An Overlooked Cause of Hip Pain


A 28-year-old male presents to the Emergency Department with acute-on-chronic hip pain.  His past medical history includes sickle cell disease and poorly controlled asthma for which he takes daily prednisone. He has been ambulating with a cane for one year due to his hip pain. He immigrated one week ago from Puerto Rico and reports worsening hip pain since arriving.  He denies fevers, chills, weakness, or numbness.  No tobacco, alcohol, or drug use.  His radiographs are shown below.  Can you make the diagnosis? Click the answer box below. 

Figure 1. AP pelvis

Figure 1. AP pelvis

Figure 2: Lateral view of left hip 

Figure 2: Lateral view of left hip 

Figure 3: Lateral view of right hip

Figure 3: Lateral view of right hip

Avascular necrosis (AVN) of the bilateral femoral heads

This patient’s AVN is more advanced on the right hip compared to the left, with demonstrated right-sided cortical collapse, subchondral cyst formation, and remodeling of the femoral head and acetabulum. The left hip displays increased density and sclerosis. 

Definition and Epidemiology:

Avascular necrosis (AVN) of the femoral head refers to a decrease in blood flow to the femoral head that ultimately leads to cell death, fracture, and collapse of the articular surface.  The demographics of the disease vary based on the underlying cause of AVN. Across all causes, the average age at presentation ranges from 35-45 years, and males are affected up to three times more commonly than females (Kaushik, Das, & Cui, 2012).  

Pathophysiology and Risk Factors:

The exact underlying pathophysiology of AVN is controversial, but numerous traumatic and atraumatic causes have been identified that lead to interruption of the vascular supply to the femoral head and/or direct death of osteophytes and bone marrow. Risk factors for 75-90% of cases include hip trauma (injury to medial femoral circumflex artery), chronic steroid use, and alcoholism (Mont & Hungerford, 1995). Other risk factors include gout, sickle cell disease, Legg-Calve-Perthes disease, Caisson disease (aka “the bends”), myeloproliferative disorders, hypercoagulable states, hyperlipidemia, pregnancy, and smoking (Moya-Angeler, Gianakos, Villa, Ni, & Lane, 2015).   

Making the Diagnosis:

Typically, patients present with insidious onset of pain, pain with climbing stairs, and anterior hip pain. On physical exam, presentation may range from painless range of motion to severe hip pain with internal rotation. Plain radiographs are the first-line imaging modality of choice. MRI should be obtained when radiographs are negative but clinical suspicion for AVN remains high (Table 1). Multiple staging systems have been created to characterize the breadth of this disease. The modified Ficat Classification system is the most widely utilized, but it was invented prior to the advent of MRI and relies solely on x-ray imaging (Table 2) (Mont, et al., 2006). 

Table 1. Imaging studies for AVN of the femoral head (

Table 1. Imaging studies for AVN of the femoral head (

Table 2. Modified Ficat Staging System (Ficat, 1985)

Table 2. Modified Ficat Staging System (Ficat, 1985)

Why early diagnosis matters!

AVN ultimately leads to collapse of the femoral head and severe osteoarthritis requiring total hip arthroplasty. Early diagnosis allows for surgical procedures (core decompression, bone grafting) that preserve the femoral head and may delay the need for total arthroplasty. This is especially important for the young adults most affected by this disease who are likely to outlive their joint prosthesis and require revision at a later age. AVN is often multifocal, and clinical signs and symptoms are quite subtle in the early stages. Therefore, diagnosis of atraumatic AVN at one site should prompt evaluation of other high-risk sites, or a search underlying risk factors. In particular, greater than 80% of non-traumatic AVN in the femoral head is bilateral, so imaging of the full pelvis and contralateral hip should be obtained (Hauzeur, Pasteels, & Orloff, 1987). 


