Chapter 121. Oxalic Acid

Oxalic acid and oxalates are used as bleaches, metal cleaners, and rust removers and in chemical synthesis and leather tanning. A laundry powder containing sachets of oxalic acid and potassium permanganate was reported to cause an epidemic of fatal self-poisonings in Sri Lanka. Soluble and insoluble oxalate salts are found in several species of plants.

1. Mechanism of toxicity

   1. Oxalic acid solutions are highly irritating and corrosive. Ingestion and absorption of oxalate cause acute hypocalcemia resulting from precipitation of the insoluble calcium oxalate salt. Calcium oxalate crystals may then deposit in the brain, heart, kidneys, and other sites, causing serious systemic damage.

   2. Insoluble calcium oxalate salt found in Dieffenbachia and similar plants is not absorbed, but it causes local mucous membrane irritation.

2. Toxic dose. Ingestion of 5–15 g of oxalic acid has caused death. The recommended workplace limit (ACGIH TLV-TWA) for oxalic acid vapor is 1 mg/m3 as an 8-hour time-weighted average. The level considered immediately dangerous to life or health (IDLH) is 500 mg/m3.

3. Clinical presentation. Toxicity may occur as a result of skin or eye contact, inhalation, or ingestion.

   1. Acute skin or eye contact causes irritation and burning, which may lead to serious corrosive injury if the exposure and concentration are high.

   2. Inhalation may cause sore throat, cough, and wheezing. Large exposures may lead to chemical pneumonitis or pulmonary edema.

   3. Ingestion of soluble oxalates may result in weakness, tetany, convulsions, and cardiac arrest due to profound hypocalcemia. The QT interval may be prolonged, and variable conduction defects may occur. Oxalate crystals may be found on urinalysis. Insoluble oxalate crystals are not absorbed but can cause irritation and swelling in the oropharynx and esophagus.

4. Diagnosis is based on a history of exposure and evidence of local or systemic effects or oxalate crystalluria.

   1. Specific levels. Serum oxalate levels are not available.

   2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, calcium, ECG monitoring, and urinalysis.

5. Treatment

   1. Emergency and supportive measures

      1. Protect the airway (See Airway), which may become acutely swollen and obstructed after a significant ingestion or inhalation. Administer supplemental oxygen and assist ventilation if necessary (See Airway and Breathing).

      2. Treat coma (See Coma and stupor), seizures (See Seizures), and arrhythmias (See QRS interval prolongation, Tachycardia, and Ventricular dysrhythmias) if they occur.

      3. Monitor the ECG and vital signs for at least 6 hours after significant exposure and admit symptomatic patients to an intensive care unit.

   2. Specific drugs and antidotes. Administer 10% calcium solution (chloride or gluconate) to counteract symptomatic hypocalcemia (See Calcium).

   3. Decontamination (See Decontamination)

      1. Insoluble oxalates in plants. Flush exposed areas. For ingestions, dilute with plain water; do not induce vomiting or give charcoal.

      2. Oxalic acid or strong commercial oxalate solutions. Immediately flush with copious water. Do not induce vomiting because of the risk for aggravating corrosive injury; instead, give water to dilute, and on arrival in the hospital perform gastric lavage.

      3. Plants containing soluble oxalates. Attempt to precipitate ingested oxalate in the stomach by administering calcium (calcium chloride or gluconate, 1–2 g, or calcium carbonate [Tums], several tablets) orally or via a gastric tube. The effectiveness of activated charcoal is unknown.

   4. Enhanced elimination. Maintain high-volume urine flow (3–5 mL/kg/h) to help prevent calcium oxalate precipitation in the tubules. Oxalate is removed by hemodialysis, but the indications for this treatment are not established.