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 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).
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.
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.
>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.
Lungs extend from about 2 cm above the clavicle down to the 6th rib in the midclavicular line and 8th rib in the midaxillary line
The oblique fissure goes from the 6th rib midclavicular line to T3 in the back
The horizontal fissure (only on the right) starts at the 4th rib at the sternum and then meets the oblique fissure at the 5th rib in the midaxillary line.
The pleura generally is 2 ribs below
Insert a chest tube in the 4th or 5th intercostal space in the anterior axillary line. When making the incision, make it one rib below the intercostal space you want to insert the tube into. Also, remember to go above the rib, as the neurovascular bundles travel along the underside of the ribs.
These can be done to relieve a pneumothorax, drain a malignant pleural effusion, drain a empyema, or drain a hemopneumothorax. They can also be placed post-operatively following a thoracotomy, esophagectomy or cardiac surgery.
These are used in a pinch when a patient is suspected to have a tension pneumothorax and needs immediate decompression. A 14 or 16 gauge needle is inserted above the 2nd or 3rd rib in the midclavicular line.
When you hit your head on something (or something hits your head) there are two typical patterns of injury. The first is the coupe where the brain injury is directly under the spot that was hit. This usually happens when your head is stationary and something moving hits it (such as someone’s fist).
The second is the contre-coupe, which happens when your head is moving and hits something stationary (such as if you fall and hit your head on the wall or the floor.