sodium-bicarbonate has been researched along with Poisoning* in 45 studies
13 review(s) available for sodium-bicarbonate and Poisoning
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A Brief Review on Toxic Alcohols: Management Strategies.
The information on burden of alcohol abuse in Iran is scarce. However, the available data show that mortality rates and frequency of its use have increased in the Iranian community. In particular, Iran occupies the 1st rank in the number of outbreak incidents and victims of toxic alcohols such as methanol in the Middle East. Mortality and morbidity of toxic alcohols are high if prompt diagnosis and treatment are not initiated rapidly. On-time diagnosis, proper case finding, and standard treatment have an essential role to reduce mortality and morbidity of toxic alcohols particularly blindness and other physical and psychological disabilities. This review focuses on intoxication with methanol, ethylene glycol, and isopropanol, and their treatment. Topics: 2-Propanol; Acidosis; Alcoholism; Antidotes; Ethanol; Ethylene Glycol; Fomepizole; Humans; Iran; Methanol; Poisoning; Pyrazoles; Renal Dialysis; Sodium Bicarbonate; Solvents | 2016 |
Sodium acetate as a replacement for sodium bicarbonate in medical toxicology: a review.
Sodium bicarbonate is central to the treatment of many poisonings. When it was placed on the FDA drug shortage list in 2012, alternative treatment strategies to specific poisonings were considered. Many hospital pharmacies, poison centers, and medical toxicologists proposed sodium acetate as an adequate alternative, despite a paucity of data to support its use in medical toxicology. The intention of this review is to educate the clinician on the use of sodium acetate and to advise them on the potential adverse events when given in excess. We conducted a literature search focused on the pharmacology of sodium acetate, its use as a buffer in pathologic acidemia and dialysis baths, and potential adverse events associated with excess sodium acetate infusion. It appears safe to replace sodium bicarbonate infusion with sodium acetate on an equimolar basis. The metabolism of acetate, however, is more complex than bicarbonate. Future prospective studies will be needed to confirm the efficacy of sodium acetate in the treatment of the poisoned patient. Topics: Animals; Antidotes; Dose-Response Relationship, Drug; Drug Substitution; Emergency Medical Services; Humans; Infusions, Intravenous; Poisoning; Sodium Acetate; Sodium Bicarbonate; Vascular Resistance | 2013 |
Advances in the management of organophosphate poisoning.
Organophosphate (OP) poisoning is commonly encountered in agricultural communities. The mainstay of therapy in OP poisoning is the use of atropine. However, several other therapies have been evaluated. Although oxime has been the most studied antidote, results in humans have been disappointing and limited by the lack of well-designed, prospective, randomised controlled trials. The key factor in determining outcomes in OP poisoning appears to be the timing of antidote administration. Other adjuvants, such as magnesium, fresh frozen plasma and haemoperfusion appear promising, and need to be explored further. A multi-faceted approach may be the answer to improving outcomes in OP poisoning. This review evaluates the advances in OP management over the last 20 years. Topics: Antidotes; Atropine; Blood Component Transfusion; Chemical Warfare Agents; Cholinesterase Reactivators; Hemoperfusion; Humans; Inhalation Exposure; Magnesium Compounds; Organophosphate Poisoning; Oximes; Pesticides; Plasma; Poisoning; Sodium Bicarbonate; Suicide | 2007 |
Alkalinisation for organophosphorus pesticide poisoning.
Poisoning with organophosphorus pesticides (OPs) is an important cause of morbidity and mortality in all parts of the world, particularly developing countries. The case-fatality ratio for pesticide intentional self-poisoning is around 10-20% even when the standard antidotes (atropine, oximes and benzodiazepines) are used. Alternative treatments have been trialled in an attempt to improve outcomes from acute OP poisoning, one of which is plasma alkalinisation. Animal and preliminary human research has suggested benefit from plasma alkalinisation with sodium bicarbonate (NaHCO3) as a treatment for acute OP poisoning.. To determine the efficacy of alkalinisation, in particular NaHCO3, for the treatment of acute OP poisoning.. We searched MEDLINE (1966-2004), EMBASE (1980-2004), the Controlled Trials Register of the Cochrane Collaboration, Current Awareness in Clinical Toxicology, Info Trac, http://www.google.com.au, and Science Citation Index of studies identified by the previous searches. We also manually reviewed the bibliographies of identified articles and personally contacted experts in the field.. Randomised controlled trials and controlled clinical trials of symptomatic patients following acute OP poisoning treated with alkalinisation. The quality of studies and eligibility for inclusion was assessed using criteria by Jadad and Schulz.. Studies were identified and both authors independently extracted data which was recorded on a pre-designed form. Study design, including the method of randomisation, participant characteristics, type of intervention and outcomes were recorded. Outcomes were discussed, but unfortunately specific analyses could not be performed, given the poor quality of the studies identified.. Five studies were identified but none satisfied inclusion criteria. NaHCO3 was used in each of these to induce alkalinisation. Two studies were uncontrolled, two studies were historically controlled and one study was randomised but poorly concealed. Marked heterogeneity between subjects and treatments was noted - for example, a different regimen of NaHCO3 was used in each study. While there may have been a trend towards improved outcomes (lower total dose of atropine and shorter length of stay), these were not statistically significant.. There is insufficient evidence to support the routine use of plasma alkalinisation for treatment of OP poisoning. Further research is required to determine the method of alkalinisation that will optimise outcomes, and the regimen which will produce the target arterial pH of 7.50 (range 7.45-7.55). This should be followed by a well-designed randomised controlled trial to determine efficacy. Topics: Humans; Organophosphate Poisoning; Pesticides; Poisoning; Sodium Bicarbonate | 2005 |
Management of the cardiovascular complications of tricyclic antidepressant poisoning : role of sodium bicarbonate.
