Transcript electrolyte imbalanc..

Electrolyte imbalance
Dr. Mohammed Al-Ghonaim
MBBS,FRCP(C)
Goals of this Tutorial
• SESSION OBJECTIVES
– Learn to effectively assess and manage various
electrolyte abnormalities (NA, K)
– Apply your knowledge to real cases!
• LEARNING METHODS
– Lecture/material review
– Interactive case scenarios
Body’s fluid compartments
Sodium disorders: body’s fluid
compartments
•
•
•
•
•
TBW = WEIGHT x .5 (women) or .6 (men)
TBW x 1/3 = ECF
TBW x 2/3 = ICF
ECF x 2/3 = Interstitial compartment
ECF x 1/4 = Intravascular compartment
What regulate Sodium balance?
Water content of
the blood HIGH
Water content of
the blood LOW
Too much water drunk
Too much salt
or sweating
Brain
produces
More ADH
Brain
produces
Less ADH
Water content
of the blood normal
High volume of water
reabsorbed by kidney
Urine output
LOW
(small volume of
Concentrated urine)
Low volume of water
reabsorbed by kidney
Urine output
HIGH
(large volume of
dilute urine)
Sodium disorders
• [Na] is a measure of Na relative to water.
• It tells you NOTHING about the total body
sodium. Abnormalities in the Na
concentration tell us that there are
abnormalities in the amount of WATER in the
ECF compartment.
Hyponateremia
• Plasma [Na+ <135
• Approach:
– Calculate serum Osmolality
• Osmolality = Osmoles/kg of water
• 2(Na+) + Glucose + BUN
• Normal is 285-295
– Determine volume status
Case Study: (1)
23 yr old male develops watery diarrhea. He
comes to your ER lightheaded and orthostatic.
On exam:
- dry MM and tachycardia.
- Neuro exam is normal and he is alert.
- Labs: Na 129, K 3, HCO3 20, BUN 4, Cr 88,
Glucose 75, Urine Na 5, Urine osm 520.
Hyponatremia
Serum OSM
Low
Hypotonic
Hyponatremia
Normal
High
Marked hyperlipidemia
(lipemia, TG >35mM)
Hyperproteinemia
(Multiple myeloma)
Hyperglycemia
Mannitol
*Note: all have ↑ADH
•SIADH: inappropriate
•Rest: appropriate
ECFv *
Low
Renal loss (UNa > 20)
Extra-renal loss (UNa <10)
•Diuretics
•Bleeding
•Thiazide
•Burns
•K-sparing
•GI (N/V, diarrhea)
•ACE-I, ARB
•Pancreatitis
•IV RTA, Hypoaldo
• Cerebral salt wasting
Normal
•Hypothyroidism
•AI
•SIADH
•Reset Osmostat
•Water Intoxication
1° Polydipsia
TURP post-op
High
•CHF
•Cirrhosis
•Nephrosis
Hyponateremia
• Hyponatremia with high osmolality: [Na] is low since
water will flow into the ECF compartment as a result
of hyperglycemia for example.
– The calculated and measured osm will be elevated in that
case. Na will decrease by approx 1.6 meq/dL for every 100
mg/dl increase in glucose above 100.
– In the case of mannitol the measured osm will be high but
the calculated osm will be low.
Case Study: (1) continue
• Diagnosis:
– First step: calculate osmolality
• Low (
)
– Second step: Volume status
• Low ECF volume
• Treatment:
– Acute vs Chronic
– Any neurological symptoms
Case study-2
• 72 yr old woman with DM presents to ER with
polyuria and polydipsia x 5 days.
• Normal physical examination.
• Labs:
– Na 129, K 4.2, Cl 89, HCO2 3.4, BUN 5, Cr 88, Glucose 780.
• What is the osm?
• Why is he hyponatremic?
• What is the corrected Na?
• What is the treatment
Case study-3
• A 50 yr old male with h/o hyperlipidemia has
the following labs:
• Na 125, M-Osm 270, TGs 1000, total protein
85.
Case study-4
• 72 yr old male who is a heavy smoker presents with
cough and hemoptysis.
• His physical exam is completely normal in terms of
volume status.
• CXR reveals a 6 cm left sided chest mass.
• Labs: Na 125, K 4.2, Cr 1.1, M OSM 270, Urine Na is
45. He takes no meds. TSH and am cortisol are
normal.
• What is causing the hyponatremia
Case Study: (5)
• A 72-year-old woman presents with a 2-day history
of presyncope when rising from a chair.
– Over the last week she has had a bout of viral gastroenteritis with
diarrhea.
