Hypokalemiacauses n Decreased K intake Low calorie diets

  • Slides: 27
Download presentation
Hypokalemia-causes n Decreased K intake – Low calorie diets – rare n Increased K

Hypokalemia-causes n Decreased K intake – Low calorie diets – rare n Increased K entry into cells – – – – Alkalosis Increased insulin Increased Catecholamines Channelopathies Increased RBC production Hypothermia Chlorquine intox

Hypokalemia n Increased GI losses – Vomiting, Diarrhea, NG tube, laxatives n Increased Urinary

Hypokalemia n Increased GI losses – Vomiting, Diarrhea, NG tube, laxatives n Increased Urinary losses – – – – – Diuretics Mineralocorticoid excess Nonreabsorbable ions Metabolic acidosis Hypo. Mg Nephropathies Ampho B Polyuria Licorice

Hypokalemia Increased Sweat Losses n Dialysis n Plasmaphoresis n

Hypokalemia Increased Sweat Losses n Dialysis n Plasmaphoresis n

Presentation n Neuro muscular K 2 -2. 5 – Weakness prox > distal, loss

Presentation n Neuro muscular K 2 -2. 5 – Weakness prox > distal, loss of reflexes n Cardiac – Arrhythmias – EKG n. U Hyper waves, prolonged QT, small T wave K+ K+ K+ K+ Hypo T wave K+

Familial Periodic Paralysis n Types – Hyper Kalemic – Hyper. PP – Hypo Kalemic

Familial Periodic Paralysis n Types – Hyper Kalemic – Hyper. PP – Hypo Kalemic – Hypo. PP – Thyrotoxic- TPP n Genetic mutation – Autosomal dominant and sporadic

Channelopathies n n Inability to find a decent TV program despite having cable and

Channelopathies n n Inability to find a decent TV program despite having cable and 150 channels to chose from. Functional disturbances of ion channels in the cell membrane – “Flaccid muscle weakness due to under excitability of sarcolemma. ”

Hypo. PP n Rare, potentially fatal episodes of muscle weakness – Asian population Acute

Hypo. PP n Rare, potentially fatal episodes of muscle weakness – Asian population Acute attacks due to K+ moving into cells n Precipitated by exercise, carbs, stress n K level n – Low – Normal* (low K + Rhabdo) n Often self limiting

Treating K problems ABCs n IV – O 2 – Monitor n Stat labs

Treating K problems ABCs n IV – O 2 – Monitor n Stat labs n Check Mg, CPK, TFTs n Oral K is good for non life threatening hypo. K n – Watch N/V – Use PO KCl if hypo K is due to loss of Cl

Hypo. PP - Rx n Administer K+ – 10 -20 meq/hr IV (Higher via

Hypo. PP - Rx n Administer K+ – 10 -20 meq/hr IV (Higher via central line if severe) – 40 -60 meq PO x 2 Check the K+ q 15 -30 min n Rx thyrotoxicosis w/ propanolol n

Hypo. PP - Discharge Daily oral K does not prevent attacks n Carbonic anhydrase

Hypo. PP - Discharge Daily oral K does not prevent attacks n Carbonic anhydrase inhibitors. Acetozolamide n Low carb diet n Consult/referral n

Caveats – K problems n 1 meq decrease in K represents 300 meq deficit*

Caveats – K problems n 1 meq decrease in K represents 300 meq deficit* – If hypo K is due to loss – Remember, 98% of K is in the ICF n 0. 1 drop in p. H raises K by 0. 6 – Think of acid/base problems n Is this primary or secondary problem?

Dangers in Rx PP n Check the type before starting K – Must confirm

Dangers in Rx PP n Check the type before starting K – Must confirm if hypo, hyper or nl n Remember this is a cellular shift – Rebound hyper K can occur if you are too aggressive w/ K replacement n Watch for respiratory insufficiency !

