Scaphoid Shift Test

Scaphoid-Shift

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)

  1. Use the same hand as the patient’s affected hand (suspicious of a right scaphoid problem? Use your right hand to test)
  2. 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)
  3. 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
  4. 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
    1. At this point, the patient is likely no longer your friend
  5. Note the degree of shift, any crepitus or clunk, and pain evoked.
  6. Remember to compare this to the opposite wrist

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)

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.

Brachial Plexus Part 1 – anatomical relations

brachial_plexus

The brachial plexus is the bane of many med students’ existence during any sort of neuro block. So many nerves, so many connections, so many seemingly arbitrary names of different sections. It’s just a woven mess of misery. (especially when they start getting into the “where is the lesion” questions)

Thus I’ve decided to have a couple posts about the brachial plexus, hopefully demystifying it to some extent. This first doodle is about the brachial plexus and its anatomical relationship to some of the structures that show why anatomists who named the parts weren’t as crazy as they seem.

Important structures to remember because they explain why parts are named the way they are:

  1. Vertebrae
  2. Anterior and posterior scalene muscles
  3. Subclavian artery
  4. The arm (in its anatomical position)

Vertebrae: There are 7 cervical vertebrae and 12 thoracic vertebrae. To make things confusing the cervical spinal nerves exit ABOVE their named vertebrae (except for C8) while the thoracic, lumbar and sacral exit BELOW. This messes up the whole numbering system because there are SEVEN cervical vertebrae but there are EIGHT cervical spinal nerve roots. The brachial plexus generally includes the nerve roots C5-T1*
* I say generally because there’s are anatomical variations such as a “prefixed” plexus that goes from C4-C8 and a “postfixed” plexus that goes from C6-T2

Scalene Muscles: The brachial plexus is nestled between the scalenes in the neck. At this point the plexus is oriented up and down and therefore the trunks are superior (closest to your noggin), middle, and inferior.

Subclavian Artery/Anatomical Position: The artery is in front of the plexus at the level of the trunks and then the plexus starts to wrap around it (or at least seems to because we don’t keep our arms straight out to our sides in “anatomical position” at all times). The cords are named for their relationship to the artery. One is lateral (again, if the arm was held out to the side), one is posterior and one is medial (think closest to armpit).

 

Subdivisions of the Brachial Plexus

The parts are: Roots/Trunks/Divisions/Cords/Branches or, as I remember them being a classy east coast Canadian: Real/Truckers/Drink/Cold/Beer

Then you might think, “But how do I remember which of the terminal branches comes off where?” For that I think of the two “M” branches being on the M: Musculocutaneous, Median and (M)Ulnar and that the whole thing together can just be said as “MARMU” Pick the mnemonics you want, the brachial plexus is rife with them. I personally just like the sound of the word marmu.

Complex Regional Pain Syndrome

crps

Hypo/Hyperalgesia:Decreased/increased sensitivity to a usually-painful stimulus (e.g., pinprick).
Hypo/Hyperesthesia: Decreased/increased sensation to a usually-innocuous stimulus (e.g., light touch).
Allodynia: Sensation of pain from a usually-innocuous stimulus (e.g., light touch).

Complex Regional Pain Syndrome (CRPS) refers to a chronic neuropathic pain condition with a broad and varied range of  clinical presentations. CRPS patients experience severe pain out of proportion to their original injury, and this may start at the time of injury or weeks later. The pain is described as deep-seated and burning/aching/shooting. Sesnory changes are common, including hypo/hyperesthesia, hypo/hyperalgesia, and allodynia. For instance, many patients describe not being able to tolerate the sensation of bedsheets on their painful limb.

In the affected area, there is often marked edema, temperature asymmetry (usually cooler), and sweating changes (usually increased). Loss of hair and nail growth is common, and disuse of the limb can result in weakness, muscle atrophy, and contractures.

The diagnosis is made clinically, using the Budapest Criteria. Some pain physicians use a nuclear medicine test, three-phase bone scintigraphy, for CRPS diagnosis but this test is becoming less popular, since it has a low positive predictive value.

Budapest Criteria

  1. Pain, ongoing and disproportionate to any inciting event
  2. Symptoms: at least one symptom in three of the four categories:
    • Sensory: reports of hyperesthesia and/or allodynia
    • Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetr
    • Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. Physical Signs: at least one sign at time of evaluation in two or more categories:
    • Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or 
joint movement)
    • Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry
    • Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  4. No other diagnosis better explains the signs and symptoms

CRPS is classified as Type I when there is no apparent history of nerve damage, and Type II when associated with definite peripheral nerve injury. CRPS most commonly occurs following fractures and immobilization, but can happen even with little to no trauma.The pathophysiology is thought to involve autonomic dysfunction and inflammation, but much is still unknown.

CRPS affects females about 2-4 times more often than males, and onset is usually in middle age (though there are rare pediatric cases reported). It is a progressive disease that can result in spread of pain, sensory disturbances, and physical changes to other limbs.

Treatment for CRPS may involve physiotherapy, complementary medicine (e.g., acupuncture, qi gong) psychological therapies, and a variety of pharmacologic (e.g., NSAIDs, anticonvulsants, antidepressants, opioids, ketamine, bisphosphonates) and interventional procedures (nerve blocks, sympathectomy, neurostimulators). As with all things CRPS, there isn’t great evidence for any particular intervention.

