A True Orthopedic and Vascular Emergency

Case: A 76-year-old male presents after falling down a long flight of stairs. On exam the patient has multiple obvious external injuries, including a grossly deformed right shoulder with a large overlying hematoma. His chest x-ray and shoulder x-ray demonstrate a superiorly and laterally displaced right scapula, as well as a comminuted right scapular fracture and clavicle fracture. On further CT imaging, the patient has subtle widening of the scapulothoracic articulation.

OneQuestion: What potentially devastating injury should be considered in this patient?

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CITW 12: The Extra Weight

Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!

HPI: 27 year old male presents to the ED with left chest wall pain. He states he was bench pressing at the gym when he felt a “sudden twinge of pain and popping sensation” in his left upper arm and shoulder. He was unable to lift weights following this injury without experiencing excruciating pain. He subsequently noticed swelling and bruising on his left upper arm. He denies any other injuries, numbness, or weakness.

VS: HR 54, BP 112/64, RR 11, SpO2 100%, T 98.7

PE: Patient is noted to have weakness of the left arm with internal rotation and shoulder adduction. No other deficits appreciated. Neurovascularly intact.


What’s the diagnosis?

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Coming Down the Pike: Zika Virus

From the Pan American Health Organization Zika virus website: http://www.paho.org/zikavirus

What is Zika Virus?
A single-stranded RNA virus of the Flavivirdae family, genus Flavivirus. The virus was first identified in 1947 in a rhesus monkey in the Zika Forest, Uganda.

What are the signs and symptoms?
Only about 1 in 4 people infected with Zika develop signs or symptoms, which include fever, maculopapular rash, arthralgias and conjunctivitis. Additionally, Zika causes headaches, myalgias, retro-orbital pain and vomiting.

How is it transmitted?
Zika Virus is primarily transmitted through the Aedes mosquito, which also transmits Dengue and Chikungunya. Transmission is also believed to take place vertically between mother and child, and through sexual contact.

Where has it been found?
As of the January 9, 2016, the following Pan American countries have seen confirmed cases of Zika virus: Brazil, Chile, Colombia, El Salvador, French Guiana, Guatemala, Honduras, Martinique, Mexico, Panama, Puerto Rico, Paraguay, Suriname, and Venezuela. 

Countries with confirmed Zika virus outside of the Americas include: Central African Republic, Egypt, French Polynesia, Gabon, India, Indonesia, Malaysia, Nigeria, The Philippines, Sierra Leone, Tanzania, Thailand, Uganda, and Vietnam

Why is it in the news?
Zika virus made national headlines in the United States in late December 2015 when Brazillian health officials advised would-be parents to delay pregnancy over concerns that Zika virus is contributing to a spike in microcephaly. The Brazil Ministry of Health reports a twenty-fold increase in the incidence of microcephaly over the past year in areas that have had confirmed Zika virus transmission (2,782 cases in 2015 versus 147 cases in 2014). The connection was made in November 2015 when Brazilian health officials found traces of Zika virus in a deceased newborn born with microcephaly.
From the Pan American Health Organization Zika virus website, Epidemiological Alert, December 1, 2015

Additionally, Brazil has reported an increase in neurological syndromes in patients infected with Zika virus, most notably Guillain-Barré syndrome.

What is the treatment?
Supportive care: rest, fluids, antipyretics, and analgesics. Hold aspirin or NSAIDs until Dengue has been ruled out to reduce the risk of hemorrhage.

Pan American Health Organization Zika virus website: http://www.paho.org/zikavirus

Brazil warns against pregnancy due to spreading virus, CNN, December 23, 2015

Foy BD, Kobylinski KC, Foy JLC, Blitvich BJ, Travassos da Rosa A, Haddow AD, et al. Probable non–vector-borne transmission of Zika virus, Colorado, USA. Emerg Infect Dis. 2011 May; http://www.ncbi.nlm.nih.gov/pubmed/21529401

Pan American Health Organization Epidemiological Alert: Neurological syndrome, congenital malformations, and Zika virus infection. Implications for public health in the Americas; December 1, 2015. PDF Direct Link

A new mosquito-borne threat to pregnancy women in Brazil, The Lancet, published online December 23, 2015. http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(15)00548-4/abstract

Hit Them Hard: The Use of H1 and H2 Antagonists for Acute Allergic Symptoms

This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles.