For Ficat stages 0-II, bisphosphonates are used to prevent femoral head collapse. Alendronate has been shown to reduce pain, improve articular function, and slow collapse progression in adults with AVN in some trials, but other studies have shown no benefit (Luo, Lin, Zhong, Yan, & Wang, 2014). In these early stages, operative interventions such as core decompression and/or bone grafting are available to stimulate angiogenesis and promote healing.  For post-collapse stages (Ficat III-IV), operative interventions are required and include total hip replacement, hip resurfacing, or arthrodesis.

Case Resolution:

This patient was diagnosed with bilateral AVN at Ficat stage IV in his right hip and Ficat stage II in his left hip. His sickle cell disease and use of chronic oral steroids increased his risk for this condition. Ultimately, his hip pain did not require acute intervention or hospital admission, so he was referred to the orthopedic outpatient clinic for follow up and will require operative intervention.


  • Consider AVN in the differential diagnosis when patients present with insidious onset of pain, pain with climbing stairs, and/or anterior hip pain
  • Plain films are first-line imaging, but MRI (not CT) is gold standard for diagnosis
  • Early diagnosis may allow for surgical interventions that delay the need for total hip arthroplasty

    Faculty Reviewer: Dr. Jeff Feden


Ficat, R. (1985). Idiopathic Bone Necrosis of the Femoral Head. Early Diagnosis and Treatment. J Bone Joint Surg Br, 3-9.

Hauzeur, J., Pasteels, J., & Orloff, S. (1987). Bilateral non-traumatic aseptic osteonecrosis in the femoral head. An experimental study of incidence. J Bone Joint Surg Am, 1221-5.

Kaushik, A., Das, A., & Cui, Q. (2012). Osteonecrosis of the femoral head: An update in year 2012. World J Orthop, 49-57.

Luo, R.-b., Lin, T., Zhong, H.-M., Yan, S.-G., & Wang, J.-A. (2014). Evidence for Using Alendronate to Treat Adult Avascular Necrosis of the Femoral Head: A Systematic Review. Med Sci Monit, 2439-2447.

Mont, M., & Hungerford, D. (1995). Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am, 459.

Mont, M., Marulanda, G., Jones, L., Saleh, K., Gordon, N., Hungerford, D., & Steinberg, M. (2006). Systematic analysis of classification systems for osteonecrosis of the femoral head. J Bone Joint Surg Am, 16-26.

Moya-Angeler, J., Gianakos, A., Villa, J., Ni, A., & Lane, J. (2015). Current concepts on osteonecrosis of the femoral head. World J Orthop, 590-601.

Super Glued Shut


3-year-old boy presents with super glue in his right eye. He was being watched by his aunt who left the room for 20 min and came back to find him playing with a tube of super glue. He had gotten some on his left cheek, left eyelashes and in his right eye. They had flushed with water at home and were able to get his left eyelid open. On arrival, he is inconsolable in mom’s arms.

Image 1: Super glued eye. Source:

Image 1: Super glued eye. Source:

Recommendations from the Super Glue Corporation:

Should Super Glue bond to any body part where acetone should not be applied, such as the lips or eyes, the following steps will help you get out of any sticky situation!


Immerse bonded areas in warm, soapy water. Peel or roll skin apart; a spatula or teaspoon handle or even a pencil will help. Remove cured adhesive with warm, soapy water (may take several applications). Fingernail polish remover with an acetone base has also been successful for removal of cured adhesive from skin.


If lips are accidentally stuck together, apply a generous amount of warm water and encourage maximum wetting and pressure from saliva from inside the mouth. Peel or roll (do not pull) lips apart. It is almost impossible to swallow the adhesive as a liquid. The adhesive solidifies upon contact with saliva (moisture) and could adhere to the inside of the mouth. Saliva will lift the adhesive in 1-2 days, avoid swallowing the adhesive after detachment.


In the event that eyelids are stuck together or bonded to the eyeball, wash thoroughly with warm water and apply a gauze patch. The eye will open without further action within 1-4 days. To our knowledge there has never been a documented case of adhesive in the eye causing permanent damage. Do not try to force eyes open.


