Answer to Orthopaedic Question

Question #1 – What are the muscles that make up the rotator cuff?

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Answer – Supraspinatus, Infraspinatus, Teres Minor, and Subscapularis

Picture1

 

Question #2 – What is AT LEAST one maneuver to assess each of these muscles

Keep in mind, there are several maneuvers of the shoulder and many overlap into other structures.  These are the more common individual maneuvers that I think general practice PAs need to know.

Supraspinatus

Drop Arm test

Description – Patient is seated with examiner to the front. Examiner grasps the patient’s wrist and passively abducts the patient’s shoulder to 90 degrees. Examiner releases the patient’s arm with instructions to slowly lower the arm. Test is positive if the patient is unable to lower his or her arm in a smooth, controlled fashion

Infraspinatus

Dropping Sign

Description – The patient stands with the arm at the side with the elbow at 90 degrees and the humerus medially rotated to 45 degrees. Patient then resists external rotation. Pain or the inability to resist medial rotation indicates a positive test for an infraspinatus strain.

Teres Minor

Hornblower (Patte) Test

Description – Elevate the patient’s arm to 90 degrees in the scapular plane and then flex the elbow to 90 degrees, and the patient is asked to laterally rotate the shoulder. A positive test occurs with weakness and/or pain.

Subscapularis

Lift Off (Gerber) Test

Description – The patient stands and places the dorsum of the hand against mid-lumbar spine. The patient then lifts hand away from the back. An inability to perform this action indicates subscapularis weakness or injury.


References

  1. Physical Therapy Haven – Shoulder
  2. iOrtho App

#14 – Ankle Sprains



Epidemiology

  • 25,000 ankle sprains each day in United States
  • Up to 30% of outpatient sports medicine clinics
  • Ankle injuries are the most common type of injury in high school athletes

Anatomy

  • Lateral
    • Lateral Collateral Complex
      • Anterior talofibular ligament (most common)
      • Calcaneofibular ligament (2nd most common)
      • Posterior talofibular ligament
    • Mechanism of Injury
      • Inversions with either dorsiflexion or plantarflexion

Picture1

  • Medial
    • Deltoid Complex
      • Posterior tibiotalar ligament
      • Tibiocalcaneal ligament
      • Tibionavicular ligament
      • Anterior tibiotalar ligament
    • Mechanism of Injury
      • Forced eversion

Picture12png

  • Syndesmotic (high ankle sprain)
    • Distal Tibiofibular Syndesmosis
      • Anterior-inferior tibiofibular ligament
      • Posterior-inferior tibiofibular ligament
      • Transverse tibiofibular ligament
      • Interosseous membrane
      • Interosseous ligament
      • Inferior transverse ligament
    • Mechanism of Injury
      • External rotation with dorsiflexion

Picture2

Important History Questions

  • What was the mechanism of injury?
  • Could you walk immediately after the injury?
  • Can you walk now?
  • Any previous history of ankle injuries?

Physical Exam

  • Observation
    • Swelling or ecchymosis
    • Ambulation to exam room
  • Palpation
    • Bony
      • Entire fibula (from lateral malleolus to fibular head)
      • Lateral malleolus
      • 5th metatarsal
      • Navicular
    • Soft Tissue
      • Palpate each ligament based on mechanism
    • Special Maneuvers
      • Lateral Injuries
        • Anterior drawer
          • Stabilize proximal leg to the ankle and grasp calcaneous and apply anterior force
        • Talar tilt
          • Stabilize proximal leg to ankle and grasp calcaneous and apply inversion force
      • Syndesmotic Injuries
        • Squeeze test (Hopkin’s test)
          • Compression of tibia and fibula at mid calf
        • External rotation stress test (Kleiger’s test)
          • Stabilize proximal leg to the ankle and applying external rotation force to the forefoot

Grading and Classifications

Screen Shot 2016-05-24 at 1.23.12 PM

Indications for Radiography

  • Ottawa Rules of Foot and Ankle
    • Published in 1996 and showed reduction of ankle x-rays by 28% if none of the following are present:
      • Posterior lateral malleolar tenderness
      • Posterior medial malleolar tenderness
      • Base of 5th metatarsal tenderness
      • Navicular tenderness
      • Inability to ambulate both immediately and in the ED

Picture1

  • Views
    • Standard three views (AP, Lateral, Mortise)

Picture1

  • Varus stress view

Picture1

  • MRI
    • Used for clinically suspicious of syndesmotic injury with normal radiographs

