Renal replacement therapy (RRT) is a process of removing waste products and excess free water from the blood during renal failure and critical illness.
Common indications for RRT can be remembered with the mnemonic AEIOU:
- (Metabolic) Acidosis
- Electrolyte abnormalities (especially severe hyperkalemia)
- Ingestions/toxins (aspirin, lithium, methanol, ethylene glycol)
- (Volume) Overload
There are many different variations of RRT, but the main principles behind it can be quite simple.
In hemodialysis, diffusion is responsible for removing unwanted solutes and water. The setup involves a semipermeable membrane that can allow water and some water-soluble molecules to pass. Blood will flow on one side of the membrane, under pressure, while the dialysate (contains glucose and some electrolytes) generally flows on the other side in the opposite direction. This creates a suitable concentration gradient for unwanted molecules to pass into the dialysate, while excess water is forced across the membrane based on the amount of pressure is applied by the dialysis circuit.
In hemofiltration, blood is pushed across a semipermeable membrane, under pressure. Most of the plasma water is able to pass through the membrane, while unwanted molecules get stuck in the membrane (convection). A substitution fluid may be added back to the blood, in order to dilute out waste molecules (e.g., urea), replace useful molecules (e.g., bicarbonate), and to avoid losing too much fluid from the patient’s circulation.
Some modes of RRT will involve both hemodialysis and hemofiltration. Others only use one of these mechanisms.
- Butcher BW, Liu KD. 2013. Renal replacement therapy and rhabdomyolysis. In: Critical Care Secrets (Parsons and Wiener-Kronish, Eds.) Mosby, Philadelpia PA.
- Hoste E, Vanommeslaeghe. 2017. Renal replacement therapy. In: Textbook of Critical Care (Vincent, Abraham, Moore, Kochanek, and Fink, Eds.) Elsevier, Philadelphia PA.
- Ricci Z, Romagnoli S, Ronco C. 2015. Extracorporeal support therapies. In: Miller’s Anesthesia (Miller, Ed.) Elsevier/Saunders, Philadelphia PA.
Waveform capnography is a commonly used monitor in the operating room, and is increasingly seen in non-operating room environments too! The capnographic waveform can be described as having several phases:
- Phase 0 (inspiratory baseline) represents the inspiratory phase of the respiratory cycle.
- Phase 1 is the initial part of expiration, when dead space gases are being exhaled. Since the exhaled gas in this phase did not take part in gas exchange, the PCO2 is 0.
- Phase 2 (expiratory upstroke) involves exhaled gases from alveoli reaching the detector. There is a sharp rise in PCO2 during this phase.
- Phase 3 is a (more or less) flat plateau showing continued exhalation of alveolar gas. The last, maximal part of this phase is the end-tidal point (ETCO2), which is usually 35-40 mmHg. ETCO2 tends to be 2-5 mmHg lower than PaCO2, though this difference can be increased/decreased under a variety of conditions, such as ventilation-perfusion mismatch.
The shape of the capnograph waveform can tell you a lot!
- A slanting upslope can represent airway obstruction (e.g., chronic obstructed pulmonary disease, bronchospasm, blocked endotracheal tube).
- In patients paralyzed with a neuromuscular blocker, as the paralytic wears off they may try to breathe asynchronously against the ventilator, producing a notch called a ‘curare cleft.’
- Quantitative capnography during resuscitation can be very useful. During CPR, there should be a visible waveform during high quality chest compressions; its absence may indicate accidental esophageal intubation
- A sudden loss is bad, as it means that the tube is fully obstructed or disconnected or that there has been a sudden loss of circulation
- You can also just simply tell is someone is hypo- or hyperventilating
- Dorsch JA, Dorsch SE. 2007. Gas monitoring. In: Understanding anesthesia equipment (Dorsch and Dorsch, Eds.) Lippincott Williams & Wilkins, Philadelphia PA.
- Kodali BS. 2013. Capnography outside the operating rooms. Anesthesiology; 118:192.
Tumescent solution is also called “Klein’s Solution” after the physician who characterized the recipe and the use of it.
It’s called “tumescent” because it makes things tumescent, which is a fancy word for swollen. Tumescent is a dilute solution of lidocaine, epinephrine, and sodium bicarbonate that is injected in the subcutaneous tissue (fat). The epinephrine is the most important ingredient as it causes vasoconstriction, this means that the blood loss that could be a big problem for large procedures like burn surgery and liposuction becomes much less of a big deal.