The adhesive will attach itself to the eye protein and will disassociate from it over time, usually within several hours. Periods of weeping and double vision may be experienced until clearance is achieved. Use of water to wash eyes repeatedly may assist in aiding more rapid removal of the adhesive.


ED Management:

In the ED, with a screaming child and nervous parents, you may elect to try and remove the glue rather than patch the eye and send them home.  Article by Danish authors recommends surgical eyelid opening if necessary (specifically for bilateral glued shut), but if easily done in the ED, it makes sense to try and remove the glue and open the eyes.

The Procedure:

1. Calm the patient. Child life Specialists, IN versed, conscious sedation if necessary

2. Gather your supplies

Image 2: The supplies

Image 2: The supplies

a. Erythromycin ointment (lubricates and loosens the glue)

b. Soft cotton swab

c. 4x4s

d. Paperclips for eyelid holders

e. Tetracaine drops

f. Fluorescein drops and wood’s lamp

3. Numb the eye with Tetracaine drops, put a ribbon of erythromycin on the eyelid

4. Trim the lashes if necessary to open the lid, do not pull the lids apart if they are glued shut

5. Use cotton swab to gently wipe away chunks of glue on the cornea/sclera (it should be mobile and not adherent to the surface of the eye), if adherent to the surface of the eye, do not force it off or your will scratch the cornea

6. Rinse the eyes with saline or water, Morgan lens if cooperative patient

7. Do a thorough woods lamp exam after fluorescein administration

8. Call ophthalmology if you have any complications, adherent glue to the eye surface or shut lids

After ED Care:

1. Erythromycin ointment x 3 days

2. Ophthalmology follow-up

3. Patch if eyelids remain glued shut or glue still adherent to cornea/sclera

Faculty Reviewer: Dr. Chris Merritt

Further Resources on the Topic:

Reddy SC. Superglue injuries of the eye. International Journal of Ophthalmology. 2012;5(5):634-637. doi:10.3980/j.issn.2222-3959.2012.05.18.

Asynchrony PEM: Topics in Pediatric Neurology

This week in our Neurology etc. block, we're going to focus on a few important pediatric neurology topics: febrile seizures, headache, head injury, and stroke (gah!). The first three, you'll see all the time. The last -- hopefully you'll never see, but if you do, you've got to recognize it.

By the end, you should know (among other things):

  • Do all kids with complex febrile seizure need an LP? 
  • Should pediatric stroke patients receive tPA? (double gaah!!) 
  • Which headaches are concerning, and which just need a dose of acetaminophen and a kiss from Boo-Boo Bunny? 
  • Knocked on the noggin': does 'LOC' equal 'head CT' (and not just because it rhymes)?

Theme song: OneRepublic's "Kids" -- admittedly not neuro-specific, but we got the pediatric part down!
Yeah, perfect disasters
Yeah, we were swinging, swinging from the rafters...

(Yup, we're discussing pediatric head trauma...)

Time to get those synapses firing -- let's go!


a) From EM Cases: Emergency Management of Febrile Seizures  Read the show notes; listen to the podcast if you have time.

b) From Annals of EM, article in press: Do all children who present with a complex febrile seizure need an LP? (pdf in Canvas for Brown readers.) DOI:



From PEM Playbook: Pediatric Headache: Some Relief for All Detailed show notes or 30 minute podcast -- your pick. Clear and thoughtful advice!



Courtesy of Dr. Turcotte-Benedict : a few resources on Pediatric Head Injury/TBI.

a) Here is a podcast on Pediatric Head Injury from EM Cases. This 1 hour podcast reviews pediatric minor and major head injury, the Kupperman PECARN head injury guideline, and the CATCH study. Detailed show notes if you're short on time.

b) More EM Cases: summarizes some of the literature on pediatric minor head trauma.

c) Don't Forget the Bubbles has a quick and to the point review of Traumatic Brain Injury



a) From EMDocs (2015): Pediatric Stroke

b) Interesting quick video from Mayo Clinic's EM Blog (Hat tip to our Mayo EM colleagues). Pecha Kucha format, fast and to-the-point. 

c) Children Don't Have Strokes? Just Ask Jared.  A family's account of the presentation and aftermath of a stroke in a healthy seven-year-old. NY Times, 2010.



