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Entries in Myths (4)

Thursday
Dec292011

Myth Buster Episode 3 - Digital Nerve blocks and adrenaline / epinephrine

This age old myth has been taught over the generations, handed down from from medical eminence to medical students & junior doctors alike. Having been told the same thing recently by a resident in plastics, I thought I would attempt to debunk it here. 

Where it Came From

Several publications of case reports in the 1940s cited digital nerve blocks with epinephrine as a cause for gangrene of the finger in the post-op period. This was further propagated in the surgical texts of the day (see references below). 

It is widely accepted now (including by the authors) that the actual cause of the gangrene was thermal injury secondary to boiling hot soaks in boric acid solution post-operatively, which was recommneded practice back in the day. 

Current evidence

Numerous reviews have examnied this - most recently this study by Chowdhry et al in the December 2010 edition  of the journal of Plastic and Reconstructive Surgery :

BACKGROUND:

Epinephrine in digital blocks has been condemned by traditional medical theory. The authors provide a retrospective review of 1111 cases involving digital block anesthesia with epinephrine in conjunction with an extensive literature review.

METHODS:

The authors conducted a retrospective review of 1111 cases involving digital and hand surgery. Observations were made concerning the location of and indication for surgery, age, sex, type of block used, type and dose of anesthetic, use of epinephrine and concentration, use of a tourniquet, follow-up, and complications. Dorsal and transthecal techniques were used exclusively. Patients with vascular compromise did not receive epinephrine and were excluded from the study.

RESULTS:

One thousand one hundred eleven cases were reviewed, distributed among 692 male patients and 419 female patients. Sites of surgery ranged throughout the hand and all fingers for a variety of indications. Five hundred patients received injections of 1% plain lidocaine with a dosage range of 2 to 10 cc and an average of 5.7 cc. Six hundred eleven patients received injections of 1% lidocaine with epinephrine (1:100,000) in a dose range of 0.5 to 10 cc and an average dose of 4.33 cc. Nine hundred eighty-six patients (88.75 percent) followed up in the clinic. No patients suffered from digital gangrene in the epinephrine group.

CONCLUSIONS:

After reviewing 1111 cases, there were no complications associated with the use of epinephrine in digital blocks. The authors suggest that correct application of epinephrine in digital blocks is appropriate, and defend its use.

Plast Reconstr Surg. 2010 Dec;126(6):2031-4.

Myth de-bunked.

The following caveats apply:

- digital blocks may be contraindicated in patients with disease processes involving the digital vessels at the base of the proximal phalanx

- adrenaline / epinephrine should be used cautiously in patients wth known cardiac disease, hypertension & peripheral vascular disease. 

 

References

Plast Reconstr Surg. 2010 Dec;126(6):2031-4.

Kaufman, P. A. Gangrene following digital nerve block anesthesia. Arch. Surg. 42: 929, 1941. 

McLaughlin, C. W., Jr. Postoperative gangrene of the finger following digital nerve block anesthesia. Am. J. Surg. 55: 588, 1942. 

O’Neill, E. E., and Byrne, J. J. Gangrene of the finger following digital nerve block. Am. J. Surg. 64: 80, 1944. 

Bunnell, S. Surgery of the Hand, 1st Ed. London: Lippin- cott, 1944. Pp. 100–105.

 

Sunday
Dec182011

Myth Buster Episode 2 Hypertension and Epistaxis

Blood Spatter

Not infrequently we will see patients who present to the ED with a nose bleed. The usual measures will be employed (pressure, ice packs, packing, tampons), and then someone really clever notices that the blood pressure is elevated. All manner of blood pressure lowering drugs are then employed - GTN, labetelol, metoprolol, to name but a few, in order to reduce the blood pressure, and therefore reduce the pressure on that standing column of blood that connects the heart to the Kiesselbach's plexus. We've gone from permissive hypotension (penetrating trauma) to "active hypotension" for epistaxis.

The hypertensive emergencies include:

- hypertensive encephalopathy

- intracranial haemorrhage (including SAH)

- aortic dissection

- acute pulmonary oedema

- acute kidney injury

- pre-eclampsia

Not a hypertensive emergency

- epistaxis

I would love to know who the first person was, that suggested that giving blood pressure lowering drugs to patients who are acutely externally haemorrhaging is somehow a good idea. In my experience, standing in front of a patient actively hosing from their nose, holding a Rapid Rhino is more than enough to get their pressure up.