The other interesting thing is that since fat is relatively avascular compared to other tissues, the “safe amount” of tumescent is much higher than what is normally stated for injections of lidocaine or epinephrine.
For example, it was reported by Klein that the toxic dose of lidocaine for tumescent solution is 35 mg/kg of body weight.
There are a few different recipes for tumescent anesthesia, the one presented in the doodle is the one first outlined by Klein, some use more or less lidocaine or epinephrine.
- Kucera IJ1, Lambert TJ, Klein JA, Watkins RG, Hoover JM, Kaye AD. Liposuction: contemporary issues for the anesthesiologist. J Clin Anesth. 2006, 18(5): 379-87.
- Klein JA. The tumescent technique. Anesthesia and modified liposuction technique. Dermatol Clin. 1990, 8(3): 425-37.
- Klein JA. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast Reconstr Surg. 1993, 92: 1085-100.
The jugular venous pulse/pressure (JVP) is a favourite topic on the wards!
The jugular veins fill with blood and pulsate in relation to filling in the right atrium. Since the JVP correlates well with central venous pressure, it’s used as an indirect marker of intravascular fluid status.
Traditionally, the right internal jugular (IJ) vein is used in JVP measurement; it’s preferred since it is directly in line with the superior vena cava and right atrium. The external jugular (EJ) vein is not commonly used to assess the JVP because it has more valves and an indirect course to the right atrium, but EJ is easier to see than IJ, and JVP measurements from both sites correlate fairly well. The left-sided jugular veins are also uncommonly used, since they can be inadvertently compressed by other structures and thus be less accurate!
Learners on the ward are often asked how to identify the JVP and distinguish it from carotid artery pulsations. The mnemonic POLICE describes the distinguishing features of the JVP:
- Palpation: The carotid pulse is easy felt but the JVP is not.
- Occlusion: Gentle pressure applied above the clavicle will dampen the JVP but will not affect the carotid pulse.
- Location: The IJ lies lateral to the common carotid, starting between the sternal and clavicular heads of the sternocleidomastoid (SCM), goes under the SCM, and when it emerges again can be followed up to the angle of the jaw. The EJ is easier to spot because it crosses SCM superficially.
- Inspiration: JVP height usually goes down with inspiration (increased venous return) and is at its highest during expiration.
- (Kussmaul’s Sign describes a paradoxical rise in JVP during inspiration that happens in right-sided heart failure or tamponade)
- Contour: The JVP has a biphasic waveform, while carotid pulse only beats once.
- Erection/Position: Sitting up erect will drop the meniscus of the JVP, while lying supine will increase filling of the JVP.
To measure the JVP, the patient lies supine in bed at a 30 – 45 degree angle, with their head turned slightly leftward and jaw relaxed. A hard light source (e.g., penlight) pointed tangential to the patient’s neck will accentuate the visibility of the veins. Once the highest point of JVP pulsation is seen, measure high how it is at its maximum, in terms of centimeters above the sternal angle (aka Angle of Louis, at the 2nd costal cartilage). The JVP normally is 4 cm above the sternal angle or lower; increased in fluid overload and decreased in hypovolemia.
- Beigel R et al. 2013. Noninvasive evaluation of right atrial pressure. Journal of the American Society of Echocardiography: 26;1033.
- Chua Chiaco JMS, Parikh NI, Fergusson DJ. 2013. The jugular venous pressure revisited. Cleveland Clinic Journal of Medicine. 80;638.
- Cook DJ, Simel DL. 1996. Does this patient have abnormal central venous pressure? Journal of the American Medical Association: 275;630.
- Vinayak AG, Pohlman AS. 2006. Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients. Archives of Internal Medicine: 166;2132.
- Wang CS et al. 2005. Does this dyspneic patient in the emergency department have congestive heart failure? Journal of the American Medical Association: 294;1944.
For being such a small anatomic location, people find it very difficult to describe where on the hand or digits things are actually happening when there is an injury.
I think part of it stems back to medical school when we are taught that the digits all have numbers, the thumb is D1, index D2 and so forth. The problem comes when people say “the 3rd finger” and all of the sudden one has no idea whether they are talking about the long finger (D3) or the ring finger (D4 but then, the thumb doesn’t count as a finger, does it?)
Which finger (digit?!) is which?
This is why it’s always best to call digits by their names, this even goes for metacarpals. It is totally OK, and generally less confusing to call a bone the index finger metacarpal.
