Tag Archives: pharm

quick reference: opiod conversion

1 Sep

for a quick sense of what is an equivalent dose across different opiates:

  • morphine 10 mg IV
  • hydromorphone 1.5 mg IV
  • fentanyl 200 mcg IV

 

  • hydromorphone 7.5 mg PO
  • oxycodone 15-20 mg PO
  • hydrocodone 30-45 mg PO
  • codeine 180-200 mg PO

References: e-med journal article; emedicine; picture

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topical NSAIDs

13 Aug

quick hit review in July’s EP Monthly:

 

topical NSAIDs:

  • as effective as oral NSAIDs for pain relief (NNT for 50% pain relief with topical gel = 11)
  • adverse GI side effects less common
  • risk of renal injury not clearly defined, but less systemic absorption (6-10% vs. 85% oral)

 

1% diclofenac gel (Voltaren):

  • typically QID, up to 32 g/day
  • 100g tube costs ~$45  (the 1.5% solution costs way more)

 

BOTTOM LINE:

Worth knowing about, especially in those with significant GI issues taking NSAIDs, with focal musculoskeletal issues.  Keep the cost in mind, though.

 

References: EPmonthly mag + picture

 

 

Anbesol for babies: why worry?

23 Jun

Dapsone and topical anesthetic agents (benzocaine, the active ingredient in anbesol) are the most common causes of acquired methemoglobinemia

Acquired methemoglobinemia is a result of certain ingested drugs leading to a state of oxidized (ferric state Fe+++) of hemoglobin, which are unable to bind oxygen. The remaining hemoglobin groups have an increased oxygen affinity causing a left shift.

The overall result is a functional anemia.

There are two ways for methemoglobin to be reduced back to hemoglobin:

  1. NADH-dependent catalyzed by cytochrome b5 reductase (b5R)
  2. NADPH generated by glucose-6 phosphate dehydrogenase (G6PD), but in order for this pathway to be activated, an extrinsically administered electron acceptor is required (methylene blue and riboflavin)

Infants are more susceptible to the development of methemoglobinemia because their erythrocyte cytochrome b5 reductase activity is 50-60% of adult activity

Treatment includes administration of intravenous methylene blue, 1 to 2 mg/kg, given over five minutes

Source: uptodate.com

Submitted by K Estes.

Myth Buster: Egg allergies and Propofol

18 Jun

 

Bottom line: there is no confirmed report of propofol-induced anaphylaxis in egg-allergic patients.

 

Propofol is made up of an oil water emulsion using soybean oil (10%) and egg lecithin (1.2%).

 

Lecithin (from the Greek lekithos, which means egg yolk) is a purified phosphatide found in egg yolk.

 

Egg allergy is most common during childhood and is usually outgrown by adulthood. The five major allergens that have been characterized originate from the egg white. Chicken serum albumin is the major allergen that has been described from the egg yolk.

 

The cases documented of anaphylaxis that have been associated with propofol were never followed with formal skin testing.

 

Now that we are on the topic… what about allergies to soy? Should you be worried that patients with soy allergies will have anaphylaxis to propofol?

 

Refined soy oil, such that is used to make propofol, is safe for people with soy allergy because the allergenic proteins are removed during the refining process.

 

Source: Anesthesia in the patient with multiple drug allergies: are all allergies the same? Current Opinion in Anaesthesiology. June 2011. Issue: Volume 24 (3), p 320-325; picture

 

Submitted by K Estes.

quick & dirty epinephrine drip

2 Jun

great post from ALiEM covers this handy tip:

10-SECOND RECAP:

In a pinch, here’s a quick way to get an IV epi drip started until the pharmacy/PYXIS/IV pump setup catches up to your need.

  • Grab the code cart epi (its 1 mg)
  • Inject the whole 1 mg into a 1 Liter NS bag 
  • Hang your new Liter bag of 1 mcg/mL concentration epi
  • Run wide open until desired initial stabilization/BP
  • Titrate to effect

 

TO MAKE YOU FEEL MORE COMFORTABLE ABOUT THIS:

ANAPHYLAXIS:

  • starting drip is 1-4 mcg/min IV
  • a wide-open 18-gauge IV will deliver ~20-30 mL/min (or 20-30 mcg/min) of epinephrine
  • recommended push-dose epi is 0.1 mg (or 100 mcg) over 5 minutes, which is 20 mcg/min avg.

 

RESUSCITATION/PRESSOR DOSING:

  • dose is 2-10 mcg/min IV   (or 2-20 mcg/min, depending on your source)

 

There you go.  Good to have in your back pocket.

