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This design was actually originally made for an event, but I’m reposting it here because it’s useful and I like it and I haven’t had a chance to draw anything new recently.
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
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
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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.
Suppurative (infectious) flexor tenosynovitis is a medical emergency because the tendon sheath is a closed space and too much swelling can lead to compartment syndrome and necrosis.
* You can’t really get these complications in extensor tendons as it is an open space (no tendon sheath)
There are 4 cardinal signs of flexor tenosynovitis (Kanavel’s Signs)
- Tenderness along the whole tendon sheath (late sign)
- Finger held in flexion
- Fusiform swelling (sausage finger)
- Pain with passive extension *this is the earliest finding
It is usually caused by some sort of inoculation, but this can be something very small and the patient may not be aware that he/she had ever been injured (can also be caused by local or hematogenous spread). It’s not unreasonable to get an x-ray to rule out other things and if there’s a fever or they seem very unwell, you can do blood cultures. You also probably want to start the patient on some broad spectrum antibiotics such as vancomycin + ciprofloxacin (or ceftriaxone).
Treatment is tendon sheath drainage and debridement as well as antibiotics.
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The Glasgow Coma Scale is a scoring system used to evaluate someone’s level of consciousness. It is scored out of 15 with 15 being totally awake and alert and 3 being totally not.
The important thing to remember is that the lowest score possible is 3.
Absolutely anything can score a 3, however if you are a living, breathing human being, hopefully you are scoring well up into the 10s.
Generally the GSC is applied in trauma situations and can be used as part of the decision making process of such thing things like should this patient be intubated?
- ≥13 correlates with mild brain injury (or being ok)
- 9-12 correlates with moderate injury
- ≤8 represents severe brain injury – you should probably consider intubating them as they most likely cannot protect their airway
Thanks to Mike for the guest doodle!
Meningitis is very literally inflammation of the meninges. Something swollen in a closed space is never good, so it’s important to not miss meningitis when it presents.
Classic triad of meningitis
- Neck stiffness
- Mental status change – in babies this can be an increase in somnolence or irritability (unconsolably crying)
- E. coli*
- GBS (Group B strep)*
- Neisseria meningitidis
- Strep pneumoniae
- Staph aureus
- Gram neg bacilli
- Haemophilus influenza
- Viral (“aseptic”)
* These are the common ones in the neonatal period
- Positive Gram stain
- CSF white blood cell (WBC) count >1000/uL with a predominance of neutrophils
- Low CSF glucose concentration <40 mg/dL (2.2 mmol/L)
- Empiric treatment: high doses of a 3rd generation cephalosporin (cefotaxime, ceftriaxone) and vancomycin (this covers antibiotic-resistant S. pneumoniae, N. meningitidis, and Hib)
When you see someone with suspected pneumonia you think “well, they have pneumonia, but how sick are they reaaalllly?” (you would ideally think this while cocking an eyebrow and tilting your head slightly)
To help you determine whether you send the person home on their merry way or admit them to hospital, you can use the CURB-65 pneumonia severity score.
- Urea >7
- Respiratory rate >30 breaths per minute
- Blood pressure <90 systolic or <60 diastolic
- 65 years or older
Each of the five criteria is worth 1 point, add them together:
- 0 – 1 points: mild pneumonia (there’s only a 3% chance that your patient will go home and die, leaving you racked with guilt)
- 2 points: moderate (9% risk of dying) – you should probably hospitalize this person
- 3 – 5 points: severe (13-53% chance of dying) – you better admit this person, maybe even to the ICU
Lim WS, van der Eerden MM, Laing R, et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax. 2003 May;58(5):377-82.
Lim WS, Baudouin SV, George RC, et al. BTS guidelines for the management of community acquired pneumonia in adults: update 2009. Thorax. 2009 Oct;64 Suppl 3:iii1-55.
Surface anatomy of the lungs
- 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.
A tension pneumothorax is recognized by:
- Decreased breath sounds on the affected side
- Distended neck veins
- Trachea deviating away from affected side
The Salter-Harris fracture classification has to be just about the most sensible classification systems in medicine, as least as far as the mnemonic goes. It is a system used to grade growth plate fractures and conveniently uses Salter’s name as the way to remember.
- SEPARATED (the bone and the growth plate have come apart) – but it actually looks normal on x-ray (you can only tell on physical exam)
- Fracture ABOVE the growth plate
- Fracture LOWER (below) the growth plate – fracture extends to the articular surface
- Fracture THROUGH the growth plate
- Fracture ERASING/compressing/squashing the growth plate – this is the worst kind because with disruption of the growth plate comes disruption of growth. Some odd things can cause these ones like frostbite, electric shock and irradiation. They’re hard to see on x-rays but show up on MRIs.