SplintER Series: Pain in the Snuff Box

Scaphoid Fracture
 
A 16-year-old male presents to the ED after injuring his wrist during a track meet. The patient was running hurdles when he fell forward, planting his wrist into the ground. The imaging is shown below (courtesy of Dr. Hani Makky ALSALAM, Radiopaedia.org).
Scaphoid fracture (Image 2).

  • Pearl: The scaphoid is the most frequently fractured carpal bone [1,2].
  • Pearl: Fractures occur at the waist, proximal third, and distal portion: 65%, 25%, and 10% respectively [3].

Image 2. Fracture of scaphoid. Case courtesy of Dr. Hani Makky ALSALAM, Radiopaedia.org, rID: 10398 (arrow added by authors).

Occurs when there is an axial load across hyper-dorsiflexed, pronated and ulnar deviated wrists or from a fall on the outstretched hand (FOOSH) [1-3].

Snuff box tenderness, scaphoid tubercle tenderness over the volar aspect of the wrist, and/or positive scaphoid compression test (pain reproduced with an axial load applied through thumb metacarpal) [4-6].

Snuff Box

Image 3. Location of scaphoid tubercle (S) at the base of the thenar eminence (left) and the location of the snuffbox (SB) on the radial aspect of the wrist (right). Images by authors.

Plain film imaging with anterior-posterior, oblique, and lateral views to assess for injury.

  • Pearl: There is also a scaphoid view that is recommended if the department technician is trained. This image is a posterior-anterior view of the scaphoid that is obtained with the wrist in ulnar deviation [7].

Abnormal exam: If not neurovascularly intact or if there is an open fracture, consult orthopedics in the ED.

Identified scaphoid fracture: Thumb spica splint and prompt orthopedic follow-up usually within 1-3 days as though some fractures only require immobilization for treatment; surgery may be required for some fracture patterns [1-3,6].

Suspicion for fracture without radiographic evidence: Place in thumb spica splint and repeat imaging in 14 days to evaluate for occult fracture. If negative again at that time with high clinical suspicion, the patient should have an outpatient MRI [1-3,6].

  • Pearl: Initial imaging can miss 5-20% of fractures [8].

Classic complications include vascular necrosis (AVN), and scaphoid nonunion advanced collapse (SNAC). Associated fractures and dislocation of the surrounding carpal bones, distal radius, ligamentous disruption may be seen as other pathology occurs secondary to a FOOSH [1-4,6].

  • Pearl: AVN is of high concern and directly correlated to the site of fracture. The scaphoid receives blood supply via retrograde flow – the more proximal the fracture, the higher the risk of AVN [1-4,6].
  • Pearl: SNAC occurs when the proximal scaphoid remains attached to the lunate and the distal fragment rotates into flexion. This results in early osteoarthritis between the distal scaphoid and radial styloid, leading to pain and decreased functionality [9].

 

References & Resources:

For a review of other causes of traumatic wrist pain check out the SplintER archives.

  1. Tada K, Ikeda K, Okamoto S, Hachinota A, Yamamoto D, Tsuchiya H. Scaphoid Fracture–Overview and Conservative Treatment. Hand Surg. 2015;20(2):204-209. PMID 26051761.
  2. Sabbagh MD, Morsy M, Moran SL. Diagnosis and Management of Acute Scaphoid Fractures. Hand Clin. 2019;35(3):259-269. PMID 31178084.
  3. Gupta V, Rijal L, Jawed A. Managing scaphoid fractures. How we do it?. J Clin Orthop Trauma. 2013;4(1):3-10. PMID 26403769.
  4. Basu A, Lomnassey LM, Demos TC, et al: Your Diagnosis? scaphoid fracture. Orthopedics 28:177, 2005. PMID 15751361
  5. Watson HK, Weinzweig J. Physical examination of the wrist. Hand Clin. 1997;13(1):17-34. PMID 9048180.
  6. Stapczynski, JS, Tintinalli, JE. Wrist injuries. In Tintinalli’s emergency medicine: A comprehensive study guide, 8th Edition. New York, NY: McGraw-Hill Education; 2016: 1853-1854
  7. Cheung GC, Lever CJ, Morris AD. X-ray diagnosis of acute scaphoid fractures. J Hand Surg Br. 2006;31(1):104-109.PMID 16257481.
  8. Ashmead D 4th, Watson HK, Damon C, Herber S, Paly W. Scapholunate advanced collapse wrist salvage. J Hand Surg Am. 1994;19(5):741-750. PMID 7806794.
  9. Moritomo H, Tada K, Yoshida T, Masatomi T. The relationship between the site of nonunion of the scaphoid and scaphoid nonunion advanced collapse (SNAC). J Bone Joint Surg Br. 1999;81(5):871-876. PMID: 10530853.
  10.  

