Losing faith in evidence-based medicine: Etomidate and sepsis

In an era where evidence-based medicine is the goal, it is vitally important for practitioners to understand how to prioritize and interpret the onslaught of data coming at us.

This fact was driven home for me with a recent publication. Several weeks ago an article was published in Critical Care Medicine entitled “Etomidate is associated with mortality and adrenal insufficiency in sepsis: A meta-analysis.”

The point of this post is not to debate if etomidate should be used to intubate septic patients. Etomidate very well may kill people with sepsis. I just don’t know from the data currently available. Using this meta-analysis as an example, the goal is to point out two important areas where we could stand to sharpen our literature evaluation skills.

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By Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP|2016-11-11T18:43:14-08:00Nov 20, 2012|Infectious Disease, Tox & Medications|

PV card: PE Severity Index (PESI) score

Do you send some of your low-risk patients with pulmonary embolism home?

This is a controversial issue which warrants a look at risk stratification tools. The primary one used is the validated Pulmonary Embolism Severity Index (PESI) score. In Lancet 2011, the authors looked at whether PESI class I and II (low risk) patients could be managed safely as outpatients. It turns out in their study, regardless of whether their PESI class I and II patients were treated as outpatients and inpatients, all fared equally well from a complications standpoint (recurrent clot, bleeding from anticoagulation).

I like the validated PESI scoring system to risk-stratify patients as low vs high risk for complications. I, however, do caution people to look closely at the exclusion criteria for this study before applying this to all ED patients.

The exclusion filter was so strict that they likely have captured a very narrow and unrealistic scope of patients to be widely applicable. It makes sense from a research standpoint to have these criteria to achieve internal validity but the question is external validity. Two exclusion criteria that struck me as awfully strict were: (1) needing parenteral opioids or (2) active alcohol or drug abuse.

Bottom line

For me, this study alone seems not have enough external validity to decide about the decision to treat PE patients as inpatient vs outpatient. Although I think that ultimately some can be managed as outpatients, I’d like to see more studies.

PV Card: PESI Score for Pulmonary Embolism

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See other ALiEM (PV) Cards.

By Michelle Lin, MD|2021-10-08T09:35:48-07:00Nov 17, 2012|ALiEM Cards, Cardiovascular, Pulmonary|

Identify the antihypertensive agent:

1. Rapid acting systemic and coronary artery vasodilator with minimal effects on cardiac conductivity or inotropy. Well studied in pregnancy. Caution in patients with left ventricular failure, liver cirrhosis

Answer: Nicardipine

2. Predominantly dilates the venous system. Useful in patients with cardiac ischemia, pulmonary edema, or congestive heart failure. Caution in patients with right ventricular failure

Answer: Nitroglycerin

3. Drug of choice in eclampsia, pre-eclampsia, and aortic dissection. Contraindicated in patients with congestive heart failure and heart block

Answer: Labetalol

4. Decreases peripheral vascular resistance and increases collateral coronary blood flow in an uncontrolled and unpredictable manner and may result in serious complications. Drug of choice during pregnancy

Answer: Nifedipine

5. Direct arterial vasodilator that increases cardiac output and heart rate (Reflex response). Patient may develop lupus like syndrome. Not to be used as first line in the ED

Answer: Hydralyzine

6. Arterial vasodilator that delays atrioventricular conduction and has a negative inotropic effect

Answer: Verapamil

7. Rapid onset of effect after oral administration (30 mins) with little change in cardiac output or reflex tachycardia. Adverse effect may include cough, angioedema. Toxic during first trimester.

Answer: Captopril

8. Only for patients with subarachnoid hemorrhage. Not to be given IV only PO or NG tube

Answer: Nimodipine

9. The only parenteral angiotensin-converting enzyme inhibitor. May cause azotemia in older patients after MI

Answer: Enalapril

10. Oral or transdermal decreases peripheral vascular resistance. May cause sedation and bradycardia

Answer: Clonidine

11. Used in patients who are volume overloaded but not in patients who are hypertensive and volume depleted

Answer: Diuretics

12. Drug of choice for pheochromocytoma, MAOI crisis, and cocaine overdose

Answer: Phentolamine

Reference:
1. Richard S. Irwin, James M. Rippe. Manual of Intensive Care Medicine; 4th ed
2. Marx: Rosen’s Emergency Medicine, 7th ed (Chapter 82- Hypertension: Richard O. Gray)

By Javier Benitez, MD|2016-11-11T11:52:01-08:00Nov 14, 2012|Cardiovascular|

Trick of the Trade: Persistent paracentesis leakage

Dr. Matt Borloz (Carilion Clinic) recently emailed me his recent trick in fixing a persistently leaking paracentesis site. Read about his experience:

A patient with advanced alcoholic cirrhosis with ascitic fluid leaking from a paracentesis puncture site from a procedure done 2 days prior. Dermabond had initially been applied post-procedure, but it had come loose, and ascitic fluid had been saturating dressing after dressing.

