Subtalar Dislocations


A 24 year-old male presents with right foot pain after falling off of a 12 foot ladder, his foot locked in supination, with obvious deformed (Figure 1). Pulses, sensation, and motor function intact distally. X-rays are ordered (Figure 2).

Figure 1: Right foot physical examination findings.  Pictures:

Figure 1: Right foot physical examination findings.


Figure 2: Plain films of right foot.

Figure 2: Plain films of right foot.


Subtalar dislocation


This is a rare injury; it accounts for approximately 1 – 2% of all dislocations. This can look similar to an ankle dislocation on examination, but the tibiotalar joint and mortise are intact.

These injuries typically from a high energy mechanism such as a fall from height or high energy motor vehicle collision (MVC). Typically to cause this dislocation, an axial load is applied when the patient has a plantar flexed foot. Patients may get these injuries from lower energy mechanisms such as sport injuries or fall from standing, especially if the patient is elderly or obese. Most injuries tend to be male (3:1 ratio) and in the third decade of life.

Subtalar dislocation is the disruption of the articulation of both the talocalcaneal and the talonavicular joints with an intact ankle joint mortis. This involves disruption of the surrounding ligaments: interosseous talocalcaneal ligament (most important), anterior talocalcaneal ligament, posterior talocalcaneal ligament, lateral talocalcaneal ligament, and medial talocalcaneal ligament.

Approximately 25% of these injuries are open upon presentation to the ED. There is high risk of skin necrosis from tenting over malleolus or talar head, which can convert these injuries to open dislocations.

Types of Subtalar Dislocations

The vast majority of subtalar dislocations are either medial (85%) or lateral (15%). Anterior and posterior dislocations can also occur.

Medial Subtalar Dislocation

This is the most common type of subtalar dislocation. It typically results from an inversion injury with a plantar flexed foot. It is sometimes called “basketball foot” as this is a common mechanism. Another term for this injury is “acquired clubfoot.” On physical exam, you will find that the foot is inverted, the calcaneus is displaced medially, and the foot is locked in supination.

On AP x-ray, the calcaneus will be displaced medially (Figure 3). Lateral x-ray will show that the talar head is superior to the navicular (Figure 4).

Figure 3: AP view of medial subtalar dislocation.

Figure 3: AP view of medial subtalar dislocation.

Figure 4: Lateral view of medial subtalar dislocation showing that the head of the talus is superior to the navicular.

Figure 4: Lateral view of medial subtalar dislocation showing that the head of the talus is superior to the navicular.

Lateral Subtalar Dislocation

Lateral subtalar dislocations account for around 15% of subtalar dislocations. On physical examination, you will find that the foot is everted, the calcaneus is lateral to talus, and the foot is locked in pronation. AP x-ray will show lateral displacement of the calcaneus (Figure 5). On lateral views, the talar head with be inferior to the navicular (Figure 6). Lateral dislocations tend to result from higher mechanism injuries; therefore, these injuries are more likely to be open and have more associated injuries.

Figure 5: AP view of a lateral subtalar dislocation.

Figure 5: AP view of a lateral subtalar dislocation.

Figure 6: Lateral view of lateral subtalar dislocation showing the head of the talus is inferior to the navicular

Figure 6: Lateral view of lateral subtalar dislocation showing the head of the talus is inferior to the navicular

Figure 7: Physical exam findings for a lateral subtalar dislocation.

Figure 7: Physical exam findings for a lateral subtalar dislocation.

Anterior and Posterior Dislocations

There are case reports of anterior and posterior dislocations, but these are exceedingly rare. They account for around 1% of subtalar dislocations.

Reduction technique

Reduction should be attempted rapidly due to the threat of skin necrosis if dislocation is prolonged. Reduction should occur prior to obtaining radiographs (either immediately upon presentation to the ED or in the field) if the foot has obvious neurovascular compromise such as absent or thready dorsalis pedis or posterior tibial pulse, decreased capillary refill, or lack of sensation to the bottom of the foot. Obtaining a thorough vascular and sensory exam of the foot before and after any reduction attempts is key. Often procedural sedation is necessary to perform this procedure. The approach to reduction is as follows:

  • Knee bent at 90 degrees to relax gastrocnemius and soleus muscles

  • Apply traction at heel and counter-traction to thigh

  • Accentuate deformity followed by reversal.

    • Medial dislocations: Further invert, pull traction, and then evert

    • Lateral dislocations: Further evert, pull traction, and then invert

  • Apply a splint – short posterior slab splint with side gussets

  • If reduction is successful, then obtain post-reduction x-rays and CT scan of foot and ankle. It is recommended that the patient is non-weight bearing in short leg cast for 4 to 6 weeks.