Picture1

Management

  • Orthopaedic Referral
    • Fracture
    • Dislocation/Subluxation
    • Syndesmotic injury
    • Tendon rupture
    • Uncertain diagnosis
  • Non-operative
    • Low ankle
      • RICE
        • Cryotherapy 20 min every 2 hours for 48 hours
      • May use crutches and NWB up to 10 days (Grade II and III)
        • Early immobilization = better recovery
        • Cast vs CAM Boot vs Aircast
      • NSAIDs for pain control
      • Refer to physical therapy for grade II and III for rehabilitation exercises
    • Syndesmotic
      • CAM Boot vs short leg cast for 2-3 weeks
  • Operative
    • Indications
      • Low Ankle
        • Any grade with continued pain and instability despite extensive non-operative management
        • Any grade with bony avulsion
      • Syndesmotic
        • Instability on radiographs
        • Continued pain despite conservative pain
        • Associated ankle fracture
    • Procedures
      • Low Ankle
        • Modified Brostrum
          • Anatomic shortening and reinsertion of the ATFL and CFL
        • Tendon transfer and tenodesis
      • Syndesmotic
        • Screw fixation
        • Suture button

Athlete Return to Play

Screen Shot 2016-05-24 at 1.32.40 PM

Cottage Physician

Picture1


References

  1. American College of Sports Medicine. Fact Sheets: Ankle Sprains. http://www.acsm.org/public-information/brochures-fact-sheets/fact-sheets.  Accessed May 23, 2016.
  2. Wheeless’ Textbook of Orthopaedics. Ankle Sprain. http://www.wheelessonline.com/ortho/ankle_sprain.  Accessed May 23, 2016.
  3. Low Ankle Sprain.  http://www.orthobullets.com/foot-and-ankle/7028/low-ankle-sprain.  Accessed May 23, 2016.
  4. High Ankle Sprain.  http://www.orthobullets.com/foot-and-ankle/7029/high-ankle-sprain.  Accessed May 23, 2016.
  5. Stiell I. Ottawa ankle rules. Can Fam Physician. 1996;42:478-80.
  6. Tiemstra JD. Update on Acute Ankle Sprains.  Am Fam Physician.  2012;85(12):1170-1176.
  7. De Brucker Y, Jager T, Devos H, Boulet CG, Kichouh M, De Maeseneer M, Shahabpour M, de May J. Trauma mechanism in ankle fracture: Let’s do the twisthttp://posterng.netkey.at/esr/viewing/index.php?module=viewing_poster&task=viewsection&pi=121495&ti=402298&searchkey=.  Accessed May 24, 2016.
  8. Stress view of ankle – with deltoid ligament tearhttp://radiopaedia.org/cases/stress-view-of-ankle-with-deltoid-ligament-tear.  Accessed May 24, 2016.
  9. Hocutt JE, Jaffe R, Rylander CR, Beebe JK. Cryotherapy in ankle sprains. Am J Sports Med. 1982;10(5):316-9.
  10. Seah R, Mani-babu S. Managing ankle sprains in primary care: what is best practice? A systematic review of the last 10 years of evidence. Br Med Bull. 2011;97:105-35.
  11. Bleakley CM, O’connor SR, Tully MA, et al. Effect of accelerated rehabilitation on function after ankle sprain: randomised controlled trial. BMJ. 2010;340:c1964.
  12. Tsao LY.  Radsource.  High Ankle Sprain. http://radsource.us/high-ankle-sprains/.  Accessed May 24, 2016.

Answer to Neuro Question

19yo male is brought into the emergency department by EMS after getting into an altercation and getting knocked unconscious.  He unsure of how long he was out, but he came to once EMS arrived.  He denies any nausea, vomiting, or vision changes.  He is drowsy/lethargic with his eyes closed, but is arousable to voice.  He can carry on a conversation, but he needs frequent redirection and he does not know where he is.  While talking with him, the nurse starts an IV and he tries to swat her away with his opposite hand.

 

What is the classic score we use and what is his score?

The Glasgow Coma Scale (GCS) was first devised in 1974 and has been the predominant neurologic scoring system since.  It takes into account 3 main variables and each variable has a point score attached to it.  The maximum score is 15 and the minimum score is 3 (3T if intubated).

