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METABOLIC ACIDOSIS
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Objectives Review physiology of acid-base balance Determine gap versus non-anion gap metabolic acidosis Overview of RTAs Practice with clinical vignettes
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Normal Physiology Daily production of acid (H + ) mostly from diet Balanced by renal excretion of acids and/or reclamation of base (HCO 3 - )
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Metabolic Acidosis Disorder 1) Overproduction of acids = ↑H + 2) Increased extra-renal loss of base = ↓ HCO 3 - 3) Decrease in renal acid secretion = ↑H + 4) Poor renal absorption of base = ↓ HCO 3 -
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Expected Compensation
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Acid/Base Formulas Winter’s Formula (CO2) = 1.5 [HCO 3 - ] + 8 ± 2 Anion Gap = Na + – Cl - + HCO 3 - Correct for hypoalbuminemia Increase AG by 2.5 for every 1 decrease in albumin Unmeasured Anions = Lactate, Phosphate, Sulfate ∆ Anion gap / ∆ [HCO 3 - ]
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Elevated Anion Gap (>12) “MUDPILES” Methanol Uremia Diabetic ketoacidosis / Starvation ketoacidosis Paraldehyde Isoniazid / Iron Lactic acidosis Ethanol / Ethylene glycol Salicylates CO, cyanide, hydrogen sulfide, sulfur, theophylline, toluene
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Non-anion Gap Metabolic Acidosis “HARD UP” Hyperalimentation Acetazolamide Renal tubular acidosis (RTA) Diarrhea Ureteral diversion Pancreatic fistula
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Low Anion Gap (<3) Increase in unmeasured cations Hyper-Ca Hyper-Mg Hyper-K Lithium intoxication Paraproteinemia Decrease in unmeasured anions Hypoalbuminemia Dilution
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Urine Anion Gap UAG= (U Na + U K + U NH4 ) – (U Cl - U HCO3 ) POSITIVE if renal disease NEGATIVE if normal or GI bicarbonate losses
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Proximal (type 2) RTA Impaired proximal tubule HCO 3 - reabsorption In steady state distal nephron can accommodate and acidify urine pH < 5.5 Hypokalemia Increased NaHCO 3 to the distal tubules Increased aldosterone activity reabsorbing Na+ and secreting K+
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Distal (type 1) RTA Impaired distal secretion of H + Causes impairment in regeneration of HCO 3 - Unable to acidify urine pH < 5.5 Associated with hypo-K Associated with nephrocalcinosis and nephrolithiasis Increase in urinary luminal Ca 2+ from bone mineral dissolution for buffering systems High urine pH decreases solubility of Ca 2+ phosphate complexes
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Hyperkalemic (type 4) RTA Decreased H + and K + secretion Urine pH < 5.5 Etiology due to mild/moderate CKD, DM, autoimmune disorders Deficiency of circulating aldosterone Impairment of distal luminal electronegativity in the cortical collecting duct
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RTA Review Proximal (type 2) Poor HCO 3 reclamation Normal / hypo-K Urine pH < 5.5 (variable) HCO 3 14-20 Distal (type 1) Reduced H + secretion Normal / hypo-K Urine pH > 5.5 (constant) HCO 3 <10 mEq/L Nephrocalcinosis Hyperkalemic (type 4) Aldosterone deficiency Reduced H + secretion Hyperkalemia Urine pH < 5.3 HCO 3 >15 RTA of Renal Failure Decreased renal mass Hyperkalemia Urine pH < 5.5 Abnormal renal function
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Approach to Acid/Base Disorders 1. Acidemia or Alkalemia 2. ∆ PCO 2 and serum HCO 3 from normal (-osis) 3. Calculate anion gap 4. PCO 2 and HCO 3 compensation – Winter’s: Expected pCO2 = 1.5 [HCO 3 - ] + 8 +/- 2 – Delta-Delta = Measured AG – 12 / 24 – [HCO 3 - ] – Metabolic Alkalosis: Expected pCO2 = 0.7 [HCO 3 - ] + 20 mmHg (range +/- 5) 5. Differential Diagnosis 6. Treat underlying condition unless pH within critical range
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Delta-Delta
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ABG Warm-Up pH / PaCO 2 / HCO 3 7.28 / 50 / 23 7.10 / 38 / 14 7.48 / 55 / 34 → Respiratory Acidosis → Metabolic Acidosis → Metabolic Alkalosis + Respiratory compensation
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Case #1 60 y/o woman with HTN, admitted after 7 days of severe vomiting. Appears ill, hypotensive with tachycardia (+) Rebound tenderness w/ no bowel sounds BMP – 140/3.2/80/11/90/3<90 ABG – 7.29 / 24 AG Metabolic acidosis + Metabolic alkalosis
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Case #2 64 y/o man admitted to ICU for PNA and septic shock. 4 days of SOB and fever Afebrile, BP 85/50, HR 110, RR 22 (+) Crackles and heart murmur, pedal edema BMP – 135/4.8/103/10/22/1.4<115, Albumin=3.8 ABG – 6.94 / 48 / 51 AG Metabolic acidosis + Respiratory acidosis
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Case #3 15 y/o male with no reported PMH Complains of light sensitivity Short stature based on growth chart, bowed-legs Initial labs: 145/3.9/108/14/12/0.8<99 UA with pH=5.3 What next?
