Article

Baking soda misuse as a home remedy: Case experience of the California Poison Control System

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Abstract

Baking soda is a common household product promoted by the manufacturer as an antacid. It contains sodium bicarbonate and has the potential for significant toxicity when ingested in excessive amounts. Characterizing the patterns and outcomes from the misuse of baking soda as a home remedy can guide the clinical assessment and preventative counselling of patients at risk for use of this product. We conducted a retrospective review of all symptomatic cases involving ingestion and misuse of a baking soda powder product that were reported to the California Poison Control System between the years 2000 and 2012. Of the 192 cases we identified, 55·8% were female, ages ranged 2 months to 79 years, and the most common reasons for misuse included antacid (60·4%), 'beat a urine drug test' (11·5%) and treat a UTI (4·7%). Most cases (55·2%) had significant symptoms warranting a medical evaluation, whereas 12 patients required hospital admission developed either electrolyte imbalances, metabolic alkalosis or respiratory depression. Misuse of baking soda can result in serious electrolyte and acid/base imbalances. Patients at highest risk of toxicity may include those who chronically use an antacid, those who use the method to 'beat' urine drug screens, pregnant women and young children. Self-treatment with baking soda as a home remedy may also mask or delay medical care thereby complicating or exacerbating an existing medical problem. We suggest that healthcare providers counsel high-risk patients about the potential complications of misuse of baking soda as a home remedy.

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... Hypothetically, soluble base treatment could exacerbate vascular calcification, however no examination has been acted in people to test this impact [16]. ( Nonetheless, treatment with sodium bicarbonate might be related with some reactions, for example, hypokalemia, ionized hypocalcaemia, hypercapnia, prolongation of the QTc stretch, an ascent in the urinary discharge of sodium, and the possibility to disintegrate vascular calcifications on constant organization [17]. ...
... Thyroid brokenness and dyslipidemia in CKD may additionally expand CVD chance prompting expanded bleakness and mortality [16]. Dyslipidemia with higher LDL and lower HDL cholesterol is related with atherosclerotic vascular infection that expansion the danger of CVD occasions [17]. Proteinuria related with movement of renal infection, expand hazard for cardiovascular occasions as myocardial ischemia as it expanded hazard for atherosclerotic occasions and increment cardiovascular mortality [17]). ...
... Dyslipidemia with higher LDL and lower HDL cholesterol is related with atherosclerotic vascular infection that expansion the danger of CVD occasions [17]. Proteinuria related with movement of renal infection, expand hazard for cardiovascular occasions as myocardial ischemia as it expanded hazard for atherosclerotic occasions and increment cardiovascular mortality [17]). Microalbuminuria may possibly be related with constant aggravation [18]. ...
... Hypothetically, soluble base treatment could exacerbate vascular calcification, however no examination has been acted in people to test this impact [16]. ( Nonetheless, treatment with sodium bicarbonate might be related with some reactions, for example, hypokalemia, ionized hypocalcaemia, hypercapnia, prolongation of the QTc stretch, an ascent in the urinary discharge of sodium, and the possibility to disintegrate vascular calcifications on constant organization [17]. ...
... Thyroid brokenness and dyslipidemia in CKD may additionally expand CVD chance prompting expanded bleakness and mortality [16]. Dyslipidemia with higher LDL and lower HDL cholesterol is related with atherosclerotic vascular infection that expansion the danger of CVD occasions [17]. Proteinuria related with movement of renal infection, expand hazard for cardiovascular occasions as myocardial ischemia as it expanded hazard for atherosclerotic occasions and increment cardiovascular mortality [17]). ...
... Dyslipidemia with higher LDL and lower HDL cholesterol is related with atherosclerotic vascular infection that expansion the danger of CVD occasions [17]. Proteinuria related with movement of renal infection, expand hazard for cardiovascular occasions as myocardial ischemia as it expanded hazard for atherosclerotic occasions and increment cardiovascular mortality [17]). Microalbuminuria may possibly be related with constant aggravation [18]. ...
... It is a widely available household product used for cooking, baking, personal care and cleaning purposes [3]. It has long been used also as a home remedy for heartburn and indigestion, and also misused as an agent to "beat a urine drug test" and to treat urinary infections [4]. In clinical medicine it's used to treat severe metabolic acidosis, hyperkalemia, dysrhythmias, tricyclics and diphenhydramine overdose [1,5]. ...