  • Eye opening
    1. 4 points – Spontaneous
    2. 3 points – To speech
    3. 2 points – To pain
    4. 1 point – None
  • Verbal Response
    1. 5 points – Oriented
    2. 4 points – Confused conversation
      1. Not sure where they are, or what their name is
    3. 3 points – Inappropriate words
      1. They speak real words, but they are not in context
    4. 2 points – Incomprehensible sounds
    5. 1 point – None
  • Motor Response
    1. 6 points – Obeys commands
    2. 5 points – Localizes to pain
      1. Crosses midline/clavicles to remove painful stimuli
    3. 4 points – Withdrawal to pain
      1. Moves extremity/head away from painful stimuli
    4. 3 points – Decorticate (flexor) posturing
    5. 2 points – Decerebrate (extensor) posturing
    6. 1 point – None

Our patient’s score is 3E + 4V + 5M = 12

How good is it?

The GCS was never designed to be used for acute injury.  It was created to monitor changes in neurologic status of patients in a neurosurgical unit and was not designed to have the 3 individual variables combined into one score.  Here are the important limitations of the GCS.

  • The GCS is NOT reliable
    1. It is made up of subjective elements that are open to the interpretation of each provider assessing the patient and has been repeated shown to have poor inter-rater reliability.
      1. One study showed only a 38% accuracy between raters and were 2 or more points off 33% of the time.
  • Providers CAN’T remember the scale
    1. It has too many elements and is regarded as too complicated to be easily, and rapidly applied to patients
    2. In 2003, it was discovered that 25% of British hospitals were using the original 12-point scale instead of the current 13-point scale without anyone noticing.
  • The GCS is only GROSSLY predictive
    1. It is not designed to predict outcomes of patients with acute neurologic injury.
  • The GCS is NOT equal to the sum of its parts
    1. The original creators vehemently opposed the summed total score because it assumes that each variable is equal to the others in terms of importance
      1. Example
        1. GCS of 4 with 1E + 1V + 2M = 48% mortality
        2. GCS of 4 with 1E + 2V + 1M = 27% mortality
        3. GCS of 4 with 2E + 1V + 1M = 19% mortality

Are there any other scoring systems out there?

The motor subscale of the GCS has been proven to be most predictive of outcomes in patients with neurologic trauma and injury.  This has led to debate about whether to do away with the other 2 subscales and use just the motor score (since it has been shown to close to linear in regards to survival).

Healy C. J Trauma. 2003.

Healy C. J Trauma. 2003.

But this is still 6 points and some argue can be further simplified.  One study broke down the 6-point motor subscale and found that only 3 of those were statistically important.  Those are:

  • Obeys commands
  • Localizes to pain
  • Withdrawal to pain or less

This new Simplified Motor Scale can be remembered by the acronym TROLL (Test Responsiveness: Obeys, Localizes, Less).  2 other simplified scores have also been created to help quickly determine neurologic status.  These are:

  1. AVPU
    1. Alert
    2. Responds to verbal stimuli
    3. Responds to painful stimuli
    4. Unresponsive
  2. ACDU
    1. Alert
    2. Confused
    3. Drowsy
    4. Unresponsive

There is another, although more complicated, score called the FOUR score, which has 4 components and stands for Full Outline of UnResponsiveness.  Unfortunately, it is even more complicated than the GCS (in the original study it was performed by neurologic specialists, not general practitioners) and it performed just as poorly in external validation studies as the GCS.

Wijdicks EF. Ann Neurol. 2005.

Wijdicks EF. Ann Neurol. 2005.

 

Bottom Line

GCS is essentially worthless clinically even when it is calculated correctly.  Simplified scores give just as much information, are easier to use, and are just as predictive. But….you will always be asked “what is the patient’s GCS”, in spite of the growing evidence against it.


References

  1. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2(7872):81-4.
  2. Green SM. Cheerio, laddie! Bidding farewell to the Glasgow Coma Scale. Ann Emerg Med. 2011;58(5):427-30.
  3. Teasdale G, Jennett B, Murray L, Murray G. Glasgow coma scale: to sum or not to sum. Lancet. 1983;2(8351):678.
  4. Zuercher M, Ummenhofer W, Baltussen A, Walder B. The use of Glasgow Coma Scale in injury assessment: a critical review. Brain Inj. 2009;23(5):371-84.
  5. Healey C, Osler TM, Rogers FB, et al. Improving the Glasgow Coma Scale score: motor score alone is a better predictor. J Trauma. 2003;54(4):671-8.
  6. Gill M, Windemuth R, Steele R, Green SM. A comparison of the Glasgow Coma Scale score to simplified alternative scores for the prediction of traumatic brain injury outcomes. Ann Emerg Med. 2005;45(1):37-42.
  7. Mcnarry AF, Goldhill DR. Simple bedside assessment of level of consciousness: comparison of two simple assessment scales with the Glasgow Coma scale. Anaesthesia. 2004;59(1):34-7.
  8. Wijdicks EF, Bamlet WR, Maramattom BV, Manno EM, Mcclelland RL. Validation of a new coma scale: The FOUR score. Ann Neurol. 2005;58(4):585-93.
  9. Fischer M, Rüegg S, Czaplinski A, et al. Inter-rater reliability of the Full Outline of UnResponsiveness score and the Glasgow Coma Scale in critically ill patients: a prospective observational study. Crit Care. 2010;14(2):R64.