Experimental studies suggest that both alkalinisation and sodium loading are effective in reducing cardiotoxicity independently. Species and experimental differences may explain why sodium bicarbonate appears to work by sodium loading in some studies and by a pH change in others. In the only case series, the administration of intravenous sodium bicarbonate to achieve a systemic pH of 7.5-7.55 reduced QRS prolongation, reversed hypotension (although colloid was also given) and improved mental status in patients with moderate to severe tricyclic antidepressant poisoning. This clinical study supports the use of sodium bicarbonate in the management of the cardiovascular complications of tricyclic antidepressant poisoning. However, the clinical indications and dosing recommendations remain to be clarified. Hypotension should be managed initially by administration of colloid or crystalloid solutions, guided by central venous pressure monitoring. Based on experimental and clinical studies, sodium bicarbonate should then be administered. If hypotension persists despite adequate filling pressure and sodium bicarbonate administration, inotropic support should be initiated. In a non-randomised controlled trial in rats, epinephrine resulted in a higher survival rate and was superior to norepinephrine both when the drugs were used alone or when epinephrine was used in combination with sodium bicarbonate. Sodium bicarbonate alone resulted in a modest increase in survival rate but this increased markedly when sodium bicarbonate was used with epinephrine or norepinephrine. Clinical studies suggest benefit from norepinephrine and dopamine; in an uncontrolled study the former appeared more effective. Glucagon has also been of benefit. Experimental studies suggest extracorporeal circulation membrane oxygenation is also of potential value. The immediate treatment of arrhythmias involves correcting hypoxia, electrolyte abnormalities, hypotension and acidosis. Administration of sodium bicarbonate may resolve arrhythmias even in the absence of acidosis and, only if this therapy fails, should conventional antiarrhythmic drugs be used. The class 1b agent phenytoin may reverse conduction defects and may be used for resistant ventricular tachycardia. There is also limited evidence for benefit from magnesium infusion. However, class 1a and 1c antiarrhythmic drugs should be avoided since they worsen sodium channel blockade, further slow conduction velocity and depress contractility. Topics: Alkalosis, Respiratory; Anti-Arrhythmia Agents; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Humans; Hypotension; Poisoning; Sodium Bicarbonate | 2005 |
How to position our practice?
Topics: Antidepressive Agents, Tricyclic; Antidotes; Clinical Medicine; Consensus; Drug Overdose; Evidence-Based Medicine; Guidelines as Topic; Humans; Poison Control Centers; Poisoning; Sodium Bicarbonate; Toxicology; Treatment Outcome | 2004 |
Does urine alkalinization increase salicylate elimination? If so, why?
Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. Experimental and clinical studies confirm that urinary alkalinization increases salicylate elimination, although the mechanisms by which this occurs have not been elucidated. The conventional view is that ionisation of a weak acid, such as salicylic acid, is increased in an alkaline environment. Since the ionisation constant (pKa) is a logarithmic function then, theoretically, a small change in urine pH will have a disproportionately larger effect on salicylate clearance. Hence, elimination of salicylic acid by the kidneys is increased substantially in alkaline urine. However, as salicylic acid is almost completely ionised within physiological pH limits, alkalinization of the urine could not, therefore, significantly increase the extent of ionisation further and the conventional view of the mechanism by which alkalinization is effective is patently impossible. Further experimental studies are required to clarify the mechanisms by which urine alkalinization enhances salicylate elimination. Topics: Adolescent; Adult; Animals; Female; Half-Life; Humans; Hydrogen-Ion Concentration; Male; Metabolic Clearance Rate; Middle Aged; Poisoning; Salicylates; Sodium Bicarbonate | 2003 |
[Severe flecainide acetate poisoning. Apropos of a case].
Poisoning with flecainide acetate is rare and associated with a high mortality. This usually occurs after massive ingestion but can also be observed during therapeutic overdose in patients with renal failure or with amiodarone therapy. The prognostic depends on the haemodynamic and rhythmic effects of the overdose one sign of which is widening of the QRS complexes. Major sodium bicarbonate or lactate infusion is the generally prescribed treatment. The authors report one case of a patient with renal failure on amiodarone who survived a severe flecainide acetate overdose. Topics: Aged; Amiodarone; Anti-Arrhythmia Agents; Atrial Flutter; Biological Availability; Calcium Gluconate; Charcoal; Combined Modality Therapy; Consciousness Disorders; Diabetic Nephropathies; Drug Interactions; Drug Therapy, Combination; Flecainide; Heart Block; Hemofiltration; Humans; Hypertension; Hypotension; Intestinal Pseudo-Obstruction; Kidney Failure, Chronic; Male; Poisoning; Pulmonary Edema; Renal Dialysis; Respiration, Artificial; Sodium Bicarbonate; Sodium Channel Blockers; Uremia | 1999 |
Poisoning by sodium channel blocking agents.
Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others. Topics: Action Potentials; Drug-Related Side Effects and Adverse Reactions; Heart; Heart Diseases; Humans; Poisoning; Sodium Bicarbonate; Sodium Channel Blockers; Sodium Channels | 1997 |
Baking soda: a potentially fatal home remedy.
We present a case of a six-week-old infant who developed life-threatening complications after unintentional sodium bicarbonate intoxication. Baking soda was being used by the mother as a home remedy to "help the baby burp." A review of the literature regarding the use (or misuse) of baking soda follows. Our patient, along with the other noted case reports, emphasizes the need for warnings on baking soda products whose labels recommend its use as an antacid. Poisonings must be high in the differential diagnosis of any patient, regardless of age, who presents with altered mental status or status epilepticus. Topics: Drug Labeling; Female; Humans; Hypernatremia; Infant; Infant Care; Medicine, Traditional; Poisoning; Sodium Bicarbonate | 1995 |
[Therapy of acute salicylate poisoning].
Poisoning with salicylic acid and its derivatives is a quite common event, leading to possibly life-threatening complications. A case of fatal intoxication of a sixty-year old patient with acetylsalicylic acid is described and the therapeutic options are discussed. In acute poisoning it is mandatory to initiate simple and effective measures first. This gives time for discussing and planning the more laborious procedures. The initial treatment of salicylate poisoning is based on the prevention of further absorption by a sufficiently large quantity of orally administered activated charcoal (approximately 1 g/kg b.w.). Given repeatedly, activated charcoal may enhance non-renal clearance of salicylates. Intravenously administered sodium bicarbonate counteracts the metabolic acidosis. Moreover, bicarbonate therapy limits tissue distribution of the drug and enhances its renal excretion. The availability of glycine for salicylic acid metabolism may be limited in poisoning because glycine has been used for forming the conjugation product salicyluric acid. Glycine may be administered orally to overcome this bottleneck. Gastric lavage has been proven to be of limited efficacy. This efficacy is further diminished if gastric lavage is performed late after drug ingestion. When it is performed, however, activated charcoal should be administered before and after gastric lavage. Whenever the more simple treatment options fail, hemodialysis or hemoperfusion should be additionally considered since these procedures are effective in removing salicylates from the body. Topics: Aspirin; Charcoal; Coma; Fatal Outcome; Female; Fever; Gastric Lavage; Glycine; Hemoperfusion; Humans; Middle Aged; Poisoning; Renal Dialysis; Salicylates; Sodium Bicarbonate | 1993 |
Methanol poisoning: two cases with similar plasma methanol concentrations but different outcomes.