 

References: ALiEM post; Epocrates; uptodate.com; picture

Isopropyl Alcohol (part 2) – Management

18 May

(check out the previous post for some initial isopropyl alcohol tidbits)

WHAT TO ORDER, WHAT TO LOOK FOR:

Tests to obtain — The following tests should be obtained in all poisoned patients:

  • POC glucose
  • Acetaminophen and salicylate levels, to rule out these common co-ingestions
  • Electrocardiogram (ECG), to rule out conduction system poisoning by drugs that affect the QRS or QTc intervals
  • Pregnancy test in women of childbearing age
  • Serum isopropyl alcohol and acetone levels (or serum osmolality, if direct serum drug levels are unavailable). 
  • Basic electrolytes, with calculation of anion gap
  • BUN and creatinine
  • Serum and urine ketones
  • Arterial or venous blood gas

 

Elevated Osmolar Gap. The absence of a high anion gap metabolic acidosis four to six hours post-ingestion enables the clinician to distinguish from other alcohols.

 

Serum concentrations of at least 100 mg/dL (17 mmol/L) are necessary to cause a decreased level of consciousness. 

Both isopropyl alcohol and acetone will raise the osmolal gap.

The plasma osmolal gap cannot distinguish among isopropyl alcohol, methanol, and ethylene glycol poisoning, and so cannot be used to exclude ingestion of these more toxic alcohols.

 Calculated Sosm   =   (2 x serum [Na])  +  [glucose]/18  + [BUN]/2.8

 

MANAGEMENT – ABC’s, then…

Decontamination — There is no role for gastrointestinal (GI) decontamination in most cases of isolated isopropyl alcohol intoxication. Its rapid absorption after oral ingestion and its low toxicity make such interventions unnecessary.

 

Alcohol dehydrogenase (ADH) inhibition — Since acetone (the primary metabolite) is less toxic than isopropyl alcohol (the parent alcohol), there is no indication for ADH inhibition with fomepizole or ethanol following isopropyl alcohol exposure

 

Disposition – Symptoms from isopropyl alcohol manifest quickly. Therefore, patients with unintentional ingestions can be discharged after two hours if they remain asymptomatic and isopropyl alcohol is known to be the only substance involved.

 

Submitted by Christina Brown.

 

References: uptodate.com; Trullas JC, Aguilo S, Castro P, Nogue S. Life-threatening isopropyl alcohol intoxication: is hemodialysis really necessary? Vet Hum Toxicol 2004; 46:282.; Stremski E, Hennes H. Accidental isopropanol ingestion in children. Pediatr Emerg Care 2000; 16:238.;  Bekka R, Borron SW, Astier A, et al. Treatment of methanol and isopropanol poisoning with intravenous fomepizole. J Toxicol Clin Toxicol 2001; 39:59.;  Su M, Hoffman RS, Nelson LS. Error in an emergency medicine textbook: isopropyl alcohol toxicity. Acad Emerg Med 2002; 9:175.; picture

Isopropyl Alcohol (part 1) – Recognition

15 May

ISOPROPYL ALCOHOL – Central nervous system (CNS) inebriant and depressant.  Toxicity and treatment resemble that of ethanol.

 

EPIDEMIOLOGY – Fatality from isolated isopropyl alcohol toxicity is rare, but can result from injury due to inebriant effects, untreated coma with airway compromise, or rarely, cardiovascular depression and shock following massive ingestion. 

 

PHARMACOLOGY AND TOXICOLOGY — a CNS depressant whose toxicity closely resembles that of ethanol, with which it shares strong structural similarity.  

In untreated animals, the median lethal dose lies between 4 and 8 g/kg.

Isopropyl alcohol does NOT cause an elevated anion gap acidosis, unlike the toxic alcohols methanol and ethylene glycol.  Why?  Because Ketones cannot be oxidized to carboxylic acids.

Isopropyl alcohol is metabolized by the alcohol dehydrogenase family of enzymes to acetone. 

Following ingestion, the elimination of acetone is slower than its formation, and this metabolic end-product accumulates.  Acetone itself is a mild CNS depressant and may exacerbate the CNS depression caused by isopropyl alcohol.  It is also responsible for the marked ketosis that is present in most isopropyl alcohol ingestions.

 

KINETICS – Peak serum concentration and clinical effects occur approximately one to two hours after ingestion.

 

CLINICAL FEATURES OF OVERDOSE

Symptoms – nausea, vomiting, and abdominal pain.

Signs – CNS Depressive effects peak within the first hour after ingestion.  Can cause an alteration in mental status similar to that seen in ethanol intoxication.

A fruity breath odor is often perceptible, suggesting acetone accumulation.

Following massive ingestion, signs of shock may be present, as may hematemesis (gastric irritant), pulmonary edema, and hemorrhagic tracheobronchitis.

 

Submitted by Christina Brown.
References: uptodate.com; Trullas JC, Aguilo S, Castro P, Nogue S. Life-threatening isopropyl alcohol intoxication: is hemodialysis really necessary? Vet Hum Toxicol 2004; 46:282. Stremski E, Hennes H. Accidental isopropanol ingestion in children. Pediatr Emerg Care 2000; 16:238. Bekka R, Borron SW, Astier A, et al. Treatment of methanol and isopropanol poisoning with intravenous fomepizole. J Toxicol Clin Toxicol 2001; 39:59.  Su M, Hoffman RS, Nelson LS. Error in an emergency medicine textbook: isopropyl alcohol toxicity. Acad Emerg Med 2002; 9:175.; picture