Neuro Question

19yo male is brought into the emergency department by EMS after getting into an altercation and getting knocked unconscious.  He unsure of how long he was out, but he came to once EMS arrived.  He denies any nausea, vomiting, or vision changes.  He is drowsy/lethargic with his eyes closed, but is arousable to voice.  He can carry on a conversation, but he needs frequent redirection and he does not know where he is.  While talking with him, the nurse starts an IV and he tries to swat her away with his opposite hand.

 

What is the classic score we use and what is his score?

How good is it?

Are there any other scoring systems out there?

 

#13 – Transient Ischemic Attacks



***LISTEN TO THE PODCAST HERE***



Epidemiology

  • Estimated to be 50-80 per 100,000, or 240,000 per year

Definition

  • Original
    • Neurologic deficits lasting for < 24 hours
      • Can still have permanent tissue injury
Picture1

Ay H. Ann Neuro. 2005;57(5):679-86

  • Consensus from American Heart Association and American Stroke Association
    • Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction
    • Benefits
      • Tissue damage can be seen on imaging (more objective)
        • Thus, encourages early neurodiagnostic tests

Pathophysiology

  • 3 main causes
    • Intrinsic, vessel abnormality
      • Atherosclerosis, lipohyalinosis, dissection, malformation, inflammation
    • Embolic from distal source
    • Inadequate cerebral blood flow
      • Decreased perfusion pressure or increased blood viscosity

Classifications

  • 3 main types
    • Large artery, low-flow
      • Brief (minutes to a few hours), recurrent, and sterotyped due to specific vessel it effects
        • Often due to stenotic internal carotid, middle cerebral, or vertebral-basilar junction
    • Embolic
      • Discrete, infrequent, prolonged (several hours) episode
    • Lacunar, small vessel
      • Stenosis of intracerebral penetrating vessels from middle cerebral, basilar, or vertebral arteries
      • HTN and DMII main culprits

Signs and Symptoms

  • All depends on the vessels being effected
  • 2 Global Regions
    • Anterior Circulation
      • Internal carotid arteries
        • Anterior cerebral artery (contralateral LE>UE weakness)
        • Middle cerebral artery (contralateral face/UE>LE)
    • Posterior Circulation
      • Vertebral arteries
        • Basilar artery (crossed deficits, ataxis, visual disturbances)
          • Cerebellar arteries (dizziness, N/V, visual disturbances)
        • Posterior cerebral artery (visual disturbances, contralateral hemiplegia)
UpToDate

UpToDate

  • Disabling symptoms that suggest stroke
    • Complete hemianopsia
    • Severe aphasia
    • Visual/sensory extinction
    • Any weakness limiting sustained effort against gravity
    • NIHSS ≥ 5
    • Inability to walk
    • Modified Rankin Score ≥ 1
    • Any deficit considered potentially disabling to patient or family

Stroke Mimics

  • Seizures
  • Migraine auras
  • Syncope
  • Peripheral vestibulopathies
  • Pressure/position related peripheral neuropathies
  • Metabolic derangements
    • Hypo/hyperglycemia, renal, liver, pulmonary

Initial Evaluation

  • Laboratory studies
    • BMP, CBC, NH4, LFT, PT/PTT/INR
  • EKG
  • Brain imaging
    • Preferred – Brain MRI with diffusion-weighted imaging
    • Suboptimal – Non-contrast head CT
    • CT perfusion scans becoming an option

ABCD2 Score

  • Used to estimate the risk of ischemic stroke in the first 48 hours after TIA
  • 2-day stroke risk
    • 0-3 – 1%
    • 4-5 – 4%
    • ≥ 6 – 8%
UpToDate

UpToDate

Admit or Outpatient???