ACEP free CME: Pediatric Neurologic Emergencies -- a 45-minute audio lecture.


That's it for this week -- Brown residents, remember to complete the module in Canvas for credit!  See you in two!


Fingertip Amputations: What YOU need to know


A maintenance worker raised her hand blindly into a utility closet to fix a broken light and her hand hit part of a rapidly moving conveyor belt. She immediately pulls her hand back, but it is too late, blood is everywhere and her fingertip is found on the floor. EMS brings the patient along with her amputated fingertip to the emergency department. The patient anxiously inquires if the amputated part can be reattached. Is reattachment an option, and what actions should the physician take to ensure proper care of this traumatic event?

Image 1: Amputated right ring finger

Image 1: Amputated right ring finger

Image 2: Amputated right ring finger with multiple phalanx fractures

Image 2: Amputated right ring finger with multiple phalanx fractures

Fingertip Amputations:

Unfortunately, fingertip injuries are exceedingly common in the emergency department (ED). Fingertip amputation is defined by an injury that occurs distal to the tendon insertions on the distal phalanx. Most will involve some kind of repair in the ED, and many will also require definitive operative care by a hand surgeon. Goals of care include pain reduction, preservation of sensation, and bony support for nail growth.

While some hand surgeons will attempt re-implantation of an amputated fingertip, success rates remain exceedingly low.[i] However, patients should be reassured that they will likely maintain most functionality of their hand.

Injuries involving minor tissue loss (usually less than 1 cm squared) without exposed bone may be allowed to heal by secondary intention. Options for more significant injuries include revision amputation (rongeuring of bone) with primary closure, skin grafting, and flap reconstruction.

Most of these injuries will require a digital nerve block for pain control and repair. Literature describes numerous methods of achieving a sufficient block, but you might consider a wing block to achieve full anesthesia of the distal fingertip. This technique involves injecting just proximal to the nail bed fold medially and laterally. Before performing a digital nerve block, ensure you fully assess the neurovascular status of the digit.  (For more information on the wing block:

Hemostasis can be difficult to achieve with fingertip injuries. A quick and simple solution to hemostasis can be achieved by wrapping a Penrose drain around the finger proximally and securing the drain with a clamp (Image 3).[ii]

Image 3: Utilizing Penrose drain as a tourniquet

Image 3: Utilizing Penrose drain as a tourniquet

In general, most fingertip injuries should be referred for consultation with a hand specialist. The majority of these injuries can be followed up with a hand surgeon in 5-7 days. However, some patients may require evaluation in the emergency department, particularly those with associated infection, tendon injury, or significant bone exposure.[iii]

As always, with any wound, assess tetanus status and administer a tetanus booster if indicated. Antibiotics are not necessary with clean wounds, but they may be considered for contaminated or open/complex wounds.[iv] Patients should also be counseled to avoid tobacco use as it can impair healing.

All fingertip amputations should be evaluated for subungual hematoma and nail bed laceration. For those with subungual hematoma, trephination should be considered if the hematoma is acute (<48 hours) and painful. It should be performed with electrocautery or boring technique with a small gauge needle. It is not recommended to use a heated paper clip given concerns for safety.[v] If the nail bed is intact, it is not necessary to remove the nail after trephination.

For those with nail bed lacerations, the nail should be removed, and the laceration should be meticulously repaired. If the nail remains intact, it can be placed back over the nail bed after repair to act as a splint. If no amputation occurred, the patient should be aware that a new nail will likely grow again, but this may take as long as three to twelve months.[vi]

Case Conclusion:

Our patient’s fingertip was amputated proximal to the nail bed so the bone was further debrided and the wound was closed with sutures. She underwent definitive surgery (for repair of multiple displaced phalanx fractures) approximately two weeks later. Three months after the injury, she then underwent a nail ablation (removal of nail plate and matrix) of her amputated fingertip after her nail began to regrow and cause pain at the site.

