Laundry Detergent is Delicious Candy

Children, rumor has it, are curious, persistent, and nefarious creatures.  Furthermore, the entire natural environment must first be tasted.  Thus, age-old cautionary guidance regarding home safety for children to prevent exposure to potentially hazardous materials.

So, naturally, laundry detergent would be kept safely out of reach of children – particularly the pre-packaged pod systems, which are candy-like and perfect for oral consumption – correct?

Nope!

According to this data from the National Poison Data System, in just a single year, there were 17,230 calls for pediatric exposure to laundry detergent pods in just two years, between January 2012 and December 2013.  The majority – 79.7% of cases – were secondary to ingestion.  4.4% of patients with an ingestion were judged to necessitate hospitalization, including 102 requiring intubation.  One death was reported – but the autopsy showed intracranial bleeding of uncertain/unlikely relation to the ingestion of detergent.

The authors specifically call out Procter & Gamble, maker of Tide Pods, for failure to place adequate warning labels or safety latches on their packaging – although, frankly, the ultimate responsibility lay with parents.  Keep cleaning supplies safely out of reach!

“Pediatric Exposure to Laundry Detergent Pods”
http://pediatrics.aappublications.org/content/early/2014/11/05/peds.2014-0057.abstract

No, You Can’t Get Drunk Off Tampons

Yet another bit of YouTube lunacy debunked – the concerning “recent phenomenon” amongst adolescents and young adults to use alternate methods of ethanol absorption to decrease detectability, or increase the rate of intoxication.

Such as “tampons soaked in vodka”.  In the vagina.

So, how viable is this strategy?  A toxicologist from USC investigates this strategy in vitro with a relatively straightforward study – simply measuring the maximum quantity of alcohol that could be absorbed by a tampon prior to insertion.  Commercially available tampons, with the applicator attached, maxed out at 15mL.  Minus the applicator, tampons absorbed up to 31mL – but obviously lost any insertion potential.

Disregarding the likely local irritation and discomfort of this method of administration, 15mL is clearly not enough to result in any appreciable level of intoxication – even assuming complete absorption across the vaginal mucosa, which is another topic of entirely reasonable uncertainty.

Another media-hyped “danger” that clearly isn’t.

“A New Clandestine Route of Ethanol Administration? Volume of Vodka Absorbed in Commercially Available Tampons. An in vitro study”
http://www.ncbi.nlm.nih.gov/pubmed/24928406

Bleeders Bleed, and Snakebites Don’t Help

A guest post by Justin Hensley (@EBMGoneWild) of Evidence-Based Medicine Gone Wild.

As the population ages, and the drug companies convince more and more  people to take drugs, new trends start showing up in medicine. One of them is patients taking antiplatelet and anticoagulant medications having other problems. Certainly there has been trauma literature on patients taking those medications, and now there is a toxicologic study.

In said study, the authors went back into their huge rattlesnake bite database in Arizona to identify those patients who were taking antiplatelet and/or anticoagulant medications. Comically, there were patients who had multiple snakebites, but they were only enrolled for their first bite. Also one patient was taking aspirin, clopidogrel, and warfarin, to go ahead and knock out any chance of hemostasis. They then looked for “early bleeding”, “late bleeding” or bleeding “at any time.” Major bleeding was markedly increased over controls, as was early bleeding and late bleeding. Length of stay and use of antivenom was not significantly different, however.


Take home messages? Antivenom does not correct coagulopathies secondary to medications, and late bleeding is much higher in patients on those medications, so laboratory observation of those patients should be extended. Also, avoid traipsing through rattlesnake country if you’re on blood thinners.
Bleeding Following Rattlesnake Envenomation in Patients With Preenvenomation Use of Antiplatelet or Anticoagulant Medications.

“Bleeding Following Rattlesnake Envenomation in Patients With Preenvenomation Use of Antiplatelet or Anticoagulant Medications.”
http://www.ncbi.nlm.nih.gov/pubmed/24628755

An Abbreviated IV Acetylcysteine Regime for Acute APAP Toxicity. Short, Sweet, and…. Safe?

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.
Anyone who has perused the literature on APAP toxicity will notice the protocols we use to guide us in the diagnosis and treatment of acute APAP overdose are based primarily on ultra-conservative estimates of risk rather than true clinical data. As a result we are left with acetylcysteine (NAC) treatment regimes that, though effective are cumbersome and convoluted. The current IV NAC regime consists of 3 different weight-based doses over various time periods within the first 25 hours. This regime is costly and frequently causes vomiting and anaphylactoid reactions. In a move towards practicality, authors from the Royal Infirmary of Edinburgh (the birthplace of the Rumack-Matthew Nomogram) performed a RCT comparing this traditional dosing scheme to a far more rational one.