– She is drinking 2–3 L of water per day
• Medications:
– Hydrochlorothiazide, 25 mg/d, for HTN
• On examination:
– She had postural hypotension, JVP is low
• Labs:
– sodium 128 mmol/L, potassium 3.1 mmol/L, creatinine 125 mmol/L
and urea nitrogen 10 mmol/L.
Hypernateremia
• Plasma [Na] >145
• Caused primarily by Na+ gain, or water deficit
• Etiology:
– Impaired thirst
– Water loss
• Renal
• Extra renal
– Na+ gain
– Trans cellular shift
Hypernateremia
Case study: (1)
•
•
•
•
•
•
76 yrs old male
HTN,DM II, dementia
Admitted to ICU with septic shock, intubated
Called to see due to Na154,
Bp 125/76mmHg,
Urine out put 1.3 L/day
Case study: (2)
•
•
•
•
•
•
25 yrs old male presented with polyuria
Found to have Na 156
Bp 110/67 mmHg, low JVP
Urine out put=6 L/day
Urine osmolality 100
Calculate the osmolar excretion rate
– 6 x 100 = 600 Mosmole
• Replace the fluid deficit
• Dx Diabetes insipidis (central Vs nephrogenic)
Potassium disorders
• Potassium is one of the body's major ions.
– 98% of the body's potassium is intracellular
– Total body potassium stores 50 mEq/kg (ie,
approximately 3500 mEq in a 70-kg person).
• potassium homeostasis:
– GI absorption is complete
• daily intake of 1 mEq/kg/d (60-100 mEq)
– 90% of this excess is excreted through the kidneys
– 10% is excreted through the gut
• Normal K level: 3.5 – 5.0
Hypokalemia
• K < 3.5 mEq/L
• Clinical manifestations:
– Fatigue
– Cramps
– Constipation
– Weakness / Paralysis
– Parasthesias
– Arrhythmias
EKG Changes in Hypokalemia
– Flattened T waves
– ST depressions
– Prominent U waves
– Prolonged QT
– Prolonged PR interval
Pathophysiology of hypokalemia
• Deficient intake (Poor potassium intake)
• Due to a shift from extracellular to
intracellular
• Increased excretion
– Renal
– Extra renal
Case study: (1)
• 35 yrs old male
• HTN on treatment
• Found to have hypokalemia (K=2.9) referred
for evaluation.
• HCO3=29
• Urine K (spot)= 30
How to asses kidney response?
• Urinary excertion of K
– U k < 15 mmol/l in hypokalemia
– U k > 200 mmol/l in hyperkalemia
• TTKG < 2 in hypokalemia
•
>8 in hyperkalemia
Approach to Hypokalemia
• Step 1: Redistribution or depletion?
– Redistribution causes
• Insulin therapy (usually in DKA)
• Beta 2 agonists (e.g. albuterol)
• Metabolic alkalosis
– Replacement of potassium in these settings may
lead to overshoot and hyperkalemia
Approach to Hypokalemia
• Step 1: Redistribution or depletion?
– Depletion causes (common)
•
•
•
•
•
•
•
GI tract losses (diarrhea, vomiting)
Loop/thiazide diuretic therapy
Other medications (e.g. amphotericin B)
Osmotic diuresis (DKA)
Endocrinopathies (mineralocorticoid excess)
Salt wasting nephropathies/RTA’s
Magnesium deficiency
Approach to Hypokalemia
• Step 2: Estimate the deficit
– For every 100 mEq below normal, serum K+
usually drops by 0.3 mEq/L
• Highly variable from patient to patient, however!!
• For every 10 mEq below normal, serum K+ usually drops
by 0.1 mEq
Approach to Hypokalemia
• Step 3: Choose route to replace K+
– In nearly all situations, ORAL replacement is
PREFERRED over IV replacement
• Oral is quicker
• Oral is less dangerous
• Increase dietary intake
– Potatoes / Bananas
– Choose IV therapy ONLY in patients who are NPO
(for whatever reason) or who have severe
depletion
Approach to Hypokalemia
• Step 5: Choose dose/timing
– Mild/moderate hypokalemia
• 3.0 to 3.5 mEq/L
• 60-80 mEq PO (or IV) QD, divided doses
• Sometimes will require up to 160 mEq QD (severe diarrhea, IV
diuretics)
• Avoid too much PO at once
– GI upset or just poor response
• Usually divide as BID or TID dosing
– Severe hypokalemia (< 3.0 mEq/L)
• Can use combination of IV and PO
• Avoid more than 60-80 mEq PO in a single dose
• Avoid IV infusion rates faster than 20 mEq/hour—can cause
arrhythmia!!!