This blog post reviews the article by Lin, R. Curry, A. Pesola, G. et al. “Improved Outcomes in Patients With Acute Allergic Syndromes Who Are Treated With Combined H1 and H2 Antagonists.” Annals of Emergency Medicine, November 2000; 36(5):462-8.

Main Points:

  1. In this randomized, double blinded, placebo controlled trial of 91 patients presenting with acute allergic symptoms fewer patients in the active arm (ranitidine + diphenhydramine) had signs of cutaneous involvement such as urticaria at 2 hours compared to the placebo group (placebo + diphenhydramine).
  1. There was no significant difference, however, between the placebo group and active group with regards to the absence of erythema or angioedema at two hours.


Many patients present to the emergency department with acute allergic syndromes. Anti-histamines, primarily diphenhydramine, are the mainstay therapy in most mild cases and are both safe and cost effective. The addition of H2 antagonists such as ranitidine to diphenhydramine may help improve clinical outcomes and expedite management in the emergency department. The primary goals of this study were to look for resolution of urticaria and angioedema at two hours from presentation. This study was well balanced in its patient recruitment and overall provides insight into real-world application of a second agent for management of allergic symptoms.


The methodology within this study was rigorous, though the sample size was small. This trial was a randomized, double blinded, placebo controlled trial that enrolled 91 patients at an academic emergency department in New York, NY. Enrollment was based on a convenience sampling associated with the study physicians’ scheduling. Patients were enrolled in this study if they were adults who presented with acute urticaria, acute angioedema, acute unexplained stridor or acute pruritic rash following an exposure to a food, drug or contact with latex. Patients underwent vital sign monitoring, examination for physical findings such as: presence and extent of urticaria and erythema, presence of angioedema, wheezing, stridor, abdominal distention or tenderness, as well as symptom scoring. This data collection occurred at presentation, at 1 hour and 2 hours.

This study demonstrated a statistically significant difference, p=0.03, in the resolution of urticaria in the active group compared to the placebo group at two hours. One significant limitation in this study is that the treating physician was able to administer supplemental medications such as epinephrine, corticosteroids, bronchodilators and additional doses of antihistamine at their discretion with significantly more participants in the ranitidine arm receiving epinephrine, 17, compared to 9 in the placebo arm. The placebo arm had more use of additional antihistamine, 10, compared to 2 in the ranitidine arm. These additional therapies are documented in table 3; however, it is unclear if the severity of illness was equal between the two groups. The authors do note in their discussion that there was no observed covariate effect for epinephrine administration with respect to urticaria resolution.

Level of Evidence:

This study was graded a level I based on the ACEP Clinical Policy Grading Scheme


Within the sample groups there was significant history of asthma as well as other nonasthmatic atopic conditions which supports the theory that certain individuals are genetically predisposed to allergic syndromes.

Source Articles:

Lin, R. Curry, A. Pesola, G. et al. “Improved Outcomes in Patients With Acute Allergic Syndromes Who Are Treated With Combined H1 and H2 Antagonists.” Annals of Emergency Medicine, November 2000; 36(5):462-8.

Faculty Reviewer: Dr. Siket

52 Articles: Lysis vs Transfer for PCI (NEJM 2003)

ST segments:
a lytic in my hand,
or transfer?

-Unknown, 2015

This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles.


Andersen et al., NEJM 2003.  A Comparison of Coronary Angioplasty with Fibrinolytic Therapy in Acute Myocardial Infarction.

Main Points:

  1. This prospective randomly-controlled trial investigated whether patients with STEMIs who presented to community hospitals would benefit from transport to specialized centers for percutaneous coronary intervention (PCI) rather than remaining at the local hospital for fibrinolysis. The authors demonstrated an almost 5% reduction in reinfarction rate at 30 days between the two groups.
  1.  STEMI patients that presented to community centers and received aspirin+metoprolol+heparin+PCI within 2 hours, including transfer time, had statistically significantly fewer reinfarctions at 30 days than the STEMI patients who remained at the initial facility andon alteplase+aspirin+metoprolol+heparin.  Ultimately, PCI was shown to be superior to fibrinolytic if available in a timely fashion.