Topics: Adolescent; Bicarbonates; Blood Gas Analysis; Blood Urea Nitrogen; Electrolytes; Ethanol; Female; Humans; Infusions, Intravenous; Intubation, Gastrointestinal; Methanol; Osmolar Concentration; Poisoning; Renal Dialysis; Sodium; Sodium Bicarbonate; Sodium Chloride; Treatment Outcome | 1993 |
Methanol intoxication. How to help patients who have been exposed to toxic solvents.
Methanol intoxication can be a challenge, in part because it is relatively uncommon but also because of the pharmacokinetics involved. A patient may not experience symptoms and thus may not present for treatment for several hours, or even a day or two, after exposure to the toxic substance. Yet, the interval between ingestion and treatment is one of the most important factors in determining patient outcome. Typical symptoms of methanol intoxication include lethargy, vertigo, vomiting, blurred vision, and decreased visual acuity. Treatment focuses on prevention of methanol conversion to its toxic metabolites, correction of metabolic acidosis, and elimination of the toxic substances from the system. Ethanol and bicarbonate administration and hemodialysis have been effective. Topics: Acidosis, Lactic; Bicarbonates; Ethanol; Humans; Metabolic Clearance Rate; Methanol; Poisoning; Prognosis; Renal Dialysis; Sodium; Sodium Bicarbonate | 1993 |
2 trial(s) available for sodium-bicarbonate and Poisoning
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Potential role of paraffin oil gastric lavage in acute aluminum phosphide poisoning: a randomized controlled trial.
Aluminum phosphide (ALP) poisoning is a true medical emergency associated with high mortality. The lack of a specific antidote for ALP poisoning mandates searching for new treatment modalities. This study aimed to evaluate the effectiveness and safety of gastric decontamination by paraffin oil in cases with acute ALP poisoning. This study was a randomized, controlled, parallel-group, single-blind, phase II clinical trial conducted over a period of 6 months. Sixty-two patients with acute ALP poisoning were randomly allocated into two equivalent groups. In both groups, the standard ALP treatment was given. Gastric decontamination in the control group was performed by saline and sodium bicarbonate 8.4%, while in the intervention group, it was done by paraffin oil and sodium bicarbonate 8.4%. All patients were subjected to history taking, clinical examination, and laboratory investigations. The outcomes were evaluated. The median age of the studied patients was 20 years. Most of the studied cases were females, single, and from rural areas. The median delay time was 1 h. All patients included in the study alleged ingestion of ALP during suicidal attempts. Twelve hours after admission, many clinical and laboratory findings were significantly better in the intervention group. The need for intubation, mechanical ventilation, and total amount of vasopressors was significantly lower, and the mortality rate was non-significantly lower in the intervention group compared to the control. The median length of hospital stay was significantly shorter in the control group. Gastric decontamination with paraffin oil and sodium bicarbonate 8.4% could be valuable in reducing ALP poisoning severity, the need for intubation, mechanical ventilation, and vasopressors. Topics: Adult; Aluminum Compounds; Female; Gastric Lavage; Humans; Male; Oils; Paraffin; Pesticides; Phosphines; Poisoning; Single-Blind Method; Sodium Bicarbonate; Young Adult | 2022 |
Tricyclic antidepressant poisoning treated by magnesium sulfate: a randomized, clinical trial.
Tricyclic antidepressant (TCA) poisoning is a major problem in medicine, with a high morbidity and mortality rate. The main cause of fatality is cardiac arrhythmias resulting from intoxication. Sodium bicarbonate is the drug of choice, but severe poisoning necessitates further interventions. Magnesium sulfate seems to be effective in this condition. In a randomized, clinical trial, we evaluated all patients with a history of TCA intoxication referred to the Loghman Hakim Hospital Poison Center. The patients were randomly divided into two groups: one treated by bicarbonate infusion (control group) and the other (case group) by the infusion of magnesium sulfate in addition to the treatment in the first group. Seventy-two patients were recruited into the study (36 cases and 36 controls). Mean duration of intensive care unit stay in the cases and controls were 25.63 ± 9.33 and 82.67 ± 21.66 hours, respectively (P < 0.001). Mortality rate in the case group was 13.9% and 33.3% in the other group (P = 0.052). Magnesium sulfate can be an effective drug in the treatment of TCA poisoning; however, several randomized, clinical trials are still necessary to confirm this. Topics: Antidepressive Agents, Tricyclic; Humans; Iran; Magnesium Sulfate; Poisoning; Sodium Bicarbonate; Treatment Outcome | 2012 |
30 other study(ies) available for sodium-bicarbonate and Poisoning
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Acetaminophen and Acetylsalicylic Acid Exposure in a Preterm Infant after Maternal Overdose.
Here, we review the case of a 26 1/7 weeks' gestation premature female infant born to a mother who intentionally ingested a large quantity of Tylenol, aspirin, quetiapine, and prenatal vitamins. The neonate subsequently had markedly elevated levels of both Tylenol and aspirin when checked on the first day of life. While overall clinically stable, the neonate did demonstrate coagulopathy as evidenced by abnormal coagulation studies. Both poison control and a pediatric gastroenterologist/hepatologist were consulted. She successfully tolerated a course of N-acetylcysteine; her subsequent Tylenol level was markedly decreased and the neonate exhibited no further effects of toxicity. The salicylate level decreased on its own accord. To our knowledge, this is the first report of a neonate at 26 weeks' gestation that has been successfully managed for supratherapeutic concentrations of acetaminophen and acetylsalicylic acid secondary to maternal ingestion. While rare, this case may serve as a reference for the effectiveness of N-acetylcysteine in premature infants in such instances. Topics: Acetaminophen; Antidepressive Agents; Antidotes; Aspirin; Cystine; Drug Overdose; Female; Humans; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Maternal Exposure; Poisoning; Pregnancy; Quetiapine Fumarate; Sodium Bicarbonate; Suicide, Attempted | 2019 |
Bridging the Gap.
Topics: Acid-Base Equilibrium; Adult; Blood Chemical Analysis; Ethylene Glycol; Fomepizole; Humans; Male; Osmolar Concentration; Poisoning; Renal Dialysis; Sodium Bicarbonate | 2019 |
A Methanol Intoxication Outbreak From Recreational Ingestion of Fracking Fluid.
