Fluid and ElectrolytesDe Jesus, Anthony

De Robles, ShellaDe Silos, Jeriel

general data• EC, 41/F• Paraňaque

• CC: loose watery stools

patient profile• CLD 2° to Schistosomiasis with sign of portal

hypertension– splenomegaly, portal gastropathy,

gastroesophageal varices

history of present illness• 2 days PTA (08/05) – patient and

grandchildren had– Breakfast: bread– Lunch: rice and sardines– Dinner: rice and salted fish– Water Source: NAWASA, not boiled

Patient was asymptomatic

history of present illness• 1 day PTA (08/06) – patient and grandchildren

developed diarrhea– loose watery, non-bloody, non-mucoid, non-foul

smelling, profuse, >15 x– (-) vomiting, (-) fever– No consult done– Water therapy and bed rest

history of present illness• On day of admission (08/08) – persistence of

diarrhea, >10x, (+) abdominal pain and bilateral leg weakness, 1 episode of vomiting, (-) fever

PGH-ER

Review of systems• (-) headache, (-) decrease in appetite, (-) fever, (-)

pallor• (-) cough, (-) difficulty of breathing• (-) chest pain, (-) palpitations• (-) melena/hematochezia• (-) frothy urine (-) tea colored urine, (-) change in

urine output• (-) numbness (-) paresthesia• (-) weight loss, (-) polyuria (-) polydipsia

past medical history• (-) HPN, DM, allergy, asthma, PTB• June 2009 – admitted for UGIB, s/p RBL x 4

Family medical history• (-) HPN, DM, allergy, asthma, PTB, Ca

OB History• G7P7 (7007), no complications

Personal and social history• Housewife• 6 pack-years of smoking• Occasional alcohol beverage drinker• Denies use of illicit drugs

DEMS (Triage)- patient arrived very weak,

unable to speak- BP 70 palp, HR 120s, RR 16 T

afebrile- Cold clammy extremities, faint

pulses

A>Hypovolemic Shock 2° GI lossesAGE prob 1) cholera 2) amoebicCLD 2° to Schistosomiasis (1999)

with portal hypertension

P> Fast drip pNSS (double line) 1.750 cc pNSSPlaced on NPO, Monitor: VS q1/Temp q4/UO q4Labs requested: 1) ABG; 2) CBC with PBS; 3) Fecalysis/FOBT; 4) BUN, Crea, Na, K, Cl; 5) U/A

DEMS (Triage)• Patient reassessed after 1.750cc of pNSS– More able to speak– BP 90/60, HR 104, RR 20 T afebrile– No hypotensive episode since then– (+) 3 episodes of watery diarrhea

• Referred to Gen Med• Laboratory results

ABGpH 7.244pCO 2 28.7PO2 108HCO3 12.6,BEb -12.9O2 sat 97.59%

CBCWBC 14.24 high Neu 0.900 Lym 0.069 Mon 0.099)RBC 5.64Hgb 118 lowHct 0.395 lowMCV 70.0 lowMCH 20.9 lowMCHC 299 lowRDW 19.7 highPlt 129 Retics 0.025

PBShypochromic, anisocytosis ++, poikilocytosis ++, no toxic granules seen

Blood ChemBUN 8.83Crea 138Alb 32Na 137K 2.8Cl 100AST 50ALT 44Glucose 7.44

Urinalysis Yellow, cloudy, SG 1.030, pH 6,(-)sugar,(-)proteinRBC 30-40/hpf , WBC 3-4/hpf, Epithelial cells +1 , bacteria +2, Mucus Thread rare, fatty cast , (-) crystal

FecalysisDark yellow , watery consistency, (-) RBC/hpf , WBC 0-1/hpf , no ova or parasites seen , (-) occult blood

ABG• pH 7.240• pCO2 28.7• PO2 108• HCO3 12.6,• BEb -12.9• O2 sat 97.59%

• Na 137• Cl 100

Pure high anion gap metabolic acidosis

Blood Chemistry• BUN 8.83 high• Crea 138 high• Alb 32 • Na 137• K 2.8 low• Cl 100• AST 50 high• ALT 44• Glucose 7.44 high

BUN/crea = 15Pre-renal azotemia ?

HypokalemiaK+ deficit =(desired –actual)/0.27 x 100K+ deficit = (3.5 -2.8)/0.27 x100 = 260 meqs

Stress Hyperglycemia

CBC, PBSWBC 14.24 high Neu 0.900 Lym 0.069 Mon 0.099RBC 5.64Hgb 118 lowHct 0.395 low•MCV 70.0 low•MCH 20.9 low•MCHC 299 low•RDW 19.7 highPlt 129 Retics 0.025

PBShypochromic, anisocytosis ++, poikilocytosis ++, no toxic granules seen

• Leukocytosis predominantly neutrophilic = bacterial infection?