  • Recommend admission for:
    • ABCD2 ≥ 3
    • ABCD2 ≤ 2 and unsure if work-up can be completed in 48 hours as outpatient
    • ABCD2 ≤ 2 and other evidence that this is caused by focal ischemia

Definitive Work-Up

  • Neuroimaging within 24 hours of symptom onset
    • Brain MRI with diffusion-weight imaging
  • Neurovascular evaluation
    • Preferred – 4-vessel catheter angiography
    • Options – CTA, MRA, CDUS, TCD
  • Cardiac Evaluation
    • Reasonable to perform if neurovascular work-up is negative
    • TTE if:
      • Patient ≥ 45 years
      • High suspicion of left ventricular thrombus
      • TEE is contraindicated
    • TEE preferred if:
      • Patient < 45 years without history of CVD
      • Patients with atrial fibrillation
      • Patients with mechanical valve
      • Patients with suspected aortic pathology
      • High pretest probability of cardiac embolic source
UpToDate

UpToDate

Secondary Stroke Prevention

  • Medical Management
    • Hypertension
    • Antiplatelet (ASA and clopidogrel)
    • Statins (intensive therapy)
    • Lifestyle modifications
  • Large artery disease
    • Carotid
      • Revascularization
        • Endarterectomy
        • Stenting
    • Extracranial vertebral
      • Angioplasty and stenting
    • Intracranial cerebral vessels
      • Intensive medical management
  • Small artery disease
    • Intensive medical management
  • Cardiogenic embolism
    • Atrial fibrillation
      • Lifelong anticoagulation
    • Myocardial infarction and left ventricular thrombus
      • Anticoagulation for at least 3 months
    • Mitral valve disease (prolapse, calcification)
      • Antiplatelet

Recent Study (video explanation)

One-Year Risk of Stroke after Transient Ischemic Attack or Minor Stroke (TIA Registry Investigators)

  • 4789 patients, 61 sites in 21 countries
  • Patients
    • ≥ 18 years and had a TIA or minor stroke in the last 7 days
      • Mean age – 66years
      • 70% had HTN and DM
      • 87% sought attention within 24 hours
    • Modified Rankin scale ≤ 1
  • Timeline
    • 2-day, 7-day, 30-day, 90-day, and 1-year (following for 5-years)
    • Followed median 27.2 months
  • Outcomes
    • Primary (composite)
      • Death from CV causes
      • Nonfatal stroke
      • Nonfatal ACS
    • Secondary
      • Individual components of primary
      • TIA recurrence
      • Death from any cause
      • Bleeding
  • Results
    • Primary
      • 2% incidence of major fatal or nonfatal CV events
      • Estimate of stroke risk was 5.1%
        • Highest in 1st 90-days
    • Patients with ABCD2 score ≤ 3 still had a 20% early recurrent stroke
    • Higher ABCD2 score, large artery atherosclerosis, and multiple infarctions on imaging are strong independent predictors of recurrent events
    • Risk of recurrent stroke was less than half of expected historical cohorts
      • Attributed to faster and more aggressive secondary prevention
Amarenco P. NEJM. 2016;374(16):1533-42

Amarenco P. NEJM. 2016;374(16):1533-42

Cottage Physician

Cottage Physician - 1893

Cottage Physician – 1893


References

  1. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics–2014 update: a report from the American Heart Association. Circulation. 2014;129(3):e28-e292.
  2. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40(6):2276-93.
  3. Furie KL, Ay H. Initial evaluation and management of transient ischemic attacks and minor ischemic stroke.  In: UpToDate.  Waltham, MA.
  4. Ay H, Koroshetz WJ, Benner T, et al. Transient ischemic attack with infarction: a unique syndrome?. Ann Neurol. 2005;57(5):679-86.
  5. Quinn TJ, Dawson J, Walters MR, Lees KR. Reliability of the modified Rankin Scale: a systematic review. Stroke. 2009;40(10):3393-5.
  6. Levine SR, Khatri P, Broderick JP, et al. Review, historical context, and clarifications of the NINDS rt-PA stroke trials exclusion criteria: Part 1: rapidly improving stroke symptoms. Stroke. 2013;44(9):2500-5.
  7. Brott T, Adams HP, Olinger CP, et al. Measurements of acute cerebral infarction: a clinical examination scale. Stroke. 1989;20(7):864-70.
  8. Johnston SC, Rothwell PM, Nguyen-huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007;369(9558):283-92.
  9. Johnston SC, Nguyen-huynh MN, Schwarz ME, et al. National Stroke Association guidelines for the management of transient ischemic attacks. Ann Neurol. 2006;60(3):301-13.
  10. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(7):2160-236.
  11. Whitlock RP, Sun JC, Fremes SE, Rubens FD, Teoh KH. Antithrombotic and thrombolytic therapy for valvular disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e576S-600S.
  12. Amarenco P, Lavallée PC, Labreuche J, et al. One-Year Risk of Stroke after Transient Ischemic Attack or Minor Stroke. N Engl J Med. 2016;374(16):1533-42.