scholarly journals Accidental transdermal methanol poisoning presenting to a regional emergency department

CJEM ◽  
2019 ◽  
Vol 21 (3) ◽  
pp. 435-437
Author(s):  
Chelsea R. Beaton ◽  
Clinton Meyer

Learning Points:•Know and identify clinical presentations of toxic alcohols.•Understand the differential diagnosis of high anion gap metabolic acidosis.•Appreciate the importance of history and clinical findings in establishing methanol toxicity diagnoses, especially in centres where laboratory testing is unavailable.•Recognize the value of provincial poison centres in supporting emergency physicians in the diagnosis and management of poisonings and overdoses.

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Emily A. Kiernan ◽  
Julie A. Fritzges ◽  
Kathryn A. Henry ◽  
Kenneth D. Katz

Massive acetaminophen (N-acetyl-p-aminophenol; APAP) ingestion is characterized by a rapid onset of mitochondrial dysfunction, including metabolic acidosis, lactemia, and altered mental status without hepatotoxicity which may not respond to the standard doses of N-acetylcysteine (NAC). A 64-year-old woman without medical history presented comatose after an ingestion of 208 tablets of Tylenol PM™ (APAP 500 mg and diphenhydramine 25 mg). The initial APAP concentration measured 1,017 µg/mL (therapeutic range 10-30 µg/mL), and elevated anion gap metabolic acidosis, lactemia, and 5-oxoprolinemia were detected. High-dose intravenous (IV) NAC, 4-methylpyrazole (4-MP), and hemodialysis (HD) were initiated. She was transferred to a liver transplant center and continued both NAC and HD therapies until complete resolution of metabolic acidosis and coma without developing hepatitis. She was discharged without sequelae. This is the fourth highest APAP concentration recorded in a surviving patient. Moreover, this is the first report of a novel “triple therapy” using NAC, 4-MP, and HD in the setting of massive APAP ingestion that presents with coma, elevated anion gap metabolic acidosis, and lactemia. Emergency physicians should recognize these critically ill patients and consider high-dose NAC, 4-MP, and HD to be initiated in the emergency department (ED).


CJEM ◽  
2010 ◽  
Vol 12 (05) ◽  
pp. 449-452 ◽  
Author(s):  
Thomas J. Green ◽  
Jan Jaap Bijlsma ◽  
David D. Sweet

ABSTRACTThe workup of the emergency patient with a raised anion gap metabolic acidosis includes assessment of the components of “MUDPILES” (methanol; uremia; diabetic ketoacidosis; paraldehyde; isoniazid, iron or inborn errors of metabolism; lactic acid; ethylene glycol; salicylates). This approach is usually sufficient for the majority of cases in the emergency department; however, there are many other etiologies not addressed in this mnemonic. Organic acids including 5-oxoproline (pyroglutamic acid) are rare but important causes of anion gap metabolic acidosis. We present the case of a patient with profound metabolic acidosis with raised anion gap, due to pyroglutamic acid in the setting of malnutrition and chronic ingestion of acetaminophen.


1999 ◽  
Vol 135 (6) ◽  
pp. 751-755 ◽  
Author(s):  
John M. Lorenz ◽  
Leonard I. Kleinman ◽  
Katherine Markarian ◽  
Maria Oliver ◽  
Jaime Fernandez

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
H. R. Sawe ◽  
J. A. Mfinanga ◽  
F. H. Ringo ◽  
V. Mwafongo ◽  
T. A. Reynolds ◽  
...  

Background. Traditional uvulectomy is performed as a cultural ritual or purported medical remedy. We describe the associated emergency department (ED) presentations and outcomes.Methods.This was a subgroup analysis of a retrospective review of all pediatric visits to our ED in 2012. Trained abstracters recorded demographics, clinical presentations, and outcomes.Results. Complete data were available for 5540/5774 (96%) visits and 56 (1.0%, 95% CI: 0.7–1.3%) were related to recent uvulectomy, median age 1.3 years (interquartile range: 7 months–2 years) and 30 (54%) were male. Presenting complaints included cough (82%), fever (46%), and hematemesis (38%). Clinical findings included fever (54%), tachypnea (30%), and tachycardia (25%). 35 patients (63%, 95% CI: 49–75%) received intravenous antibiotics, 11 (20%, 95% CI: 10–32%) required blood transfusion, and 3 (5%, 95% CI: 1–15%) had surgical intervention. All were admitted to the hospital and 12 (21%, 95% CI: 12–34%) died. By comparison, 498 (9.1%, 95% CI: 8–10%) of the 5484 children presenting for reasons unrelated to uvulectomy died (p=0.003).Conclusion. In our cohort, traditional uvulectomy was associated with significant morbidity and mortality. Emergency care providers should advocate for legal and public health interventions to eliminate this dangerous practice.