... Baking soda products contain 59 mEq sodium and bicarbonate per teaspoonful [4]. The short-term administration of large amounts of sodium bicarbonate to normal individuals usually results in very rapid renal excretion of the entire alkali load with minimal increase in the bicarbonate concentration [10,11]. ...
... Reduced cerebral blood flow, cerebral vasoconstriction and CSF alkalosis has also been observed [8,13,14]. Myocardial irritability can lead to supraventricular and ventricular arrhythmias [4,9,15]. Respiratory failure is caused by compensatory hypoventilation, decreased tissue oxygen delivery from a left shift of oxygen dissociation curve (Bohr effect), and decreased sensitivity of peripheral chemoreceptors to hypoxia [16][17][18]. ...
... In addition, abrupt cessation of sodium bicarbonate might also result in adverse effect. Interestingly, several articles exist in the literature reporting the toxicity of chronic ingestion of sodium bicarbonate [44][45][46][47]. Indeed, baking soda, a common household product containing sodium bicarbonate has frequently been taken as an antacid to relieve heartburn. ...
... As expected, excessive ingestion of baking soda results in serious electrolyte imbalance requiring medical attention. Gastrointestinal symptoms such as abdominal pain, diarrhea, vomiting are frequently reported in this patients coupled with other symptoms including lethargy and weakness [45]. Respiratory compensation was also noticed with blood hypercapnia. ...
... Respiratory compensation was also noticed with blood hypercapnia. Adverse effects were already reported in patients taking less than two teaspoons of baking soda with one teaspoon containing 4.8 g of sodium bicarbonate [45]. ...
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Despite recent therapeutic progress, cancer remains a major cause of death in industrialized countries. As a consequence, alternative treatments attract the attention of a growing number of patients. Among these therapies, the use of sodium bicarbonate to fight cancer has gained considerable interest. According to self-medication reports available on the internet, sodium bicarbonate is viewed by many patients as a simple, costless and efficient anti-cancer agent. Although no clinical study has demonstrated an anti-cancer activity of sodium bicarbonate up to date, emerging experimental reports indicate, that sodium bicarbonate may slow the progression of cancer. Here, we highlight the rationale to use sodium bicarbonate in cancer therapy and further enumerate experimental evidence for its anti-tumoral activity. Finally, we speculate about a future role of sodium bicarbonate in cancer therapy.
... As a strong base, it serves as a buffer to neutralize acid, and its consumer use stems from its properties as a deodorizing, degreasing, and cleaning agent. Sodium bicarbonate toxicity manifesting as metabolic alkalosis has previously been reported following oral ingestion in the setting of dyspepsia [1,2]. However, its use as a non-ingested agent, like a toothpaste additive, has not been reported as a potential cause of toxicity. ...
... This explains the higher risk of alkalosis with a product that is widely available over the counter to all the population. Sodium bicarbonate toxicity is mostly related with its use as antacid and in smaller proportions as a strategy to cause false negative illicit drug tests and to treat UTIs [1][2][3]. Nonetheless, physicians should be aware of this common but underreported use of toxicity related to baking soda exposure. Springer Nature journal content, brought to you courtesy of Springer Nature Customer Service Center GmbH ("Springer Nature"). ...
Article
Full-text available
Background: Sodium bicarbonate, in the form of baking soda, is widely used as a home remedy, and as an additive for personal and household cleaning products. Its toxicity has previously been reported following oral ingestion in the setting of dyspepsia. However, its use as a non-ingested agent, like a toothpaste additive, has not been reported as a potential cause of toxicity. Case presentation: We are reporting a case of an 80-year-old woman who presented with chronic metabolic alkalosis and hypokalemia secondary to exogenous alkali exposure from baking soda as a toothpaste additive, which might have represented an underreported ingestion of the substance. Conclusions: Considering that one teaspoon of baking soda provides approximately 59 m-equivalents (mEq) of bicarbonate, specific questioning on its general use should be pursued in similar cases of chloride resistant metabolic alkalosis.
... 2,6,12-14 A retrospective review of all symptomatic cases reported to the California Poison Control system between 2000-2012 found that the most common reasons for reports were antacid misuse (60.4%), attempts to alter urine drug testing (11.5%), and urinary tract infection treatment (4.7%). 12 There have been other reports of baking soda toxicity in the setting of pica and topical use in an infant with diaper rash. 3,15 Our patient was unable to articulate his reasons for ingestion. ...
