Acid Base Disorders

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    Introduction

     

     

    Anion Gap Metabolic Acidosis

    Lactic Acidosis

    • Type A = tissue hypoperfusion is present.
      • Tissues lack oxygen, undergo anaerobic metabolism = lactic acid created. (2ndary to shock)
    • Type B = due to medications/toxins, accummulate lactate without tissue hypoxia.
      • Acetaminophen overdose (Esp if poorly nourished)
      • Cyanide
      • Ethylene Glycol
      • Linesolid
      • Mangosteen juice
      • Metformin (Most Common)
        • If renal function impaired
      • Methanole
      • NRTI (HIV drugs)
      • Propelene Glycol
      • Propofol
        • If high doses > 4mg/kg/hr for >48hrs = Type B acidosis (rhabdo, hyperlipidemia, J-point elevation on ECG... tx is supportive).  Dialysis if acidosis very severe. 
      • Salicylates
      • Thamine Deficiency
      • Systemic Disease: Liver failure, G6PD, Pregnancy
    • D-Lactic Acidosis
      • D-isomer accummulates in pts with short-gut syndrome (Jejuno-ilial bypass OR small bowel resection)
      • Excess carbohydrates reaching colon metabolized to D-lactate
      • Lactate assay does not measure this?? (Unsure)
      • Symptoms: Intermittent confusion, slurred speech, ataxia
      • Treatment: Abx against bowel flora (metro or neomycin, restrict carbohydrates)

     

    Ketoacidosis

    • Can have normal anion gap if euvolemic
    • Glycosuria from DKA = polyuria, polydipsia = water, sodium, K+ losses, = volume depletion
      • Pre-renal azotemia, ketoacids not cleared, built up.
    • If fluid replete, ketones in urine, no anion gap. 
    • Bicarb usually not needed, can metabolize ketoacids back to bicarb once fluid replete.
      • Bicarb only indicated in extreme acidosis (pH < 7.0 or if critically ill < 7.1-7.2)

     

    Alcoholic Ketoacidosis

    • B-hydroxybutirate is predominant ketone.
      • This ketone is not detected by nitroprusside assay on urine dipstick
      • Also present in DKA (but have also acetoacetate, which is on the urine dipstick)
    • Giving IV glucose or improved caloric intake reverses ketoacidosis
    • For chronic alcoholism --> give thiamine.

     

    Methanol & Ethyelene Glycol

    • Lethal intoxications that cause severe AG metabolic acidosis
    • Cause osmolar gap
    • (see ICU --> toxins)

     

    Normal Anion Gap Metabolic Acidosis

    • Acidosis without an unmeasured anion
    • Causes:
      • Urine diversion (gastrointestinal conduit - i.e. ilial conduit)
      • Failure of kidneys to excrete acid load
      • GI loss of bicarb (diarrhea, laxative abuse)
    • Workup:
      • HISTORY is the most important diagnostic test
      • Look at kidney causes (Renal Tubular Acidosis)
        • Renal Tubular Acidosis (If renal function normal)
        • CKD (if abnormal renal function)

     

    Renal Tubular Acidosis

    • Kidney fails to excrete acid load (but normal renal function)
    • 3 Categories
      • 1.  Type IV - distal RTA - Hypoaldosteronism (most common!!! By far!)
        • Often very mild acidosis
        • Hyperkalemia
        • In distal nephron ENaC channel reabsorbs sodium, excretes potassium, and excretes hydrogen.
          • Lack of aldosterone, lack of ENaC --> cannot excrete hydrogen
        • Treatment:
          • Treat Hyperkalemia
          • Treat underlying cause (i.e. reduce dose of contributing meds - i.e. decr. ACEi)
          • Diuretic
          • NOT aldosterone (giving aldosterone worsens hypertension + edema)
      • 2.  Type II - Proximal RTA
        • Proximal tubule not working
        • Normally reabsorbs glucose, phosphate, amino acids, citrate, potassium.  If not functional, will waste these electrolytes.
          • Urine dip stick positive for glucose, low PO4, low serum K+, low HCO3
          • Eventually when bicarb falls very low, distal nephron (which is still working) creates ammonia --->> can make acid urine!!! (when low serum bicarb)
          • Hallmark: additional disorders (glucose, K+, HCO3, PO4)
          • NOTE: acetazolamide (used for glaucoma, high altitude), causes localized proximal tubule defect (just waste bicarb)
          • Causes:  (bold = most common)
            • Meds: Tenofovir, Ifosfamide, amyloidosis, multiple myeloma, renal transplant, heavy metal toxicity (Cadmium, copper, lead mercury), Wilson's Disease.
          • Treatment:
            • Very difficult to treat.
            • Alkali therapy?
      • 3.  Type I - Distal RTA (dRTA)
        • Suspected RTA, but do not have glycosuria (hallmark of pRTA)
        • Have hypokalemia
        • No matter how low HCO3 or pH gets, cannot make acid urine
        • Urine pH ALWAYS > 5.5 (can never acidify urine)
        • Symptoms:
          • Kidney Stones & Bone Disease
          • Bone used as buffer, increases calcium filtration, causing nephrocalcinosis
        • Causes: (none are common, but bold = more common)
          • Familial (Sjogren's, SLE, RA)
          • Cirrhosis
          • Meds (Amphotericin B, Ifosphamide, Lithium)
          • Hypercalciuria
          • Hyperglobulinemia
        • Treatment:
          • Correct K+ deficit
          • Alkali therapy 
      • NOTE: Topiramate inhibits carbonic anhydrase in proximal & distal tubule
        • Mixed acidosis pRTA + dRTA
        • High risk of CaPO4 renal stones (high urinary pH, hypocitraturia) (citrate absorbed in proximal tubule, is natural calcium chelator, stone inhibitor).

