Author Archives: Ali

Severity (Classification) of Burns

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burn_depth

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

  1. 1st degree: just in the epidermis
    • Pink, hot, no blisters
    • Like a typical sunburn
  2. 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
  3. 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
  1. 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.
  2. 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.
  3. 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. 

The Standard Drink

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standard_drink

A “standard drink” is a measure of pure ethanol consumed. One standard drink represents 10 grams of pure ethanol.

This means that based on the alcohol percentage of certain drinks, the “standard” size changes. The important thing to be aware of is to think of it as a Standard Drink because the size that equals 10 g of ethanol isn’t necessarily the standard size that is served. This is why it’s a good habit when asking “how many glasses of _______ do you drink” to ask about the size of the glass.

This design was actually originally made for an event, but I’m reposting it here because it’s useful and I like it and I haven’t had a chance to draw anything new recently.

Maculopapular Childhood Rashes

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rashes

BUY THIS AS A STUDY CARD

A kid without a rash just isn’t a kid.

Chicken Pox

  • Incubation: 10-21d, infective until crusted over
  • Rash: vesicles on macules (dewdrops on rosepetals),
  • Very pruritic!
  • Other symptoms: 1-3d prodrome of fever and respiratory symptoms
  • Treatment: supportive, acyclovir for severe disease, VZIG for post-exposure prophylaxis
  • Complications: 1st or 2nd trimester = congenital varicella syndrome

Roseola

  • Incubation: 5-15d
  • Rash: pink macules and maculopapules, starts on neck.
  • Non-pruritic!
  • Other symptoms: HIGH FEVER, cough, respiratory symptoms, erythematous pharynx, tonsils & TMs
  • Treatment: supportive
  • Complications: febrile seizures
  • * Generally affects kids <5 years old

Measles

  • Incubation: 10-14d, dx with measles IgM
  • Rash: maculopapular, starts on face.
  • Non-pruritic!
  • Other symptoms: the 3 Cs
    • 1) Cough 2) Coryza (runny nose) 3) Conjunctivitis
    • Koplik spots in mouth 1-2d before rash
  • Treatment: supportive, prophylactic Ig
  • Complications: secondary bacterial infection, encephalitis (1:1000), subacute sclerosing panencephalitis (1:100000)

Rubella aka German Measles

  • Incubation: 14-21d, infective 5d before rash and 7d after
  • Rash: pink maculopapular, starts on face.
  • Pruritic!
  • Other symptoms: non-specific
  • Treatment: supportive
  • Complications: congenital rubella syndrome (very bad*), first four months of pregnancy highest risk (this is why we check rubella immunity status in prenatal screening)

* Congenital Rubella Syndrome
“Blueberry muffin baby” (purpura). Cataracts/congenital glaucoma, congenital heart disease, hepatosplenomegaly, jaundice, microcephaly, developmental delay

Fifth Disease aka Erythema Infectiosum

  • Incubation: 4-14d, infective prior to onset of rash
  • Rash: slapped cheeks (raised uniform maculopapular lesions on cheeks), may appear on extensor surfaces
  • Usually not pruritic
  • Other symptoms: flu-like illness ~3d prior to rash
  • Treatment: supportive, blood transfusions if aplastic crisis
  • Complications: arthritis (10%), vasculitis
    • Aplastic crisis: reticulocytopenia, not bad in normal people, very bad anemia if you already have chronic hemolytic anemia
    • During pregnancy: fetal hydrops/fetal loss

* This is a good one to actually know the virus name! PARVOVIRUS B19

Other rash descriptors to think about

  • Sandpaper rash: scarlet fever (Group A Strep), they also have strawberry tongue, fever and sore throat
  • Pink macules with central clearing: erythema marginatum (one of the major Jones criteria for rheumatic fever)
  • Palpable purpura: Henoch-Schonlein Purpura
  • Non-blanching petechiae: BAD (meningococcal disease), could be other things too, but need to rule out meningitis

The 6 Hs of Pulseless Electrical Activity (PEA)

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6-Hs

When you find someone without a pulse but then hook up the monitor and there is a rhythm, your first thought it probably “CRAP!” But as you start CPR, you need to be thinking about what caused it because not much will help the person except correcting the underlying problem.

So like most of medicine, there is a handy mnemonic for remembering the main causes: The 6 Hs and 5Ts

The 6 Hs

  1. Hypoglycemia
  2. H+ (acidosis)
  3. Hyperkalemia/Hypokalemia (potassium disturbances only get counted once)
  4. Hypovolemia
  5. Hypoxia
  6. Hypothermia

The 5 Ts

  1. Trauma
  2. Tension pneumothorax
  3. Tamponade
  4. Toxins
  5. Thrombosis

(I’ll make a T doodle at a later date)

The other handy mnemonic for the Hs I learned from this video (so I take no credit for it): Diabetic crashing with a wide QRS

  • Diabetic = Hypoglycemia or H+ acidosis
  • Crashing = bad vitals
    • Low BP +/- tachycardia (hypovolemia)
    • Low O2 (hypoxia)
    • Low temperature (hypothermia)
  • Wide QRS = hyperkalemia

Vertebral Disc Prolapse (slipped disc)

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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.