Treating Blood Pressure in Intracranial Hemorrhage

hemorrhagic stroke equal podcast

Blood pressure control in the setting of ischemic stroke has a clearly recognized benefit in patient outcomes. The impact of blood pressure control in hemorrhagic stroke is not as well understood. The ACEP E-QUAL Network podcast, a partnership with ALiEM to promote clinical practice improvements, reviewed this topic with Dr. Latha Ganti (University of Central Florida College of Medicine). Dr. Ganti addressed the evidence behind recommended blood pressure targets and the available medications to achieve control. We present highlights from this discussion with Dr. Jason Woods.

 

What is the goal of blood pressure control in hemorrhagic stroke?

Management of blood pressure in intracranial hemorrhage (ICH) raises questions about the benefit of limiting hematoma expansion while maintaining cerebral perfusion. While it seems intuitive that hypertension should be controlled to limit hematoma expansion, patients with hemorrhagic stroke may be dependent on higher blood pressures for adequate perfusion.

Does lowering blood pressure lead to perihematomal ischemia?

ICH Adapt studies did not show evidence of decreased cerebral blood flow in perihematomal tissue and demonstrated that there is likely preservation of autoregulation which prevents ischemia [1].

Does lowering BP help prevent hematoma expansion and improve outcomes?

The risk of hematoma expansion is highest within the first couple of hours following initial bleeding. Hematoma expansion is clearly associated with worse outcomes. Scoring tools exist to estimate the risk of hematoma expansion. The “spot sign,” seen on source images from a computed tomography angiogram of the brain, suggests an area of dynamic bleeding.

  • ICH ADAPT: no difference in hematoma expansion or clinical outcome with acute blood pressure lowering [2].
  • INTERACT 2: intensive lowering of blood pressure did not result in a significant reduction in mortality or severe disability [3].
  • ATACH 2: intensive lowering of blood pressure did not improve functional outcomes but was associated with increased renal dysfunction [4].

What is the optimal systolic blood pressure (SBP) target?

AHA Guidelines 2015

  • ICH patients with SBP 150-220 mmHg, lower to 14 mmHg is safe
  • ICH patients with SBP > 220 mmHg, aggressive reduction with continuous infusion may be reasonable

So what’s the right thing to do? If data suggests that lowering may not be as beneficial, what should the target blood pressure be?

  • Target SBP 140-160 mmHg is a reasonable target

What medications are preferred for blood pressure control in ICH?

The ideal agent for blood pressure management in ICH would have a quick onset, but short duration, to allow titration.

Recommended first-line:

  • Labetalol
    • Onset < 5 min
    • Duration of effect 2-4 hr
    • IV bolus dose: 20 mg, followed by 20-80 mg every 10 min to a total dose of 300 mg.
    • Infusion dose: 0.5 mg-2 mg/min
    • Avoid in: asthma, COPD, heart failure, AV block
  • Nicardipine
    • Onset 1-2 min
    • Half-life ~ 40 min
    • Infusion dose: 0.5-1 mcg/kg/min, max 3 mcg/kg/min
  • Clevidipine
    • Onset 1-4 min
    • Duration of effect 5-15 min
    • Infusion dose: 1 mg/hr, up to 21 mg/hr, titrate by 2.5 mg/hr every 5-10 min
    • Avoid in: severe aortic stenosis, and lipid metabolism dysfunction or known allergy to eggs or soy (delivered as lipid emulsion)

Available second-line (mostly off-label, not preferred)

  • Esmolol
  • Fenoldopam
  • Hydralazine
  • Enalaprilat

Conclusions

When it comes to blood pressure: keep it simple.

  • Target SBP 140-160 mmHg
  • Top three drugs: Labetalol, Nicardipine, Clevidipine

Although labetalol has common contraindications, it is available as a bolus dose. In a clinical setting where drips may not be readily available, Labetalol can be easier to get.

Interested in more ACEP-EQUAL podcasts?

Listen to the other ACEP E-QUAL podcasts on our Soundcloud account.

References

  1. Butcher K, Jeerakathil T, Emery D, et al. The Intracerebral Haemorrhage Acutely Decreasing Arterial Pressure Trial: ICH ADAPT. Int J Stroke. 2010;5(3):227-233. PMID: 20536619
  2. Butcher KS, Jeerakathil T, Hill M, et al. The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial. Stroke. 2013;44(3):620-626. PMID: 23391776
  3. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368(25):2355-2365. PMID: 23713578
  4. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016;375(11):1033-1043. PMID: 27276234
By |2020-10-09T09:47:57-07:00Oct 23, 2020|Academic, Emergency Medicine, Neurology|

