A kid without a rash just isn’t a kid.
- 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
- Incubation: 5-15d
- Rash: pink macules and maculopapules, starts on neck.
- Other symptoms: HIGH FEVER, cough, respiratory symptoms, erythematous pharynx, tonsils & TMs
- Treatment: supportive
- Complications: febrile seizures
- * Generally affects kids <5 years old
- Incubation: 10-14d, dx with measles IgM
- Rash: maculopapular, starts on face.
- 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.
- 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
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
- H+ (acidosis)
- Hyperkalemia/Hypokalemia (potassium disturbances only get counted once)
The 5 Ts
- Tension pneumothorax
(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
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.
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.
- Epidural (above the dura, right under the skull)
- Subdural (below the dura, above the arachnoid)
- Subarachnoid (below the arachnoid, above the brain)
- Intraventricular (in the ventricles)
- 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.
|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)
||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
General anesthesia has a bunch of different steps:
- Pre-oxygenation/Pre-induction (some people don’t count this as a step)
- Induction (putting them “to sleep”)
- Maintenance (keeping them asleep)
- 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.
Shock is “a syndrome resulting from failure of the cardiovascular system to maintain adequate tissue perfusion.”
Weil-Shubin Classification of Shock
- Cardiogenic - Poor cardiac function reduces forward blood flow.
- Hypovolemic – Loss of intravascular volume caused by: hemorrhage, dehydration, third space loss, vomiting, diarrhea.
- Obstructive – Impair cardiac filling due to external restriction. Caused by cardiac tamponade, tension pneumothorax, pulmonary embolus.
- Distributive – Primarily characterized by loss of peripheral vascular tone. Caused by septic, anaphylactic, adrenal insufficiency, neurogenic, liver failure.
- α1: Vasoconstriction
- α2: Inhibits norepinephrine release, decreases BP, sedative effects
- β1: Positive inoptrope (increases cardiac contractility and stroke volume)
- β2: Vasodilation, broncodilation
- Effects: Causes vasoconstriction and increases cardiac output. Inotrope effect predominates at low doses (< 4.0 mcg/min).
- Disadvantages: Associated with lactic acidosis, hyperglycemia, pulmonary hypertension, tachyarrythmias, and compromised hepatosplanchnic perfusion.
- Use: First-line agent for cardiac arrest and anaphylaxis. Second-line agent for vasopressor and inotrope effects, when other agents have failed.
- Effects: Potent vasoconstrictor. Causes a minor increase in stroke volume and cardiac output.
- Disadvantages: May decrease renal blood flow and increase myocardial oxygen demand. Extravasation at site of intravenous administration may lead to tissue necrosis.
- Use: First line therapy for maintenance of blood pressure.
- Effects: Increases heart rate, cardiac output. Bronchodilator. Some anti-emetic effects. Longer duration than epinephrine. Has indirect actions on adrenergic system.
- Disadvantages: Epedrine losses effect with subsequent doses since part of its effect is indirect, by icreasing NE release, which becomes depleted
- Use: Common vasopressor during anesthesia, but only a temporizing agent in acute shock.
- Effects are dose-dependent:
- < 5 mcg/kg/min – Acts at dopamine receptors only, with mild inotrope effect. Vasodilatory effects purported to improve perfusion through renal and mesenteric vessels; however, there is no clear clinical benefit of dopamine on organ function.
- 5-10 mcg/kg/min – Predominantly β1 adrenergic effects. Increases cardiac contractility and heart rate.
- >10 mcg/kg/min – Predominately α1 effects, causing arterial vasoconstriction and increased blood pressure. Overall decrease in renal and splanchnic blood flow at this dose.
- Disadvantages: Has a high propensity for tachycardia and dysrythmias. Potential for prolactin suppression and immunosuppression.
- Use: First line vasopressor for shock, but may be associated with more adverse outcomes than norepinephrine.
- Effects: Racemic mixture. where the L-isomer acts at α1/β1 receptors and D-isomer acts at β1/β2 receptors. Increases cardiac output and decreases systemic/pulmonary cascular resistance. Can increase splanchnic blood flow and decrease endogenous glucose production.
- Disadvantages: May cause mismatch in myocardial oxygen delivery and requirement. Vasodilation undesirable in septic patients.
- Use: A ‘gold standard‘ inotropic agent in cardiogenic shock with low output and increased afterload. In sepsis, vasodilatory effects should be counteracted by co-administration with norepinephrine.
- Effects: Acts at β2 and dopamine receptors. Causes vasodilation and decreased afterload. Has some positive inotrope effect. Bronchodilatory. Unlike dopamine, dopexamine is not associated with pituitary suppression.
- Disadvantages: Not widely accepted in practice.
- Use: Like dobutamine, useful for cardiogenic shock with decreased output and high afterload.
- Effects: Classic selective α1 agonist, causing vasoconstriction. Rapid onset and short duration.
- Disadvantages: Can reduce hepatosplanchnic perfusion. May cause significant reflex bradycardia.
- Use: Generally considered a temporary vasopressor until more definitive therapy is begun. Useful for vasdilated patients with adequate cardiac output, for whom other vasopressors present risk of tachyarrhythmias.
- Effects: Arousable sedation with preserved respiratory drive. Improved tissue perfusion and renal function. General sympathetic inhibition.
- Disadvantages: Bradycardia and hypotension.
- Use: Not used in acute shock setting, but may be useful in later critical care setting.
Vasopressin (not actually an adrenergic drug)
- Effects: Acts on V1 receptors to cause vasoconstriction. Increases vasculature response to catecholamines.
- Disadvantages: May cause tachycardia and tachyarrythmias. Excessive vasoconstriction can impair oxygen delivery and and cause limb ischemia.
- Use: May be used to augment norepinephrine or other agents. Not typically used alone.
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.
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
- Stratum corneum: The outmost layer, made of dead keratinocytes with a layer of protein around them (they have undergone keratinization)
- 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)
- Stratum granulosum: the keratinocytes are still on the move, by this point they have kertahyalin granules
- Stratum spinosum: the keratinocytes migrating up, they have nice oval nuclei
- 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.
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
- 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
- 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
Thumb fractures, and by this I mean 1st metacarpal fractures, have a couple of distinct patterns that are different from the other metacarpals.
Type I: Bennett Fracture
- This fracture is intra-articular on the ulnar side of the first metacarpal, basically making a little triangle
- It’s that little ulnar fragment that stays attached to the trapezium by the virtue of the volar ligament
- The distal aspect of the metacarpal gets supinated and dislocated radially no thanks to the adductor pollicis
- The fragment gets pulled proximally by the abductor pollicis brevis and abductor pollicis longus
Type II: Rolando Fracture
- You can think of this fracture as a really busted up Bennett’s (comminuted). It is also intra-articular and usually makes a Y or T shape
- These kind generally heal poorly but thankfully are fairly rare
Type III: Other extra-articular fractures
- This is basically any other 1st metacarpal fracture (all the extra-articular ones)
- They are the most common, but don’t have fancy names, just lame ones like “transverse“, “oblique“, etc.
- These really only exist in paediatrics and involve the proximal physis (growth plate)
Treatment: it’s best to treat Bennett and Rolando Fractures with thumb spica splints and then refer them to your friendly neighbourhood plastic surgeon or orthopaedic surgeon as they might need pinning or an open reduction.