Table of contents
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Introduction
- NOTE: For interpretation of arterial blood gasses, go to:
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).
- 1. Type IV - distal RTA - Hypoaldosteronism (most common!!! By far!)
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.
- Hypervolemia - Aldosterone is ON
- 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
-
- Check urinary chloride (down in vomiting)
- 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.
- Two mechanisms:
- 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
- Bartter syndrome (mnemonic: B- BAD: a lot worse than Gitelman)
- GI Losses of Acid (NG suction, vomiting)
- 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.
- Replace chloride if chloride-responsive (usually dehydrated anyway)
- 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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