These authors propose the initial bolus dose of NAC to be infused over a longer period (2 hours vs 15 min) followed by a maintenance infusion delivered over 12 hours in contrast to the traditional 24. They theorized that these modifications would reduce the amount of adverse reactions, primarily due to the initial rate at which NAC is infused and at the same time, limit the duration of treatment required. In a 2X2 factorial design, the authors also examined the effects of ondansetron on the rates of adverse reactions in both the traditional and modified NAC regimes.

From September 2010 to December 2012, 222 patients underwent randomization at three different UK hospitals. The authors found that both the modified dosing regiment and ondansetron prophylaxis decreased the rate of vomiting and retching in patients undergoing treatment for acute APAP intoxication. More impressively the modified dose regime seemed to dramatically reduce the incidence of serious anaphylactoid reactions from a frighteningly high 31% to 5%.

As far as safety is concerned there was no difference between the traditional and modified dosing regimes in the number of patients with an elevation in AST levels or microRNA miR-122 harpega(a more sensitive marker of hepatic injury as per the authors’ claims). There was an interesting increase in both AST levels and microRNA miR-122 levels in those given ondansetron when compared to placebo. Though this did not translate into any long term hepatic injuries and it is unclear if this increase was just noise secondary to the small sample size, the authors warn against its prophylactic use before further studies are performed to assess its safety.

Given that the Rumack-Mathews Nomogram was designed to be highly sensitive at the cost of its specificity, and very few patients above treatment threshold go on to clinically relevant hepatic toxicity, it is hard to say how many of these patients actually benefited from treatment. In addition 30% of this population were under the 4 hr 200mg/L level and were only treated because of the recent changes in the UK guidelines to lower the treatment threshold to 100mg/L. Due to the poor specificity and small sample size, it is difficult to truly assess the safety of this refined protocol. Using surrogate endpoints thought to be more sensitive for hepatic injury like a 50% rise in AST  (in contrast to the more traditional measurement of AST > 1000 IU) and microRNA miR-122, may provide us with some idea of efficacy, but does not answer the more pressing question. Are the patients treated with this modified regime at a higher risk for clinically relevant hepatic injury? This would require a much larger study population.

“Reduction of adverse effects from intravenous acetylcysteine treatment for paracetamol poisoning: a randomised controlled trial”
www.ncbi.nlm.nih.gov/pubmed/24290406

 

Where Is My: Coffee. Where is it.

Most modern vices seem to be, at the minimum, associated with some substantial harms.  Excessive sun exposure, rich western diets, scotch, sloth, etc.  And, then there’s coffee.

This is a review article covering the evidence behind various cardiovascular associations uncovered regarding the consumption of coffee.  After noting coffee contains thousands of compounds, the most prominent of which are caffeine, alcohols, antioxidants, and anti-inflammatories, the authors review the effects on various cardio-metabolic risk factors.

In brief, coffee consumption conferred:

  • No observed effect on blood pressure.
  • Decreased association with Type II diabetes.
  • Uncertain relationship with serum lipds.
  • A U-shaped relationship with congestive heart failure.
  • Decreased incidence of coronary heart disease.
  • Fewer cardiac arrhythmias.
  • Reduced risk of stroke.
  • Decreased risk of death.

Obviously, many of these findings are observational and potentially confounded by many other factors.  But, at the least – despair not of your coffee addiction.

“Effects of Habitual Coffee Consumption on Cardiometabolic Disease, Cardiovascular Health, and All-cause Mortality”
www.ncbi.nlm.nih.gov/pubmed/23871889

Levamisole-Induced Vasculitis

Let the good times roll – unless, of course, those good times are cut with levamisole.

This short case report from my good friends across the street at Baylor showcases a couple lovely pictures of the purpuric and necrotizing skin lesions associated with the anti-helminth levamisole – which, for some reason, is an increasingly popular additive to cocaine.  They are quite distressing and usually present following several courses of failed outpatient antibiotics.


I don’t think I specifically ever saw the exact patient these authors report upon, but it’s not a unique presentation in our county healthcare system.  This article is open-access for all to view without an institutional subscription.