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By Michelle Lin, MD|2016-11-11T18:43:16-08:00Nov 6, 2012|Gastrointestinal, Tricks of the Trade|

Mythbuster: Urgent dialysis following IV contrast?

Have you ever had to promise the radiologist that you would arrange emergent dialysis for your end-stage renal disease (ESRD) patient after receiving IV contrast?

This myth is even perpetuated in the field of nursing. In fact, what prompted this post was overhearing this very topic discussed between a nurse and a recent graduate nurse trainee.
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By Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP|2019-02-19T18:47:01-08:00Oct 31, 2012|Renal, Tox & Medications|

Where’s the best place to suffer cardiac arrest? Seattle? Las Vegas? Who’s going to give me mouth-to-mouth resuscitation? Will someone know how to use an automatic external defibrillator (AED)?

Where is the BEST place to experience a cardiac arrest???

As luck would have it, the best place would be at the ACEP Scientific Assembly. On the first day of Scientific Assembly, an exhibitor collapsed in the convention center without a pulse. At a conference with thousands of emergency physicians, several Good Samaritans immediately sprung into action. An attendee used a CPR mask while another operated an AED. They were able to revive their patient, where he is reportedly doing well at a local hospital.

Congratulations to Drs. David Pigott, Jared Shell, Jerry Edwards and everyone else involved on a job well done!

By Fred Wu, MHS, PA-C|2019-02-19T18:05:51-08:00Oct 17, 2012|Cardiovascular|

How many times have you given your patient IM ceftriaxone for that presumed gonococcal infection? … still counting? Many of us learned (or at least thought we learned) that ceftriaxone has to be administered IM to get the ‘depot’ effect.

Myth Busted

There doesn’t appear to be a true depot effect. IV and IM ceftriaxone have very similar pharmacokinetic profiles. Let me prove it to you, straight from the FDA-approved ceftriaxone package insert.

Table 1: Average plasma concentration (mcg/mL) as measured over time after 500 mg of ceftriaxone administration

Ceftriaxone route	0.5 hr	1 hr	2 hr	4 hr	6 hr	8 hr	12 hr	16 hr	24 hr
IV	82	59	48	37	29	23	15	10	5
IM	22	33	38	35	30	26	16	unknown	5

Table 2: Average urine concentration (mcg/mL) as measured over time after 500 mg of ceftriaxone administration

Ceftriaxone route	0-2 hrs	2-4 hrs	4-8 hrs	8-12 hrs	12-24 hrs	24-48 hrs
IV	526	366	142	87	70	15
IM	115	425	308	127	96	28

The plasma concentrations are almost identical after IM and IV administration through 24 hours (Table 1).
Even the urinary concentrations are similar up to 24-48 hours after a dose (Table 2).
The volume of distribution is the same for both parenteral routes, too. This means that its penetration into the “affected area” is similar.
According to a 2012 CDC Report the minimum inhibitory concentration (MIC) for N. gonorrhoeae strains to ceftriaxone is 0.125 mcg/mL. IV therapy provides concentrations above this resistance cutoff well after 24-48 hours, similar to IM therapy.

Trick of the Trade

If the patient already has an IV line, we can give IV ceftriaxone for gonorrhea instead of IM.

In fact, the Japanese Society for Sexually Transmitted Diseases has recommended monotherapy with a single IV dose of 1 g ceftriaxone since 2008. (Aoki 2021)

While most of the time patients with STD (or STI, if you prefer) complaints don’t have an IV line established, occasionally they do. My hospital stocks 1 gm and 2 gm premixed IV bags of ceftriaxone, so we could potentially just give 1 gm IV in these rare cases to ensure adequate levels (even 500 mg might be just fine).

Of course, the other way to avoid the painful injection is to mix the ceftriaxone with lidocaine… or avoid contracting gonorrhea altogether.

Disclaimer

This post is intended for educational purposes to explore the kinetic data for IM and IV therapy. The CDC guidelines should be followed for treatment of STDs.

References

Product Information: ROCEPHIN(R) IV, IM injection, ceftriaxone sodium IV, IM injection. Genentech USA, Inc. (per Manufacturer), South San Francisco, CA, 2010.
Workowski KA, Berman S; Centers for Disease Control and Prevention (CDC). Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep 2010;59(RR-12):1-110. [PMID: 21160459]. Free MMWR PDF download.

Original: October 9, 2012; Last Updated: December 24, 2021

By Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP|2022-02-03T10:29:27-08:00Oct 9, 2012|Infectious Disease, Tox & Medications, Tricks of the Trade|

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