Fingertip injuries are traumatic events for patients but when properly managed in the emergency department, patients can enjoy a return of nearly full function of their hand.

Final Pearls:

  • Digital nerve blocks are typically the best method for anesthesia; consider the wing block.
  • Bleeding can often be difficult to control; consider a penrose drain as a fast tourniquet.
  • Always evaluate for subungual hematomas if the injury is acute, painful, and without a path for drainage.

Faculty Reviewer: Dr. Jeff Feden


[i] Butler DP, Murugesan L, Ruston J, Woollard AC, Jemec B. The outcomes of digital tip amputation replacement as a composite graft in a paediatric population. J Hand Surg Eur Vol. 2016 Feb;41(2):164-70.

[ii] Aslan G, Sarifakioğlu N, Bingül F. Simple and effective device for finger tourniquet: a rolled penrose drain. Plast Reconstr Surg. 2003 Apr 15;111(5):1758-9.

[iii] Van beek AL, Kassan MA, Adson MH, Dale V. Management of acute fingernail injuries. Hand Clin. 1990;6(1):23-35.

[iv] Altergott C, Garcia FJ, Nager AL. Pediatric fingertip injuries: do prophylactic antibiotics alter infection rates? Pediatr Emerg Care 2008; 24:148.

[v] Antevy PM, Saladino RA. Management of finger injuries. In: Textbook of Pediatric Emergency Procedures, 2nd, King C, Henretig FM. (Eds), Lippincott Williams & Wilkins, Philadelphia 2008. p.939

[vi] Gellman H. Fingertip-nail bed injuries in children: current concepts and controversies of treatment. J Craniofac Surg 2009; 20:1033.

Cardiotoxicity of Opioids


Loperamide, sold over-the-counter as Imodium among others, is a medication to decrease the frequency of diarrhea. The medication was first synthesized in 1969, first used medically after FDA approval in 1976, and first sold OTC in 1988. Loperamide was recently listed on the WHO’s List of Essential Medicines, due to its affordability and widespread use for patients with inflammatory bowel disease, gastroenteritis, irritable bowel syndrome, and traveler’s diarrhea.


Loperamide is an opioid-receptor agonist, decreasing the tone of intestinal smooth muscles, and subsequently allowing more water to be absorbed from fecal matter. The effects of loperamide are limited by the actions of P-glycoprotein (P-gp), a cell membrane protein that pumps xenobiotics back into the intestinal lumen, preventing further absorption. This effect is also noticed in the blood-brain barrier where P-gp prevents loperamide from affecting the central nervous system.


Appropriate dosing is 4 mg initially, followed by 2 mg after each subsequent loose stool, with a recommended daily maximum of 16 mg. When taken in large quantities, the levels of P-gp in the CNS and gut are overwhelmed, and the medication is able to cross the blood-brain barrier, eliciting opiate-like effects. A report from the National Poison Data System showed a 91% increase in loperamide exposures from 2010-2015, notable for 23 ingestion deaths, with 8 being solely attributed to loperamide. During this timeframe, on-line drug forums with user-generated content noted significant opportunity for misuse by patients seeking euphoria or withdrawal symptom relief. Furthermore, the low cost, legal status, and lack of social stigma also precluded this medication to misuse.

An FDA June 2016 report linked the abuse/misuse of loperamide to serious cardiac events, and urged health care providers to ‘consider loperamide as a possible cause of unexplained cardiac events including QT interval prolongation, torsades de pointes or other ventricular arrhythmias, syncope, and cardiac arrest.

Cardiac Effects of Loperamide: 

In cardiac tissue, loperamide has been shown to inhibit the human Ether-a-go-go Related Gene (hERG) product, a slow K channel. Resultantly, this prolongs phase 3 of the action potential, preventing repolarization, and lengthening the QTc interval.