Levamisole-adulterated Cocaine Induced Vasculitis with Skin Ulcerations”

http://www.escholarship.org/uc/item/4rd630zt



Bonus link nomination for best article title ever:

Don’t ß-Blockade Cocaine Chest Pain

Or, specifically, ignore this evidence that says you can.

There may be some mythology to the hypothesis that non-selective ß-receptor blockade is contraindicated in the setting of cocaine chest pain.  After all, the supporting evidence consists only of small, laboratory case series – and other outcomes-oriented data suggests ß-blockade is cardioprotective, as we already know.  However, this study is a perfect example of inappropriately extending a conclusion from retrospective data.

These authors identified 378 patients from retrospective chart review, selecting patients with chief complaints of chest pain and positive toxicology tests for cocaine.  Unfortunately, urine toxicology tests for cocaine stay positive for days following the initial episode of cocaine use.  Therefore, there is no way from these chart review methods to reliably differentiate the acuity of the cocaine intoxication.  

This is important because a major flaw in retrospective reviews, such as this, is a confounding selection bias.  If all cocaine chest pain patients are not created equal – the neurohormonal effects of cocaine last on the minutes to hours while their drug tests are positive for days – then providers may be selecting patients for beta blocker use/non-use based on acuity information this review cannot detect.  If providers are excluding patients from beta-blockers based on the acuity of their intoxication – as many sensible providers might – and only using beta-blockers in non-acute presentations, then this study may not include any of the population of interest.

The authors’ statement of “We have found that BB use in the acute management of cocaine-associated chest pain did not increase the incidence of MI” cannot be defended as accurate, as it is based on indefensible assumptions.

“Safety of β-blockers in the acute management of cocaine-associated chest pain”
http://www.ncbi.nlm.nih.gov/pubmed/23122421

Tramadol: A Myth of Safety

For me, tramadol lands squarely in the gap between oral analgesics I might use for “no pain” – ibuprofen, acetaminophen – and analgesics I might use for “real pain” – hydrocodone derivatives.  The literature describing the analgesic properties of tramadol is bizarre, with multiple comparisons with placebo, nerve blocks, adjunctive epidural anesthesia, etc., and very few head-to-head comparisons to the sorts of medications we routinely use.  When there are comparative efficacy reports, they typically conclude that tramadol is effective…just as effective as the NSAIDs its being compared with.

The theory I’ve heard people use when considering use of tramadol is that it has a better safety profile than hydrocodone and is less dependence-forming.  These claims may be true, but I do not believe they are true to the extent that it is clinically relevant.  Tramadol still generates an opioid withdrawal syndrome and, as this article describes, overdose/abuse still results in apnea with need for ventilatory support.

Additionally, tramadol is a GABA antagonist, lowering seizure threshold.  Of the 525 patients overdosing primarily on tramadol retrospectively identified at this Iranian hospital, 19 experienced apnea and 242 (46.1%) experienced seizures.  This is retrospective and co-ingestants cannot be fully ruled out, but the propensity for seizure is far more surprising than the incidence of apnea.

Tramadol has a role in pain control prescribing, but, in my practice, that role is tiny.

“Tramadol-induced apnea”
http://www.ncbi.nlm.nih.gov/pubmed/22809771

The Wrong Way To Quit Drinking

This week’s NEJM Case Records is an Emergency Department & Toxicology patient – I won’t ruin the final diagnosis for you – who uses a mysterious South American alcoholism cure to attempt to rehabilitate himself after a night of heavy drinking.

Obviously, it wouldn’t be a case report if the patient in question didn’t end up in the ICU!  There are nice, educational discussions of several toxodromes, antidotes, and various options for preventing end-organ damage in a subset of uncommonly seen poisonings.

Case 22-2012: A 34-Year-Old Man with Intractable Vomiting after Ingestion of an Unknown Substance
http://www.ncbi.nlm.nih.gov/pubmed/22808962

Happy Holidays!

Holiday break – intermittent and ineloquent blogging will be the norm.  I count 209 blog posts for the year – more than enough to keep anyone busy reading the archives.

But, if you’re done with those, Life In The Fast Lane has a lovely Christmas-themed blog post with great articles including:

What was wrong with Tiny Tim?”
http://www.ncbi.nlm.nih.gov/pubmed/1340779

Children’s Nomenclatural Adventurism and Medical Evaluation study”
http://www.ncbi.nlm.nih.gov/pubmed/20415998

No poinsettia this Christmas”
http://www.ncbi.nlm.nih.gov/pubmed/16866065