Studies conducted over the years have largely debunked the connection between epistaxis and hypertension (see links below), however, pockets of resistance still remain.

Eur Arch Otorhinolaryngol. 2011 Dec;268(12):1749-53. Epub 2011 Jun 9.

Blood Press. 2003;12(3):145-8.

Int J Cardiol. 2009 May 29;134(3):e107-9. Epub 2008 May 21.

Wednesday
Dec142011

Myth Busters Episode 1...Recent negative angiogram makes ACS unlikely

You are presented with a 54 year old man, who has a 6 hour history of central chest pain at rest, very similar to his exertional angina. He has no risk factors for coronary artery disease (aside from having a heart - don't get me started on risk factors - a rant for another time...). A recent angio from a year ago showed no imminently threatening stenoses of his major vessels. He is clinically well, and is pain free by the time you examine him. You try to refer to cardiology, but the resident / registrar reassuringly tells you that a single troponin is sufficient given his recent normal angio...

Reasons why this is really not the case...

1) Angiography of the coronary vessels  focuses on stenoses of the relatively larger epicardial vessels, not the branches. Management of stenoses in these much smaller vessels is medical rather than interventional, and therefore they may not be routinely described in the report.

2) Diabetics have microvascular disease - these vessels cannot be visualised at all.

3) Vasospasm cannot be predicted by prior angiography

4) Studies have shown that lesions can progress by up to 20% a year. That non critical stenosis may look very different after 6 months...

5) Considering the pathophysiology of STEMI - most are caused by plaque rupture, which further down-stream, may occlude a 50% stenosed vessel, which was previously described as non-flow limiting. It is with Vulcan like logic that one may sumise that the size of the ruptured plaque cannot possibly be predicted on prior angiography.

So, normal recent angio does not exclude the risk of new acute coronary syndrome for the patient in front of you, and if the history sounds like it could be ischaemia / infarction, treat the patient accordingly... 

J Am Coll Cardiol. 1988 Jul;12(1):56-62.

Circulation. 2005 Jan 18;111(2):143-9. Epub 2004 Dec 27.

J Am Coll Cardiol. 2002 Mar 6;39(5):847-51

J Cardiothorac Surg. 2010 Oct 26;5:91.

Thursday
Dec082011

Sedation in Traumatic Brain Injury

Head over to Cliff Reids brilliant Resus.me site for an overview of a systematic review of RCTs related to sedation in patients with severe traumatic brain injury

After a disagreement with an anaesthetist on the use of ketamine in head injured patients, I decided to look at the evidence.

So, why don’t we use Ketamine in RSI for Head Injury?

Answer : 3 Studies from the 1970’s

Study 1 Cerebrospinal fluid during dissociative anesthesia with ketamine. (Gardner AE et al, Anesthesiology 1971 35:226-228)

2 patients requiring pneumo-ventriculograms given 2mg/kg intravenous ketamine and allowed to breathe spontaneously.

Result

Patient 1 - obstructed CSF pathway with glioma, had rise in CSF pressure from 31.5mmHg to 84mmHg

Patient 2 (normal CSF pathway) CSF pressure increased from 3.2mmHg to 13.7mmHg. Cerebral perfusion pressure increased by 3.6mmHg

Both patients had rises in BP, HR, RR

Study 2 Ketamine anesthesia in patients with intracranial pathology (Shapiro et al, Br J Anesthesia 1972 44:1200-1204)

Seven patients with CSF shunts given 2mg/Kg IV or 4mg/Kg IM.

Result

2 patients with normal CSF  pathways and no rise in ICP initially showed a small rise in ICP which ultimately remained below 10mmHg. There was an increase in CPP from 14 to 121 mmHg in one, and a decrease of 5mmHg to 83mmHg in the other

The 5 patients with obstructed CSF pathways all exhibited increased ICP and decreased CPP

Study 3 The effects of ketamine on cerebral circulation and metabolism in man (Takeshita et al, Anesthesiology 1972;36:69-75)

3mg/Kg ketamine given to healthy volunteers.

Result

Increased cerebral blood flow and reduction in cerebrovascular resistance suggesting vasodilation

Cerebral perfusion increased by 14mmHg to 88mmHg, with no metabolic effect,

Slight rise in PaCO2

Summary of Argument against Ketamine

Ketamine had deleterious effects on ICP without maintaining CPP in patients with obstructed CSF pathways

Ketamine generally improves CPP in normal patients.