Hypokalemia and hyperkalemia indore pedicon 2014 final

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Dr Rajesh Kulkarni B.J.Medical College,Pune MD,MRCPCH(UK) WHEN EVERYTHING IS NOT O.

description

POTASSIUM DISTURBANCES,HYPOKALEMIA,HYPERKALEMIA,CHILDREN

Transcript of Hypokalemia and hyperkalemia indore pedicon 2014 final

Page 1: Hypokalemia and hyperkalemia indore pedicon 2014 final

Dr Rajesh KulkarniB.J.Medical College,PuneMD,MRCPCH(UK)

WHEN EVERYTHING IS NOT O.

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CASE 1

Rahul a 2 year old boy with moderate VSD on Tab Furosemide 3 mg/kg/day since last 18 months.He had 8 episodes of diarrhea since today morning and was brought to the ED.

On examination,the pediatric resident noted “some”dehydration.He also noted abdominal distension with sluggish bowel sounds.

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CASE 1 CONTD..

Rahul was started on plan “B” management of dehydration.(ORS 75 ml/kg over 4 hours)

An ECG was done(for heart disease) and routine tests including electrolytes were ordered.

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CASE 1—CONTD..

ECG:

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CASE 1 CONTD..

LAB: Na 131 mEq/L, K 2 mEq/L

RISK FACTORS FOR HYPOKALEMIA

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CASE SCENARIO 2

Vinita is a 7 year old girl, known c/o type 1 diabetes on insulin. She is admitted to the PICU with Severe DKA and given IV fluids and insulin as per hospital protocol.

Her initial investigations show K of 4.4 mEq/L and the on duty resident feels she might get hyperkalemia if he adds more potassium to the fluids

After 4 hours she c/o severe weakness and inability to move her limbs. Her DTR are absent.

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POTASSIUM

Most abundant cation in human body ,Normal serum value 3.5 to 5.5 mEq/L.

Regulates intracellular enzyme function and helps to determine neuromuscular & cardiovascular tissue excitability.

90 % of total body K+ : Intracellular ( predominantly in

muscle ) 10 % : Extracellular fluid

< 1 % : Plasma

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HOW INTRACELLULAR K+ CONTENT IS MAINTAINED

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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

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CLINICAL FEATURES

Muscle weakness and flaccid paralysis Depressed or absent deep-tendon reflexes.

Hypoactive bowel sounds or ileus,constipation

Severe hypokalemia : Bradycardia with cardiovascular collapse, cardiac arrhythmias and acute respiratory failure from muscle paralysis

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SIC WALT

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FACTORS THAT DECREASE K+LEVELS

Aldosterone (Increases sodium resorption, and increases K+ excretion)

Insulin (Stimulates K+ entry into cells by increasing sodium efflux)

Beta-adrenergic agents(Increases skeletal muscle uptake of K+ )

Alkalosis (Enhances cellular K+ uptake)

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Due to

Decreased net intake :Uncommon

Shift into cells

Increased net loss

Cause is usually apparent on HISTORY and physical examination.

DIAGNOSIS – ETIOLOGY

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HISTORY

Increased excretion : Medications (eg, diuretics,  antibiotics ) Polyuria Vomiting or diarrhea Shift of potassium into the intracellular space Recurrent episodes of paralysis Use of high doses of insulin High-dose beta-agonist therapy (e.g, for

Asthma)

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WHAT IF CAUSE IS NOT APPARENT?? Urinary K excretion(spot test)

ABG

TTKG=(Urine K+/Plasma K+) / (Urine Osm/Plasma Osm)

Hypokalemia with extra renal losses,TTKG is <2 (kidney conserves K+)

Hypokalemia with high TTKG suggests renal loss (Not accurate if urine dilute or urine sodium <25 mmol/L)

(Manual of Pediatric Emergencies and Critical Care 2nd ed)

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FIRST LINE INVESTIGATIONS

Serum Electrolytes, Urinary Potassium ECG Initially : flattening of t wave depression of ST Segment development of prominent

u waves Severe hypokalemia : increased amplitude of

p wave increased QRS

duration

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SECOND LINE TESTS

Biochemical tests

Serum renin, aldosterone, and cortisol

24-hour urine aldosterone, cortisol, sodium, and potassium

Serum anion gap

Drug screen in urine and/or serum Hormones

Thyroid Function Tests Radiology

Pituitary imaging to evaluate for Cushing syndrome

Adrenal imaging to evaluate for adenoma

Evaluation for renal artery stenosis

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MANAGEMENT

Reduction of potassium losses

Replenishment of potassium stores

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REDUCTION OF POTASSIUM LOSSES

