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Sodyum Bikarbonat

Clinical Effects:

  • USES: Sodium bicarbonate is used to treat metabolic acidosis, hyperkalemia, to treat QRS widening and dysrhythmias resulting from drugs that cause sodium channel blockade, to prevent contrast-induce nephropathy, and to alkalinize the urine. It is also present in antacids, mouthwash and baking soda. It is also an additive in meat processing and used to clean and neutralize acidity in vegetables. PHARMACOLOGY: Sodium bicarbonate dissociates to provide bicarbonate ions. Bicarbonate neutralizes hydrogen ion concentration and raises blood and urinary pH. Dissociated sodium ions help to overcome sodium channel blockade from certain sodium channel blocking drugs. TOXICOLOGY: Toxic effects from sodium bicarbonate are secondary to the sodium and bicarbonate ions which causes hypernatremia, alkalosis, and other secondary effects. EPIDEMIOLOGY: Sodium bicarbonate is extremely common in the environment and potential exposures are very common but rarely serious. Indeed, it is given as a treatment for many seriously ill patients. However, fatalities, though very rare, can occur with exposures, especially in small children. OVERDOSE: MILD TO MODERATE TOXICITY: Gastrointestinal symptoms are common, including nausea, vomiting, belching, flatulence, and gastric distention. Mild metabolic effects are possible, including alkalosis, hypocalcemia, hypokalemia and hypernatremia with associated dizziness, weakness and irritability. SEVERE TOXICITY: Severe alkalemia may result in impaired oxygen release from hemoglobin, hypocalcemia tetany, paradoxical intracellular acidosis (from elevated pCO2), and hypokalemia. Hypernatremia and hyperosmolality can cause seizures and coma. Excessive sodium bicarbonate may also cause congestive heart failure exacerbation and pulmonary edema. Electrolyte abnormalities secondary to sodium bicarbonate administration may lead to QT prolongation and cardiac dysrhythmias. Severe gastric distention can rarely lead to stomach rupture with severe abdominal pain and hematemesis. Parenteral sodium bicarbonate extravasation may lead to tissue inflammation and necrosis. Inhalational exposures may cause pulmonary irritation, especially if exposed to higher concentrations as in some fire extinguishers. Dermal and eye exposures may cause some mild irritation. ADVERSE EFFECTS: Adverse events include gastrointestinal symptoms such as nausea, vomiting, belching, and flatulence from oral exposures and mild electrolyte abnormalities (hypokalemia, hypocalcemia, hypernatremia) and metabolic alkalosis.

Range of Toxicity:

  • BASIC FORMULATION: Per the manufacturer, baking soda products contain 41.8 mEq (952 mg) of sodium per teaspoonful and 1 gram of sodium bicarbonate = 11.9 mEq of sodium. Therefore, 41.8 mEq sodium/1 teaspoonful of sodium bicarbonate X 1 gram of sodium bicarbonate/11.9 mEq sodium = 3.512 grams of sodium bicarbonate per 1 teaspoonful. ADULT EXPOSURE: Adults with normal renal function can tolerate up to 1700 mEq daily with minimal symptoms. Alkalosis occurred in 10% of patients treated with 380 mEq sodium bicarbonate/day in combination with calcium carbonate. PEDIATRIC EXPOSURE: Life-threatening alkalosis has occurred after one tablespoonful (15 mL) in a 4 month-old infant. Much larger amounts are needed to cause hypernatremia (10 to 20 g/kg). In terms of lethal hypernatremia (serum Na greater than 185 mEq/L), it is estimated that a 3-year-old child would have to ingest about 4 tablespoonfuls/day for 10 days. DERMAL EXPOSURE: Topical application of sodium bicarbonate to denuded perineum resulted in toxicity to a 7 week old infant. THERAPEUTIC DOSE: Doses in adults and children vary depending on the route of administration and indication. In cardiac arrest, typical doses are in the 1 mEq/kg/dose range and repeated doses are guided by arterial blood gases. In hyperkalemia, initial dose IV is 50 mEq over 5 minutes. In patients with chronic renal failure with plasma HCO3 less than 15 mEq/L, initial doses start with 20 to 6 mEq/day in divided doses. In patients with renal tubular acidosis, oral doses range from 0.5 to 0 mEq/kg/day. Adult antacid dosing is from 325 mg to 2 g up to 4 times a day.


