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.
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
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 actualnot 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 (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)
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 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:
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.
References
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.
Today’s post follows up on one of the first ones on this site, about abdominal paracentesis!
Paracentesis is the process of drawing out fluid from the peritoneum. It is useful for diagnosing ascites when its cause is unclear, and the procedure be used to therapeutically remove large volumes of ascites fluid.
While it is overall a quite safe procedure, the risks of paracentesis include: bleeding, bowel or bladder perforation, persistent ascites fluid leak, infection.
Paracentesis is usually done in a lateral decubitus position (or supine, for large volumes). The level of the ascites fluid is percussed and a needle is inserted in either in the midline (2-3 cm below umbilicus) or lateral lower quadrant (lateral to rectus abdominus muscle, 2-4 cm superomedial to anterior superior iliac spine). This positioning prevents puncture of the inferior epigastric arteries; visible superficial veins and surgical scars should be avoided too. To reduce risk of ascites fluid leak, the needle is inserted either with a z-tracking technique, or at a 45-degree angle.
Lee SY, Pormento JG. 2009. Abdominal paracentesis and thoracentesis. Surgical Laparoscopy, Endoscopy & Percutaneous Techniques; 19:e32.
McGibbon A, Chen GI, Peltekian KM, Veldhuyzen van Zanten S. 2007. An evidence-based manual for abdominal paracentesis. Digestive Disease Science; 52:3307.
Thomson TW, Shaffer RW, White B, Setnik GS. 2006. Paracentesis. NEJM; 355:e21.
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.
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
(Adapted from Jackson II & Becker, 2014)
Approach to bleeding
(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.
