Acquired Nevomelanocytic Nevi (aka moles)

Posted on April 7, 2014 by Ali

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

Posted on February 10, 2014 by Ali

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.

PHACE Syndrome (hemangiomas)

Posted on February 4, 2014 by Ali

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
Hemangiomas
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

Brachial Plexus Part 1 – anatomical relations

Posted on February 1, 2014 by Ali

The brachial plexus is the bane of many med students’ existence during any sort of neuro block. So many nerves, so many connections, so many seemingly arbitrary names of different sections. It’s just a woven mess of misery. (especially when they start getting into the “where is the lesion” questions)

Thus I’ve decided to have a couple posts about the brachial plexus, hopefully demystifying it to some extent. This first doodle is about the brachial plexus and its anatomical relationship to some of the structures that show why anatomists who named the parts weren’t as crazy as they seem.

Important structures to remember because they explain why parts are named the way they are:

Vertebrae
Anterior and posterior scalene muscles
Subclavian artery
The arm (in its anatomical position)

Vertebrae: There are 7 cervical vertebrae and 12 thoracic vertebrae. To make things confusing the cervical spinal nerves exit ABOVE their named vertebrae (except for C8) while the thoracic, lumbar and sacral exit BELOW. This messes up the whole numbering system because there are SEVEN cervical vertebrae but there are EIGHT cervical spinal nerve roots. The brachial plexus generally includes the nerve roots C5-T1*
* I say generally because there’s are anatomical variations such as a “prefixed” plexus that goes from C4-C8 and a “postfixed” plexus that goes from C6-T2

Scalene Muscles: The brachial plexus is nestled between the scalenes in the neck. At this point the plexus is oriented up and down and therefore the trunks are superior (closest to your noggin), middle, and inferior.

Subclavian Artery/Anatomical Position: The artery is in front of the plexus at the level of the trunks and then the plexus starts to wrap around it (or at least seems to because we don’t keep our arms straight out to our sides in “anatomical position” at all times). The cords are named for their relationship to the artery. One is lateral (again, if the arm was held out to the side), one is posterior and one is medial (think closest to armpit).

Subdivisions of the Brachial Plexus

The parts are: Roots/Trunks/Divisions/Cords/Branches or, as I remember them being a classy east coast Canadian: Real/Truckers/Drink/Cold/Beer

Then you might think, “But how do I remember which of the terminal branches comes off where?” For that I think of the two “M” branches being on the M: Musculocutaneous, Median and (M)Ulnar and that the whole thing together can just be said as “MARMU” Pick the mnemonics you want, the brachial plexus is rife with them. I personally just like the sound of the word marmu.

Complex Regional Pain Syndrome

Posted on December 17, 2013 by Mike

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.

Budapest Criteria

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.

Types of sutures (and when to use them)

Posted on October 20, 2013 by Ali

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:

	50% Strength	Gone	Reactivity	Use
Ethibond (coated polyethylene)	indef	n/an/a	+	Tendon
Mersilene (uncoated polyethylene)	indef	n/a	+	Tendon
Nylon	20%/y	n/a	+	Skin
Silk	1 year	>2y	++++	Vessel ligation, drains
Prolene (polypropylene)	indef	n/a	–	Skin
Steel	indef	n/a	–	Tendon, sternum
Fast Gut	6d	20d	++++	Skin
Plain Gut	7d	70d	++++	Skin
Chromic Gut	28d	90d	++++	Oral mucosa
Monocryl (Poliglecaprone 25)	7d	110d	+++	Skin, subcuticular
PDS (Polydioxanone)	21d	100d	++	Internal organs, fascia
Vicryl (Polyglactin 910)	21d	90d	++	Skin, soft tissue

Key:
* Monofilament
* Braided

The “Safe Position” for the Hand

Posted on August 12, 2013 by Ali

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)

Severity (Classification) of Burns

Posted on July 21, 2013 by Ali

Burns are typically classified by their depth into (or through) the skin.

