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.