2. 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.
3. 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.
6. 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.
7. 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
9. HYPOKALEMIA
Defined
mEq/L
as plasma concentration of K+ < 3.5
Mild
Hypokalemia : 3.0 – 3.5 mEq/L :
asymptomatic
Hypokalemia
2.5 to 3.0 mEq/L : Moderate, may
be symptomatic
Hypokalemia
symptomatic
< 2.5 mEq/L : Severe, may be
10. 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
12. 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)
13. DIAGNOSIS – ETIOLOGY
Due to
Decreased net intake :Uncommon
Shift into cells
Increased net loss
Cause is usually apparent on HISTORY and
physical examination.
14. 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)
15. 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)
16.
17.
18. 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
19. 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
21. 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
22. 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?)
23. 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!!!)
25. 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)
26. 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
28. 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
31. 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).
32. IS THIS LAB REPORT CORRECT?
Fictitious Hyperkalemia :
hemolysis,
"milking" of extremities ,
thrombocytosis or leucocytosis.
34. 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 potassiumsparing diuretics).
36. 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.
37. INVESTIGATIONS
FIRST LINE:
Serum electrolyte tests.
Serum BUN and creatinine tests
Urinalysis (UA),ECG,TTKG<6 s/o renal
cause
SELECTED CASES
ABG,Serum Uric Acid, CPK and calcium
measurements),CBC,Urine electrolytes
Urine myoglobin test ,Specific drug level
tests for suspected toxicity
43. 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
44.
45. 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)
46. 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.)
47.
48. 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.
49. 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
50. C BIG K DROP
C : Calcium Gluconate
B: Bicarbonate
I,G : Insulin and Glucose
K: Kayexelate
D: Diuretics and Dialysis
51. 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+
52. 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.
53. REFERENCES
Clinical manifestations and treatment of
hypokalemia .David Mount.Avaialble from
http://www.uptodate.com/contents/clinical-manifestations-and-t
.
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.
54. 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
55. 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
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