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Case #4 44 y/o female with cirrhosis, HD#2 for fever and abdominal pain Meds: Spironolactone, Lasix, Lactulose Tm=100.8, BP 74/55, HR 72 Appears cachetic Abdomen distended, (+) TTP, 1+ BLE edema BMP – 128/5.1/104/12/20/1.3<84, Albumin=1.4 ABG – 7.25 / 28 / 78 AG Metabolic acidosis
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Case #5 66 y/o man with type II DM, HTN 8 days of diarrhea, abdominal pain, decreased PO Grandson w/ similar symptoms 1 week ago Meds: Enalapril, Atenolol, HCTZ, Metformin Normal vitals, (+) FOBT BMP – 136/3.9/114/13/21/1.2<128, Albumin=4 Urine pH=6, U Na =32, U K =21, U Cl =80 ABG – 7.27 / 30 / 90 Non-anion gap Metabolic acidosis
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Metabolic Alkalosis Metabolic Alkalosis Initiation: Net loss of H + Net addition of HCO3 - (alkali ingestion) External loss of fluid containing Cl - (contraction alkalosis) Maintenance mechanisms: Cl - depletion K + depletion Hypercapnea Rarely; primary disorders of specific ion channels in the Loop of Henle, distal tubule or collecting ducts
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Chloride Depletion Selective Cl - (eg nasogastric suction) produces a major increase in serum bicarbonate Low urine chloride K + depletion sustains the metabolic alkalosis Increases H + secretion via H + / K + ATPase Increase NH 4 + production and excretion
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Sources of Cl - responsive alkalosis Vomiting and NG suction Diarrhea Congenital Chloride Diarrhea Villous Adenoma Diuretics Loop diuretics Metolazone Thiazides Post-hypercapneic state
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Chloride-resistant Metabolic Alkalosis Mineralocorticoid excess 1 ° hyperaldosternism Adenoma Cushing’s syndrome ACTH tumor Renin tumor Androgenetic syndrome Fludrocortisone treatment Apparent excess of mineralocorticoid Licorice or Altoids (Glycyrrhizic acid) Liddle’s syndrome 11B-Hydroxysteroid dehydrogenase deficiency High-dose Glucocorticoids Normotensive Severe K + deficiency Bartter’s and Gitelman’s
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Exogenous Alkali Persistent metabolic alkalosis when the body is deficient in K + or Cl - stores Hypercalcemia Milk alkali syndrome (Ca 2+ containing antacids) Alkali administration Massive pRBC transfusion >10U (Citrate) Refeeding syndrome
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Management of Metabolic Alkalosis Treat underlying condition If severe pH > 7.60 treat with hemodialysis Chloride Responsive Normal Saline or ½ Normal Saline Rate 50-100 cc/hr over maintenance rate Replete K + PPIs minimize gastric losses If diuretic induced can use K + sparing diuretics to limit alkalosis
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Management of Metabolic Alkalosis Chloride Resistant: In a patient in an edematous state Acetazolamide Mineralocorticoid excess; restoration of normal mineralocorticoid activity Surgical Removal K + sparing diuretics + K + supplements Bartter’s and Gitelman’s syndrome K + sparing diuretics + K + supplements NSAIDs (Bartter’s)
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