  • Support: MANAGEMENT OF MILD TO MODERATE TOXICITY: For mild or moderate exposures, supportive care is the mainstay of treatment. Correct electrolyte abnormalities. Irrigate exposed eyes. Wash exposed skin. Administer inhaled beta agonists for bronchospasm. MANAGEMENT OF SEVERE TOXICITY: For patients with severe toxicity, supportive care is the mainstay of treatment. Hypotension can be treated with fluid boluses and pressors as necessary. Electrolyte abnormalities may be corrected as needed, but care must be taken not to correct serum sodium levels too quickly (which may cause seizures). Administration of 5% dextrose and half normal to normal saline with rates of administration usually at 2/3 of daily maintenance is critical. In addition, supplementation of potassium may be necessary. Acetazolamide may selectively correct alkalosis by promoting urinary bicarbonate excretion. However, it should NOT be used if serum potassium is less than 3.5 mEq/L. Treat seizures by correcting electrolyte abnormalities and administering benzodiazepines, add propofol or barbiturates if seizures persist or recur. INHALATION: Move the patient from the toxic environment to fresh air. Supportive care with supplemental oxygen and assisted ventilation as needed. Patients that develop bronchospasm can be treated with inhaled beta adrenergic agonists. PARENTERAL: Aspirate as much fluid from the aria as possible before removing the IV catheter. Extravasation injuries may require close monitoring and supportive care for pain and tissue injury. Severe extravasation that leads to tissue inflammation/necrosis or compartment syndromes may require surgical intervention.
  • Decontamination: PREHOSPITAL: GI decontamination is not indicated. Irrigate exposed eyes. Wash skin with soap and water. HOSPITAL: GI decontamination is not indicated. Irrigate exposed eyes. Wash skin with soap and water.
  • Metabolic alkalosis: Most patients do well with gradual correction of their metabolic acidosis by administration of a combination of 0.9% saline and 0.45% saline and intravenous potassium repletion. In patients with very severe alkalemia (pH greater than 7.6 in unstable patients not responding to hydration), therapy with ammonium chloride or dilute HCl may be considered, but this is rarely necessary. Ammonium chloride diluted in NS may be given IV over 12 to 24 hours. This requires close monitoring of blood pH, electrolytes, and BUN. The dose is calculated by determining the hydrogen ion deficit and bicarbonate excess using the following formula: Serum HCO3 level minus normal HCO3 level x 0.5 x body weight (kg) = amount of acid needed. Alternatively, one may treat SEVERE alkalemia with dilute (0.1 normal) HCl through a central venous catheter. HCl should be given as a 0.1 NS in 1 L of 5% dextrose or 0.225% sodium chloride IV over 6 to 24 hours at a rate of 10 mEq/hr up to 100 mEq/day. The dose calculated should be the same as listed above for ammonium chloride.
  • Ventricular arrhythmia: Primary treatment is correction of electrolyte abnormalities, particularly hypokalemia. Institute continuous cardiac monitoring and obtain an ECG. Evaluate for electrolyte abnormalities (particularly hypokalemia, hypocalcemia, and hypomagnesemia) and correct as needed. Lidocaine and amiodarone are general first line agents for stable monomorphic ventricular tachycardia.
  • Acute lung injury: Maintain adequate ventilation and oxygenation with appropriate monitoring. If a patient does develop acute lung injury, ventilation with small tidal volumes (6 mL/kg) is preferred. Antibiotics are only indicated when there is evidence of infection. Experimental therapies include partial liquid ventilation and the use of calfactant.
  • Cerebral edema: For patients with cerebral edema and elevated intracranial pressure, emergent treatment includes head elevation, administration of mannitol, and hyperventilation if there is evidence of herniation. Monitoring intracranial pressures, cerebral perfusion pressures, and cerebral blood flow may be needed. Mechanical decompression with ventriculostomy with CSF drainage, or craniectomy may be useful.
  • Antidote: There is no specific antidote for sodium bicarbonate.
  • Monitoring of patient: Monitor serum electrolytes and renal function. In symptomatic patients or those with metabolic alkalosis monitor arterial or venous pH, urinary electrolytes and pH, and ECG. Depending on the patient’s symptoms and electrolyte abnormalities, continuous cardiac monitoring, pulse oximetry, mental status checks, and head CT may be indicated.
  • Enhanced elimination procedure: Hemodialysis may be considered for seriously ill patients, especially those with renal insufficiency, with the use of high chloride, low acetate dialysate to remove bicarbonate and sodium and replace chloride deficits when other measures are ineffective.
  • Patient disposition: HOME CRITERIA: Older children or adults with unintentional ingestions with minimal to no symptoms may be managed at home. OBSERVATION CRITERIA: Patients should be sent to a healthcare facility if their exposure to sodium bicarbonate was a self-harm attempt or if the patient is symptomatic. They should be observed for 4 to 6 hours and be clearly improving or asymptomatic prior to discharge. Electrolytes should also be within normal limits or normalizing. In young children, minimal exposures can be symptomatic so any such exposures should be sent in for observation and lab work. ADMISSION CRITERIA: Patients with severe symptoms or getting worse after an observation period of 4 to 6 hours should be admitted to the hospital. Depending on the severity of their symptoms, ICU admission may be warranted (eg, for intubated patients or patients with severe metabolic or electrolyte abnormalities). Patients should not be discharged until they are clearly improving or asymptomatic. CONSULT CRITERIA: Patients admitted to the ICU may require consult by a critical care specialists. A nephrologist may be helpful in managing metabolic and electrolyte abnormalities. Consult a medical toxicologist or poison center for patients with severe toxicity or in whom the diagnosis is unclear.
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