Associated injuries

Given that most of these injuries occur from a high degree force to the foot, it is not surprising that many of patients have other foot and ankle injuries in addition to the subtalar dislocation. Approximately 55% of medial subtalar dislocations and 72% of lateral dislocations have associated injuries. Common associated injuries include osteochondral lesions of the talus, subtalar debris, ankle fractures, 5th metatarsal fracture, navicular fracture, and cuboid fracture. Given the high percentage of associated injuries and that some of the associated injuries are difficult to see on plain radiographs, it is recommended to get a CT scan of the ankle and foot after reduction. In a case series of 9 patients, CT scan showed additional injuries missed on plain film in 100% of cases, and the CT changed the treatment in 44% of the cases. Fortunately, neurovascular injury and chronic subtalar joint instability are rare complications.


Approximately 30% of injuries are not reducible by closed means. In medial dislocations, the capsule of the talonavicular joint, peroneal tendons, or the extensor digitorum brevis (EDB) muscle can block reduction. The talar head can “button hole” through the EDB which blocks reduction. In lateral dislocations, the posterior tibialis tendon, flexor halluces longus, or flexor digitorum longus can be interposed into the joint space and block reduction. These injuries are also associated with contusions or lacerations of the posterior tibial artery and nerve.

Open subtalar dislocations have an infection rate of approximately 30% even with aggressive irrigation in the OR. Appropriate antibiotics prophylaxis should be given immediately upon recognizing an open fracture. Cefazolin is sufficient coverage for skin flora in most cases without obvious contamination and with minimal soft tissue damage. If the patient is high risk for MRSA, vancomycin coverage can also be added. For patients with severe soft tissue injury or gross contamination coverage should be expanded to ampicillin-sulbactam, cefoxitin, or cefotetan. If there is exposure to water, then Pseudomonas coverage should be added with an agent like cefepime. If fecal contamination is possible or there is concern for clostridial exposure (agricultural injuries), then high dose penicillin should be used as an adjunct.

Figure 8: Open medial subtalar dislocation.

Figure 8: Open medial subtalar dislocation.

There also is a risk of avascular necrosis of the talus or navicular after a subtalar dislocation. This is a rare complication more likely to occur after lateral subtalar dislocation. This is more common with tibiotalar dislocation when the ankle mortise is disrupted.

Many patients will go on to have chronic pain in their ankle (30 - 63%); intraarticular debris fragments and open injuries increase the risk of this.

Take Home Points

  • Subtalar dislocations often occur after a high mechanism injury to the foot while it is plantar flexed

  • Medial subtalar dislocations are more common

  • Lateral subtalar dislocations are more likely to be open and to have other associated injuries

  • Open dislocations have very high infection risk even with prompt and appropriate care

  • Fast reduction is key. Put the knee at 90 degrees, apply traction, recreate the injury and then reverse it

  • Get appropriate antibiotics on board quickly for open fractures

  • Approximately 30% of the time, closed reduction is impossible as the dislocated bone is caught on adjacent structures

  • Get a CT scan after reduction to look for other injuries

Faculty Reviewer: Dr. Mark Greve


  1. Bryant, J. and Levis, J.T. 2009. Subtalar dislocation. Western Journal of Emergency Medicine, 10(2).

  2. Bibbo, C., Lin, S.S., and Abidi, N. 2001. Missed and associated injuries after subtalar dislocation: the role of CT. Foot and Ankle International, 22(4).

  3. DeLee, C. 1982. Subtalar dislocation of the foot. The Journal of Bone and Joint Surgery, 64(3): 433-437.

  4. Gustilo RB, Anderson JT. 1976. Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg Am, 58:453.

  5. Gustilo RB, Gruninger RP, Davis T. 1987. Classification of type III (severe) open fractures relative to treatment and results. Orthopedics, 10:1781.

  6. Horning, J. 2009. Subtalar dislocation. Orthopedics, 32(12): 904.

  7. Melenevsky, Y., Mackey, R.A., Abrahams, B., and Thomson, N.B. 2014. Talar fractures and dislocations: a radiologist’s guide to timely diagnosis and classification. Retrieved 7/29/17 from

  8. Schmitt, SK. 2018. Osteomyelitis associated with open fractures in adults: preventative antibiotics after open fractures. UpToDate, retrieved on 1/24/19 from