It is now an established tenet that timely PCI in an experienced center by experienced interventionalists is the best treatment for STEMI.  Historically, with no PCI available at the presenting facility, STEMI patients received anticoagulation and fibrinolytics.  But there were obvious and dangerous concerns in applying a “PCI-or-bust” policy universally, as there are only so many PCI centers to drive patients to, and “time is myocardium.”  So the best treatment for the patient with a STEMI in the middle of the proverbial forest was unknown.  Lyse or transfer?  This study made significant progress towards helping us answer this question.


1572 patients were enrolled, 1129 from 24 referral hospitals and 443 from 5 PCI centers.  All of these patients were randomly assigned to receive lysis & anticoagulation (LA) or anticoagulation & PCI (APCI), with the patients from the referral hospitals therefore being transferred for their PCI.  And yes, patients who presented to PCI centers and were assigned LA therefore did not receive PCI.  Risk characteristics of all the patients were similar.  LA patients received 300mg aspirin PO, 20mg metoprolol IV, an “accelerated” alteplase treatment (15mg bolus + 0.75mg/kg over 30min + 0.5mg/kg over the next 60min), and unfractionated heparin for 48h (5000U bolus + infusion titrated to aPTT 70-90sec).  APCI patients received 300mg aspirin IV, 20mg metoprolol IV, unfractionated heparin (10,000U bolus + infusion during procedure to activated clotting time 350-450s).  In patients receiving PCI, GPIIb/IIIa blockers were given at discretion of proceduralist, arteries were treated only if stenosed >30% or if TIMI “flow grade” was <3, non-infarct-related arteries were NOT intervened on, and all patient received Ticlodipine (500mg) or Clopidogrel (75mg) for 1 month afterwards.  The primary endpoint was a composite of death from any cause, clinical reinfarction, or disabling stroke at 30 days follow up.


  • For patients presenting to PCI centers, there was a 45% reduction in composite outcome with PCI, from 12.3% in the LA group to 6.7% in the APCI group (P = 0.05).
  • For patients presenting to referral hospitals, there was a 40% reduction in the composite outcome with PCI, from 14.2% in the LA group to 8.5% in the APCI group (P = 0.002)
  • Driving the difference within the composite outcome was clinical reinfarction: 1.6% in all APCI vs 6.3% in all LA (P =  0.001).  Differences in death and stroke rates at 30 days were not statistically significantly different between all APCI and all LA patients, whether they were transferred to a PCI center or were already there.
  • The median distance from referral site to PCI center was 50 km
  • Transfer was highly protocolized, with emphasis on shaving-off every precious second of ischemic time.  This cooperation and efficiency resulted in 96% of referral patients landing on the nearest participating PCI table in 2 hours or less.
  • The study was stopped after the 1129 patients, when the third interim analysis showed referral APCIs were reinfarcting less than the referral LAs; this was built into the design as a study cutoff as it implies that APCI is better in both settings.


  • The bottom line is the balance between the proven benefits of PCI and the ischemic time on the myocardium.  There are many variables at play in the “lyse vs transfer (vs both)” decision (see below). These variables include: location and severity of the ischemia, comorbidities and stability of the patient, EMS capabilities, distance, receiving PCI center experience, available medications, etc.  The decision may not always be clear, every patient is probably different, and there is an overwhelming amount of research on this topic.  Do your best.
  • Implementing the airtight transfer logistics they executed here is an obstacle, science aside.
  • In hindsight, your heart has to go out (no pun intended) to the 12.3% of LA patients who presented to a PCI center, got heparin & alteplase, and had a poor outcome.  Their willingness to participate has certainly saved lives.
  • Did you notice that the referred APCI patients did not receive fibrinolysis, only asa, metoprolol, and UFH?  The older research on immediate PCI after fibrinolysis showed no benefit and increased adverse effects.  New and ongoing research on “facilitated PCI,” or PCI after fibrinolysis, using ever-advancing interventional equipment and techniques, may be changing this for some high risk patients for whom PCI is not available within 90 minutes.  For further reading, see these:

Herrmann HC, et al.  Benefit of facilitated percutaneous coronary intervention in high-risk ST-segment elevation myocardial infarction patients presenting to nonpercutaneous coronary intervention hospitals.  JACC Cardiovac Interv.  2009 Oct;2(10):917-24.

