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 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)
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).
Hypo/Hyperalgesia:Decreased/increased sensitivity to a usually-painful stimulus (e.g., pinprick).
Hypo/Hyperesthesia: Decreased/increased sensation to a usually-innocuous stimulus (e.g., light touch).
Allodynia: Sensation of pain from a usually-innocuous stimulus (e.g., light touch).
Complex Regional Pain Syndrome (CRPS) refers to a chronic neuropathic pain condition with a broad and varied range of clinical presentations. CRPS patients experience severe pain out of proportion to their original injury, and this may start at the time of injury or weeks later. The pain is described as deep-seated and burning/aching/shooting. Sesnory changes are common, including hypo/hyperesthesia, hypo/hyperalgesia, and allodynia. For instance, many patients describe not being able to tolerate the sensation of bedsheets on their painful limb.
In the affected area, there is often marked edema, temperature asymmetry (usually cooler), and sweating changes (usually increased). Loss of hair and nail growth is common, and disuse of the limb can result in weakness, muscle atrophy, and contractures.
The diagnosis is made clinically, using the Budapest Criteria. Some pain physicians use a nuclear medicine test, three-phase bone scintigraphy, for CRPS diagnosis but this test is becoming less popular, since it has a low positive predictive value.
- Pain, ongoing and disproportionate to any inciting event
- Symptoms: at least one symptom in three of the four categories:
- Sensory: reports of hyperesthesia and/or allodynia
- Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetr
- Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry
- Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
- Physical Signs: at least one sign at time of evaluation in two or more categories:
- Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint movement)
- Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry
- Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry
- Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
- No other diagnosis better explains the signs and symptoms
CRPS is classified as Type I when there is no apparent history of nerve damage, and Type II when associated with definite peripheral nerve injury. CRPS most commonly occurs following fractures and immobilization, but can happen even with little to no trauma.The pathophysiology is thought to involve autonomic dysfunction and inflammation, but much is still unknown.
CRPS affects females about 2-4 times more often than males, and onset is usually in middle age (though there are rare pediatric cases reported). It is a progressive disease that can result in spread of pain, sensory disturbances, and physical changes to other limbs.
Treatment for CRPS may involve physiotherapy, complementary medicine (e.g., acupuncture, qi gong) psychological therapies, and a variety of pharmacologic (e.g., NSAIDs, anticonvulsants, antidepressants, opioids, ketamine, bisphosphonates) and interventional procedures (nerve blocks, sympathectomy, neurostimulators). As with all things CRPS, there isn’t great evidence for any particular intervention.
- Harden RN, Bruehl S, Perez RSGM, Birklein F, Marinus J, Maihofner C, Lubenow T, Buvanendran A, Mackey S, Graciosa J, Mogilevski M, Ramsden C, Chont M, Vatine J-J. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for Complex Regional Pain Syndrome. Pain; 150:268.
- Hord E-D. Complex regional pain syndrome. In: Massachusetts General Hospital Handbook of Pain Management (Eds: Ballantyne JC, Fields HL). Lippincott Williams & Wilkins.
- Moon JY, Park SY, Kim YC, Lee SC, Nahm FS, Kim H, Oh SW. 2012. Analysis of patterns of three-phase bone scintigraphy for patients with complex regional pain syndrome diagnosed using the proposed research criteria (the ‘Budapest Criteria’). British Journal of Anesthesia; 108:655.
- O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome – an overview of systematic reviews. Cochrane Database of Systematic Reviews; 4:CD009416.
- Schwartzman RJ, Erwin KL, Alexander GM. 2009. The natural history of complex regional pain syndrome. Clinical Journal of Pain; 25:273.
- Smith H, Popp AJ. The patient with chronic pain syndromes. In: A Guide to the Primary Care of Neurological Disorders (Eds: Popp AJ, Deshaies EM). Thieme.
- Tran DQH, Duong S, Bertini P, Finlayson RJ. Treatment of complex regional pain syndrome: a review of the evidence. Canadian Journal of Anesthesiology; 57:149.
There are many types of sutures and they differ by size, material and needle. I made this handy chart to help remember how long each type of material lasts in the body and what it’s commonly used for:
|Silk||1 year||>2y||++++||Vessel ligation, drains|
|Chromic Gut||28d||90d||++++||Oral mucosa|
|21d||100d||++||Internal organs, fascia|
|21d||90d||++||Skin, soft tissue|
People can be whiners sometimes. Their hand will be in a cast for some break and you’ll take it off and they will say, “my hand is stiiiiifffff”
It’s not just them, the mechanics of their hand is working against them and if the cast wasn’t positioned properly, it can make matters much worse as far as stiffness is concerned. This is why when a hand or wrist is being casted or splinted, care is taken to put it in the position that will minimize stiffness.
The “safe position” is also known as the intrinsic plus position as it favours the weaker motions of MCP flexion and IP extension that are difficult to recover.
Wrist: The weight of your hand, gravity and resting muscle tension all work together to pull the wrist into flexion. When the wrist is flexed, there is more tension on the extrinsic extensor muscles and they pull the MCP joints into extension. The extrinsic flexors are stronger than the extensors and pull the IP joints into flexion. Taking the tension off the extensors limits their pull across the MCP joints.
The position of flexed wrist, extended MCP joints and flexed IP joints is known as intrinsic minus.
Metacarpal Phalangeal (MCP) Joint: These joints are a little funny due to the collateral ligaments on either side. These ligaments pass slightly above the axis of rotation of the joint, this means that when the joint is flexed, they’re at their longest and when the joint is extended, they’re at their shortest. This is due to the famed “CAM EFFECT.” Though often quoted, you have to wonder, what is a cam*? This website explains it well.
* This does not apply to all those people who remember basic mechanical principles or were trained in something more hands-on than neuroscience
Interphalangeal (IP) Joints: The ligaments around the IP joints are at maximum stretch when they are fully extended (aka 0 degrees)
A prolapsed (slipped) disc is when the squishy innards of the disc (nucleus pulposus) bulge out past the stiffer wall of the disc (annulus fibrosis). The problem is that sometimes when this happens, the bulge can impinge the spinal cord or the spinal nerve root. This could result in an anterior cord syndrome (remember this doodle) or it could just knock out the nerve root, resulting in a specific radiculopathy (check out this doodle for where to check for numbness and weakness).
The tricky thing to remember is that though, for example, the L3 root exits at L3, if the L3,4 disc herniates, it doesn’t hit the L3 root but the L4.
Slipped L3,4 disc = L4 nerve injury
The disc hits the nerve after it has branched off the spinal cord, but before it has exited the vertebral canal.