... Most commonly, patients present with nausea, vomiting, and abdominal pain; 16 however,1-5% of patients will present with neurologic symptoms such as lethargy, drowsiness, nystagmus, seizures, weakness and rarely coma. 12 Cardiac arrhythmias and cardiopulmonary arrest have been reported, as well as a case of a pregnant woman at 37 weeks gestation with baking soda pica who presented with rhabdomyolysis and peripartum cardiomyopathy. 5,15,17 Spontaneous rupture of the stomach after sodium bicarbonate ingestion, thought to be due to increased CO 2 production following bicarbonate reaction with acidic gastric contents, has also been reported. ...
Article
Full-text available
Baking soda is a readily available household product composed of sodium bicarbonate. It can be used as a home remedy to treat dyspepsia. If used in excessive amounts, baking soda has the potential to cause a variety of serious metabolic abnormalities. We believe this is the first reported case of hemorrhagic encephalopathy induced by baking soda ingestion. Healthcare providers should be aware of the dangers of baking soda misuse and the associated adverse effects. [West J Emerg Med. 2016;17(5)619-622.]
... They first demonstrated that utilisation of 'buffer therapy' in the form of bicarbonate acts to increase tumour pH e without an appreciable effect on systemic pH via a 'compensated metabolic alkalosis' [101]. Past concerns have been raised over the chronic use of bicarbonate due to detrimental effects arising from disrupted pH homeostasis however it is important to note that these observations typically stemmed from an uncontrolled 'self-dosing' of bicarbonate [102]. Therefore, demonstration of controlled bicarbonate therapy specifically targeting tumour pH e without harming systemic pH is reassuring. ...
Article
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... Use of sweeteners and/or flavoring agents or even other alternatives may increase the compliance [122]. However, oral use of such systemic buffers requires large quantity to be consumed, which may not be without attendant risks of toxicity due to severe electrolyte imbalance [130,131]. Use in titrated concentrations may be recommended as these agents have shown dramatic anticancer effects even in lower concentrations than the optimal desired [7]. ...
Article
Several tumors exhibit pH gradient reversal, with acidification of extracellular pH (pHe) and alkalinization of intracellular pH (pHi). The pH gradient reversal is evident even during the preliminary stages of tumorigenesis and is crucial for survival and propagation of tumors, irrespective of their pathology, genetics and origins. Moreover, this hallmark seems to be present ubiquitously in all malignant tumors. Based on these facts, we propose a new emerging hallmark of cancer "pH gradient reversal". Normalizing pH gradient reversal through inhibition of various proton transporters such as Na+-H+ exchanger (NHE), Vacuolar-type H+-ATPase (V-ATPase), H+/K+-ATPases and carbonic anhydrases (CAs) has demonstrated substantial therapeutic benefits. Indeed, inhibition of NHE1 is now being regarded as the latest concept in cancer treatment. A recent patent deals with the utilization of cis-Urocanic acid to acidify the pHi and induce apoptosis in tumors. Another patent reports therapeutic benefit by inhibiting Lactate Dehydrogenase - 5 (LDH-5) in various cancers. Several patents have been formulated by designing drugs activated through acidic pHe providing a cancer specific action. The purpose of this review is to analyze the available literature and help design selective therapies that could be a valuable adjunct to the conventional therapies or even replace them.
... A recent retrospective review of symptomatic cases involving ingestion of baking soda powder (household sodium bicarbonate) reports that 192 cases were notified to the California Poison Control System between the years 2000 and 2012 and concludes that misuse of baking soda may result in severe acid-base and electrolyte alterations or respiratory depression, particularly in children, pregnant women, alcoholics, and patients on diuretics and when baking soda is used regularly as an antacid or to alter urine drugs screen tests [93]. Therapy with sodium bicarbonate may be associated with some side effects, such as hypokalemia, ionized hypocalcemia, hypercapnia, hemodynamic instability, particularly during hemodialysis sessions, prolongation of the QTc interval, a rise in the urinary excretion of sodium, and the potential to deteriorate vascular calcifications on chronic administration (Table 4). ...
