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
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
- 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
- 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)
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.
- 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)
- 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.
Hypothermia is when you get really cold. Generally, hypothermia is defined as a core temperature less than 35C (95F). The Swiss staging system is fairly commonly used for correlating core temperature and clinical signs:
- Stage I (35 – 32C; 90 – 95F): conscious, shivering
- Stage II (28 – 32C; 82 – 90F): altered mental status, not shivering
- Stage III (24 – 28C; 75 – 82F): unconscious, not shivering, vital signs present
- Stage IV (< 24C; < 75F): apparent death (but resuscitation possible!)
- Stage V (< 13.7C; < 58F): death due to irreversible hypothermia
Healthy people have fairly effective mechanisms for maintaining a normal temperature (37C; 99F) (e.g., shivering, peripheral vasoconstriction) but these can be overwhelmed by extreme cold (Primary Hypothermia). Some comorbid patients can develop hypothermia even in a warm environment (Secondary Hypothermia). For instance, severely-burned patients can have increased heat loss, while acute spinal cord injury can impair peripheral thermoregulation.
For the development of hypothermia, it is sometimes helpful to remember that heat can be lost by 4 physical mechanisms:
- Radiation: heat exchange by infrared electromagnetic radiation
- Evaporation: molecules converting from liquid to gas phase (e.g., sweat)
- Convection: heat exchange by air/fluid currents
- Conduction: heat exchange by direct contact with a colder surface
- Brown DJA, Brugger H, Boyd J, Paal P. 2012. Accidental hypothermia. NEJM; 367:1930.
- Zafran K, Mechem CC. 2017. Accidental hypothermia in adults. In: UpToDate.
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 carpal bone ossify aka turn into bone aka magically become visible on an x-ray in a predictable order.
The easiest way to remember is that it starts at the capitate (smack dab in the middle) and then goes in a ulnarly-directed spiral. I was going to say “clockwise” or “counter-clockwise” but that would depend on which side of which hand you were looking at. So capitate, followed by hamate and then down to triquetrum and so on. Except for the pisiform, being a sesamoid bone it gets left behind and only develops years later.
- Capitate: 1-3 months
- Hamate: 2-4 months
- Distal radius: 1 year
- Triquetrum: 2-3 years
- Lunate: 2-4 years
- Scaphoid: 4-6 years
- Trapezium: 4-6 years
- Trapezoid: 4-6 years
- Distal ulna: 5-6 years
- Pisiform: 8-12 years
I included the distal radius and distal ulna in there for good measure.
I know I could have been fancier with changing the length of the metacarpals or their growth plates, but it was more fun to make the animated gif.
The scaphoid shift test aka midcarpal shift test is a variation of the Watson Test for scaphoid instability. A positive test can be caused by scapholunate ligament laxity or injury.
The Watson test evaluates scaphoid instability as the wrist is moved from radial to ulnar deviation (it’s not an “active” test)
To do the scaphoid shift test (as described by Lane in 1993)
- Use the same hand as the patient’s affected hand (suspicious of a right scaphoid problem? Use your right hand to test)
- Place your hand on the patient’s so that your thumb is over the volar surface of the scaphoid tubercle (the distal pole). Don’t apply any pressure (remember this area is probably at least a little sore and you want to remain friends for now)
- Gently move the wrist through ulnar/radial deviation (you can be fancy and consider this your Watson Test) and flexion/extension to relax the patient
- With the patient’s wrist in neutral extension and neutral (or slight radial deviation), forcefully and quickly push the scaphoid tubercle in the dorsal direction
- At this point, the patient is likely no longer your friend
- Note the degree of shift, any crepitus or clunk, and pain evoked.
- Remember to compare this to the opposite wrist
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.