MUDPILES n Methanol/Ethylene glycol – Certainly possible – Pt denied – No visual sx

MUDPILES n Methanol/Ethylene glycol – Certainly possible – Pt denied – No visual sx – No Ca oxalate xtals – Woods lamp – Osm gap

MUDPILES n Uremia – BUN/Creat OK n DKA – Not a diabetic, Glucose OK

MUDPILES n Uremia – BUN/Creat OK n DKA – Not a diabetic, Glucose OK n Paraldahyde – No pungent odor n Isoniazid – No hx TB Rx

MUDPILES n Lactic Acidosis – Abd pain -> dead gut – Decreased perfusion –

MUDPILES n Lactic Acidosis – Abd pain -> dead gut – Decreased perfusion – Liver failure – Alcohols – Meds – Inborn errors – Lactate -> 27

MUDPILES n Ethanol - Alcohol Ketoacidosis – Binge drinker, Not eating n Salicylates –

MUDPILES n Ethanol - Alcohol Ketoacidosis – Binge drinker, Not eating n Salicylates – No Hx of ASA use

Hospital Course Developed DTs n + C. Dif culture n Feeding tube placed n

Hospital Course Developed DTs n + C. Dif culture n Feeding tube placed n acute alcoholic hepatitis and severe dehydration and metabolic disarray with severe hypokalemia, hypophosphatemia, hypomagnesemia, acute renal failure, lactic acidosis, n

Alcohol ketoacidosis Uncommon, often missed n Binge drinkers n

Alcohol ketoacidosis Uncommon, often missed n Binge drinkers n

AKA - 3 factors 1. 2. 3. Alcohol intake Decreased caloric intake Volume depletion

AKA - 3 factors 1. 2. 3. Alcohol intake Decreased caloric intake Volume depletion Results in starvation physiology

AKA n Decreased caloric intake – Counter regulatory hormone release – Epinephrine, cortisol, growth

AKA n Decreased caloric intake – Counter regulatory hormone release – Epinephrine, cortisol, growth hormone – Elevated glucagon, decreased insulin – Promotes lipolysis and fatty acid mobilization n Volume depletion – Elevated glucagon, decreased insulin

AKA n Alcohol intake – Oxidation of ETOH-> ->acetate – NAD->NADH which raises glucagon,

AKA n Alcohol intake – Oxidation of ETOH-> ->acetate – NAD->NADH which raises glucagon, decreases insulin – Promotes betahydoxybutyrate vs acetoacetate – Decreased gluconeogenisis

AKA n Symptoms – N, V, abd pain – Dyspnea, tremulousness – Muscle pain,

AKA n Symptoms – N, V, abd pain – Dyspnea, tremulousness – Muscle pain, fever, diarrhea, syncope, Sz n Physical – Tacycardia, tachypnea, abdominal pain, – Hepatomegaly, hypotension

AKA n Differential Dx – – – – Cholecystitis Peptic ulcer, gastritis Mesenteric ischemia

AKA n Differential Dx – – – – Cholecystitis Peptic ulcer, gastritis Mesenteric ischemia Pacreatitis Withdrawal syndromes Metabolic acidosis DKA Methanol, Ethylene glycol

AKA - labs n p. H –low, high or nl – Metabolic acidosis ->

AKA - labs n p. H –low, high or nl – Metabolic acidosis -> ketones – Metabolic alkalosis -> vomiting – Respiratory alkalosis -> hyperventilation n Serum ketones low, high or nl – Betahydoxybutyrate Lytes –abnormal n Lactate – mildly elevated n

AKA-treatment Volume replace n Carbohydrate replacement n – D 5 NS n Fix electrolyte

AKA-treatment Volume replace n Carbohydrate replacement n – D 5 NS n Fix electrolyte abnormalities – K, Mg, acidosis n Address associated problems – Withdrawal, Wernikes, GI bleed, hepatitis, pancreatitis, pneumonia, rhabdo, etc.

I have never been lost, but I will admit to being confused for several

I have never been lost, but I will admit to being confused for several weeks.