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.
- 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.
- Remember to compare this to the opposite wrist
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)
BUY THIS AS A STUDY CARD
Scaphoid fractures are very common but due to its weird blood supply, the scaphoid is prone to not healing well (review the anatomy of the scaphoid in this doodle). This is why fractures of the scaphoid and even SUSPECTED fractures of the scaphoid are treated very conservatively.
Even if you’re suspicious of a fracture but don’t see one on x-ray, that’s enough to subject someone to a cast for 2 weeks and then bring them back to re-x-ray.
This doodle goes through the basic algorithm for treating scaphoid fractures centred around a timeline to show how long the treatment course can be. There are of course nuances to the management, so take a person’s work and hobbies and handedness into consideration. Also, don’t be afraid to consult your friendly hand/wrist specialist.
The scaphoid bone is one of the eight carpal bones of the wrist (you can check out this doodle for a refresher).
The scaphoid is the most commonly fractured carpal bone, accounting for almost 70% of fractures. It tends to be young males who break their scaphoid this is both an anatomical thing: younger kids get ligament injuries and older folks break their distal radius and a lifestyle thing: falling on outstretched hands (skateboarding, snowboarding) or throwing a punch both place a lot of force across the scaphoid leading to fractures.
The bad thing about scaphoid fractures is that the blood supply (from a branch of the radial artery) comes from distal to proximal. Since most fractures happen at the waist of the scaphoid the likelihood of having poor blood supply to the fracture site is quite high. It doesn’t help matters that around 80% of the scaphoid is articular surface (joint surface), so if it doesn’t heel well, it can lead to problems with arthritis of the wrist later on.
Scaphoid fractures present with a pretty classic story and the person is usually swollen and bruised and will have tenderness in their “snuffbox.” So even if the x-ray doesn’t show a fracture, it’s best to treat with a cast for comfort and safety and then recheck them in 2 week’s time (this will be discussed in a separate post).
The Z-Plasty is one of the most fundamental local flaps. It’s a variation of a transposition flap (meaning simply that it was rotated into a defect right next to it).
The trick is that all three limbs need to be equal and that the angles should be equal.
If the angle between the central limb and the lateral limb is 60°, then there should be an increase of the central limb by 75% (ex: 2cm -> 3.5cm)*
Since the Z-Plasty lengthens and changes the line of tension, it is great for releasing scar contractures.
* If you want you can measure the doodle, it’s pretty close to a 75% increase which I found really cool (in that I created it by rotating the flaps). MATHMAGIC!
Nevi (or moles) are very, very common. They are generally well-circumscribed dark spots (or “papules” to use the dermatological terminology) that can appear at any time in someone’s life.
Histologically they are composed of groups of melanocytic nevus cells and can be found in the epidermis, dermis or both.
The problem with nevi is that they are pigmented and people tend to get worried about pigmented things on the skin (for good reason as melanoma can be a pretty scary disease).
Common acquired nevi are grouped into three categories (I’ll leave out congenital and dysplastic nevi for now)
- Junctional: the nevus cells are completely in the epidermis, just above the dermal-epidermal junction. Clinically they are <1 cm, flat or minimally elevated and dark in colour.
- Compound: the nevus cells are in both the epidermis and the papillary dermis (top layer of the dermis), and cross the basement membrane. Clinically they are raised, and a medium-brown colour.
- Dermal: the nevus cells are completely in the dermis. Clinically they are raised and almost always pigment less as the cells lose their capacity for melanization when in the dermis. They usually have telangectasia and may or may not have hair. They don’t tend to appear until the 2nd or 3rd decades of life.
Pierre-Robin Sequence is not a syndrome, it’s a sequence. While it is a collection of features, one happens because of the one that came before.
The features are:
- Retrognathia/micrognathia (posterior mandible or very small mandible)
- Glossoptosis (downwards/posterior displacement of the tongue due to the small mandible
- Airway obstruction (because the tongue is in the way)
Pierre-Robin Sequence is associated with cleft palate (50% of children with the sequence have cleft palate). There are two proposed theories:
- The first is that the tongue simply gets in the way of the palate from fusing
- The second is that the tongue prevents the newly fused palate from staying fused (this is currently the more popular theory)
PRS, though not a syndrome itself, is associated with multiple syndromes including Stickler Syndrome, velocardiofacial syndrome, fetal alcohol syndrome and Treacher Collins Syndrome.
There are no shortage of congenital syndromes that are acronyms arranged into some sort of vaguely pronounceable word. There will be lots of doodles about these, but we’ll start off with a more uncommon one – PHACE Syndrome.
PHACE Syndrome is a collection of findings that go along with large infantile hemangiomas. They’re the more worrisome (but less obviously disfiguring) things you need to look for when you see a baby with a large hemangioma on the face or multiple hemangiomas.
- Posterior fossa brain malformations
- Arterial anomalies
- Cardiac anomalies and coarctation of the aorta
- Eye abnormalities
- Sternal cleft
The most common symptom of PHACE is cerebrovascular abnormalities, followed by cardiac anomalies (coarctation, aortic arch anomalies, VSDs). If you suspect PHACE, do clinical exam of the skin and eyes and MRI of the head, neck and chest.
Other cool facts
- PHACE occurs in full-term normal birth weight infants (other hemangiomas tend to occur in preterm infants)
- Quite common, more girls than boys (8:1)
- Don’t confuse it with Strurge-Weber (port wine stain, associated with the facial dermatomes)
- Port wine stains don’t proliferate and then regress like an infantile hemangioma