Single-patient methanol intoxications are a common clinical presentation, but outbreaks are rare and usually occur in settings in which there is limited access to ethanol and methanol is consumed as a substitute. In this case report, we describe an outbreak of methanol intoxications that was challenging from a public health perspective and discuss strategies for managing such an outbreak. Topics: Acid-Base Equilibrium; Acidosis; Adult; Antidotes; Disease Outbreaks; Eating; Fomepizole; Humans; Hydraulic Fracking; Leucovorin; Male; Manitoba; Methanol; Middle Aged; Nausea; Poisoning; Pyrazoles; Renal Dialysis; Sodium Bicarbonate; Solvents; Vomiting; Young Adult | 2017 |
Development and Optimization of Gastro-Retentive Controlled-Release Tablet of Calcium-Disodium Edentate and its In Vivo Gamma Scintigraphic Evaluation.
Medical management of heavy metal toxicity, including radioactive ones, is a cause for concern because of their increased use in energy production, healthcare, and mining. Though chelating agents like EDTA and DTPA in parenteral form are available, no suitable oral formulation is there that can trap ingested heavy metal toxicants in the stomach itself, preventing their systemic absorption. The objective of the present study was to develop and optimize gastro-retentive controlled-release tablets of calcium-disodium edentate (Ca-Na2EDTA). Gastro-retentive tablet of Ca-Na2EDTA was prepared by direct compression method. Thirteen tablet formulations were designed using HPMC-K4M, sodium chloride, and carbopol-934 along with effervescing agents sodium bicarbonate and citric acid. Tablet swelling ability, in vitro buoyancy, and drug dissolution studies were conducted in 0.1 N HCl at 37 ± 0.5°C. Ca-Na2EDTA was radiolabeled with technetium-99m for scintigraphy-based in vivo evaluation. Formula F8 (Ca-Na2EDTA 200 mg, carbopol 100 mg, avicel 55 mg, citric acid 30 mg, NaHCO3 70 mg, NaCl 100 mg, and HPMC 95 mg) was found to be optimum in terms of excellent floating properties and sustained drug release. F8 fitted best for Korsmeyer-Peppas equation with an R (2) value of 0.993. Gamma scintigraphy in humans showed mean gastric retention period of 6 h. Stability studies carried out in accordance with ICH guidelines and analyzed at time intervals of 0, 1, 2, 4, and 6 months have indicated insignificant difference in tablet hardness, drug content, total floating duration, or matrix integrity of the optimized formulation. Gastro-retentive, controlled-release tablet of Ca-Na2EDTA was successfully developed using effervescent technique as a potential oral antidote for neutralizing ingested heavy metal toxicity. Topics: Administration, Oral; Adult; Animals; Antidotes; Biological Availability; Cellulose; Chemistry, Pharmaceutical; Citric Acid; Delayed-Action Preparations; Edetic Acid; Gastric Mucosa; Hardness; Heavy Metal Poisoning; Humans; Middle Aged; Poisoning; Rabbits; Sodium Bicarbonate; Solubility; Tablets; Young Adult | 2015 |
Hypertonic sodium bicarbonate versus intravenous lipid emulsion in a rabbit model of intravenous flecainide toxicity: no difference, no sink.
The use of intravenous lipid emulsion (ILE) as an antidote in non-local, anaesthetic drug toxicity has generated considerable interest. Flecainide is a lipophilic anti-arrhythmic with a significant cardiotoxic profile, with blockade of sodium and potassium channels causing arrhythmias and shock in severe toxicity. ILE has been proposed as a treatment option in severe flecainide toxicity refractory to other modalities.. We compared the effects of ILE and hypertonic sodium bicarbonate in a rabbit model of flecainide toxicity.. Twenty sedated and ventilated New Zealand White Rabbits received flecainide infusion titrated to a mean arterial pressure (MAP) of 60% baseline, which was defined as toxicity. The rabbits then received either sodium bicarbonate or ILE, and the flecainide infusion was reduced in an attempt to model ongoing enteric absorption. MAP and heart rate were recorded every minute for 15 min and plasma flecainide concentration was measured at toxicity and 15 min. ECG QRS duration was recorded at baseline, toxicity and at 5, 10 and 15 min post-toxicity.. No difference was observed in heart rate (p = 0.2804), MAP (p = 0.1802) or QRS duration (p = 0.7471) between groups. The immediate rate of rise in MAP was greatest in the bicarbonate group in the 5 min immediately post-toxicity.. In this study, no differences were observed between an active control of hypertonic sodium bicarbonate and ILE for the primary endpoint of MAP at 15 min nor for QRS duration at any timepoint. There was a transient rapid increase in blood pressure seen in the sodium bicarbonate group that was not sustained. No increase was seen in blood concentration of flecainide in the ILE group, suggesting no 'lipid sink' for flecainide in this model. More research is warranted to define any role for ILE in flecainide toxicity. Topics: Animals; Anti-Arrhythmia Agents; Antidotes; Blood Pressure; Disease Models, Animal; Endpoint Determination; Fat Emulsions, Intravenous; Female; Flecainide; Heart Rate; Hypertonic Solutions; Male; Poisoning; Rabbits; Sodium Bicarbonate | 2013 |
Death due to acute salicylate intoxication despite dialysis.
Salicylate poisoning is a common problem with appreciable morbidity and mortality. We present a case of a patient with a large aspirin ingestion who expired despite aggressive hemodialysis (HD).. A 35-year-old man arrived at the Emergency Department 7.5 h after ingesting 400 tablets of 325-mg aspirin. He was afebrile, the respiratory rate (RR) was 30 breaths/min, heart rate (HR) 120 beats/min, blood pressure (BP) 125/76 mm Hg, and oxygen saturation 99% on room air. His salicylate concentration was 89.6 mg/dL. His initial arterial blood gas: pH 7.48, pCO(2) 21 mm Hg, PaO(2) 97 mm Hg, and bicarbonate 15.8 mmol/L. His initial serum chemistry panel was normal. He received activated charcoal and intravenous hydration with sodium bicarbonate. Two hours after arrival, salicylate concentration was 91.6 mg/dL. The patient became agitated and HD was initiated; 22 h after presentation, repeat salicylate concentration was 88.4 mg/dL and his creatinine was 3.9 mg/dL. A second run of HD was performed. After this, his temperature had risen to 39.06°C (102.3°F), BP 122/64 mm Hg, HR 168 beats/min, RR 43 breaths/min, and oxygen saturation 95% (2 L nasal cannula). His confusion increased, and he died 40 h after his ingestion.. HD is widely advocated in managing severe salicylate intoxications, however, no consensus exists for the duration and best mode of therapy. Patients with severe salicylate poisonings may require extended durations of HD to effectively mitigate toxicity. Additional study is warranted to determine optimal therapy in severe salicylate intoxications. Topics: Adult; Charcoal; Fatal Outcome; Humans; Male; Poisoning; Renal Dialysis; Salicylic Acid; Sodium Bicarbonate; Suicide | 2011 |
Successful treatment of methemoglobinemia and acute renal failure after indoxacarb poisoning.