SplintER Series: A Case of Inability to Move the Knee

Normal knee radiograph

29-year-old F presents to ED with acute onset knee pain. Reports hearing an audible “pop” after twisting her leg while running down the stairs at home. She explains that her right knee is stuck, and she can neither flex nor extend it. An image is shown below (courtesy of Andrew Murphy, Radiopaedia.org)

 

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SAEM Clinical Image Series: Pitching Pain

pitching pain

A twenty-year-old right-handed male presented to the emergency department with a past medical history of right coracoid impingement, and three months of increasing right shoulder pain that became suddenly worse. He had a right shoulder arthroscopy nine months ago and played a full season as his baseball team’s pitcher over the past four months. He endorsed no exacerbating symptoms other than movement and has only taken naproxen over the counter for this pain. He denied any family history of clotting disorders.

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SAEM Clinical Image Series: Knee Pain

knee

A fifty-six-year-old male with a past medical history of legal blindness and remote right quadricep tendon rupture presents to the emergency department via emergency medical services (EMS) after a mechanical fall, complaining of left knee pain. According to the patient, he is in his regular state of health and was walking with his cane when he had a mechanical fall on the sidewalk after tripping on an unknown object and falling onto his left knee.

The patient did not hit his head, did not lose consciousness, and has no head, neck, or back pain. The patient states that he fell directly onto his knee and felt a popping upon hitting the ground, and remembers all events surrounding the incident. The patient was not ambulatory prior to coming to the emergency department.

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Anticoagulant Reversal in Hemorrhagic Stroke

anticoagulant equal podcast

Acute management of cerebrovascular accidents can be challenging enough, but questions about anticoagulant reversal in the setting of hemorrhagic stroke add another layer of complexity. The ACEP E-QUAL Network podcast, a partnership with ALiEM to promote clinical practice improvements, reviewed this topic with Dr. Joshua Goldstein (Massachusetts General Hospital, Harvard Medical School). Dr. Goldstein addressed common anticoagulants and their reversal agents, summarizing available literature to inform clinical practice. We present highlights from this discussion with Dr. Jason Woods.

 

What is the goal of anticoagulant reversal?

Since it is impossible to go back in time to prevent intracranial hemorrhage (ICH), the focus of management for hemorrhagic stroke should be to prevent further bleeding and allow brain tissue an opportunity to recover. The goal of anticoagulant reversal in patients with ICH is to decrease ongoing bleeding.

Warfarin

Warfarin is a vitamin K antagonist. Since vitamin K is required for the processing of coagulation factors II, VII, IX, and X, patients on warfarin have decreased amounts of these factors in circulation. To increase the availability of these factors, countering the effect of warfarin therapy can be two-fold:

  1. Replenish vitamin K to allow the production of new factors.
  2. Provide replacement of these factors directly.

Vitamin K supplementation will not provide immediate effect, and it may take up to 24 hours for the production of new coagulation factors. While it should be given early, patients also require factor replacement acutely.

Fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC) can be given to supplement coagulation factors.

  • FFP carries each of the 4 needed factors in addition to other clotting factors.
    • The cost of FFP is low.
    • Transfusion will take some time as it will require ~ 1 L volume.
  • PCC, marketed as Kaycentra in the US, consists of concentrated Factor II, VII, IX, X, and proteins C and S.
    • The cost of PCC is higher.
    • Transfusion is quick, ~70 mL, and leads to rapid correction of INR.

Studies have shown PCC to be associated with faster INR reversal, less ICH expansion, and a non-statistical trend toward decreased mortality [1]. PCC does carry a theoretical risk of thromboembolism given the rapid correction, but no evidence exists to suggest that this is the case.

Direct Oral Anticoagulants (DOACs)

There are 2 categories of DOACs:

  1. Factor II inhibitors (e.g., dabigatran)
  2. Factor Xa inhibitors (e.g., rivaroxaban, apixaban, edoxaban)

Approach to reversal: remove the inhibitor to allow normal function of already existent Factor II or Xa

  • Time
    • Time can be thought of as a reversal agent. Most DOACs have a half-life ~12 hours. If the timing of the last dose is known and it was hours ago, there may not be much medication left to reverse.
  • Monoclonal antibodies
    • Reversal of dabigatran can be achieved with the use of a monoclonal antibody, idarucizumab, to bind up circulating inhibitor.
    • Reversal of Factor Xa inhibitors can similarly be attempted with the use of monoclonal antibody andexanet. Andexanet is notably more expensive than idarucizumab.
  • PCC
    • PCC can be used off-label to outcompete circulating inhibitor with extra coagulation factors and increase the number of functional factors.

It should be noted that there are no reliable tests for measuring DOAC activity.

