This is not an exhaustive overview of the muscles of the arm and forearm, but it demonstrates some of the tricky relationships that often catch people up. Some of the key points of compression are also noted and the muscles are coloured per their innervation. One thing not mentioned in the doodle that is important to notice is the way that the aponeurosis of the biceps veers medially (ulnarly) this is why it is also a supinator and not just an elbow flexor.
The branches of the three main terminal branches of the brachial plexus can be difficult to remember. Even worse is trying to remember where all of those pesky compression points are and why it is that you get some symptoms with some and not others.
This diagram attempts to clarify the branches of the radial, median, and ulnar nerves and where they can get squished along the way. There are of course, slight anatomic variations, but this is a good starting point. I’ve even included where the famed Martin-Gruber anastomosis and the Riche-Cannieu anastomosis are, since they can make an otherwise (totally not) straightforward examination of a median or ulnar nerve palsy more muddied since both carry motor fibers between the two nerves.
Most interestingly is John Struthers, whose namesake structures compress the median nerve as a ligament and the ulnar nerve as an arcade.
I’ve drawn the brachial plexus before showing more of its anatomical relationships (which is actually why the trunks and cords are named as they are). As I’m gearing up studying, I created this more schematic diagram of the plexus, including the distal targets (mostly the muscles but some sensory too).
Hopefully this will help you figure out “where is the lesion?” when you are faced with a brachial plexus question on your exams (and in life) as well.
I’ve also included a printable version for your printing and pasting-up-to-the-wall-to-passively-absorb pleasure.
Long thoracic: serratus anterior Dorsal scapular: rhomboids, levator scapulae Suprascapular: supraspinatus, infraspinatus, sensory to the AC & GH joints Nerve to subclavius: subclavius Lateral pectoral: pec major (clavicular head), sensation to pec Superior subscapular: subscapularis (upper part) Thoracodorsal (aka middle subscapular): lat dorsi Inferior subscapular: subscapularis (lower part), teres major Medial pectoral: pec minor, pec major (sternocostal head) Medial cutaneous n. of arm: sensory to medial surface of arm (tiny area) Medial cutaneous n. of forearm (antebrachial cutaneous): sensory to skin over biceps and medial forearm
The most common use for vancomycin is in invasive Gram positive infections
You need to consider
Infection site
Patient weight
Kidney function
Pathogen susceptibility
Pharmacokinetics
Vancomycin has bad oral bioavailability so it’s almost never used as a pill
Occasionally it is orally to supplement C. diff infections (because that’s going on in the GI tract)
Volume of distribution: IV serum 0.4-1 L / kg
Normally vancomycin doesn’t cross the blood brain barrier very well, but in the setting of meningitis the inflamed meninges increases permeability
Adverse effects
Redman syndrome: A histamine-like flushing during or immediately after dose. Occurs mostly on the face and neck. This is NOT life threatening
Treatment: anti-histamine, pause infusion, then restart at a slower rate
If the reaction is severe, stop the infusion, give antihistamines, wait until symptoms resolve before restarting. When you restart, give the infusion reaaaalllllly slooooooowly (over more than 4 hours)
Nephrotoxicity
Dosing
This is where vancomycin can get tricky, because you are aiming for a target trough (between dose) serum concentrations.
Generally the target is 10 mcg/ml, but this may need to be higher for treating MRSA or osteomyelitis
Trough concentrations should be measured 30 minutes before the 4th dose any time a course of vanco is started or the dose is changed
Monitor creatinine at least once a week (remember that whole nephrotoxicity bit)
Starting dose should be 15-20 mg/kg (based on actualnot ideal body weight) every 12 hours. This usually works out to 1-2 g IV Q12H. If the kidneys are not working well, reduce the dose.
References
UpToDate.com “Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults”
Tumescent solution is also called “Klein’s Solution” after the physician who characterized the recipe and the use of it.
It’s called “tumescent” because it makes things tumescent, which is a fancy word for swollen. Tumescent is a dilute solution of lidocaine, epinephrine, and sodium bicarbonate that is injected in the subcutaneous tissue (fat). The epinephrine is the most important ingredient as it causes vasoconstriction, this means that the blood loss that could be a big problem for large procedures like burn surgery and liposuction becomes much less of a big deal.
