USED CARS mnemonic for non-anion gap metabolic acidosis (NAGMA):
Why “USED CARS”?
• Ureterosigmoidostomy
• Saline & Chloride infusion (excessive).. chloride offsets AG
• Endocrine disorders (Addison’s disease aka adrenal insufficiency, hypoaldosteronism)
• Diarrhea
• Carbonic anhydrase inhibitors
• Ammonium chloride
• Renal tubular acidosis
• Spironolactone
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U – Ureteroenteric fistula (or diversion surgery)
• Why NAGMA?
• Ureter attached directly to colon; bicarbonate lost into bowel, chloride absorbed, causing hyperchloremic acidosis.
• Symptoms:
• History of bladder/colon surgery, urine-like smell from stool, chronic acidosis.
• Labs: Normal AG, elevated chloride, chronic metabolic acidosis.
• ED Management:
• Identify, refer to urology or general surgery for definitive repair.
• Correct electrolyte disturbances (usually potassium, bicarbonate).
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S – Saline Infusion (Excessive)
• What: Excessive infusion of normal saline (0.9% NaCl).
• Why (Pathophysiology): High chloride content of NS dilutes bicarbonate → hyperchloremic metabolic acidosis (common in hospitalized patients).
• Symptoms: Usually subtle (fatigue, mild confusion, fluid overload signs).
• Labs: Normal AG, hyperchloremia, normal renal function initially.
• ED Management:
• Switch to balanced solutions (Lactated Ringer’s, Plasmalyte).
• Monitor fluid and electrolyte balance.
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E – Endocrine Disorders (Addison’s Disease/Adrenal Insufficiency):
• Why: Lack of aldosterone = inability to excrete acid & retain sodium.
• Clinical Clues: Weakness, fatigue, low BP, dizziness, hyperpigmentation (skin darkening), abdominal pain.
• Labs: Low sodium, high potassium, normal anion gap, metabolic acidosis.
• ED Management:
• IV fluids (Normal saline), hydrocortisone, monitor electrolytes closely.
• Admit for adrenal crisis management.
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D – Diarrhea
• Pathophysiology: Loss of bicarbonate-rich fluids via stool → bicarbonate depletion.
• Clinical Clues: Frequent watery stools, dehydration signs (tachycardia, low BP).
• Labs: Normal anion gap, hypokalemia common, hyperchloremia.
• ED Management:
• Aggressive fluid resuscitation (often NS or LR).
• Electrolyte replacement (especially potassium).
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C – Carbonic Anhydrase Inhibitors (Acetazolamide)
• Mechanism: Prevent bicarbonate reabsorption → bicarbonate loss → acidosis.
• Clinical clues: Medication history (glaucoma treatment, altitude sickness prophylaxis, idiopathic intracranial hypertension).
• Labs: Normal AG, mild hypokalemia, mild hyperchloremia.
• ED Management:
• Stop offending medication, supportive care, and electrolyte replacement.
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A – Ammonium Chloride Ingestion
• Mechanism: Direct chloride ingestion overwhelms bicarbonate buffers.
• Rare cause today, often historical or industrial exposure.
• Clinical clues: History of ingestion, occupational exposures, metabolic symptoms (nausea, vomiting, confusion).
• Labs: Normal AG, hyperchloremia.
• ED Management:
• Supportive care, stop exposure.
• Correct metabolic acidosis if severe (sodium bicarbonate IV if severe).
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R – Renal Tubular Acidosis (RTA)
• Mechanism: Kidneys fail to reabsorb bicarbonate or excrete acid properly.
• Bicarbonate replacement.
• Potassium correction (careful monitoring).
• Referral to nephrology.
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R – Renal Tubular Acidosis (Already covered above)
• Included in detail in the “A” section, given its complexity.
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S – Spironolactone (and other Aldosterone Antagonists)
• Mechanism: Blocks aldosterone receptors → reduced acid and potassium excretion.
• Clinical clues:
Use in CHF, cirrhosis, hypertension treatment.
• Hold spironolactone, manage hyperkalemia aggressively (calcium gluconate, insulin/dextrose, albuterol, kayexalate).
• Consider bicarbonate if severely acidotic.