• Anemia

• Microcytic• Hypochromic

• Reticulocyte index = 0.025 x (0.395/0.45) x 100 = 2.19 / 1.5 =1.46

Iron Deficiency Anemia

Urinalysisyellow, cloudy, SG 1.030, pH 6, (-)sugar, (-)proteinRBC 30-40/hpf, WBC 3-4/hpf, epithelial cells +1 , bacteria +2, Mucus Thread rare, fatty cast , (-) crystal

Fecalysis /FOBTDark yellow , watery consistency, (-) RBC/hpf,WBC 0-1/hpf, no ova or parasites seen,(-) occult blood

Gen MedA> AGE prob 1) bacterial (cholera vs ETEC) 2) amoebic Hypovolemic Shock 2° to GI losses, resolved CLD 2° to Schistosomiasis (1999) with signs of portal hypertension Prerenal Azotemia Hypokalemia Stress Hyperglycemia Anemia prob 1) Nutritional 2) Chronic Disease

Gen MedCiprofloxacin 500 mg/tab 1 tab BIDMetronidazole 500 mg/tab 1 tab q6Praziquantel (still for procurement)ORS vol/vol replacementFeSO4 + FA 1 tab TID

HypokalemiaTherapeutic Goals:• to prevent life-threatening complications (arrhthymias, respiratory failure)• correct the K+ deficit• minimize on-going losses through treatment of underlying cause (AGE)

– Hypomagnesemia should be sought and corrected to allow effective K+ repletion

Using the old formula:K+ deficit = (desired –actual)/0.27 x 100 = (3.5 -2.8)/0.27 x100 = 260 meqsNew Paradigm:4.0 to 3.0 = 200 meqs deficit3.0 to 2.0 = 400 meqs deficit<2.0 = 600 meqs deficit Since K+ is 2.8 = 400 meqs deficit

HypokalemiaOral Therapy– safer– larger doses can be given

IV Therapy– For patients with imminently life-

treatening hypokalemia and those unable to take anything by mouth

• MAX conc:– 40 meqs/L via a peripheral vein– 100 meq/L via a central vein

• Rate of Infusion– 20 meq/hr unless paralysis or

malignant ventricular arrhythmias are present

HypokalemiaCorrect half of the deficit in 24 hours, the rest for the next 3 days

K+ deficit = 400 meqs correct 200 meqs for the first 24 hours

Oral KCl 10 meqs/tab 5 tabs q6 for 4 dosesIV KCl 10% sol’n, 40 meqs/30cc, 40 meqs in 1L pNSS x 6° for 5cycles

For this patient, she was managed: KCl 10% drip 40 meqs in 1 L pNSS x x 6° for 3 cycles Oral KCl 3 tabs q8 for 3 doses then d/c

HypokalemiaFor this patient the hypokalemia was primarily due

to GI losses

Contributory Factors (Transcellular Shift)• Stress Hyperglycemia (insulin and cathecolamine

– induced transcellular shift)• Anemia(anabolic state)

Clinical Manifestations of Hypokalemia

• Symptoms inlcude:– Fatigue– Myalgia– Muscular weakness

• If severe, can lead to:– Progressive weakness– Hypoventilation– Complete paralysis• Hypokalemic periodic paralysis

Approach to Hypokalemia

ECG FindingsEarly changes:

Flattening/inversion of T waveProminent U waveST-segment depressionProlonged QU interval

Severe K depletion:Prolonged PR intervalWidening of the QRS complexIncreased risk of ventricular arrythmias

Hypokalemia

• Defined as a plasma concentration <3.5mmol/L• Causes:– Decreased intake– Redistribution into cells– Increased loss

Decreased Intake

• Starvation, clay ingestion• Normal K intake is 40-120 meq/day• Rarely the sole cause• However, can contribute to the severity if an

underlying problem is present

Redistribution Into Cells

• Maintained by the Na-K-ATPase pump in the cell membrane

• Metabolic/Respiratory alkalosis – promotes K entry into cells

• Insulin – increases the activity of the Na-K-ATPase pump

• B2-agonists – increases the activity of the Na-K-ATPase pump

Increased Losses

• GI losses usually seen in patients with: – Severe infectious diarrhea (usually secretory)– Villous adenomas– Vasoactive intestinal pepetide tumors– Laxative abuse

• Primarily due to increased urinary losses• Results in volume depletion and metabolic

alkalosis• Hypovalemia stimulates aldosterone release