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The milk-alkali syndrome became rare with the advent of modern ulcer therapy with nonabsorbable antacids, histamine2 blockers, and sucralfate. An increased frequency of this syndrome seems likely with the growing popularity of the use of calcium carbonate as an antacid or as calcium supplementation to prevent osteoporosis. We treated five patients who had six episodes of the milk-alkali syndrome; four of these cases were diagnosed between 1990 and 1992. All patients were ingesting massive quantities of calcium and absorbable alkali and were unaware of the toxic effects of these compounds. All patients presented with the triad of hypercalcemia, metabolic alkalosis, and renal failure. All metabolic abnormalities were corrected, and renal function improved with appropriate supportive measures and cessation of calcium and alkali ingestion. In two patients, the renal failure was so severe that dialysis was necessary. In four patients, either the serum amino-terminal parathyroid hormone or 1,25-dihydroxycholecalciferol levels were appropriately decreased in response to hypercalcemia. The serum carboxy-terminal parathyroid hormone levels were increased because of renal failure. Since both physicians and patients are often unaware of the calcium and alkali content of many nonprescription medicines, the diagnosis of the milk-alkali syndrome, a reversible cause of renal failure, can be missed if a detailed history of such intake is not elicited. Measurement of the serum amino-terminal parathyroid hormone and 1,25-dihydroxycholecalciferol levels may help differentiate milk-alkali syndrome from primary hyperparathyroidism.
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The case is described of a 29-year-old man with renal failure and recurrent hyperparathyroidism who 3 weeks postparathyroidectomy developed hypocalcemic tetany because he was taking one-half the prescribed dose of calcitriol. He interpreted his symptoms as those of potassium intoxication and self-administered almost 1,500 mEq sodium bicarbonate. The increase in plasma sodium and osmolarity led to increased fluid intake, and at presentation he had an ionized calcium of 0.50 mmol/L, K 5.3 mmol/L, Na 148 mmol/L, total CO2 52.6 mmol/L, pO2 51.2 mm Hg, and pH of 7.61. He had gained 7 kg in weight. All abnormalities were corrected by dialysis, using initially a calcium-free dialyzate with extra calcium infused. The case illustrates the effect of alkalosis in reducing the amount of calcium that exists in ionized form, and it is suggested that complexing of calcium as calcium bicarbonate together with the pH change contributed to the decrease in ionized calcium. It is also an example of the hazards of treating patients who devise their own therapeutic regimens.
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Oral ingestion of baking soda (sodium bicarbonate) has been used for decades as a home remedy for acid indigestion. Excessive bicarbonate ingestion places patients at risk for a variety of metabolic derangements including metabolic alkalosis, hypokalemia, hypernatremia, and even hypoxia. The clinical presentation is highly variable but can include seizures, dysrhythmias, and cardiopulmonary arrest. We present two cases of severe metabolic alkalosis in patients with unsuspected antacid overdose. The presentation and pathophysiology of antacid-related metabolic alkalosis is reviewed.
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We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis. A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices. Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.
Article
A 68-year-old man presented to the Emergency Department with a severe metabolic alkalosis after ingesting large quantities of baking soda to treat his dyspepsia. His underlying pulmonary disease and a progressively worsening mental status necessitated intubation for respiratory failure. Laboratory studies revealed a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis. The patient was successfully treated after cessation of the oral bicarbonate, initiation of intravenous hydration, and correction of electrolyte abnormalities.
Letter to Editor. Baking soda toxicity
  • Razzavi
Razzavi B. Letter to Editor. Baking soda toxicity. Am J Med, 2000;108:756-757.
Available at: http://www.armandhammer. com/solutions/solution-53
ARM & HAMMERâ Baking soda package. Available at: http://www.armandhammer. com/solutions/solution-53/Antacid.aspx. (accessed 9 October 2012).
Natural Choices for Women's Health Available at: http://www. livestrong.com/article/52007 8-baking-soda-water-for-urinary-tract infec- tions
  • L Steelsmith
Steelsmith L. Natural Choices for Women's Health. 2005. Available at: http://www. livestrong.com/article/52007 8-baking-soda-water-for-urinary-tract infec- tions/#ixzz2XHRUMGwj (accessed 12 June 2013).
Rugby Laboratories, Inc.] Drug fact sheet Available at
  • Sodium Bicarbonate
Hypocalcemic tetany and metabolic alkalosis in a dialysis patient: an unusual event
  • M Kaye
  • Pj Somerville
  • G Lowe
  • M Katis
  • W Schneider
Spontaneous rupture of the normal stomach after sodium bicarbonate ingestion
  • N Lazebnik
  • A Lellin
  • M Michowitz
Antacid Drug Products for Over-the-Counter Human Use
  • Food and Drug Administration
Food and Drug Administration. Antacid Drug Products for Over-the-Counter Human Use. Fed Reg 1994; 59.
Baking Soda: a potentially fatal home remedy
  • Nichols