Discontinue diuretics/laxatives

Use potassium-sparing diuretics like spironolactone or amiloride if diuretic therapy is required (e.g, severe heart failure)

Treat diarrhea or vomiting

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REPLENISHMENT OF POTASSIUM STORES

Patients who have mild or moderate hypokalemia ( 2.5-3.5 mEq/L) ;asymptomatic patients:

ORAL THERAPY PREFERRED

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

Dose : 0.5-2 mEq/kg PO q12hr (How to give?)

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MANAGEMENT

• In Severe Hypokalemia(Potassium <2) or symptomatic patients IV Correction required,

add: 30 meq / L of IV fluid 40 meq / L of IV fluid 50 meq / L of IV fluid 60 meq / L of IV fluid 70 meq / L of IV fluid ECG monitoring Frequent testing I.V.KCL K+ is 2 mEq/ml

(RECHECK!!!)

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CAUTION!!!

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

BOLUS OF KCL I.V. SHOULD NOT BE GIVEN

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REVISION—WHICH PATIENTS CAN HAVE HYPOKALEMIA

Neuromuscular weakness (AFP) esp.if recurrent, unable to wean off ventilator.

Unexplained abdominal distension,constipation

Children with Asthma , Heart disease and children on medications that cause polyuria or loss of K in urine

Children who have rhythm abnormalities( Bradycardia,hypotension,low volume pulse)

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HYPOKALEMIA---TAKE HOME MESSAGE

Anticipate Hypokalemia in children with diarrhea,children on diuretics,during treatment of DKA.

Uncommon causes like Bartter syndrome,RTA should be considered –look for clues in history,examination and investigations.

Oral route is safe and effective,IV only if K is less than 2.5 or symptoms present.

DOUBLE CHECK IV Potassium prescriptions

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HYPERKALEMIA

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CASE

A 2 Year old boy was brought to hospital with h/o loose motions and vomiting since 3 days.

He has not passed urine since 24 hours.

BUN 160 mg/dl ,Creatinine 5.4 mg/dl

Na 123 mEq/L ,K 7.5 mEq/L

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HYPERKALEMIA

K+ above 5.5 mEq/L, Premature infants /young children upto 6.5

mEq/L normal.

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FACTORS INCREASING K+

Alpha-adrenergic agents(Impairs cellular K+ uptake)

Acidosis (Impairs cellular K+ uptake)

Cell damage (Intracellular K+ release)

Hypoaldosteronism

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CLINICAL MANIFESTATIONS

Patient may be ASYMPTOMATIC or may have NONSPECIFIC symptoms or may present with arrythmia/ CARDIAC ARREST

Respiratory failure and weakness that progresses to paralysis.

Nausea, vomiting, and paresthesias (eg, tingling).

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IS THIS LAB REPORT CORRECT?

Fictitious Hyperkalemia : hemolysis, "milking" of extremities , thrombocytosis or leucocytosis.

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TRUE HYPERKALEMIA

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DECREASED EXCRETION

Most common cause is Oliguric renal failure.

Other causes include Primary adrenal disease (e g, Addison

disease, salt-wasting forms of congenital adrenal hyperplasia),

Hyporeninemic hypoaldosteronism, Renal tubular disease

(pseudohypoaldosteronism I[or II), or Medications (e g, ACE inhibitors,

angiotensin II blockers, spironolactone or other potassium-sparing diuretics).

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INCREASED K+ INTAKE

Intravenous or oral potassium supplementation.

Packed RBCs (PRBCs)transfusion

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TRANSCELLULAR SHIFTS

Acidosis most common cause

Process that leads to cellular injury or death (eg, Tumor lysis syndrome, massive hemolysis) can cause hyperkalemia

Other causes include propofol ("propofol infusion syndrome"),toxins (digitalis intoxication), succinylcholine, beta-adrenergic blockade, strenuous or prolonged exercise, insulin deficiency, malignant hyperthermia, and hyperkalemic periodic paralysis.