The other interesting thing is that since fat is relatively avascular compared to other tissues, the “safe amount” of tumescent is much higher than what is normally stated for injections of lidocaine or epinephrine.
For example, it was reported by Klein that the toxic dose of lidocaine for tumescent solution is 35 mg/kg of body weight.
There are a few different recipes for tumescent anesthesia, the one presented in the doodle is the one first outlined by Klein, some use more or less lidocaine or epinephrine.
References
Kucera IJ1, Lambert TJ, Klein JA, Watkins RG, Hoover JM, Kaye AD. Liposuction: contemporary issues for the anesthesiologist. J Clin Anesth. 2006, 18(5): 379-87.
Klein JA. The tumescent technique. Anesthesia and modified liposuction technique. Dermatol Clin. 1990, 8(3): 425-37.
Klein JA. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast Reconstr Surg. 1993, 92: 1085-100.
The carpal bone ossify aka turn into bone aka magically become visible on an x-ray in a predictable order.
The easiest way to remember is that it starts at the capitate (smack dab in the middle) and then goes in a ulnarly-directed spiral. I was going to say “clockwise” or “counter-clockwise” but that would depend on which side of which hand you were looking at. So capitate, followed by hamate and then down to triquetrum and so on. Except for the pisiform, being a sesamoid bone it gets left behind and only develops years later.
Capitate: 1-3 months
Hamate: 2-4 months
Distal radius: 1 year
Triquetrum: 2-3 years
Lunate: 2-4 years
Scaphoid: 4-6 years
Trapezium: 4-6 years
Trapezoid: 4-6 years
Distal ulna: 5-6 years
Pisiform: 8-12 years
I included the distal radius and distal ulna in there for good measure.
I know I could have been fancier with changing the length of the metacarpals or their growth plates, but it was more fun to make the animated gif.
The scaphoid shift test aka midcarpal shift test is a variation of the Watson Test for scaphoid instability. A positive test can be caused by scapholunate ligament laxity or injury.
The Watson test evaluates scaphoid instability as the wrist is moved from radial to ulnar deviation (it’s not an “active” test)
To do the scaphoid shift test (as described by Lane in 1993)
Use the same hand as the patient’s affected hand (suspicious of a right scaphoid problem? Use your right hand to test)
Place your hand on the patient’s so that your thumb is over the volar surface of the scaphoid tubercle (the distal pole). Don’t apply any pressure (remember this area is probably at least a little sore and you want to remain friends for now)
Gently move the wrist through ulnar/radial deviation (you can be fancy and consider this your Watson Test) and flexion/extension to relax the patient
With the patient’s wrist in neutral extension and neutral (or slight radial deviation), forcefully and quickly push the scaphoid tubercle in the dorsal direction
At this point, the patient is likely no longer your friend
Note the degree of shift, any crepitus or clunk, and pain evoked.
For being such a small anatomic location, people find it very difficult to describe where on the hand or digits things are actually happening when there is an injury.
I think part of it stems back to medical school when we are taught that the digits all have numbers, the thumb is D1, index D2 and so forth. The problem comes when people say “the 3rd finger” and all of the sudden one has no idea whether they are talking about the long finger (D3) or the ring finger (D4 but then, the thumb doesn’t count as a finger, does it?)
Which finger (digit?!) is which?
This is why it’s always best to call digits by their names, this even goes for metacarpals. It is totally OK, and generally less confusing to call a bone the index finger metacarpal.
Thumb = D1
Index = D2
Long = D3
Ring = D4
Small = D5
Which side of the hand?
The same goes for which side of the hand the problem is on. There is no lateral or medial side to the hand. One could argue that it’s how someone is in anatomical position, so obviously the small finger side is medial, unfortunately very few people walk around in anatomic position and it’s their thumbs that point to the body.
So best to describe side by two things that stay put regardless of how someone has their hands in space: the radius and the ulna.