  9. Weatherford, B. 2017. Subtalar dislocations. Retrieved on 7/29/17 from

  10. Weir, A. 2015. MR:EM subtalar dislocation. Retrieved on 7/29/17 from

  11. Wheeless, C.R. 2012. Wheeless’ Textbook of Orthopaedics: Sub Talar Dislocation. Retrieved on 7/29/17 from

  12. Yoder, W., Nelson, P., Bowen, M., and Frania, S. 2011. Chapter 11: Talocalcaneal navicular dislocation. Retrieved on 7/29/17 from

AEM Early Access 25: Randomized Clinical Trial Comparing Procedural Amnesia and Respiratory Depression Between Moderate and Deep Sedation With Propofol in the Emergency Department

Welcome to the twenty-fifth episode of AEM Early Access, a FOAMed podcast collaboration between the Academic Emergency Medicine Journal and Brown Emergency Medicine. Each month, we'll give you digital open access to an recent AEM Article or Article in Press, with an author interview podcast and suggested supportive educational materials for EM learners.

Find this podcast series on iTunes here.

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Randomized Clinical Trial Comparing Procedural Amnesia and Respiratory Depression Between Moderate and Deep Sedation With Propofol in the Emergency Department. Alexandra Schick, MD, Brian Driver, MD, Johanna C. Moore, MD/MPH, Erik Fagerstrom, and James R. Miner, MD



Alexandra Schick, MD

Resident Physician, Brown Emergency Medicine

Twitter: @allie_schickMD


Objectives: The objective was to determine if there is a difference in procedural amnesia and adverse respiratory events (AREs) between the target sedation levels of moderate (MS) and deep (DS) procedural sedation.

Methods: This was a prospective, randomized clinical trial of consenting adult patients planning to undergo DS with propofol between March 5, 2015, and May 24, 2017. Patients were randomized to a target sedation level of MS or DS using the American Society of Anesthesiologist's definitions. Drug doses, vital signs, observer's assessment of alertness/sedation (OAAS) score, end-tidal CO2 (ETCO2 ), and the need for supportive airway maneuvers (SAMs; bag-valve mask use, repositioning, and stimulation to induce respirations) were monitored continuously. A standardized image was shown every 30 seconds starting 3 minutes before the procedure continuing until the patient had returned to baseline after the procedure. Recall and recognition of images were assessed 10 minutes after the sedation. Subclinical respiratory depression (RD) was defined as SaO2 ≤ 91%, change in ETCO2 ≥ 10 mm Hg, or absent ETCO2 at any time. The occurrence of RD with a SAM was defined as an ARE. Patient satisfaction, pain, and perceived recollection and physician assessment of procedure difficulty were collected using visual analog scales (VASs). Data were analyzed with descriptive statistics and Wilcoxon rank-sum test.

Results: A total of 107 patients were enrolled: 54 randomized to target MS and 53 to DS. Of the patients randomized to target MS, 50% achieved MS and 50% achieved DS. In the target DS group, 77% achieved DS and 23% achieved MS. The median total propofol dose (mg/kg) was lower in the MS group: MS 1.4 (95% confidence interval [CI] = 1.3-1.6, IQR = 1) versus DS 1.8 (95% CI = 1.6-2.0, IQR = 0.9). There were no differences in median OAAS during the procedure (MS 2.4 and DS 2.8), lowest OAAS (MS 2 and DS 2), percentage of images recalled (MS 4.7% vs. DS 3.8%, p = 0.73), or percentage of images recognized (MS 61.1% vs. DS 55%, p = 0.52). In the MS group, 41% patients had any AREs compared to 42% in the DS group (p = 0.77, 95% CI difference = -0.12 to 0.24). The total number of AREs was 23% lower in the MS group (p = 0.01, 95% CI = -0.41 to -0.04). There was no difference in patient-reported pain, satisfaction, or recollection VAS scores. Provider's rating of procedural difficulty and procedural success were similar in both groups.

Conclusions: Targeting MS or DS did not reliably result in the intended sedation level. Targeting MS, however, resulted in a lower rate of total AREs and fewer patients had multiple AREs with no difference in procedural recall. As seen in previous reports, patients who achieved MS had less AREs than those who achieved DS. Our study suggests that a target of MS provides adequate amnesia with less need for supportive airway interventions than a target level of DS, despite the fact that it often does not result in intended sedation level.

FPIES: Expanding the Differential for Hypotension in the Pediatric Patient


An 8-month-old male, full term, infant with no significant past medical history presents to the ED for nausea, vomiting, and non-bloody diarrhea for the past several hours. His family has slowly been introducing new foods into his diet. There are no known sick contacts. He is well-appearing, hemodynamically stable, and tolerating PO in the ED. After some observation, the patient was discharged with the diagnosis of viral gastroenteritis.