We report a case of systemic toxicity induced by indoxacarb, an oxadiazine insecticide. Previous reports have suggested the occurrence of methemoglobinemia after indoxacarb ingestion, but no case of indoxacarb-induced systemic toxicity, such as acute renal failure, has been reported thus far.. A 71-year-old woman presented with indoxacarb poisoning, resulting in methemoglobinemia and acute renal failure. The methemoglobinemia improved after methylene blue administration, but rapidly progressive acute renal failure occurred 7 h after admission. She was treated with continuous veno-venous hemofiltration and intravenous sodium bicarbonate and recovered successfully.. Ingestion of indoxacarb may produce not only methemoglobinemia, but also systemic toxicities like acute renal failure, which can be successfully treated with aggressive therapy such as continuous veno-venous hemofiltration. Physicians should be alert to acute renal failure as a possible complication of indoxacarb ingestion, and treat it accordingly. Topics: Acute Kidney Injury; Aged; Female; Hemofiltration; Humans; Injections, Intravenous; Insecticides; Methemoglobinemia; Oxazines; Poisoning; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome | 2011 |
Cyanide poisoning caused by ingestion of apricot seeds.
To report diagnostic, clinical and therapeutic aspects of cyanide intoxication resulting from ingestion of cyanogenic glucoside-containing apricot seeds.. Thirteen patients admitted to the Pediatric Intensive Care Unit (PICU) of Erciyes University between 2005 and 2009 with cyanide intoxication associated with ingestion of apricot seeds were reviewed retrospectively.. Of the 13 patients, four were male. The mean time of onset of symptoms was 60 minutes (range 20 minutes to 3 hours). On admission, all patients underwent gastric lavage and received activated charcoal. In addition to signs of mild poisoning related to cyanide intoxication, there was severe intoxication requiring mechanical ventilation (in four cases), hypotension (in two), coma (in two) and convulsions (in one). Metabolic acidosis (lactic acidosis) was detected in nine patients and these were treated with sodium bicarbonate. Hyperglycaemia occurred in nine patients and blood glucose levels normalised spontaneously in six but three required insulin therapy for 3-6 hours. Six patients received antidote treatment: high-dose hydroxocobalamin in four and two were treated with a cyanide antidote kit in addition to high-dose hydroxocobalamin. One patient required anticonvulsive therapy. All patients recovered and were discharged from the PICU within a mean (SD, range) 3.1 (1.7, 2-6) days.. Cyanide poisoning associated with ingestion of apricot seeds is an important poison in children, many of whom require intensive care. Topics: Acidosis; Antidotes; Charcoal; Child; Child, Preschool; Coma; Cyanides; Eating; Female; Gastric Lavage; Hematinics; Humans; Hydroxocobalamin; Hyperglycemia; Insulin; Male; Poisoning; Prunus; Respiratory Insufficiency; Retrospective Studies; Seeds; Seizures; Sodium Bicarbonate; Turkey | 2010 |
The poison pen: bedside diagnosis of urinary diquat.
Diquat is a bipyridyl herbicide with nephrotoxic effects. This in vitro study demonstrates a colorimetric test for detection of diquat in human urine. Urine specimens using ten concentrations of diquat herbicide solution and controls for urine and glyphosate were prepared. A two-step assay (addition of bicarbonate followed by sodium dithionite) was performed, with a resulting color change of the original solution for each specimen. Color change intensity was noted immediately and after 30 min, by gross visual inspection. A green color with concentration-dependent intensity was detected in all specimens, in which concentrations of diquat solution ranged from 0.73 to 730 mg/L. This colorimetric effect disappeared after 30 min. The sodium bicarbonate/dithionite test may be useful as a qualitative bedside technique for the detection of urinary diquat in the appropriate clinical setting. Topics: Biomarkers; Colorimetry; Diquat; Dithionite; Herbicides; Humans; Point-of-Care Systems; Poisoning; Predictive Value of Tests; Reproducibility of Results; Sodium Bicarbonate | 2010 |
A simplified acute physiology score in the prediction of acute aluminum phosphide poisoning outcome.
Aluminum phosphide (AlP) is used as a fumigant. It produces phosphine gas, which is a mitochondrial poison. Unfortunately, there is no known antidote for AlP intoxication, and also, there are few data about its prognostic factors.. The aim of this study was to determine the impact of the Simplified Acute Physiology Score II (SAPS II ) in the prediction of outcome in patients with acute AlP poisoning requiring admission to the Intensive Care Unit (ICU).. This was a prospective study in patients with acute AlP poisoning, admitted to the ICU over a period of 12 months. The demographic data were collected and SAPSII was recorded. The patients were divided into survival and non-survival groups due to outcome.. The data were expressed as mean ± SD for continuous or discrete variables and as frequency and percentage for categorical variables. The results were compared between the two groups using SPSS software. Results : During the study period, 39 subjects were admitted to the ICU with acute AlP poisoning. All 39 patients required endotracheal intubation and mechanical ventilation in addition to gastric decontamination with sodium bicarbonate, permanganate potassium, and activated charcoal, therapy with MgSO 4 and calcium gluconate and adequate hydration. Among these patients, 26 (66.7%) died. SAPSII was significantly higher in the non-survival group than in the survival group (11.88 ± 4.22 vs. 4.31 ± 2.06, respectively) (P < 0.001).. SAPSII calculated within the first 24 hours was recognized as a good prognostic indicator among patients with acute AlP poisoning requiring ICU admission. Topics: Adolescent; Adult; Aluminum Compounds; Antidotes; Charcoal; Female; Forecasting; Humans; Male; Middle Aged; Pesticides; Phosphines; Poisoning; Potassium Permanganate; Prospective Studies; Severity of Illness Index; Sodium Bicarbonate; Treatment Outcome; Young Adult | 2010 |
Metformin overdose with a resultant serum pH of 6.59: survival without sequalae.