Intracranial Hemorrhages

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For the most part, bleeding in the brain (intracranial hemorrhage) is a pretty bad thing. Though like most things in medicine, there are varying degrees of badness, all with different mechanisms that help us sort of why we really wouldn’t want something to happen.

Intracranial hemorrhages are categorized into 5 subtypes, and are given obvious sounding names depending on where the bleed is in the brain and in relation to the layers of the meninges.

  1. Epidural (above the dura, right under the skull)
  2. Subdural (below the dura, above the arachnoid)
  3. Subarachnoid (below the arachnoid, above the brain)
  4. Intraventricular (in the ventricles)
  5. Intraparenchymal (in the meat* of brain)

* The brain is not meaty, “parenchyma” means the functional part of the organ

The poor pia mater did not get any hemorrhage named after it, but if you want you can think of intraparenchymal as “subpial” just so it doesn’t feel left out.

Telling them apart

The most confusing thing, and thing that likes to get asked the most on exams, is the difference between epidural and subdural hematomas.

Epidural Subdural Subarachnoid
Above the dura Below the dura Below the arachnoid
Respects suture lines Doesn’t respect suture lines No respect for anything
High force trauma Low force trauma Aneurysm rupture or high force trauma
Arterial blood (commonly the middle meningeal artery) Venous (from venous plexus) Arterial from the circle of Willis
Lentiform (lens-shaped) or biconcave on CT Cresent (banana-shaped) on CT Lining surface, going into fissures and sulci and sella (death-star)
Acute presentation May be insidious (worsening headache over days) Acute presentation (thunderclap headache)

The reason intraventricular and intraparenchymal aren’t included in the table as they each have a bunch of causes, but for both of them trauma is a potential cause as well as hypertension and stroke. It’s good to remember that premature infants are at a much higher risk of intraventricular hemorrhages.

Blood on CTs

  • New blood: bright white
  • 1-2 weeks: isodense
  • Old blood (2-3 weeks): dark grey

Induction Agents in Anesthesia

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General anesthesia has a bunch of different steps:

  1. Pre-oxygenation/Pre-induction (some people don’t count this as a step)
  2. Induction (putting them “to sleep”)
  3. Maintenance (keeping them asleep)
  4. Emergence (waking them up)

In North America, many physicians like to use a combination of an analgesic and a sedative followed by the induction agent propofol. Sometimes other agents are used for induction such as etomidate or ketamine, particularly if there is a worry about hemodynamic instability as propofol not uncommonly can cause bradycardia and/or hypotension.

If the patient is going to be intubated, a paralytic (muscle relaxant) is also used to relax the vocal cords to prevent unnecessary trauma as the tube is passed through them. Competitive acetyl choline (ACh) receptor antagonists such as rocuronium or succinylcholine are used for this. The main difference between the two is that succinylcholine is a depolarizing agent – meaning that when it first binds to the ACh receptor, it causes a contraction, whereas rocuronium is non-depolarizing – so when it binds nothing happens. So with this pesky contraction thing why would any one choose succinylcholine? The nice thing is that the half-life is much much shorter than rocuronium, so if things don’t work out quite the way you want them to, or you just want something fast, you don’t need to continue to help the patient breath.

Innervation of the lower leg

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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:

  1. Superficial peroneal nerve
  2. Deep peroneal nerve
  3. Sural nerve
  4. Saphenous nerve
  5. Calcaneal branch of the tibial nerve
  6. Medial branch of plantar nerve
  7. 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.

Layers of the Epidermis

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The epidermis is divided into five layers. From outside to inside (dermis). The stem cells are located in the stratum basale and migrate outwards in their differentiation process

  1. Stratum corneum: The outmost layer, made of dead keratinocytes with a layer of protein around them (they have undergone keratinization)
  2. Stratum lucidum: Also dead keratinocytes (there is no real distinction here other than that the poor keratinocytes have died but have not finished the keratinization process)
  3. Stratum granulosum: the keratinocytes are still on the move, by this point they have kertahyalin granules
  4. Stratum spinosum: the keratinocytes migrating up, they have nice oval nuclei
  5. Stratum basale: Single layer of proliferating columnar keratinocytes, melanocytes (pigmented cells) and Merkel cells (mechanoreceptors) also live here

Of note, Langerhans cells, which are specialized antigen-presenting cells are present in all layers of the epidermis but are mostly in the stratum spinosum.

Extensor Compartments and Extensor Zones of the Hand

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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.

  1. 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
  2. Second compartment
    • ECRB (extensor carpi radialis brevis): attaches to 3rd MC
    • ECRL (extensor carpis radialis longus): attaches to 2nd MC
  3. Third compartment
    • EPL (extensor pollicis longus): passes around Lister’s tubercle of radius and inserts on distal phalanx of thumb (extends thumb IPJ)
  4. 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)
  5. Fifth compartment
    • EDM (extensor digiti minimi): attaches to extensor expansion of little finger
  6. 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