fluid and electrolytes de jesus, anthony de robles, shella de silos, jeriel
TRANSCRIPT
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Fluid and Electrolytes
De Jesus, AnthonyDe Robles, Shella
De Silos, Jeriel
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general data
• EC, 41/F• Paraňaque
• CC: loose watery stools
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patient profile
• CLD 2° to Schistosomiasis with sign of portal hypertension– splenomegaly, portal gastropathy,
gastroesophageal varices
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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
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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
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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
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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
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past medical history
• (-) HPN, DM, allergy, asthma, PTB• June 2009 – admitted for UGIB, s/p RBL x 4
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Family medical history
• (-) HPN, DM, allergy, asthma, PTB, Ca
OB History
• G7P7 (7007), no complications
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Personal and social history
• Housewife• 6 pack-years of smoking• Occasional alcohol beverage drinker• Denies use of illicit drugs
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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
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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
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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
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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
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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
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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
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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
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Fecalysis /FOBT
Dark yellow , watery consistency, (-) RBC/hpf,WBC 0-1/hpf, no ova or parasites seen,(-) occult blood
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Gen Med
A> 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
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Gen Med
Ciprofloxacin 500 mg/tab 1 tab BIDMetronidazole 500 mg/tab 1 tab q6Praziquantel (still for procurement)ORS vol/vol replacementFeSO4 + FA 1 tab TID
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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
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Hypokalemia
Oral 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
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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
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Hypokalemia
For 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)
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Clinical Manifestations of Hypokalemia
• Symptoms inlcude:– Fatigue– Myalgia– Muscular weakness
• If severe, can lead to:– Progressive weakness– Hypoventilation– Complete paralysis• Hypokalemic periodic paralysis
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Approach to Hypokalemia
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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
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Hypokalemia
• Defined as a plasma concentration <3.5mmol/L• Causes:– Decreased intake– Redistribution into cells– Increased loss
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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
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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
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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