case presentation hypokalemic man
TRANSCRIPT
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CASE PRESENTATION
DR ANEELA HUSSAIN
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Faizullah
45 yrs
Male married
Shershah resident
Known diabetic since 5 yrs on oralhypoglycemics.
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Presenting complaints
Diarrhea 1 week
vomiting 1 week
weakness all four limbs 1 day
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Pt was having profuse diarrhea since 1 week,
yellow, watery, 10 to 15 episodes, associated
with abdominal cramps around the umbilicus.
Vomiting more than 10 times per day, in
moderate amount, projectile, watery,
Had i/v infusions and medicines but the
ailment continued
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Since one day pt noticed weakness in his arms
he was unable hold his arms up and hold
objects in his hands which progressed acutely
to involve his legs and he was unable to stand
up from sitting position and in a days span he
was unable to move his limbs in bed even
could only with difficulty move his fingers andtoes and sway legs a bit from side to side on
the bed surface.
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However there was no difficulty to
swallow, no respiratory distress, no urinary or
fecal incontinence or retention, no fever, no
ptosis or opthalmoplegia and no improvement
on resting.
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Systemic review
Past hx
Family hx Personal hx
unremarkable
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GPE
Middle aged male, average height and built,
conscious, oriented x 3
A J CL E JVP LN .. Negative
T A/F
P 80/min
R- 18/min BP - 110/60
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CNS EXAM
GCS 15/15
PUPILS- BERL
Cranial nerves normal.
Motor system
Bulk . normal
Tone..
Power 2/5 Reflexes. 1+
Plantars.
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Sensory
Pain
Touch
Vibration
Position
Cerebellar . No nystagmus
SOMI Negative.
normal
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CHEST. NVB , No added sounds.
CVS.. Normal
ABDOMEN. No visceromegaly
No
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Differentials..??
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Acute flaccid paralysis
Hypokalemic paralysis?
Botulism??
Polio?
GBS?
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LABS..
HB..13.7
TLC.. 8000
PLT. 266000
Na 128 cr 5.2
K.. 1.3 BUN.. 103 ( urea216) Cl.. 105 Rbs.. 768
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PT ..14 secs
INR. 1.08 Serum ketones negative
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Bilirubin0.4
Direct bilirubin0.2
SPGT 29 GGT 27
ALK P..220
SGOT..19
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URINE D/R.
sp gravity. 1.015
PH.. 5.0 RBCS. 1-2
PUS cells.. 30-35
Nitrates.. + Yeast. nil
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CXR P/A
normal
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ECG
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Diagnosis.?
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HYPOKALEMIC PARALYSIS
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Rx
I/V normal saline started according to out put
and losses plus
25-35 ml/kg/ 24 hrs
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K+ deficit
Expected k+ - actual k+ x 0.4 x wt 4.5 - 1.8 x 0.4x 65
70 meq/l plus add daily requirement of 65
meq 135 meq/l
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Dont give more than 20 meq/hr.
If giving thru peads chamber
1000 ml N/s add 60 meq
300 ml 20 meq.
75 d/ min then repeat. And check k+ every 6 hrly
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NA 143 146 143 141
K 1.8 3.7 3.7 3.3
CL 107 110 121 105
UREA 174 165 186 80
CR 5.0 4.7 3.5 1.7
GLUCOSE 768 496 533 153
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Patient discharged home in good health.
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HYPOKALEMIA
MEDSCAPE
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Potassium is one of the body's major ions.
Nearly 98% of the body's potassium is
intracellular. The ratio of intracellular to
extracellular potassium is important indetermining the cellular membrane potential.
cardiovascular and neuromuscular systems
effected.
MEDSCAPE
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The kidney determines potassium
homeostasis, and excess potassium is excreted
in the urine.
The reference range for serum potassium level
is 3.5-5 mEq/L, with total body potassium
stores of approximately 50 mEq/kg (ie,
approximately 3500 mEq in a 70-kg person).
MEDSCAPE
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Hypokalemia is defined as a potassium level
less than 3.5 mEq/L.
Moderate hypokalemia is a serum level of 2.5-
3 mEq/L.
Severe hypokalemia is defined as a level less
than 2.5 mEq/L.
MEDSCAPE
http://emedicine.medscape.com/article/242008-overviewhttp://emedicine.medscape.com/article/242008-overview -
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Hypokalemia may result from conditions as
varied as
renal
GI losses
inadequate diet
transcellular shift medications
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a constellation of symptoms that involve the
GI, renal, musculoskeletal, cardiac, and
nervous systems.
The patient's medications should be reviewed
to ascertain whether any of them could cause
hypokalemia.
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Common symptoms
Palpitations
Skeletal muscle weakness or cramping
Paralysis, paresthesias
Constipation Nausea or vomiting
Abdominal cramping
Polyuria, nocturia, or polydipsia
Psychosis, delirium, or hallucinations Depression
MEDSCAPE
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Signs
Signs of ileus
Hypotension
Ventricular arrhythmias
Cardiac arrest
Bradycardia or tachycardia
Premature atrial or ventricular beats
Hypoventilation, respiratory distress
Respiratory failure
Lethargy or other mental status changes Decreased muscle strength, fasciculations, or tetany
Decreased tendon reflexes
Cushingoid appearance
MEDSCAPE
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Causes
Renal losses Renal tubular acidosis
Hyperaldosteronism
Magnesium depletion
Leukemia (mechanism uncertain) GI losses (source may be medical or psychiatric,
ie, anorexia or bulimia) Vomiting or nasogastricsuctioning
Diarrhea
Enemas or laxative use
Ileal loop
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Medication effects Diuretics (most common cause)
Beta-adrenergic agonists
Steroids
Theophylline Aminoglycosides
Transcellular shift Insulin
Alkalosis Malnutrition or decreased dietary intake, parenteral
nutrition
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Labs to send
BUN and creatinine level
Glucose, calcium, and/or phosphorus level if coexistentelectrolyte disturbances are suspected.