Approach to Hypokalemia
• Step 6: Monitor/reassess
– Severe hypokalemia, DKA patients
• Reassess labs Q4-6 hours
– Moderate hypokalemia, IV diuresis patients
• Reassess labs BID to TID as needed
– Mild hypokalemia
• Reassess labs QD or less as needed
Summary: Hypokalemia
– PO almost always preferred over IV
– KCl is preferred preparation
– Don’t give too much too quickly
– Be gentle in renal failure patients
– Don’t forget to check magnesium levels in
refractory patients
Hyperkalemia
• Symptoms
– Usually asymptomatic
– Muscle weakness / paralysis
– EKG abnormalities
•
•
•
•
•
Peaked T waves
ST depression
1st degree AVB
QRS widening
“Sine wave sign”
Hyperkalemia
• Elevated potassium level should be evaluated
as to the following:
• Step 1: Is it real?
• Step 2: If real, why did it happen?
• Step 3: Is this an emergency?
• Step 4: Emergency Rx
Pathophysiology of Hyperkalemia
• Increase dietary intake
• shift of K from ICF to ECF such as:
– acidosis
– beta blocker
– insulin deficiency
– periodic paralysis
• Decrease renal excretion :
EKG changes in Hyperkalemia
Approach to Hyperkalemia
• Step 1: Is it real?
– Assess for/exclude pseudohyperkalemia
• Hemolysis—ask the nurse/phlebotomist/lab tech
– If suspected—order STAT repeat K+ level
• Potassium infusion—ask the nurse
– If suspected—order STAT repeat K+ level from peripheral vein AWAY
from infusion site
• Check CBC (WBC > 70,000, PLT > 1,000)
– K+ moves out of WBC’s, PLT’s after clotting
– If suspected—order STAT serum/plasma K+ levels
» if serum K+ > plasma K+ by more than 0.3mEq/L, suspect
pseudohyperkalemia
– In any case, have low threshold to repeat labs
Approach to Hyperkalemia
• Step 2: If real, why did it happen?
– Acute or chronic renal failure
– Medications (K+ sparing diuretics, ACE inhibitors,
ARB’s, BB’s, digoxin, etc.)
– Endocrinopathies
– K+ supplements or salt substitutes
– K+ in IV infusions/TPN
Approach to Hyperkalemia
• Step 3: Is this an emergency?
– How high is the potassium level?
• If serum K+ > or = 6.0 mEq/L, then treat as emergency
– Are there any EKG changes consistent with hyperkalemiainduced cardiac instability?
• If yes, then treat as emergency
• Remember, the lack of EKG changes is NOT always entirely
reassuring
Approach to Hyperkalemia
• Step 3 (con’t): EKG assessment
– Four stages of EKG changes
•
•
•
•
Peaked T waves
PR prolongation
QRS widening
Sine waves
• PEA or asystole
Approach to Hyperkalemia
• Step 4: Emergency Rx
– Part A: oppose toxic effects on cell membrane
• IV calcium infusion (gluconate preferred over chloride)
– Less toxic effects if IV extravasation
• Give 1-2, 10mL ampules of 10% Calcium gluconate over 2-5
minutes
• Keep EKG machine attached to patient!!!
– EKG changes will diminish in 1-3 minutes
– Action: Stabilization of cardiac cells. Does not lower
potassium. Used for hyperkalemia with EKG changes.
– If EKG changes do not immediately resolve, dose can be
repeated in 5 minutes.
Approach to Hyperkalemia
• Step 4 (con’t): Emergency Rx
– Part B: Shift K+ into cells
• Will buy you 1-4 hours before direct elimination methods “kick-in”
• Insulin/dextrose therapy
–
–
–
–
Give 10U regular insulin IV push, together with 1 ampule (50mL) D50 IV push
Follow this with a D 5 containing IV maintenance fluid for several hours.
Effect within 15 minutes.
Peak effect 60 min. Duration 3-4 hours.
• Adjuncts
– Beta agonist:
– Albuterol nebulizer
» Peak effect in 90 minutes
– Sodium bicarbonate 1 ampule IV push
– Onset: 30 minutes
– Duration: 60-120 minutes
Approach to Hyperkalemia
• Step 5: Emergency or non-emergency therapy
(usually takes 4-6 hours to work)
– Direct elimination of K+ from body
– Sodium polystyrene sufonate (K+ binding resin)
plus sorbitol
• Give Kayexalate 30-60 gm
– PO if patient can tolerate
– PR (retention enema) if upper GI problems
– Patient needs to have a colon for this to work!
– Hemodialysis as last resort or in severe cases
Summary: Hyperkalemia
– Make sure it’s real
– Determine emergent or not
• Degree of hyperkalemia, EKG
– Treat emergent cases with calcium gluconate,
insulin, dextrose, and kayexalate +/- dialysis
– Monitor closely for response to treatment—watch
for rebound
– Fix the cause if possible