Thumb side = RADIAL
Small finger side = ULNAR
Finally for the top and bottom (or is it back and front) of the hands: use the terms DORSAL (where the nails are) and VOLAR (or palmar)
The clotting cascade was one of the first doodles posted on Sketchy Medicine, I’ve now updated it to include some of the Novel Oral Anticoagulants (NOACs): Dabigatran, Rivaroxaban and Apixiban.
Dabigatran (Pradaxa)
Selective, reversible direct thrombin inhibitor
Is actually a prodrug that reaches peak concentration 2-3 h post ingestion
Approved (in Canada) for: Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence
T1/2: 7-17 h
CYP independent (not as many drug-drug interactions)
Excreted in urine 95% / Feces 5%
Reversal: hemodialysis?
Big trial = RELY, REMEDY
Rivaroxaban (Xarelto)
Selective, reversible direct factor Xa inhibitor
Approved (in Canada) for: Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence
T1/2: 3-9 h (relatively speedy!)
CYP3A4
Very good oral bioavailability
Almost all of it is protein-bound in the serum
Urine 70% / Feces 30%
Reversal: ???? (not hemodialysis)
Apixaban (Eliquis)
Selective, reversible direct factor Xa inhibitor
Approved (in Canada) for: Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence (only atrial fib in the USA)
T1/2: 8-15
CYP3A4
Almost all (95%) protein-bound in the serum
Urine 30% / Feces 70%
Reversal: ???? (not hemodialysis)
Reversal agents:
Hemodialysis
Only good for agents that aren’t highly protein bound (i.e. dabigatran).
Warfarin, rivaroxaban and apixaban are all mostly bound to protein in the serum, so dialysis won’t get rid of them
PCC
Plasma-derived product containing factors II, IX and X (3-factor PCC) or II, VII, IX and X (4-factor PCC) in addition to variable amounts of proteins C and S, and heparin
aPCC
Plasma-derived product containing activated factors II, VII, IX and X
Recombinant factor VIIa
Looks good in test tubes, clinical evidence lacking
Idarucizumab
Humanized monoclonal antibody against dabigatran
Andxanet alfa
Recombinant factor Xa derivative
Could theoretically be used for rivaroxaban and apixaban
Anticoagulation Assays
(Adapted from Jackson II & Becker, 2014)
Approach to bleeding
(From Siegal, 2015)
References
Jackson II LR & Becker RC. (2014). Novel oral anticoagulants: pharmacology, coagulation measures, and considerations for reversal. Journal of Thrombosis and Thrombolysis, 37(3), 380-391.
Ufer M. (2010). Comparative efficacy and safety of the novel oral anticoagulants dabigatran, rivaroxaban and apixaban in preclinical and clinical development. Thrombosis and Haemostasis. 103: 572-585.
Siegal DM. (2015). Managing target-specific oral anticoagulant associated bleeding including an update on pharmacological reversal agents. Journal of Thrombosis and Thrombolysis, 1-8.
Amyotrophic Lateral Sclerosis (ALS) is a degenerative disease of the motor neurons in the brain and spinal cord. It progressively affects all the muscles in the body but there is no known cause and no treatment. Only about 5-10% of cases are inherited while the rest are sporadic.
The neurons ALS affects are primarily the upper motor neurons. These are the ones that originate in the brain and travel down the spinal cord. These neurons then synapse with the lower motor neurons in the ventral horn, and it is the lower motor neurons that go directly to the muscles.
In ALS there are both upper motor neuron and lower motor neuron symptoms. As the neurons die, a constellation of symptoms including numbness, weakness and paralysis emerge. Eventually the paralysis progresses leading to inability to speak, swallow and breath. There is no cure for ALS and treatments only help with the symptoms, they do not slow the progression of the disease.
So you may have seen a lot of ice bucket challenges over the last few weeks but please support this cause as it is a horrible disease that up until now had almost no recognition or support. So please donate to The ALS Association (alas.org).
And in case you get tired or jaded seeing your social media full of these videos, watch this one of my father doing it. He’s not an emotional guy, but he has lost more than his fair share of friends to this disease.