Metformin, widely used in the treatment of diabetes mellitus, is known to cause lactic acidosis in both therapeutic use and after an overdose. We report the case of a 40-year-old woman who claimed to have ingested between 75 and 100 grams of metformin and subsequently developed severe lactic acidosis. She eventually developed a peak serum lactate level of 40.0 mmol/L and a serum pH nadir of 6.59 and became obtunded, hypotensive, and hypothermic. After aggressive supportive therapy with mechanical ventilation, vasopressor agents, sodium bicarbonate, and hemodialysis, her metabolic derangements steadily improved and she made a complete recovery without any residual sequelae. Her admission serum metformin concentration was later determined to be 160 microg/mL (therapeutic range is 1-2 microg/mL). There are several case reports and case series describing lactic acidosis secondary to metformin ingestion, although the exact mechanism remains unclear. The overall management of metformin overdose is reviewed. This case represents the largest reported amount of ingested metformin, the lowest serum pH, and the highest serum lactate concentration in any intentional metformin overdose survivor in the literature. Despite potentially lethal metabolic derangements, such patients can survive with aggressive supportive care. Topics: Acidosis, Lactic; Adult; Drug Overdose; Female; Humans; Hypoglycemic Agents; Hypotension; Metformin; Poisoning; Sodium Bicarbonate | 2010 |
[Severe vomiting in alcoholics'. Toxic gastritis or withdrawal?].
Topics: Acidosis; Adult; Antidotes; Diagnosis, Differential; Ethanol; Ethylene Glycol; Female; Gastritis; Humans; Poisoning; Sodium Bicarbonate; Vomiting | 2009 |
CASH as a mnemonic for indications of sodium bicarbonate for sodium channel blocker intoxication.
Topics: Adult; Anti-Arrhythmia Agents; Brugada Syndrome; Electrocardiography; Flecainide; Humans; Magnesium; Male; Poisoning; Sodium Bicarbonate | 2009 |
Management of acute paracetamol poisoning in a tertiary care hospital.
To compare the management of acute paracetamol poisoning with the best evidence available, and to determine the effect of plasma paracetamol level estimation on the management.. Descriptive study with an intervention.. Medical wards of the National Hospital of Sri Lanka, Colombo.. Patients admitted with a history of acute paracetamol poisoning.. Measurement of plasma paracetamol.. Data were obtained from the patients, medical staff and medical records. Plasma paracetamol was estimated between 4-24 hours of paracetamol ingestion. The current management practices were compared with the best evidence on acute paracetamol poisoning management.. 157 patients were included. The mean ingested dose of paracetamol was 333 mg/kg body weight. Majority of the patients (84%) were transfers. Induced emesis and activated charcoal were given to 91% of patients. N-acetylcysteine was given to 66, methionine to 55, and both to 2. Aclinically important delay in the administration of antidotes was noted; 68% of patients received antidotes after 8 hours of the acute ingestion. Only 31 (26%) had paracetamol levels above the Rumack-Matthew normogram. 74 patients received an antidote despite having a plasma paracetamol level below the toxic level according to the normogram.. Management of acute paracetamol poisoning could be improved by following best available evidence and adapting cheaper methods for plasma paracetamol estimation. Topics: Acetaminophen; Acetylcysteine; Acute Disease; Analgesics, Non-Narcotic; Antidotes; Charcoal; Emetics; Evidence-Based Medicine; Female; Hospitals, Public; Humans; Male; Methionine; Poisoning; Sodium Bicarbonate; Sri Lanka; Time Factors; Treatment Outcome; Young Adult | 2008 |
Plasma alkalinization for acute organophosphorus poisoning--is it a reality in the developing world?
Topics: Acute Disease; Alkalies; Antidotes; Clinical Trials as Topic; Developing Countries; Emergency Medicine; Humans; Hydrogen-Ion Concentration; Injections, Intravenous; Organophosphate Poisoning; Pesticides; Poisoning; Serum; Sodium Bicarbonate | 2007 |
Prolonged clinical effects in modified-release amitriptyline poisoning.
Tricyclic antidepressant poisoning is often associated with significant cardiovascular and central nervous system toxicity. Effective treatment includes the use of appropriate gastric decontamination techniques, the administration of sodium bicarbonate, and meticulous supportive care. Tricylcic antidepressant toxicity typically lasts 24-48 hours following a significant overdose.. We describe a case of tricyclic antidepressant poisoning where significant clinical toxicity (QRS prolongation, metabolic acidosis) was observed for up to 4 days following ingestion of a modified-release preparation of amitriptyline. Successful patient recovery was associated with the use of multidose activated charcoal and repeated administration of intravenous sodium bicarbonate.. Clinicians should be aware of the potential for prolonged tricyclic toxicity in patients who have ingested modified-release amitriptyline in overdose. Gastric decontamination techniques such as multidose activated charcoal and whole bowel irrigation should be considered where there is evidence of ongoing tricyclic antidepressant absorption or clinical toxicity following ingestion of a modified-release preparation. These interventions may be indicated for prolonged periods (greater than 36 hours) post ingestion. Topics: Acidosis; Adult; Amitriptyline; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Central Nervous System Diseases; Charcoal; Delayed-Action Preparations; Female; Humans; Injections, Intravenous; Poisoning; Sodium Bicarbonate; Treatment Outcome | 2006 |
The need for translational research on antidotes for pesticide poisoning.
1. Pesticide poisoning kills hundreds of thousands of people in the Asia-Pacific region each year. The majority of deaths are from deliberate self-poisoning with organophosphorus pesticides (OP), aluminium phosphide and paraquat. The current response from a public health, medical and research perspective is inadequate. 2. There are few proven or effective treatments; in addition, very little clinical research has been performed to transfer antidotes shown to work in animal studies into clinical practice. 3. The human toxicity of pesticides is poorly studied and better information may inform a more sustained and appropriate regulatory response. Further understanding may also lead to improvements in diagnosis and treatment. 4. The few effective treatments are not being recommended or delivered in an optimal and timely fashion to poisoned patients. A regional approach to facilitate appropriate pricing, packaging and delivery of antidotes is required. Topics: Animals; Antidotes; Cholinesterase Inhibitors; Humans; Immunosuppressive Agents; Organophosphate Poisoning; Oximes; Paraquat; Pesticides; Poisoning; Public Health; Sodium Bicarbonate; Sri Lanka | 2005 |
Hypertonic sodium bicarbonate for Taxus media-induced cardiac toxicity in swine.
