Peripheral nerve branches and compression neuropathy

The branches of the three main terminal branches of the brachial plexus can be difficult to remember. Even worse is trying to remember where all of those pesky compression points are and why it is that you get some symptoms with some and not others.

This diagram attempts to clarify the branches of the radial, median, and ulnar nerves and where they can get squished along the way. There are of course, slight anatomic variations, but this is a good starting point. I’ve even included where the famed Martin-Gruber anastomosis and the Riche-Cannieu anastomosis are, since they can make an otherwise (totally not) straightforward examination of a median or ulnar nerve palsy more muddied since both carry motor fibers between the two nerves.

Most interestingly is John Struthers, whose namesake structures compress the median nerve as a ligament and the ulnar nerve as an arcade.

Brachial plexus schematic with distal targets (printable diagram)

I’ve drawn the brachial plexus before showing more of its anatomical relationships (which is actually why the trunks and cords are named as they are). As I’m gearing up studying, I created this more schematic diagram of the plexus, including the distal targets (mostly the muscles but some sensory too).

Hopefully this will help you figure out “where is the lesion?” when you are faced with a brachial plexus question on your exams (and in life) as well.

I’ve also included a printable version for your printing and pasting-up-to-the-wall-to-passively-absorb pleasure.

Long thoracic: serratus anterior
Dorsal scapular: rhomboids, levator scapulae
Suprascapular: supraspinatus, infraspinatus, sensory to the AC & GH joints
Nerve to subclavius: subclavius
Lateral pectoral: pec major (clavicular head), sensation to pec
Superior subscapular: subscapularis (upper part)
Thoracodorsal (aka middle subscapular): lat dorsi
Inferior subscapular: subscapularis (lower part), teres major
Medial pectoral: pec minor, pec major (sternocostal head)
Medial cutaneous n. of arm: sensory to medial surface of arm (tiny area)
Medial cutaneous n. of forearm (antebrachial cutaneous): sensory to skin over biceps and medial forearm

Vancomycin Dosing

When to use vancomycin

The most common use for vancomycin is in invasive Gram positive infections

You need to consider

  • Infection site
  • Patient weight
  • Kidney function
  • Pathogen susceptibility

Pharmacokinetics

  • Vancomycin has bad oral bioavailability so it’s almost never used as a pill
    • Occasionally it is orally to supplement C. diff infections (because that’s going on in the GI tract)
  • Volume of distribution: IV serum 0.4-1 L / kg
  • Normally vancomycin doesn’t cross the blood brain barrier very well, but in the setting of meningitis the inflamed meninges increases permeability

Adverse effects

  • Redman syndrome: A histamine-like flushing during or immediately after dose. Occurs mostly on the face and neck. This is NOT life threatening
    • Treatment: anti-histamine, pause infusion, then restart at a slower rate
    • If the reaction is severe, stop the infusion, give antihistamines, wait until symptoms resolve before restarting. When you restart, give the infusion reaaaalllllly slooooooowly (over more than 4 hours)
  • Nephrotoxicity

Dosing

This is where vancomycin can get tricky, because you are aiming for a target trough (between dose) serum concentrations.

  • Generally the target is 10 mcg/ml, but this may need to be higher for treating MRSA or osteomyelitis
  • Trough concentrations should be measured 30 minutes before the 4th dose any time a course of vanco is started or the dose is changed
  • Monitor creatinine at least once a week (remember that whole nephrotoxicity bit)

Starting dose should be 15-20 mg/kg (based on actual not ideal body weight) every 12 hours. This usually works out to 1-2 g IV Q12H. If the kidneys are not working well, reduce the dose.

References

  • UpToDate.com “Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults”

Renal replacement therapy (dialysis)

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
  • Uremia

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.

References

  • 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

capnography 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!

For example:

  1. A slanting upslope can represent airway obstruction (e.g., chronic obstructed pulmonary disease, bronchospasm, blocked endotracheal tube).
  2. 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.’
  3. 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
  4. 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
  5. 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 (for burn surgery and liposuction and other things too)

tumescent_a

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.

References

  1. 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.
  2. Klein JA. The tumescent technique. Anesthesia and modified liposuction technique. Dermatol Clin. 1990, 8(3): 425-37.
  3. Klein JA. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast Reconstr Surg. 1993, 92: 1085-100.

Jugular Venous Pulse (JVP)

jvpThe 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.

Describing where things are on the hand

hand-descriptions

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.

  1. Thumb = D1
  2. Index = D2
  3. Long = D3
  4. Ring = D4
  5. 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)

Clotting Cascade – NOW WITH NOACs

clotting_cascade_NOAC

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.

Dabigatran (Pradaxa)

  • 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

Rivaroxaban (Xarelto)

  • 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!)
  • CYP3A4
  • Very good oral bioavailability
  • Almost all of it is protein-bound in the serum
  • Urine 70% / Feces 30%
  • Reversal: ???? (not hemodialysis)

Apixaban (Eliquis)

  • 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
  • CYP3A4
  • Almost all (95%) protein-bound in the serum
  • Urine 30% / Feces 70%
  • Reversal: ???? (not hemodialysis)

Reversal agents:

  • 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
  • PCC
    • 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
  • aPCC
    • Plasma-derived product containing activated factors II, VII, IX and X
  • Recombinant factor VIIa
    • Looks good in test tubes, clinical evidence lacking
  • Idarucizumab
    • Humanized monoclonal antibody against dabigatran
  • Andxanet alfa
    • Recombinant factor Xa derivative
    • Could theoretically be used for rivaroxaban and apixaban

Anticoagulation Assays

Effect of oral anticoagulants on coagulation assays (Jackson II & Becker, 2014)

(Adapted from Jackson II & Becker, 2014)

Approach to bleeding

Managing target-specific oral anticoagulant (Siegal, 2015)

(From Siegal, 2015)

References

  • 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.

Streptococcal Pharyngitis

strep-pharyngitis

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
  • Mastoiditis
  • 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:

  1. Fever (subjective or >38 C)
  2. Lack of cough
  3. Tender lymphadenopathy (anterior cervical)
  4. 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.

References

  • 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.
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