Six days later, the same patient presented with profuse vomiting, diarrhea, and profound lethargy. He was found to be tachycardic and hypotensive. He was taken to the critical care area for altered mental status, unstable vital signs, and undifferentiated shock. His exam was notable for lethargy, pallor, and a distended abdomen. Initial labs showed a metabolic acidosis, eosinophilia, and thrombocytosis. Stool studies and UA were unrevealing. Abdominal plain films were normal.


FPIES - What is it?

As many ED practitioners are aware, food allergies are common in the first 2 years of life, with a prevalence cited between 1-10% of the population. Most food allergies are IgE-mediated hypersensitivity reactions. Food protein-induced enterocolitis (FPIES) is a syndrome characterized by a severe non-IgE mediated food hypersensitivity reaction. FPIES is important to keep on the differential as the syndrome often goes unrecognized or is misdiagnosed at the initial (or subsequent) presentation. (1)

FPIES is characterized by profound and repetitive vomiting, and occasionally diarrhea, 1-4 hours after exposure to the causal protein. In the acute setting, this can manifest as dehydration and lethargy. More than 15% of FPIES patients will require admission for hemodynamic instability secondary to dehydration. In the chronic setting, pediatric patients can present as failure to thrive and/or unexplained weight loss. The most common food triggers in FPIES are cow milk's and soy. FPIES may be induced by solid food, including grains, meat and poultry, eggs, vegetables and fruit, seafood, and legumes. (1,3)

Though the underlying mechanism of FPIES is not clearly understood, it differs from other allergen mediated reactions as it is not triggered by an (IgE)-mediated hypersensitivity. Preliminary research indicates that there is inflammation within the lamina propria and epithelium in both the small and large intestine secondary to increased tumor necrosis factor-alpha (TNF-α) expression by activated T cells. Downstream, this causes increased intestinal permeability which contributes to pathogenesis of FPIES. (4, 8)

Figure A.

Figure A.


Patients with acute presentations tend to be sicker and may develop pallor, hypotension/shock, and/or hypothermia. Failure to thrive and weight loss are seen in patients with chronic FPIES.

  • Lethargy (70%)

  • Pallor (70%)

  • Dehydration

  • Hypotension (15%)

  • Hypothermia (25%)

  • Abdominal distension


Labs often reveal anemia, hypoalbuminemia, and an elevated white blood cell count with a left shift. Eosinophilia is often seen in chronic FPIES. Thrombocytosis was found in 65 percent of acute FPIES. Metabolic acidosis (mean pH 7.03) and methemoglobinemia have been reported in both acute and chronic FPIES. Transient methemoglobinemia was reported in about one-third of acute FPIES infants with some requiring methylene blue treatment. Methemoglobinemia may be caused by severe intestinal inflammation and reduced catalase activity resulting in increased nitrites. (5)

Diagnostic imaging studies are not part of the standard FPIES workup, but some older studies have analyzed trends. Although findings are nonspecific, it is important to be familiar with them as often these infants get imaging as part of their workup.

Findings include:

  • Air fluid levels

  • Nonspecific narrowing and thumb-printing of rectum and sigmoid colon

  • Thickening of plicae circulares in duodenum and jejunum

  • Excess luminal fluid

  • Rarely intramural gas (which can lead to misdiagnosis of NEC)

Resolution of radiographic abnormalities after dietary restriction has been documented. (1, 3, 5)


Given the clinical picture of FPIES is nonspecific, the ED physician can arrive at the diagnosis more quickly by obtaining a brief dietary history. This especially holds true if the patient has been seen multiple times in the ED prior for similar complaints. In infants, the causes of acute repetitive vomiting and severely altered mental status includes a broad differential diagnosis. Sepsis, infectious gastroenteritis, head injury, toxicologic, gut malrotation, intussusception, NEC, pyloric stenosis, as well as other metabolic and cardiogenic causes can present similarly. In patients with such symptoms, allergy as a cause is sometimes not considered by ED physicians. Diagnosis of FPIES is based on the recognition of clinical manifestations, exclusion of alternative causes, and a physician-supervised oral food challenge (OFC). Diagnosis is often made in the inpatient or primary care setting, and is based on presence of a major criterion as well as three minor criteria as seen below.

Below are some quick and dirty rules to differentiate FPIES from other diagnoses:

Food protein-induced proctocolitis: Infants are well-appearing and thriving, unlike acute FPIES children. Present with blood streaked stools in first months of life.

Anaphylaxis: Time to symptoms is much shorter (usually minutes vs. 2-4 hours). Have constellation of associated symptoms not seen in FPIES: rash, respiratory distress/stridor. Symptoms resolve with IM epinephrine.