Author(s):  
Raymond S. Douglas ◽  
Robert A. Goldberg

Although orbital disorders are not frequently encountered in the comprehensive ophthalmologist’s practice, it is essential to be able to diagnose patients with orbital disease and manage them accordingly. Various disease processes can affect the orbit. This chapter endeavors to provide a thoughtful, stepwise, and logical approach to the evaluation of orbital disease. The discussion begins with differential diagnosis, adds an intelligent history-taking and physical examination, and then focuses on efficient use of diagnostic tests to finally arrive at the correct diagnosis. The staging and management of two common orbital disorders, orbital inflammation and thyroid-associated ophthalmopathy, will also be discussed. The differential diagnosis of orbital disease is extensive, and most listings of orbital disease divide the causes between histopathologic and mechanistic categories. This type of grouping is intellectually sound and scientifically useful but does not provide a framework that the clinical practitioner can easily grasp and directly use in sorting through the differential diagnosis of any given patient. In broad terms, orbital disease can be considered in terms of location, extent, and biologic activity. The classification used in this chapter is broken down along clinical lines and takes advantage of the fact that the orbit has a somewhat limited repertoire of ways that it can respond to pathologic conditions. Orbital disease can be categorized into five basic clinical patterns: inflammatory, mass effect, structural, vascular, and functional. Although many cases cross over into several categories, the vast majority of clinical presentations fit predominantly into one of these patterns. As the clinician walks through each step of the evaluation process—history, physical examination, laboratory testing, orbital imaging—a conscious effort should be made to categorize the presentation within this framework. If the practitioner approaches orbital disease with this framework of discrete patterns of clinical presentation, then at every step of the diagnostic pathway (history, physical examination, orbital imaging studies, and special tests), he or she can draw from a defined set of differential diagnoses that characterize each pattern of orbital disease and use that information to efficiently and confidently orchestrate diagnosis and management.


2013 ◽  
Author(s):  
Ann P. O'Rourke ◽  
James Orr ◽  
Suresh Agarwal

Anticipation and early identification of conditions that alter the body's ability to compensate for acid-base disorders are vital in managing surgical patients. This review describes the general principles and classification of acid-base disorders. Metabolic acid-base disorders are presented, including metabolic acidosis and alkalosis. Respiratory acid-base disorders are also presented, including respiratory acidosis and alkalosis. Tables show the differentiation of acid-base disorders, causes of positive–anion gap acidosis, the differential diagnosis for normal–anion gap metabolic acidosis, the mechanisms associated with increased serum lactate concentration, and the differential diagnosis for metabolic alkalosis. This review contains 7 highly rendered figures, 5 tables, and 135 references.


2017 ◽  
Vol 36 (4) ◽  
pp. 229-232
Author(s):  
Susan Givens Bell

AbstractThe anion gap, in conjunction with other laboratory results, can be a useful clue in the differential diagnosis of metabolic acidosis. There are three primary causes of metabolic acidosis: loss of base, decreased renal excretion of acid, and increased acid production. Depending on the cause of metabolic acidosis, the anion gap may be elevated or normal.


Author(s):  
Stephanie Teasdale ◽  
Elham Reda

Summary We present two cases of adrenal phaeochromocytoma in patients with a previous diagnosis of neurofibromatosis type 1 (NF1). One had an adrenergic phenotype. The other had a more noradrenergic phenotype. Both had large primary tumours, which increases the likelihood of malignancy. Both also had elevated plasma-free methoxytyramine, which has been linked with malignancy even in non-SDHB phaeochromocytomas. Learning points Phaeochromocytoma can have varied clinical presentations. Methoxytyramine can be useful in the biochemical work-up of both SDHB-positive and SDHB-negative phaeochromocytoma. The utility of methoxytyramine as a marker of malignancy in NF1-related phaeochromocytoma is unclear, and cases with elevated titres warrant longer follow-up.


2019 ◽  
Vol 19 (4) ◽  
pp. 359 ◽  
Author(s):  
Abdullah M. Al Alawi ◽  
Usama Al Amri ◽  
Henrik Falhammar

Lactation ketoacidosis is an extremely rare type of high anion gap metabolic acidosis. We report two lactating women who were diagnosed with lactation ketoacidosis. The first patient presented to the Emergency Department at Royal Darwin Hospital, Darwin, Australia, in 2018 with lethargy, nausea and abdominal pain after she commenced a new diet regimen based on three meals of protein per day and free of glucose, gluten and dairy products. The second patient presented to the Emergency Department at Sultan Qaboos University Hospital, Muscat, Oman, in 2018 with headache, severe malaise, epigastric pain and worsening of gastroesophageal symptoms. Blood investigation results showed that both patients had high anion gap metabolic acidosis, ketosis and hypoglycaemia. The patients responded well to intravenous dextrose and resumption of a balanced diet. Both patients were able to continue breastfeeding and remained well on follow-up.Keywords: Breastfeeding; Starvation; Hypoglycemia; Ketosis; Acid-Base Imbalance; Metabolic Diseases; Ketone Bodies; Fasting; Case Series; Australia; Oman.


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