- Thumb = D1
- Index = D2
- Long = D3
- Ring = D4
- Small = D5
Which side of the hand?
The same goes for which side of the hand the problem is on. There is no lateral or medial side to the hand. One could argue that it’s how someone is in anatomical position, so obviously the small finger side is medial, unfortunately very few people walk around in anatomic position and it’s their thumbs that point to the body.
So best to describe side by two things that stay put regardless of how someone has their hands in space: the radius and the ulna.
- Thumb side = RADIAL
- Small finger side = ULNAR
Finally for the top and bottom (or is it back and front) of the hands: use the terms DORSAL (where the nails are) and VOLAR (or palmar)
The clotting cascade was one of the first doodles posted on Sketchy Medicine, I’ve now updated it to include some of the Novel Oral Anticoagulants (NOACs): Dabigatran, Rivaroxaban and Apixiban.
- Selective, reversible direct thrombin inhibitor
- Is actually a prodrug that reaches peak concentration 2-3 h post ingestion
- Approved (in Canada) for: Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence
- T1/2: 7-17 h
- CYP independent (not as many drug-drug interactions)
- Excreted in urine 95% / Feces 5%
- Reversal: hemodialysis?
- Big trial = RELY, REMEDY
- Selective, reversible direct factor Xa inhibitor
- Approved (in Canada) for: Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence
- T1/2: 3-9 h (relatively speedy!)
- Very good oral bioavailability
- Almost all of it is protein-bound in the serum
- Urine 70% / Feces 30%
- Reversal: ???? (not hemodialysis)
- Selective, reversible direct factor Xa inhibitor
- Approved (in Canada) for: Thromboprophylaxis in atrial fib, post-op, and treatment of VTE and VTE recurrence (only atrial fib in the USA)
- T1/2: 8-15
- Almost all (95%) protein-bound in the serum
- Urine 30% / Feces 70%
- Reversal: ???? (not hemodialysis)
- Only good for agents that aren’t highly protein bound (i.e. dabigatran).
- Warfarin, rivaroxaban and apixaban are all mostly bound to protein in the serum, so dialysis won’t get rid of them
- Plasma-derived product containing factors II, IX and X (3-factor PCC) or II, VII, IX and X (4-factor PCC) in addition to variable amounts of proteins C and S, and heparin
- Plasma-derived product containing activated factors II, VII, IX and X
- Recombinant factor VIIa
- Looks good in test tubes, clinical evidence lacking
- Humanized monoclonal antibody against dabigatran
- Andxanet alfa
- Recombinant factor Xa derivative
- Could theoretically be used for rivaroxaban and apixaban
(Adapted from Jackson II & Becker, 2014)
Approach to bleeding
(From Siegal, 2015)
- Jackson II LR & Becker RC. (2014). Novel oral anticoagulants: pharmacology, coagulation measures, and considerations for reversal. Journal of Thrombosis and Thrombolysis, 37(3), 380-391.
- Ufer M. (2010). Comparative efficacy and safety of the novel oral anticoagulants dabigatran, rivaroxaban and apixaban in preclinical and clinical development. Thrombosis and Haemostasis. 103: 572-585.
- Siegal DM. (2015). Managing target-specific oral anticoagulant associated bleeding including an update on pharmacological reversal agents. Journal of Thrombosis and Thrombolysis, 1-8.
Sore throats (pharyngitis) are a common complaint in primary and emergency care settings. Most of the time, pharyngitis is caused by viral infection (most commonly rhinovirus).
Streptococcus pyogenes, aka Lancefield group A streptococci, (GAS) is the most common bacterial cause of pharyngitis. The possible complications of GAS infection include:
- Rheumatic fever
- Post-streptococcal glomerulonephritis
- Peritonsillar/retropharyngeal abscess
- Otitis media
- Pediatric autoimmune neuropsychiatric disorder associated with Group A streptococci (PANDAS) *controversial!
Signs and symptoms
GAS pharyngitis may also include fever, chills, malaise, headache, nausea, vomiting, abdominal pain, or maculopapular rash (scarlet fever). Cough, coryza/rhinitis, and conjunctivitis are uncommon symptoms for GAS pharyngitis. However, clinically diagnosing GAS pharyngitis based on history and physical is incredibly unreliable, so patients with a convincing presentation would benefit from laboratory confirmation (i.e., throat culture, rapid antigen detection test of throat swab). The Centor and McIsaac criteria are useful for helping rule out GAS pharyngitis, but shouldn’t be used exclusively to diagnose it.