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INVESTIGATIONS

FIRST LINE: Serum electrolyte tests. Serum BUN and creatinine tests Urinalysis (UA),ECG,TTKG<6 s/o renal

causeSELECTED CASES ABG,Serum Uric Acid, CPK and calcium

measurements),CBC,Urine electrolytes Urine myoglobin test ,Specific drug

level tests for suspected toxicity

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ECG CHANGES

Tall Peaked T waves (K 6.5)

Prolonged PR, Flat or absent P waves(K 7.5)

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ECG CHANGES

Widened QRS (>0.12 Sec) ,

Sine wave pattern(S and T waves merging) (K 8.5)

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ECG CHANGES

Bradycardia, Ventricular Tachycardia (K 9.0)

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MANAGEMENT

Immediately discontinue any IV potassium containing fluid/any drugs that may cause hyperkalemia.

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STABILIZE MYOCARDIUM

IV Calcium Gluconate (10 %) 0.5 mL/kg IV over 2-4 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

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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)

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SHIFT K INTO CELLS CONTD…

Sodium bicarbonate(7.5%) IV 2 cc / kg slowly ,?Efficacy, repetition not

recommended.

A Cochrane review suggests that Dextrose/Insulin and salbutamol are the first line therapies most supported by evidence, and that a combination of

the two therapies may be more effective than either alone.

(Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev 2005;(2):CD003235.)

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INCREASE K EXCRETION

Loop or thiazide diuretics work well if kidneys are functioning normally.

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

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

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INCREASE K EXCRETION CONTD..

Hemodialysis Definitive method ,used in cases of severe

hyperkalaemia or when other treatments have

failed. K can be lowered by 1-1.5mmol/l for every

hour of dialysis

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C BIG K DROP C : Calcium Gluconate

B: Bicarbonate

I,G : Insulin and Glucose

K: Kayexelate

D: Diuretics and Dialysis

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REVISION—AT RISK CHILDREN FOR HYPERKALEMIA

Children with low or absent urine output ,hypertension ( ARF)

Children on drugs (K sparing diuretics,ACE inhibitors)

Children who have rhythm disturbances –always check K+

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HYPERKALEMIA-TAKE HOME MESSAGE

Acute Renal Failure is most common cause of hyperkalemia.

Uncommon causes like adrenal insufficiency, aldosterone deficiency should be kept in mind.

Always take hyperkalemia seriously (potentially fatal).

Calcium gluconate ,Glucose insulin therapy and salbutamol neb can be lifesaving in hyperkalemia.

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REFERENCES Clinical manifestations and treatment of

hypokalemia .David Mount.Avaialble from http://www.uptodate.com/contents/clinical-manifestations-and-treatment-of-hypokalemia.

Pediatric Hypokalemia Treatment and Management . Michael J Verive.Available from http://emedicine.medscape.com/article/907757-treatment.

Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev 2005;(2):CD003235.

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CASE HISTORY

A six month old boy was admitted to our hospital with cough and fever for 4 days, repeated vomiting and severe dehydration. Within the past three months he had suffered three similar episodes warranting hospitalization and IV fluids, but was normal between episodes and prior to onset.

Antenatal,perinatal and postnatal period was uneventful with normal development

On admission, he was in hypovolemic shock with tachycardia

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CASE CONTD..

After vigorous fluid resuscitation he was haemodynamically stabilized. Abdomen, genitalia and nervous system appeared normal.

His CBC, blood urea, and creatinine were normal but despite serum sodium being normal (135meq/l), potassium (2.5meq/l) and chloride (92meq/l) were low.

His arterial blood gas revealed metabolic alkalosis with a pH of 7.56

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CASE CONTD..

His urine electrolytes revealed increased excretion of sodium, potassium and chloride. TTKG>4

His subsequent ultrasound scan of abdomen was normal.

Serum renin was markedly elevated

(11.99ng/ml/hr) [normal range 0.15-2.33].

DIAGNOSIS

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THANK YOU

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ALTERNATIVE APPROACH TO HYPOKALEMIA

Investigations Required

Urine Potassium

ABG

Urine chloride

Renin/Aldosterone

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