  • Harden RN, Bruehl S, Perez RSGM, Birklein F, Marinus J, Maihofner C, Lubenow T, Buvanendran A, Mackey S, Graciosa J, Mogilevski M, Ramsden C, Chont M, Vatine J-J. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for Complex Regional Pain Syndrome. Pain; 150:268.
  • Hord E-D. Complex regional pain syndrome. In: Massachusetts General Hospital Handbook of Pain Management (Eds: Ballantyne JC, Fields HL). Lippincott Williams & Wilkins.
  • Moon JY, Park SY, Kim YC, Lee SC, Nahm FS, Kim H, Oh SW. 2012. Analysis of  patterns of three-phase bone scintigraphy for patients with complex regional pain syndrome diagnosed using the proposed research criteria (the ‘Budapest Criteria’). British Journal of Anesthesia; 108:655.
  • O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome – an overview of systematic reviews. Cochrane Database of Systematic Reviews; 4:CD009416.
  • Schwartzman RJ, Erwin KL, Alexander GM. 2009. The natural history of complex regional pain syndrome. Clinical Journal of Pain; 25:273.
  • Smith H, Popp AJ. The patient with chronic pain syndromes. In: A Guide to the Primary Care of Neurological Disorders (Eds: Popp AJ, Deshaies EM). Thieme.
  • Tran DQH, Duong S, Bertini P, Finlayson RJ. Treatment of complex regional pain syndrome: a review of the evidence. Canadian Journal of Anesthesiology; 57:149.

Internuclear Opthalmoplegia

ino.v2Internuclear opthalmoplegia (INO) is an impairment in lateral conjugate gaze (both eyes looking toward one side), caused by a lesion in the medial longitudinal fasciculus (MLF), and associated with multiple sclerosis.

Lateral conjugate gaze requires coordination of adduction (medial rectus muscle, CN III) in one eye and abduction (lateral rectus muscle, CN VI) in the other eye. These movements are coordinated by the paramedian pontine reticular formation (PPRF), also known as the pontine gaze centre. The pathway is as follows:

  1. To look to the left, the right frontal eye field (FEF) sends a signal to the left PPRF.
  2. The left PPRF innervates the left abducens (CN VI) nucleus, which controls the left lateral rectus muscle and causes the left eye to abduct (gaze to the left).
  3. Additionally, the left CN VI nucleus innervates the right oculomotor (CN III) nucleus, which controls the right medial rectus muscle and causes the right eye to adduct (gaze to the left). The MLF is the tract connecting the CN VI nucleus to the contralateral CN III nucleus.

In INO, there is damage to the MLF, giving a deficit in adduction of the corresponding eye during conjugate lateral gaze, but convergence (eye crossing) is classically preserved because that is controlled by a different pathway. In very mild cases of INO, the only deficit is a slowed velocity of the affected eye. For naming, a right INO (as in the sketch) involves damage to the right MLF, which means that the right eye can’t adduct to look to the left, but can abduct to look to the right.

INO may also be associated with gaze abnormalities such as nystagmus, skew deviation, and even abduction or convergence deficits.

The causes of INO include: multiple sclerosis, pontine glioma, and stroke.

  • Flaherty AW, Rost NS. 2007. Eyes and vision. In: Massachusetts General Hospital Handbook of Neurology. Lippincott Williams & Wilkins.
  • Frohman EM, Frohman TC, Zee DS, McColl R, Galetta S. 2005. The neuro-opthalmology of multiple sclerosis. The Lancet Neurology; 4:111.
  • Ropper AH, Brown RH. 2005. Disorders of ocular movement and pupillary function. In: Adams and Victor’s Principles of Neurology. McGraw-Hill.
  • Wilkinson I, Lennox G. 2005. Cranial nerve disorders. In: Essential Neurology. Blackwell.

 

Leopold Maneuvers

Leopold Maneuvers are a slick series of abdominal palpations that let you determine which way the baby is facing in a pregnant woman.

It’s akin to palm reading, but cooler and more accurate. With the four maneuvers you can figure out which part of the baby is facing towards the pelvis (presentation aka bum first/breach or head first/cephalic), if it’s facing to the right or left and how far it is into the pelvis (engagement).

Skilled physicians can even estimate the weight based on Leopold maneuvers.

Signs of Meningitis

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

  1. Fever
  2. Neck stiffness
    • Brudzinski
    • Kernig
  3. Mental status change – in babies this can be an increase in somnolence or irritability (unconsolably crying)

Important organisms:

  • Bacterial
    • Listeria*
    • E. coli*
    • GBS (Group B strep)*
    • Neisseria meningitidis
    • Strep pneumoniae
    • Staph aureus
    • Gram neg bacilli
    • Haemophilus influenza
  • Viral (“aseptic”)
    • HSV
    • Enterovirus
    • HIV
    • Mumps

* These are the common ones in the neonatal period

Bacterial:

  • 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. pneumoniaeN. meningitidis, and Hib)

Hand Exam: Motor 13/13 – Adductor Pollicis

Adductor Pollicis

  • Instruct the patient to do Froment’s sign – get the patient to forcibly grasp a piece of paper between the thumb and radial side of the index proximal phalanx
  • Origin:
    Oblique head: bases of 2nd and 3rd metacarpals, capitate and adjacent carpal bones
    Transverse head: anterior surface of body of 3rd metacarpal
  • Insertion: lateral side of base of proximal phalanx of thumb
  • Action: adducts thumb and flexes MP joint
  • Innervation: deep branch of the ulnar nerve

In a complete ulnar collateral ligament tear, the adductor pollicis can become entrapped between the remnants of the ligament

The 13 muscle groups you need to test in the hand exam:

  1. FPL
  2. FDP
  3. FDS
  4. Thenar muscles
  5. Interosseous
  6. Hypothenar muscles
  7. EPB and APL
  8. EPL
  9. EDC
  10. EIP and EDM
  11. ECRL and ECRB
  12. ECU
  13. Adductor Pollicis
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