Ellis SG, et al.  Facilitated PCI in patients with ST-elevation myocardial infarction.  N Engl J Med. 2008 Maay 22;358(21):2205-17.

Ellis SG, et al. Facilitated percutaneous coronary intervention versus primary percutaneous coronary intervention: design and rationale of the Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events (FINESSE) trial. Am Heart J. 2004; 147: E16.

Level of Evidence:

Based on the ACEP grading system for therapeutic questions this study was graded level I.


The study inclusion criteria was defined as the symptoms for greater than 30 minutes, but less than 12 hours with associated cumulative ST-segment elevation of at least 4mm in at least two contiguous leads.

Resident Reviewer: Dr. Kazakin
Faculty Reviewer: Dr. Siket

EUS: Pyloric Stenosis, Early Pregnancy, Serratus Plane block

brownsound 2
Brown Ultrasound Tape Review – 11:19:15
At this week’s BUTR, we again reviewed some great ultrasound images that were scanned over the past week.
Resident reviewer: Dr. Mike Hunihan
Faculty reviewers: Drs. Erika Constantine and Otto Liebmann
When to suspect pyloric stenosis:
– Onset between 3-5 weeks old, but can occur up to 12 weeks old.
– More commonly affects males.
– Risk factors include family history of pyloric stenosis, maternal smoking, macrolide antibiotics administered to infant, and bottle-feeding.
– Classic presentation is “hungry vomiter”; postprandial forceful non-bilious vomiting.
How to diagnose: 
– “Olive-shaped” mass that can be palpated along the R rectus sheath is pathognomonic, but rarely found.
– Ultrasound is the gold standard test when done by an experienced ultrasonographer.
– Additional studies, when ultrasound and exam are nondiagnostic, include barium swallow and upper endoscopy.
Ultrasound diagnostic criteria: 
Pyloric Muscle Thickness = >3mm
Pyloric Muscle Length = >14mm
Helpful mnemonic to remember this: Pi =3.14 (PYloric stenosis, >3mm thick, >14mm long)
Screen Shot 2015-11-30 at 12.26.58 PM Screen Shot 2015-11-30 at 12.27.12 PM
Abnormal findings: (Upper) Channel length (Lower) Muscle wall thickness
Another component of the US exam is to watch for passage of gastric contents through the pylorus. If you visualize passage of gastric contents, this is reassuring that there is no pyloric stenosis. However, sometimes you can get passage of small volumes of liquid through a tight pylorus and still have pyloric stenosis – it’s called the string sign with barium studies.
The other pertinent signs of pyloric stenosis:
1. Antral Nipple Sign: Redundant pyloric mucosa that protrudes into gastric antrum resembling a nipple.
2. Target Sign: Hypertrophied hypoechoic muscle surrounding echogenic mucosa layer, visualized in short axis.
target sign
3. Cervix Sign: Indentation of the pylorus into the fluid filled antrum. image (1)
In 2013, there was a prospective observational trial of PEM fellows performing bedside US for diagnosis of pyloric stenosis. They had a convenience sample of patients who were suspected to have pyloric stenosis based on history and physical exam, and who were ordered to have a formal ultrasound in the radiology department. The PEM fellows also performed bedside ultrasound on those same patients and compared their results to the radiology results. They enrolled 67 patients into their study, of which, 10 patients (15%) were found to have pyloric stenosis. The results of their study showed a 100% sensitivity and 100% specificity for PEM fellows performing bedside ultrasound. They had zero false positives or false negatives. This study suggests that bedside ultrasound for evaluation of pyloric stenosis is feasible for our residents, fellows, and attendings in the ED.
Sivitz, Adam B., Cena Tejani, and Stephanie G. Cohen. “Evaluation of hypertrophic pyloric stenosis by pediatric emergency physician sonography.”Academic Emergency Medicine 20.7 (2013): 646-651.

