case presentation hypokalemic man

8/4/2019 Case Presentation Hypokalemic Man

1/61

CASE PRESENTATION

DR ANEELA HUSSAIN


2/61

Faizullah

45 yrs

Male married

Shershah resident

Known diabetic since 5 yrs on oralhypoglycemics.


3/61

Presenting complaints

Diarrhea 1 week

vomiting 1 week

weakness all four limbs 1 day


4/61

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


5/61

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.


6/61

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.


7/61

Systemic review

Past hx

Family hx Personal hx

unremarkable


8/61

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


9/61

CNS EXAM

GCS 15/15

PUPILS- BERL

Cranial nerves normal.

Motor system

Bulk . normal

Tone..

Power 2/5 Reflexes. 1+

Plantars.


10/61

Sensory

Pain

Touch

Vibration

Position

Cerebellar . No nystagmus

SOMI Negative.

normal


11/61

CHEST. NVB , No added sounds.

CVS.. Normal

ABDOMEN. No visceromegaly

No


12/61

Differentials..??


13/61

Acute flaccid paralysis

Hypokalemic paralysis?

Botulism??

Polio?

GBS?


14/61

LABS..

HB..13.7

TLC.. 8000

PLT. 266000

Na 128 cr 5.2

K.. 1.3 BUN.. 103 ( urea216) Cl.. 105 Rbs.. 768


15/61

PT ..14 secs

INR. 1.08 Serum ketones negative


16/61

Bilirubin0.4

Direct bilirubin0.2

SPGT 29 GGT 27

ALK P..220

SGOT..19


17/61

URINE D/R.

sp gravity. 1.015

PH.. 5.0 RBCS. 1-2

PUS cells.. 30-35

Nitrates.. + Yeast. nil


18/61

CXR P/A

normal


19/61

ECG


20/61


21/61

Diagnosis.?


22/61

HYPOKALEMIC PARALYSIS


23/61

Rx

I/V normal saline started according to out put

and losses plus

25-35 ml/kg/ 24 hrs


24/61

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


25/61

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


26/61

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


27/61

Patient discharged home in good health.


28/61

HYPOKALEMIA

MEDSCAPE


29/61

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


30/61

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


31/61

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


33/61

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


35/61

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


36/61

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


37/61

Medication effects Diuretics (most common cause)

Beta-adrenergic agonists

Steroids

Theophylline Aminoglycosides

Transcellular shift Insulin

Alkalosis Malnutrition or decreased dietary intake, parenteral

nutrition


38/61


39/61

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


40/61

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


42/61

MEDSCAPE


43/61

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.


45/61

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


46/61

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..


48/61

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


49/61

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


50/61

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


51/61

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


52/61

Advise on d/c

Increase intake of bananas, tomatoes,

oranges, and peaches because they are high

in potassium.


53/61

HYPOKALEMIC PERIODIC PARALYSIS


54/61

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


55/61

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.


56/61

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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case presentation hypokalemic man

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