Magnesium levels are unreliable and typically do notchange management, since patients with hypokalemiaalmost always have coincident hypomagnesemia andshould be treated empirically.
Consider digoxin level if the patient is on a digitalis. Consider ABG: Alkalosis can cause potassium to shift
from extracellular to intracellular.
MEDSCAPE
http://emedicine.medscape.com/article/246366-overviewhttp://emedicine.medscape.com/article/246366-overviewhttp://emedicine.medscape.com/article/246366-overview -
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CT scan of the adrenal glands is indicated if
mineralocorticoid excess is evident (rarely
needed emergently).
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Ecg findings..
T-wave flattening or inverted T waves
Prominent U waves after T waves
ST-segment depression
Ventricular arrhythmias PVCs, torsade de
pointes, vf
Atrial arrhythmias PACs, a fib
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MEDSCAPE
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RX
Be attentive to the ABCs.
Put on cardiac monitor
Pts with 2.5-3.5 mEq/L need only oral
potassium replacement therapy.
If less than 2.5 mEq/L, intravenous potassium
should be given
Replace mg++
MEDSCAPE
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While intravenous potassium dosages of up
to 40 mEq/h have been advocated, patients
should receive no more than 20 mEq/h IV to
avoid potential deleterious effects on the
cardiac conduction system.
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Replacing potassium too quickly can cause a rapid
rise in the blood potassium level, leading to a
relative hyperkalemia with subsequent cardiac
complications. If hypokalemia is not corrected easily with
replacement therapy, search for other coexistent
metabolic abnormalities (eg, hypomagnesemia).Hypokalemia may be refractory to treatment until
hypomagnesemia is corrected.
http://emedicine.medscape.com/article/240903-overviewhttp://emedicine.medscape.com/article/240903-overview -
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Never put k+ injections in a running drip
Prepare the solution and and invert i/v drip
atleast ten times for maximum mixing
Concentration greater than 3 mmol/100 ml
can damage perepheral vessels. ( 30 mmol/l)
ROYAL HOBART HOSPITAL AUSTRALIA 2003
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HOW TO CALCULATE DEFICIT..
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RX
If potassium is:3.8-3.9, give 20 mEq of KCL
3.6-3.7, give 40 mEq of KCL
3.4-3.5, give 60 mEq of KCL3.2-3.3 , give 80 mEq of KCL
3.0-3.1 , give 100 mEq of KCL
plus
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On going loss Amount of k+ per litre of the loss
Urinary loss 20 mmol/l
diuretics 75-100 mmol/l of urine
alkalosis 75-100 mmol/l of urine
Gut loss ( diarrhea/ vomiting) 40 mmol/l of the fluid.
Pancreatic/ small intestinal fistula 100 mmol/l of fluid loss
ROYAL HOBART HOSPITAL AUSTRALIA 2003
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Take value from the chart and add deficit
calculated from the serum k+ and replace that
in 48 hrs..
Almost 75% in the first 24 hrs and the
remaining later
ROYAL HOBART HOSPITAL AUSTRALIA
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K+ deficit
Expected k+ - actual k+ x 0.4 x wt
4.5 - 1.8 x 0.4x 65
70 meq/l plus add daily requirement of 65
meq 135 meq/l
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Advise on d/c
Increase intake of bananas, tomatoes,
oranges, and peaches because they are high
in potassium.
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HYPOKALEMIC PERIODIC PARALYSIS
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The physiologic basis of flaccid weakness is
inexcitability of the muscle membrane (ie,
sarcolemma). Alteration of serum potassium
level is not the principal defect in primary PP
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Severe cases present in early childhood and
mild cases may present as late as the third
decade.
A majority of cases present before age 16
years.
Weakness may range from slight transient
weakness of an isolated muscle group tosevere generalized weakness.
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Severe attacks begin in the morning, often
with strenuous exercise or a high
carbohydrate meal on the preceding day
Mild attacks are frequent and involve only a
particular group of muscles, and may be
unilateral, partial, or monomelic. This may
affect predominantly legs; sometimes,extensor muscles are affected more than
flexors.
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Duration varies from a few hours to almost 8
days but seldom exceeds 72 hours. The
attacks are intermittent and infrequent in the
beginning but may increase in frequency untilattacks occur almost daily.
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The frequency starts diminishing by age 30
years; it rarely occurs after age 50 years.
Urinary output is decreased during the attack
because water accumulates intracellularly in
muscles.
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Permanent muscle weakness may be seen
later in the course of the disease and may
become severe. Hypertrophy of the calves has
been observed. Proximal muscle wasting,rather than hypertrophy, may be seen in
patients with permanent weakness
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Attacks may also be provoked by stress,
including infections, menstruation, lack of
sleep, and certain medications (eg, beta-
agonists, insulin, corticosteroids). Patientswake up with severe symmetrical weakness,
often with truncal involvement.
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