The Centor criteria are scored based on the presence of:
- Fever (subjective or >38 C)
- Lack of cough
- Tender lymphadenopathy (anterior cervical)
- Tonsillar exudate
The MacIsaac criteria add an extra point for patients < 14 years old (since this age group is more prone to GAS pharyngitis) and subtract a point if >45 years old. A low score on these criteria help to exclude GAS pharyngitis, but higher scores indicate a need for lab tests.
The first-line treatment for GAS pharyngitis is penicillin. Other antimicrobial agents vary between different guidelines. Guidelines vary about whether empiric treatment should be considered before lab results have confirmed a diagnosis.
- Aalbers J et al. 2011. Predicting streptococcal pharyngitis in adults in primary care: A systematic review of the diagnostic accuracy of symptoms and signs and validation of the Centor score. BMC Medicine: 9;67.
- Kociolek LK, Shulman ST. 2012. Pharyngitis. In: Annals of Internal Medicine: In the Clinic (Cotton D, Taichman D, Williams S, Eds.). ITC3-1.
- Weber R. 2014. Pharyngitis. Primary Care Clinics in Office Practice: 41;91.
- Wessels MR. 2011. Streptococcal pharyngitis. New England Journal of Medicine; 364:648.
- Worrall G. 2011. Acute sore throat. Canadian Family Physician: 57;791.
Amyotrophic Lateral Sclerosis (ALS) is a degenerative disease of the motor neurons in the brain and spinal cord. It progressively affects all the muscles in the body but there is no known cause and no treatment. Only about 5-10% of cases are inherited while the rest are sporadic.
The neurons ALS affects are primarily the upper motor neurons. These are the ones that originate in the brain and travel down the spinal cord. These neurons then synapse with the lower motor neurons in the ventral horn, and it is the lower motor neurons that go directly to the muscles.
In ALS there are both upper motor neuron and lower motor neuron symptoms. As the neurons die, a constellation of symptoms including numbness, weakness and paralysis emerge. Eventually the paralysis progresses leading to inability to speak, swallow and breath. There is no cure for ALS and treatments only help with the symptoms, they do not slow the progression of the disease.
So you may have seen a lot of ice bucket challenges over the last few weeks but please support this cause as it is a horrible disease that up until now had almost no recognition or support. So please donate to The ALS Association (alas.org).
And in case you get tired or jaded seeing your social media full of these videos, watch this one of my father doing it. He’s not an emotional guy, but he has lost more than his fair share of friends to this disease.
donate to help fund ALS research and support from Ali & Mike on Vimeo.
Volume control (VC) and pressure control (PC) are two common modes of positive pressure mechanical ventilation. In VC, the clinician sets the tidal volume that is given for every breath; pressure is allowed to vary over the course of the breath. In PC, the ventilator is programmed to deliver the same pressure throughout inspiration, so tidal volume is allowed to vary based on the pressure and timing settings, as well as the patient’s own lung compliance.
The timing of ventilation can be set according to a trigger. Continuous mandatory ventilation (CMV) involves setting the respiratory rate and having the ventilator deliver breaths at exactly that rate. This is generally used in paralyzed patients (e.g., general anesthesia), where the patient is not expected to trigger any breaths. In Synchronized Intermittent Mandatory Ventilation (SIMV), mandatory breaths are still given but they are synchronized to the patients’ own respiratory efforts (if present). Also, the patient is allowed to take additional breaths on their own. SIMV is often used to wean patients from the ventilator, by decreasing the rate of mandatory breaths and having patients take more of their breaths spontaneously.
Pressure support (PS) is another mode that is used for weaning. No mandatory breaths are programmed. The patient actively takes their own breaths, and the ventilator simply gives an additional boast of inspiratory pressure to help them out.
Positive End Expiratory Pressure (PEEP) is a setting that is used to prevent alveolar collapse, increase functional residual capacity, and generally improve gas exchange. PEEP involves programming a small amount of additional airway pressure (often ~5-10 cmH2O) to be present at the end of expiration.
- Nugent K, Nourbaksh E (Eds.). 2011. A bedside guide to mechanical ventilation. Createspace.
- Owens W. 2012. The ventilator book. First Draught.
- Kacmarek RM, Hess DR. 2008. Mechanical ventilation for the surgical patient. In: Anesthesiology (Longnecker DE, Brown DL, Newman MF, Zapol WM, Eds.). McGraw Hill, New York.
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.