To determine whether intravenous (IV) hypertonic sodium bicarbonate is effective in the reversal of QRS widening associated with severe Taxus intoxication.. Seventeen anesthetized and instrumented swine were poisoned with an IV extract of Taxus media until doubling of the QRS interval on electrocardiography was achieved. After poisoning (time zero), the animals received either 4 mL/kg IV 8.4% sodium bicarbonate (experimental group; 6 animals), a similar volume of 0.7% NaCl in 10% mannitol (mannitol group; 6 animals), or nothing (control group; 5 animals). The main outcome parameter was QRS duration. Secondary outcome parameters were mean arterial pressure (MAP), heart rate (HR), and cardiac index (CI = cardiac output/kg). Additionally, arterial pH, partial pressure of carbon dioxide (pCO(2)), and plasma-ionized calcium, sodium, and potassium were monitored.. Taxus toxicity, defined as a 100% increase in QRS duration, was produced in all animals. The animals were similar in regard to baseline and time 0 physiologic parameters as well as amount of Taxus media extract administered. From times 5 through 30 minutes, following assigned treatment, significant increases in QRS duration were detected in the experimental and mannitol groups compared with the control group. A significant lowering of MAP was found in the experimental group compared with the control group. No significant difference between groups was noted in HR or CI. The swine treated with hypertonic sodium bicarbonate had a statistically significant increase in pH, plasma sodium concentration, and base excess compared with the other groups.. Hypertonic sodium bicarbonate was ineffective in reversing the widening of QRS interval associated with Taxus poisoning in this swine model. Topics: Animals; Blood Pressure; Calcium; Disease Models, Animal; Electrocardiography; Heart Rate; Hydrogen-Ion Concentration; Hypertonic Solutions; Infusions, Intravenous; Male; Mannitol; Poisoning; Potassium; Sodium; Sodium Bicarbonate; Swine; Taxus | 2002 |
The effect of sodium bicarbonate on propranolol-induced cardiovascular toxicity in a canine model.
To evaluate the potential utility of sodium bicarbonate in an established model of acute propranolol toxicity.. Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of 1.5 mEq/kg of sodium bicarbonate solution (1 mEq/mL) followed by an infusion of 1.5 mEq/kg over the next 26 minutes (n = 6) or an equivalent timing and volume of 5% dextrose solution (n = 6) was administered in each dog. Targeted cardiovascular parameters included heart rate, mean arterial pressure, left ventricular dP/dtmax, and QRS interval.. Propranolol infusion significantly depressed heart rate (p < 0.0001), mean arterial pressure (p < 0.0001), dP/dtmax (p < 0.0001) and prolonged the QRS interval (p < 0.0001). Sodium bicarbonate failed to significantly improve these targeted parameters when compared to control animals.. In this canine model of propranolol toxicity, intravenous sodium bicarbonate appears to be an ineffective single therapy. Furthermore, these results may suggest a different mechanism of sodium channel blockade for propanolol than that of type IA antiarrhythmic agents. Topics: Animals; Bicarbonates; Blood Pressure; Cardiovascular Diseases; Disease Models, Animal; Dogs; Electrocardiography; Heart Conduction System; Heart Rate; Infusions, Intravenous; Poisoning; Propranolol; Sodium; Sodium Bicarbonate; Treatment Outcome; Ventricular Function, Left | 2000 |
Ethanol treatment in ethylene glycol poisoned patients.
Two otherwise healthy 16-y-old female patients were treated with sodium bicarbonate and ethanol after the ingestion of unknown quantities of ethylene glycol. Patient 2 was admitted twice for ethylene glycol poisoning in unrelated events. In patient 1, the maximum levels of ethylene glycol and glycolate in plasma were 14 mmol/L (0.9 g/L) and 8.2 mmol/L (0.5 g/L), respectively. In patient 2, the maximum levels of ethylene glycol in plasma during the 2 admissions were 18 mmol/L (1.1 g/L) and 45 mmol (2.8 g/L), respectively. In patient 1, a blood ethanol concentration between 130-140 mg/dL (28-30 mmol/L) was reached 3 h after the start of ethanol administration and maintained for 22 h. During this period, ethylene glycol metabolism was effectively inhibited as indicated by S-glycolate levels and that 88% of the eliminated ethylene glycol was accounted for in the urine. This suggests that ethanol therapy alone may be sufficient for patients admitted early with low serum ethylene glycol concentrations. During the admissions of patient 2, the blood ethanol concentrations were presumed to effectively inhibit ethylene glycol metabolism as judged from normal acid/base parameters. However, during the second admission the bolus infusion of ethanol was associated with respiratory arrest. During both admissions for patient 2, hemodialysis constituted the major route of ethylene glycol elimination. Topics: Adolescent; Antidotes; Ethanol; Ethylene Glycol; Female; Glycolates; Humans; Poisoning; Renal Dialysis; Sodium Bicarbonate | 1998 |
Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning.
Cardiac depression is the main adverse effect of severe tricyclic antidepressant poisoning. The aim of this study was to investigate whether treatment with epinephrine or norepinephrine increases survival as compared with standard treatment with sodium bicarbonate in experimental amitriptyline poisoning.. Nonrandomized, controlled intervention trial.. University laboratory.. Male, anesthetized, paralyzed, and mechanically ventilated Sprague-Dawley rats (n = 91).. Rats subjected to a 60-min infusion of amitriptyline (2 mg/kg/min) were treated with a continuous infusion of either epinephrine, norepinephrine, sodium bicarbonate, epinephrine plus sodium bicarbonate, norepinephrine plus sodium bicarbonate, or placebo.. Inotropic drug treatment was associated with an increased survival rate as compared with treatment with sodium bicarbonate and treatment with placebo. Epinephrine treatment was superior to norepinephrine. Additional treatment with sodium bicarbonate increased survival rate for each inotropic drug. Sodium bicarbonate and inotropic drug treatment independently increased the survival rate (p < .001 for both effects). No interaction between these two treatment effects was observed.. Both epinephrine and norepinephrine increased the survival rate in tricyclic antidepressant poisoning in rats. Sodium bicarbonate increased the survival rate independent of inotropic drug treatment. Furthermore, epinephrine was superior to norepinephrine when used both with and without sodium bicarbonate, and the most effective treatment was epinephrine plus sodium bicarbonate. Topics: Amitriptyline; Animals; Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Disease Models, Animal; Drug Combinations; Electrolytes; Epinephrine; Hemodynamics; Humans; Male; Norepinephrine; Poisoning; Rats; Rats, Sprague-Dawley; Sodium Bicarbonate; Survival Rate; Sympathomimetics | 1997 |
Cyclic antidepressant toxicity in children and adolescents.
