Approach to the patient with electrolyte disorders Hypokalemia-Hyperkalemia Zehra Eren, M.D.
Hypokalemia and hyperkalemia indore pedicon 2014 final
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Transcript of Hypokalemia and hyperkalemia indore pedicon 2014 final
Dr Rajesh KulkarniB.J.Medical College,PuneMD,MRCPCH(UK)
WHEN EVERYTHING IS NOT O.
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.
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.
CASE 1—CONTD..
ECG:
CASE 1 CONTD..
LAB: Na 131 mEq/L, K 2 mEq/L
RISK FACTORS FOR HYPOKALEMIA
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.
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
HOW INTRACELLULAR K+ CONTENT IS MAINTAINED
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
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
SIC WALT
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)
Due to
Decreased net intake :Uncommon
Shift into cells
Increased net loss
Cause is usually apparent on HISTORY and physical examination.
DIAGNOSIS – ETIOLOGY
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)
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)
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
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
MANAGEMENT
Reduction of potassium losses
Replenishment of potassium stores
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
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?)
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!!!)
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
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)
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
HYPERKALEMIA
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
HYPERKALEMIA
K+ above 5.5 mEq/L, Premature infants /young children upto 6.5
mEq/L normal.
FACTORS INCREASING K+
Alpha-adrenergic agents(Impairs cellular K+ uptake)
Acidosis (Impairs cellular K+ uptake)
Cell damage (Intracellular K+ release)
Hypoaldosteronism
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).
IS THIS LAB REPORT CORRECT?
Fictitious Hyperkalemia : hemolysis, "milking" of extremities , thrombocytosis or leucocytosis.
TRUE HYPERKALEMIA
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).
INCREASED K+ INTAKE
Intravenous or oral potassium supplementation.
Packed RBCs (PRBCs)transfusion
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.
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
ECG CHANGES
Tall Peaked T waves (K 6.5)
Prolonged PR, Flat or absent P waves(K 7.5)
ECG CHANGES
Widened QRS (>0.12 Sec) ,
Sine wave pattern(S and T waves merging) (K 8.5)
ECG CHANGES
Bradycardia, Ventricular Tachycardia (K 9.0)
MANAGEMENT
Immediately discontinue any IV potassium containing fluid/any drugs that may cause hyperkalemia.
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
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)
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.)
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.
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
C BIG K DROP C : Calcium Gluconate
B: Bicarbonate
I,G : Insulin and Glucose
K: Kayexelate
D: Diuretics and Dialysis
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+
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.
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.
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
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
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
THANK YOU
ALTERNATIVE APPROACH TO HYPOKALEMIA
Investigations Required
Urine Potassium
ABG
Urine chloride
Renin/Aldosterone