We also discussed the use of ultrasound in early pregnancy patients. From the ED perspective, our main question should be: IUP or no IUP?  If we cannot visualize a definitive IUP (gestational sac + yolk sac) then we need to be concerned about ectopic pregnancy.
But what about heterotopic pregnancy?
-A heterotopic pregnancy is the presence of both an IUP AND an ectopic pregnancy at the same time!
– In females who become pregnant by natural means, the chance is 1 in 10,000.
– In females who have assisted reproduction (IVF or even just hormone therapy) that chance increases to 1 in 1,000.

Moral of the story: When performing ultrasound in early pregnancy be sure to take a good history of any assisted reproduction techniques used for that pregnancy 
In addition to determining the location of an early pregnancy, we discussed the diagnostic criteria for non-viable IUP. A helpful review article in NEJM by Doubilet et al reviews the topic at length. 
Important measurements on US that are diagnostic for nonviable pregnancy: 
CRL >7mm with no heartbeat 
GS diameter >25mm with no embryo 
image (2)
Doubilet, Peter M., et al. “Diagnostic criteria for nonviable pregnancy early in the first trimester.” New England Journal of Medicine 369.15 (2013): 1443-1451.

Finally, we discussed a novel serratus plane nerve block that could be useful for anesthesia for axillary abscesses, rib fractures, or even chest tube placement. The aim is to block the thoracic intercostal nerves and provide anesthesia to the lateral hemithorax. The images below show the two options for serratus nerve plane block; injecting superior or inferior to the serratus anterior.
image (3)
 image (4)
Although this study gave the initial description of a serratus nerve plane block, there is still further studies to be performed. Something to keep an eye out for!
Blanco, R., et al. “Serratus plane block: a novel ultrasound‐guided thoracic wall nerve block.” Anaesthesia 68.11 (2013): 1107-1113.

CITW 10: The Persistent Rash

Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!

HPI: A 63 year old male with a history of hypertension and hemorrhagic CVA presented to the ED with 3 months of worsening rash. Per the patient, it is pruritic, painful, and started gradually on his upper extremities, and progressed to his lower extremities. He denies any oral or mucosal lesions. Prior to this, the patient has never experienced a similar rash. The patient initially saw his PCP who prescribed Keflex, which did not have an effect. The patient was then referred to a dermatologist who prescribed Dapsone and a “steroid cream” which he states he’s been compliant with despite the lack of relief. Of note, he states the rash appeared around the same time he started taking Enalapril. He denies fevers, chills, trauma, sick contacts, recent travel, shortness of breath, chest pain, abdominal pain, nausea, vomiting, diarrhea, dysuria, or any other infectious signs or symptoms. He has no known allergies to medications.

FH/SH: Non-contributory

VS: BP 147/72 HR 84 RR 13 T 98.9 O2 99% on RA

Notable PE: The skin examination; see below:


Arm 2


What’s the diagnosis?

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ACEP ’15 Pearls

Here are twelve pearls that the 4th years learned at ACEP!