We retrospectively evaluated the clinical and laboratory findings of all patients admitted to our facility during a 6.5-year period with a history of cyclic antidepressant ingestion (CAD). Outcome parameters [admission CAD concentration, arterial pH, and corrected QT (QTc) and QRS intervals] used in adult populations to predict morbidity after CAD ingestion were applied to our study population. During the study period, 45 patients (mean +/- SD age of 11.8 +/- 5.6 years) were admitted with CAD ingestion. Conduction delays were present in 17 patients, 9 of whom had QTc intervals greater than 0.43 seconds. Seven patients had generalized seizures; 7 required mechanical ventilation; 14 had Glasgow Coma Scores of 8 or lower on presentation; and one required pharmacologic support for hypotension. In our cohort, the mean admission serum CAD concentration was 461.5 +/- 477.4 ng/mL. Correlations were found between the arterial pH, the QRS interval, the QTc interval, and the admission CAD serum concentration. In an analysis of three subsets of patients (i.e., those with seizures, coma, and respiratory insufficiency), only patients who presented with seizures were found to have a significant prolongation in the QRS and QTc intervals. Pediatric patients who have ingested CADs and present with seizures would appear to be at increased risk for having conduction delays, cardiac dysrhythmias, and, presumably, attendant morbidity and mortality associated with an ingestion. Topics: Adolescent; Anticonvulsants; Antidepressive Agents, Tricyclic; Arkansas; Child; Child, Preschool; Female; Humans; Infant; Intensive Care Units, Pediatric; Male; Poisoning; Respiration, Artificial; Respiratory Insufficiency; Retrospective Studies; Seizures; Sodium Bicarbonate | 1995 |
Nebulized sodium bicarbonate in the treatment of chlorine gas inhalation.
In this two year retrospective review, 86 cases of chlorine gas inhalation from 49 medical facilities were treated with nebulized sodium bicarbonate on the recommendation of the Kentucky Regional Poison Center. Typical manifestations included cough, chest discomfort, shortness of breath, and wheezing. No patients developed pulmonary edema or respiratory insufficiency requiring ventilatory support. Sixty-three cases (73.3%) were exposures to chlorine producing acid/hypochlorite mixtures. Six (7.0%) were exposed to chlorine gas in industrial settings. Twelve (14.0%) were exposed to chlorine gas in swimming pool settings. Sixty-nine (80.2%) were treated and released from the emergency department. In 53 patients, clinical condition was clearly improved on emergency department discharge. Seventeen (19.8%) were admitted to the hospital. All admitted patients gradually improved and had a mean hospital stay of 1.4 days (range 1 to 3 days). No patients in this study deteriorated clinically after nebulized sodium bicarbonate use. Nebulized sodium bicarbonate appears safe and merits prospective evaluation in the therapy of chlorine gas inhalation. Topics: Administration, Intranasal; Adolescent; Adult; Aerosols; Aged; Child; Child, Preschool; Chlorine; Emergencies; Female; Hospitalization; Humans; Kentucky; Length of Stay; Male; Middle Aged; Poison Control Centers; Poisoning; Retrospective Studies; Sodium Bicarbonate | 1994 |
Acute toxicity from baking soda ingestion.
Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed. Topics: Acute Disease; Alkalosis; Humans; Hypokalemia; Male; Middle Aged; Poisoning; Sodium Bicarbonate | 1994 |
Drug overdose: salicylates.
Topics: Acidosis; Adult; Alkalosis, Respiratory; Bicarbonates; Charcoal; Female; Humans; Poisoning; Salicylates; Sodium; Sodium Bicarbonate; Suicide, Attempted | 1992 |
Massive diphenhydramine poisoning resulting in a wide-complex tachycardia: successful treatment with sodium bicarbonate.
Diphenhydramine poisoning is characterized most often by anticholinergic effects. Cardiotoxicity and circulatory collapse have rarely been reported after massive ingestions of diphenhydramine and other H1-receptor-blocking agents, although these substances have local anesthetic properties and have been studied as antiarrhythmics. We report the case of a patient who developed a wide-complex tachycardia as a complication of acute diphenhydramine poisoning that responded to IV sodium bicarbonate. Topics: Adolescent; Alcohol Drinking; Bicarbonates; Blood Gas Analysis; Charcoal; Diphenhydramine; Electrocardiography; Emergency Service, Hospital; Female; Gastric Lavage; Humans; Poisoning; Sodium; Sodium Bicarbonate; Suicide, Attempted; Tachycardia | 1992 |
A case of percutaneous industrial methanol toxicity.
Methanol (CH3OH) is a chemical feedstock of increasing importance as well as a commonly used solvent. In the early 1980s methanol production was introduced at a new petrochemical complex in the Saudi port of Jubail. A case is presented of a consultant supervising tank cleaning prior to methanol loading. He wore positive pressure breathing apparatus but no protective clothing. After 2-3 hours working in the confined space of the tank, he worked on deck and continued to wear his methanol-soaked clothing which eventually dried out. Visual symptoms of acute methanol toxicity presented some 8 hours after exposure. The appropriate treatment (with ethanol provided by the ship bond) was carried out in hospital and the individual recovered completely. Most reported cases of methanol toxicity are social in origin, arising from ingestion. This particular case, though unusual, does present some interesting lessons. Topics: Adult; Bicarbonates; Blood Gas Analysis; Ethanol; Humans; Infusions, Intravenous; Male; Methanol; Occupational Diseases; Poisoning; Saudi Arabia; Sodium; Sodium Bicarbonate | 1992 |
The utility of a 12-lead electrocardiogram in diagnosing a suspected antidepressant overdose.
Topics: Adolescent; Bicarbonates; Desipramine; Drug Overdose; Electrocardiography; Emergency Service, Hospital; Female; Gastric Lavage; Humans; Intensive Care Units, Pediatric; Poisoning; Sensitivity and Specificity; Sodium; Sodium Bicarbonate; Substance Abuse Detection | 1992 |
[Forced alkalic diuresis. Still a current therapy in poisoning].
Topics: Bicarbonates; Diuresis; Humans; Poisoning; Rhabdomyolysis; Sodium; Sodium Bicarbonate | 1989 |
[Poisoning by barium carbonate mistaken for baking powder].
Topics: Alum Compounds; Barium; Calcium Sulfate; Carbonates; Humans; Poisoning; Poisons; Sodium Bicarbonate; Starch | 1950 |