Infections/Sepsis: Usually present febrile (or less often hypothermic) and often with a history of sick contacts. Labs showing leukocytosis with a left shift/bandemia (vs eosinophilia in FPIES). There may be a presence of respiratory symptoms if sepsis 2/2 to PNA, viral URI. Septic patients typically do not improve with IVF alone (unlike FPIES patients).

Necrotizing enterocolitis: Systemic and abdominal symptoms seen in NEC that are not typical of FPIES include apnea, respiratory failure, temperature instability, intramural gas on abdominal radiograph. NEC is usually at a much earlier age, and often within the first few days of life.

Intestinal obstruction: There are reports of ex-laps being performed when acute FPIES was mistaken for ileus. Obstruction often presents with more pronounced distention and history of decreased to no stool output (FPIES infants can have normal stool output and/or diarrhea).

Intussusception: While the classic teaching is currant jelly stools, this is rarely present. Vomiting/discomfort waxing and waning over protracted period of time, and pain may be more predominant.

Pyloric Stenosis: Usually between 2 weeks and 2 months of life before the introduction of solid foods. There may be an olive-shaped mass in epigastrium, and ultrasound confirms the diagnosis.

Metabolic disorders: May have other features, such as hypoglycemia, hematologic abnormalities (ex, anemia, neutropenia, thrombocytopenia), liver dysfunction (hepatomegaly, jaundice), renal disease, and developmental delay.

Data shows that of FPIES patients presenting to the ED, 34% of patients undergoing abdominal imaging, 28% undergoing a septic evaluation, and 22% having a surgical consultation. Misdiagnosis and delays in diagnosis for children with food protein-induced enterocolitis syndrome were common, leading many children to undergo unnecessary investigations. (6, 7, 9)


The patient mentioned in the case earlier was subsequently admitted to the PICU for further workup and resuscitation. After many diagnoses were ruled out, and in conjunction with thorough dietary review, it was found that the patient had both of these episodes after exposure to sweet potato. The diagnoses of FPIES was made and patient was discharged to home in good health with rheumatology follow up.

For acute presentations, patients often require admission for fluid resuscitation, symptom management, and parent education. For chronic FPIES patients, it is sometimes reasonable to discharge patient to home, but this should always be done in conjunction with primary care doctor as well as expectant management and education. Often times, labs can be drawn in the emergency setting as a conduit to help the patient’s PCP rule out other causes (such as IgE-mediated allergies). (2, 3)

Faculty Reviewer: Dr. Jane Preotle



  1. Nowak-Węgrzyn A, Katz Y, Mehr SS, Koletzko S. Non-IgE-mediated gastrointestinal food allergy. J Allergy Clin Immunol 2015; 135:1114.

  2. Nowak-Węgrzyn A, Chehade M, Groetch ME, et al. International consensus guidelines for the diagnosis and management of food protein-induced enterocolitis syndrome: Executive summary-Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology. J Allergy Clin Immunol 2017; 139:1111.

  3. Mehr S, Kakakios A, Frith K, Kemp AS. Food protein-induced enterocolitis syndrome: 16-year experience. Pediatrics 2009; 123:e459.

  4. Caubet JC, Nowak-Węgrzyn A. Current understanding of the immune mechanisms of food protein-induced enterocolitis syndrome. Expert Rev Clin Immunol 2011; 7:317.

  5. Sicherer SH, Eigenmann PA, Sampson HA. Clinical features of food protein-induced enterocolitis syndrome. J Pediatr 1998; 133:214.

  6. Ruffner MA, Ruymann K, Barni S, et al. Food protein-induced enterocolitis syndrome: insights from review of a large referral population. J Allergy Clin Immunol Pract 2013; 1:343.

  7. Coates RW, Weaver KR, Lloyd R, et al. Food protein-induced enterocolitis syndrome as a cause for infant hypotension. West J Emerg Med 2011; 12:512.

  8. Sampson HA, Anderson JA. Summary and recommendations: Classification of gastrointestinal manifestations due to immunologic reactions to foods in infants and young children. J Pediatr Gastroenterol Nutr 2000; 30 Suppl:S87.

  9. Jayasooriya S, Fox AT, Murch SH. Do not laparotomize food-protein-induced enterocolitis syndrome. Pediatr Emerg Care 2007; 23:173.

  10. Figure A: Berin, M. Cecilia. Immunopathophysiology of food protein-induced enterocolitis syndrome. Journal of Allergy and Clinical Immunology, Volume 135. Issue5. 1108-1113