CASE PRESENTATION

DR ANEELA HUSSAIN

Faizullah 45 yrs Male married Shershah resident Known diabetic since 5 yrs on oral hypoglycemics.

Presenting complaints

Diarrhea 1 week vomiting 1 week weakness all four limbs 1 day

 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

 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 and toes and sway legs a bit from side to side on the bed surface.

 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.

Systemic review Past hx Family hx Personal hx

unremarkable

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

CNS EXAM
GCS 15/15 PUPILS- BERL Cranial nerves normal. Motor system
Bulk . normal Tone.. Power 2/5 Reflexes. 1+ Plantars.

 Sensory
Pain Touch Vibration Position

normal

Cerebellar . No nystagmus SOMI Negative.

CHEST. NVB , No added sounds. CVS.. Normal ABDOMEN. No visceromegaly No

Differentials..??

Acute flaccid paralysis

Hypokalemic paralysis? Botulism?? Polio? GBS?

LABS..
HB..13.7 TLC.. 8000 PLT. 266000 Na 128 K.. 1.3 Cl.. 105 cr 5.2 BUN.. 103 ( urea216) Rbs.. 768

 PT ..14 secs INR. 1.08 Serum ketones negative

Bilirubin0.4 Direct bilirubin0.2 SPGT 29 GGT 27 ALK P..220 SGOT..19

URINE D/R. sp gravity. 1.015 PH.. 5.0 RBCS. 1-2 PUS cells.. 30-35 Nitrates.. + Yeast. nil

CXR P/A

normal

ECG

Diagnosis.?

 HYPOKALEMIC PARALYSIS

Rx
I/V normal saline started according to out put and losses plus 25-35 ml/kg/ 24 hrs

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

 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

NA K CL UREA CR GLUCOSE

143 1.8 107 174 5.0 768

146 3.7 110 165 4.7 496

143 3.7 121 186 3.5 533

141 3.3 105 80 1.7 153

 Patient discharged home in good health.

HYPOKALEMIA

MEDSCAPE

 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 in determining the cellular membrane potential. cardiovascular and neuromuscular systems effected.
MEDSCAPE

 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

 Hypokalemia is defined as a potassium level less than 3.5 mEq/L. Moderate hypokalemia is a serum level of 2.53 mEq/L. Severe hypokalemia is defined as a level less than 2.5 mEq/L.

MEDSCAPE

 Hypokalemia may result from conditions as varied as renal GI losses inadequate diet transcellular shift medications

 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.

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

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

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 nasogastric suctioning Diarrhea Enemas or laxative use Ileal loop

 Medication effects
Diuretics (most common cause) Beta-adrenergic agonists Steroids Theophylline Aminoglycosides

Transcellular shift
Insulin

Alkalosis Malnutrition or decreased dietary intake, parenteral nutrition

Labs to send
BUN and creatinine level Glucose, calcium, and/or phosphorus level if coexistent electrolyte disturbances are suspected. Magnesium levels are unreliable and typically do not change management, since patients with hypokalemia almost always have coincident hypomagnesemia and should 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

 CT scan of the adrenal glands is indicated if mineralocorticoid excess is evident (rarely needed emergently).

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

MEDSCAPE

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

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.

 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.

 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

HOW TO CALCULATE DEFICIT..

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 KCL 3.2-3.3 , give 80 mEq of KCL 3.0-3.1 , give 100 mEq of KCL

plus

On going loss Urinary loss diuretics alkalosis Gut loss ( diarrhea/ vomiting) Pancreatic/ small intestinal fistula

Amount of k+ per litre of the loss 20 mmol/l 75-100 mmol/l of urine 75-100 mmol/l of urine 40 mmol/l of the fluid. 100 mmol/l of fluid loss

ROYAL HOBART HOSPITAL AUSTRALIA 2003

 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

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

Advise on d/c

Increase intake of bananas, tomatoes, oranges, and peaches because they are high in potassium.

HYPOKALEMIC PERIODIC PARALYSIS

 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

 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 to severe generalized weakness.

 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.

 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 until attacks occur almost daily.

 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.

 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

Attacks may also be provoked by stress, including infections, menstruation, lack of sleep, and certain medications (eg, betaagonists, insulin, corticosteroids). Patients wake up with severe symmetrical weakness, often with truncal involvement.