  1. You can calculate shock index (SI) to help determine mortality
  • SI= heart rate/ systolic bp
  • 0.5-0.7 normal
  • > 0.9 increased mortality
  1. Giving Bactrim to someone on ace inhibitor is a no-no due to risk of hyperkalemia
  1. AMA risk is all about the documentation. The actual disposition label and the patient’s signature do not mean much. Document on how you explained, how well the patient understood, the patient’s decision making capacity, and that you encouraged them to return.
  1.  RVU pearls: In order to get full RVU for reviewing an EKG, you need to chart 4 elements in your EKG interpretation.  Also, charting an abscess as “complex and loculated” gets you way higher RVUs.
  1. You can make a high flow nasal oxygen setup without respiratory therapy.  Attach a nasal trumpet to suction tubing using the adapter you usually use between tubing and an NG tube. Hook that to the wall oxygen and turn all the way up.
  1. You can’t use adenosine to differentiate between VT and SVT — at least 10% of VT will be adenosine responsive. Thank you Amal Mattu.
  1. Evaluating an HIV patient with no recent CD4 count? The absolute lymphocyte count (total WBC x lymphocyte percentage) can act as a surrogate. If <1000, 91% predictive of CD4<200; if >2000, 95% predictive of CD4>200
  1. Thromboelastography (TEG) may be an alternate way to test coagulation in patients, particularly those on anti-platelet agents. It may also help to determine which blood product should be given most emergently: plasma vs. plts vs. factor vs. PRBC. Not sure we have this at RIH, but it may be available at your next shop. I am sure it has limitations and etc., but at least you now know it exists.
  1. Arrhythmogenic Right Ventricular Dysplasia (ARVD) is more common than once thought. Don’t forget to look for that epsilon wave in the EKG of your syncope patients which is a small positive deflection buried at the end of the QRS. You may save that (usually young) person’s life.
  1.  Bismuth subsalicylate (Pepto Bismol) can reduce the incidence of traveler’s diarrhea up to 60%.  And it may have antimicrobial effects against C. difficile.
  1. In blunt pediatric trauma:  Neg FAST + normal lipase, and ALT and AST <100 = no need for CT Abd and Pelvis, just observation. (SE 88%, SP 98%; PPV 94%, NPV 96%, accuracy 96%).   Side note : AST alone has a negative predictive value of 71%, Lipase alone has positive predictive value 75%
  1. Pulmonary embolism is responsible for 50% of deaths after bariatric surgery.

What did you learn at #ACEP15??
Post on the comments below!

Faculty reviewer: Dr. Gita Pensa


Winter is coming… Think CO toxicity!

Much has been written on the topic of Carbon Monoxide Toxicity. I will not reiterate that CO is a colorless, tasteless, odorless gas, nor will I restate that it is among the top killers of toxins worldwide. I may tell you, however, that whenever a carbon based material undergoes incomplete combustion, CO is generated. Another tidbit commonly discussed in this context is that dichloromethane (CH2Cl2) ingestion will lead to high serum CO concentrations from metabolic conversion in the liver. There have been countless laboratory, animal and human studies which elucidate aspects of the multifactorial pathophysiology of CO toxicity which show effects from displacement of oxygen, causing hypoxic injury, binding to cytochrome, myoglobin and other proteins causing disruption in cellular respiration or function, lipid peroxidation and inflammatory effects with oxygen free radical generation, etc. most commonly manifesting in neurological, neuropsychiatric and cardiac dysfunction1. I am going to cut to the chase, as this is a blog and not a stuffy scientific manuscript, and discuss the presentation, diagnosis, treatment and outcome of patients with CO exposure and toxicity. Be warned, there is much controversy, a lot of data- some of which is contradictory- and even more anecdotal case studies. There are also medical-legal overtones and regional differences in preferred treatment modalities.

CO 1
Figure 1: Electron Transport Chain and the Effect of CO. https://www.boundless.com/biology/textbooks/boundless-biology-textbook/cellular-respiration-7/oxidative-phosphorylation-76/chemiosmosis-and-oxidative-phosphorylation-363-11589/

Case: 54 yo woman presenting with headache, nausea and blurred vision for 7-10 days. She stated that her contractor hired to re-work a botched job on her boiler advised her to go the emergency department because the CO level in her house was “sky-high”. After seeing another physician and hours after leaving her house, she presented to the emergency department. The boiler was faulty for about 2 weeks. Her examination was normal. Her labs and ECG were normal. Her COHgb concentration was 4.

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Knee Dislocations: High risk, can’t miss!

By: Dr. Maddie Boyle


A 19-year-old male presents with left knee pain. He injured his knee yesterday while wrestling with friends and was seen in a local ED where his knee was reduced. He was discharged in a knee immobilizer and now returns with complaints of increasing pain and recurrent deformity after removing the immobilizer to shower.


Imaging demonstrates lateral tibiofemoral subluxation. He has a normal neurovascular exam, including strong distal pulses. Orthopedics is consulted and performs closed reduction of his knee. His ABI is subsequently measured at 0.92, and the knee is immobilized in 20° of flexion.


Image 1

Image 2


What would you do next?

(a) Call an emergency Vascular Surgery consult
(b) Admit for serial physical exams and ABI measurements
(c) Obtain a CTA of the lower extremity
(d) Discharge home in a knee immobilizer with outpatient Orthopedic follow-up
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