1st degree: just in the epidermis
- Pink, hot, no blisters
- Like a typical sunburn
2nd degree: into dermis, painful, wet
- Superficial: unruptured blisters, hair & glands spared, erythematous (red) but blanch with pressure
- Deep: ruptured blisters, hair often gone, can convert to a 3rd
3rd degree: through the dermis aka full thickness
- Lack vascularization, dry, leathery, no sensation

Zones of a Burn

A burn isn’t a homogenous spot on the skin; more heat means more damage (who knew!)

40 – 44 C: enzymes malfunction, protein denature
>44 C: damage occurs faster than the cell can handle
Damage keeps going after the heat source is removed

Zone of Coagulation: The cells are dead and their proteins have denatured. Denatured proteins coagulate – think fried eggs. This is what forms the eschar of the burn.
Zone of Stasis: The cells aren’t quite dead but the blood supply isn’t the best. If the circulation gets worse (usually due to vessel constriction and thrombosis) the cells in this area will die too. This is why it can take a couple days for a burn to “declare” itself.
Zone of Hyperemia: “Hyperemia” means an increase in blood flow, in this case because of vasodilation. The cells in this area are alive and generally recover.

The image above shows a superficial 2nd degree burn.

Innervation of the lower leg

Posted on January 17, 2013 by Ali

The lower leg (and especially the foot) have a pretty fancy pattern of skin innervation by the terminal branches. For example, the skin of the foot is innervated by 7 separate nerves:

Superficial peroneal nerve
Deep peroneal nerve
Sural nerve
Saphenous nerve
Calcaneal branch of the tibial nerve
Medial branch of plantar nerve
Lateral branch of plantar nerve

Also good to keep in mind that the anterior compartment is innervated by the deep peroneal nerve, the lateral compartment by the superficial peroneal nerve and the posterior compartment by the tibial nerve.

Extensor Compartments and Extensor Zones of the Hand

Posted on October 21, 2012 by Ali

Extensor Compartments

There are a whole lot of wrist/finger extensors trying to fit in the wrist and anatomically these are divided into 6 compartments.

First compartment – it’s this that is affected in de Quervain tenosynovitis
- APL (abductor pollicis longus): attaches to 1st MC
- EPB (extensor pollicis brevis): attaches to base of proximal phalanx
Second compartment
- ECRB (extensor carpi radialis brevis): attaches to 3rd MC
- ECRL (extensor carpis radialis longus): attaches to 2nd MC
Third compartment
- EPL (extensor pollicis longus): passes around Lister’s tubercle of radius and inserts on distal phalanx of thumb (extends thumb IPJ)
Fourth compartment – the posterior interosseus nerve lies on the floor of this compartment
- EDC (extensor digitorum communis): no direct attachment to phalanx, attaches to the extensor expansions
- EIP (extensor indicis proprius): lies ulnar to 1st EDC tendon)
Fifth compartment
- EDM (extensor digiti minimi): attaches to extensor expansion of little finger
Sixth compartment
- ECU (extensor carpi ulnaris): attaches to base of 5th MC

Extensor Zones

Zone I: over the DIP (this is where mallet finger injuries occur)
Zone II: middle phalanx
Zone III: over the PIP
Zone IV: proximal phalanx
Zone V: over the MCP
Zone VI: dorsum of hand/metacarpals
Zone VII: over the extensor retinaculum/carpals
Zone VIII: proximal wrist

Juncturae Tendinum

This is the connections of fascia between the EDC tendons and why you can’t stick your ring finger up alone, as it prevents independent movement.
It can also lead to confusion about whether an extensor tendon has been cut as the juncture tendinum transmits MCP joint extension even if a tendon is cut (as long as it’s cut distal to the JT)
But it’s also helpful as it prevents the cut tendon from retracting up into the forearm

Sketchy Medicine

doodles for studying

Category Archives: Plastics

Acquired Nevomelanocytic Nevi (aka moles)

Pierre-Robin Sequence