Cardiotoxicity of Other Opioids: 

Propoxyphene (Darvocet when combined with acetaminophen) is a synthetic weak opioid introduced in 1957, that has subsequently been withdrawn from the US market after multiple black box warnings regarding cardiac effects. Propoxyphene exhibits Vaughn-Williams class Ic antiarrhythmic effects (more potent than lidocaine) and promotes cardiac Na channel blockade, subsequently prolonging phase 0 of the action potential, and prolonging the QRS interval. 

Methadone, commonly used in the treatment of opioid dependence since the 1960s in the US, also exhibits QTc prolongation effects. Similar to loperamide, methadone has been shown to also block the same slow K channel, precluding patients to risk of torsades de pointes.

Figure 1: Borrowed from

Figure 1: Borrowed from


When presented with ingestions of loperamide or the other aforementioned opioids with cardiac effects, after appropriate resuscitation, an ECG should be collected to assess the QRS and QTc intervals. The QTc prolongation effects of loperamide and methadone should be treated supportively with magnesium sulfate to prevent torsades de pointes. If TdP develops, the provider should consider isoproterenol (if there is intermittent bradycardia), and further transcutaneous/transvenous pacing.

Faculty Reviewer: Dr. Jason Hack 


Marraffa J, Holland M, Sullivan R, et al. Cardiac conduction disturbance after loperamide abuse. Clin Toxicol. 2014;52,952-957.

Daniulaityte R, Carlson R, Falck R. “I just wanted to tell you that loperamide WILL WORK”: a web-based study of extra-medical use of loperamide. Drug Alcohol Depend. 2013;130,241-244.

Dierksen J, Gonsoulin M, Walterscheid J. Poor man’s methadone: a case report of loperamide toxicity. Am J Forensic Med Pathol. 2015;36,268-270.

Vakkalanka J, Charlton N, Holstege C. Epidemiologic trends in loperamide abuse and misuse. Ann Emerg Med. 2017;69,73-78.

Uphadyay A, Bodar V, Malekzadegan M, et al. Loperamide induced life threatening ventricular arrhythmia. Case Rep Cardiol. 2016;1-3.

Lasoff D, Schneir A. Ventricular dysrhythmias from loperamide misuse. J Emerg Med. 2012;508-509.

Aschenbrenner D. Loperamide abuse or misuse triggers cardiac events. AJN. 2016;116,26-27.

Eggleston W, Clark K, Marraffa J. Loperamide abuse associated with cardiac dysrhythmia and death. Ann Emerg Med. 2017;69,83-86.

Gussow L. Opioid abusers using loperamide to get high or alleviate withdrawal, with fatal consequences. Emergency Medicine News. 2016;38,8.

Adler A, Viskin S, Bhuiyan Z, et al. Propoxyphene-induced torsades de pointes. Heart Rhythm. 2011;8,1952-54.

Jang D, Hoffman R, Nelson L, et al. Fatal outcome of a propoxyphene/acetaminophen (Darvocet) overdose: should it still be used in the United States? Ann Emerg Med. 2011;57,421-22.

Barkin R, Barkin S, Barkin D. Propoxyphene (Dextropropoxyphene): a critical review of a weak opioid analgesic that should remain in antiquity. Am J Ther. 2006;13,534-542.

Latta K, Ginsberg B, Barkin R. Meperidine: a critical review. Am J Ther. 2002;9,53-68.

Song M, Bae E, Baek J. QT prolongation and life threatening ventricular tachycardia in a patient injected with intravenous meperidine (Demerol). Korean Circ J. 2011;41,342-45.

Alinejad S, Kazemi T, Zamani N, et al. A systematic review of the cardiotoxicity of methadone. EXCLI Journal. 2015;14,577-600.

Caffrey C, Pinchbeck C. Methadone Induced Torsades. NUEM Blog. Retrieved from

Chen A, Ashburn M. Cardiac effects of opioid therapy. Pain Medicine. 2015;16,S27-S31.