
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Causes of Hypomagnesemia (con…)
3. Other causes: Poor intake Insulin Pancreatitis IUGR Infants of Diabetic mother Exchange transfusion
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Clinical Menifestations:
Most cases are asymptomatic Causes secondary hypocalcemia by impairing PTH release Dominant features due to hypocalcemia
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Diagnosis History Physical exam. Evaluation of urinary Mg losses ECG:
Flattening of T wave Lengthening of ST segment Arrythmias
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Correction of Hypomagnesemia
Encourage Mg++ containing foods such as Apple juice,vegetables, cereals, nuts. Inj 50% MgSO ml/Kg/ in IV drip over 24 hours or IM daily. Lower doses for a child with renal insufficiency. Oral correction for chronic cases by Mg salt tablet may be done. (Ref: Nelson + CPDT)
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Hypermagnesemia Almost always secondary to excessive intake
It is unusual except in neonates born to mother receiving IV Mg May be due to excessive use of laxatives May occur in CRF
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Clinical Manifestations
Asymptomatic until plasma level >4.5 mg/dl Inhibits acetylcholine release , producing Hypotonia Hyporeflexia Weakness Lethargy & sleepiness Hypotension & flushing
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Diagnosis History ECG changes: Prolonged PR, QRS, & QT intervals
Complete Heart block & cardiac arrest.
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Correction of Hypermagnesemia
Restrict Mg++ containing foods. Diuretics-Frusemide. Inj Cal-gluconate 1 ml/Kg may give transient benefit. Dialysis may be needed for severe cases. (Ref: Nelson + CPDT)
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