    Metabolic Alkalosis

    • One of two mechanisms:
      • Loss of H+
      • Retention of HCO3-
    • #1 --> Rule out Milk Alkali Syndrome & Hypercalcemia!!
    • Kidneys recognize Cl and HCO3 as equal, if give patient Chloride, they will get rid of extra bicarb. (if problem outside kidneys, urine chloride is low) 
    • Effects:
      • Reduces myocardial contractility
      • Promotes peripheral vasoconstriction (decreases calcium)
      • Shifts oxyhemoglobin dissociation curve to the left (Bohr effect) --> reduces tissue O2
      • Increased cellular O2 consumption (glycolytic activity increased)
    • Approach:
      • Hypervolemia - Aldosterone is ON
        • (i.e. Liddle's Syndrome (ENaC active), renin-secreting tumor, malignant HTN, renovascular HTN, primary hyperadlosteronism, liquorish)
      • Hypovolemic (Low or Normal BP)
        • GI Losses of H+ (vomiting)  --> Urine Chloride very low
        • Urinary Losses of H+
          • Diuretics (i.e. Thiazides block NaCl transporter in DCT, increased distal delivery of Na + Cl.  Na taken up by principal cell ENaC channel, causing K+ to be lost.  The intercalated cell is in the vicinity, takes up K+, secretes H+, which prevents severe hypokalemia).
        • Bicarb reabsorption
          • Dehydration causes RAAS activation.  AngII stimulates proximal Na reabsorption, and HCO3- comes along, which perpetuates metabolic alkalosis. 
    • Labs:
      • Check urinary chloride (down in vomiting)
        • Chloride-Responsive Chloride-Resistant

          Urinary Chloride < 15 mEq/L

          (some say < 20)

          Urinary Chloride > 25 mEq/L

          (some say > 20)

          EXTRA-RENAL LOSS RENAL LOSS

          1.  Loss of gastric acid

          2.  Diuretics

          3.  Volume Depletion

          4.  Post-hypercapnia

           

          NORMOTENSIVE

          Bartter syndrome and Gitelman syndrome

            (Loop                        Thiazide)

          Diuretics

          HypoK+ (kidney things K+ = acidosis)

          HypoMg++

           

          HYPERTENSIVE

          RAAS Excess

          Mineralocorticoid excess

          Replace chloride Correct cause
    • Causes:
      • GI Losses of Acid (NG suction, vomiting)
        • Chloride depletion causes HCO3 reabsorption in kidneys
      • Diuretics (Thiazide, Loop)
        • Through the loss of chloride (HCO3 reabsorption to maintain electrical neutrality)
      • Volume Depletion
        • Two mechanisms:
          • Increased renal sodium reabsorption = increased HCO3 reabsorption
          • Renin release --> aldosterone production --> Promotes H+ secretion in distal tubules.
        • Interesting: volume replacement does not correct it, but CHLORIDE replacement does.  Most resuscitation fluids have chloride so not clinically relevant.
      • Hypokalemia
        • Trans-cellular shift of H+ into cells
        • Increased H+ secretion in distal tubules.
      • Chronic CO2 retention
      • Organic Anions (citrate in blood transfusions [but need >8u], lactate in lactated Ringers, etc..), small effect
      • Consider genetic disorders
        • Bartter syndrome (mnemonic: B-  BAD: a lot worse than Gitelman)
          • Behaves like chronically on a loop diuretic
          • If not recognized in childhood, hyperkalemia and metabolic alkalosis causes problems.
          • Diagnosed typically in childhood
        • Gitelman syndrome (mnemonic: G - GOOD: less severe than Bartter)
          • Acts as if chronically on a high-dose thiazide
          • Diagnosis often made in adulthood
    • Treatments:
      • Mild metabolic alkalosis from diuretic use does not require treatment
      • Correct volume depletion with isotonic saline!! 
      • Fix Mg and K+ abnormalities!!!! (very common cause)
      • GI losses (i.e. NG suction chronically)
        • Use PPI
      • Chloride Responsive:
        • Replace chloride if chloride-responsive (usually dehydrated anyway)
          • CL deficit = 0.2 x wt (kg) x (normal - current plasma chloride)
          •  Volume of 0.9% NaCl (L) = CL deficit / 154
        • Use Potassium Chloride if hypokalemia concomitant
        • Hydrochloric Acid IV (not advisable - very sclerosing, tissue necrosis if extravasate) - prev used in ICU, but no longer needed due to PPIs.
      • Chloride Resistant
        • Fix underlying cause
        • Can use acetazolamide --> blocks HCO3 reabsorption in proximal tubule
          • Essentially creates renal-tubular acidosis - wastes bicarb.
          • 5-10 mg/kg IV (or PO) - max effect at 15 hours
          • Promotes volume + potassium depletion (fix these first before giving acetazolamide)
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