Dual Antiplatelet Therapy (DAPT)

The most common agents are aspirin and Plavix (clopidogrel). The issue with patients on these antiplatelet agents is not a lack of platelets, but the presence of medication that suppresses normal platelet function. Theoretically, if one could provide extra platelets, the inhibiting agent could be saturated and the remaining platelets provide some functional activity.

The PATCH trial demonstrated, however, that platelet transfusion led to significantly worse outcomes [2]. While there is no readily available reversal agent for DAPT, platelet transfusion should be avoided. In fact, observational data suggest that patients on single antiplatelet therapy don’t fare worse and may not need reversal like those with DAPT [3].

Conclusions

Warfarin reversal

  • IV vitamin K + PCC (or FFP)

Dabigatran reversal

  • Specific agent: Idarucizumab
  • Non-specific agent: PCC

Factor Xa inhibitor reversal

  • Specific agent: Andexanet
  • Non-specific agent: PCC

Antiplatelet reversal

  • No available agent
  • Transfusion of platelets associated with worse outcomes.

Interested in more ACEP-EQUAL podcasts?

Listen to the other ACEP E-QUAL podcasts on our Soundcloud account.

References

  1. Steiner T, Poli S, Griebe M, et al. Fresh frozen plasma versus prothrombin complex concentrate in patients with intracranial haemorrhage related to vitamin K antagonists (INCH): a randomised trial. Lancet Neurol. 2016;15(6):566-573. [PMID: 27302126]
  2. Baharoglu MI, Cordonnier C, Al-Shahi Salman R, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial. Lancet. 2016;387(10038):2605-2613. [PMID:27178479]
  3. Khan NI, Siddiqui FM, Goldstein JN, et al. Association Between Previous Use of Antiplatelet Therapy and Intracerebral Hemorrhage Outcomes. Stroke. 2017;48(7):1810-1817. [PMID:28596454]
By |2020-10-09T09:33:43-07:00Oct 16, 2020|Academic, Emergency Medicine, Neurology|

SplintER Series: A Collision at the Plate

Proximal avulsion fracture

A 17-year-old male baseball catcher presents with right knee pain after an opponent slid into home plate, striking the anteromedial aspect of the patient’s knee while it was in extension trying to block the plate. An x-ray of the tibia and fibula was obtained (courtesy of Dr. Haytham Bedier, Radiopaedia.org).

This is a proximal avulsion fracture of the styloid process of the fibula, indicating injury to the posterolateral corner (PLC) of the knee [1].

  • Pearl: In most cases, the avulsed fragment is attached to the lateral collateral ligament and/or the biceps femoris [2].

This injury usually occurs from varus stress in a hyperextended knee- think a blow to the anteromedial tibia with the knee in extension [2].

The arcuate sign is a horizontal linear lucency through the head of the fibula that represents a fracture of the styloid process [3].

  • Pearl: This injury may be confused with a Segond fracture, which is a small avulsion fracture fragment from the lateral tibial plateau associated with anterior cruciate ligament injury.

A proximal fibular avulsion fracture is commonly associated with injury to the posterior cruciate ligament, anterior cruciate ligament, popliteus, or meniscus. It is frequently seen with bone contusions and sometimes a tibial plateau fracture [2].

  • Pearl: Injury to the common peroneal nerve may occur as well. Remember to perform a thorough neurovascular examination [1].
  • Pearl: This fracture is a sign of posterolateral instability and likely internal derangement of the knee. Outpatient MRI can be used to evaluate the soft tissue components of the injury and diagnose associated injuries [2].

This injury indicates potential significant instability of the knee and requires outpatient follow-up with MRI. Operative management will be dictated on an individual basis, after evaluating MRI results. In the emergency department, place the patient in a knee immobilizer and recommend non-weight-bearing status until further imaging. Follow-up with orthopedics or sports medicine within 1 week.

  • Pearl: As always, perform a thorough neurovascular examination and consult orthopedics immediately if there is evidence of compromise. If your exam demonstrates significant instability and you are concerned about a spontaneously-reduced knee dislocation, consider ankle-brachial indices and/or further vessel imaging.

If diagnosis of this injury is delayed, posterolateral instability may develop. If not recognized and managed appropriately, this may hinder the success of a cruciate ligament reconstruction [1].

 

References and Resources:

Want more information about the knee exam? Check out the SplintER archives.

  1. Shon OJ, Park JW, Kim BJ. Current concepts of posterolateral corner injuries of the knee. Knee Surg Relat Res. 2017;29(4):256-268. PMID: 29172386
  2. Juhng SK, Lee JK, Choi SS, Yoon KH, Roh BS, Won JJ. MR evaluation of the “arcuate” sign of posterolateral knee instability. Am J Roentgenol. 2002;178(3):583-588. PMID: 11856678
  3. Strub WM. The arcuate sign. Radiology. 2007; 244(2):620-621. PMID: 17641383

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