Case Report

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American Journal of Emergency Medicine

journal homepage: www. elsevier. com/ locate/ajem

Atraumatic bilateral posterior Shoulder dislocations, a rare case of sleep deprivation

Abstract

Atraumatic bilateral shoulder posterior fracture dislocation is a very rare and Unusual presentation to emergency department (ED). Bilateral posterior shoulder dislocations are usually caused by seizures or electrical shock. The authors highlight the case of a healthy non traumatic patient who presented to the ED without any medical history who found himself in severe shoulder pain after having a nap on his bed.

Upon review of the scientific literature, it is clear that the joint most prone to traumatic dislocation is the glenohumeral joint [1]. Although unilateral dislocations are more commonly anteriorly, there is a predilec- tion for bilateral dislocations to present posteriorly. Posterior shoulder instability comprises a spectrum of disorders. This spectrum includes first-time traumatic dislocations, designated by a complete dissociation of the humeral head from the glenoid, and Recurrent dislocations or subluxations, characterized by symptomatic, excessive translation of the humeral head on the glenoid [2]. The prevalence of posterior shoulder dislocation is low, accounting for 1.7% to 4.3% of dislocations occurring in the general population [3,4]. Traditionally, the mechanisms of injury associated with posterior dislocations have been identified as Epileptic seizures, high-energy trauma, electrocution, or electroconvulsive therapy [5,6]. We present a case of atraumatic first-time bilateral posterior shoulder dislocation ina patient with no known medical history.

A 37-year-old man, with no significant medical history, was brought in by ambulance to the emergency department (ED) after awakening from a nap to find himself unable to move either of his shoulders. The patient reported lucid memories upon awakening. He had no recollection of falling out of bed and denied any history of previous falls from bed. The patient’s chief complaint was severe bilateral shoulder pain. He denied any headache or pain across his back or neck and denied paresthesia and weakness in upper and lower extremities. He reported a normal day at work, although felt tired and went home to get some rest on the couch in his home. He remembered eating and drinking normally without anything atypical that morning, denying trauma or injury, although he stated that his work at the office had been very busy recently. He had no significant medical history and denied taking any medications, smoking, alcohol, or illicit drug abuse. He was transported by emergency medical services to the ED uneventfully and was not immobilized. Emer- gency medical services did not report any suspicious events at the scene, and their history was consistent with the one obtained in the ED. His vital signs on arrival were blood pressure of 112/78, pulse of 80, respiratory rate of 18, and temperature of 97.3. His initial examination was notable for mild diaphoresis and in moderate pain after transfer from the emer- gency medical services stretcher to the ED stretcher. Venous access was established, pain control was ordered to facilitate an examination, and

blood tests were ordered. His pain improved slightly, and a physical examination was conducted. This was notable for small ecchymosis on right side of tongue, whereas the rest of his head, neck, back, heart, lungs, abdominal, and lower extremity examinations were normal. Upper extremity examination demonstrated equally appearing shoulders without ecchymosis or abrasions. On palpation, general tenderness of both shoulders was noted. The patient described limited range of motion of both shoulders due to pain, with full range of motion in his elbows, wrists, and hands. Notably, flexion of his elbow caused shoulder pain on the same side. Neurovascular examination was intact in both upper extremities. Laboratory finding were significant for a leukocytosis of 15.99, without significant left shift, and a potassium level of 2.8. All other blood work and the comprehensive metabolic panel were normal. His shoulder x-ray revealed bilateral posterior shoulder dislocations with a comminuted fracture of the inferomedial aspect of both humeral heads, consistent with an acute reverse Hill-Sachs fracture (Figs. 1 and 2).

Continuing to manage this patient in the ED, orthopedic consultation was obtained; shoulders were reduced bilaterally and subsequently placed in abduction slings with shoulders in zero degrees’ internal rotation/external rotation. At the emergency medicine team’s decision, the patient was then admitted to the medical service for further workup with neurology consultation obtained due to concerns for seizure. The patient’s head computed tomography and brain magnetic resonance were not significant to detect any relevant pathology. Initial electroen- cephalogram testing was performed for more than 5 hours during asleep and was within normal limits. A repeat electroencephalogram of similar duration to include at least 1 hour of wakefulness was also within normal limits. Patient continued to remain afebrile during hospital stay with no further hypokalemia after the initial repletion. Metabolic and infectious workup (including vitamin B₁₂, folate, Thyroid stimulating hormone , HIV, and rapid plasma reagin (RPR)) were negative for possible secondary causes of seizure. Neurology service recommended starting pa- tient on levetiracetam 500 mg twice daily due to the severe nature of his injury, and seizure was attributed to sleep deprivation.

A presentation of bilateral glenohumeral dislocation is quite rare, though bilateral posterior shoulder dislocations tend to be more common than bilateral anterior dislocations [7]. The incidence of posterior fracture- dislocations has been recorded at 0.6 per 100,000 population per year, stressing the rarity of incidence in these types of presentations [3].

The pathophysiology of bilateral posterior shoulder dislocations is notable, as it requires significant force placed on the shoulder, concur- rently. This mechanism for this injury is simultaneous bilateral shoulders adduction, flexion, and internal rotation under strain [8]. This injury has been linked to a number of atraumatic etiologies. Classically, this can occur during a convulsive seizure in patients who have seizure disorders [9,10]. Alternatively, patients with metabolic abnormalities that result

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Fig. 1. Bilateral posterior shoulder dislocations.

in seizures, such as hypoglycemia or hypocalcemia, could develop poste- rior shoulder dislocation injuries. alcohol withdrawal seizures could also cause these injuries [2]. Finally, the intense muscle contractions secondary to Electric shock or electroconvulsive shock therapy has been reported to cause posterior glenohumeral dislocation [11,12].

Because of the rarity of bilateral posterior shoulder dislocation conditions, treatment can become more challenging than with their anterior or unilateral counterparts [2]. A major threat to treatment is a missed diagnosis. The literature estimates that the diagnosis of posterior glenohumeral dislocation is missed in approximately 60% to 79% of cases [13]. A proposed explanation is that concomitant Proximal humerus fracture can confound the patient’s clinical presentation. Because of the rarity of this presentation, many physicians have a low or absent index of suspicion for this often-overlooked condition. The marked limitation of both active and passive range of motion can often lead to the incorrect diagnosis of frozen shoulder, resulting in delayed treatment of the dislocation and increased risk of more dramatic sequelae [14].

In our case, determining the etiology of significant force to cause bilateral posterior shoulder dislocations was challenging. There was no history of seizure disorders and no suggestion of significant trauma, as the chief complaint presented upon awakening from a nap. The

patient was notable for questionable history of urinary incontinence and, on physical examination, ecchymosis on his tongue, suggesting the dislocations were secondary to seizures, the etiology of which remained unclear and were potentially attributed to sleep deprivation.

Ali Pourmand MD, MPH, RDMS^? David Marcozzi MD, MHS-CL Hamid Shokoohi MD, MPH Abdulla Alhmoudi MD Samantha Olafson BA

Department of Emergency Medicine, George Washington University

Medical Center, Washington, DC 20037

?Corresponding author. Tel.: +1 202 741 2911, +1 202 320 1107

(mobile); fax: +1 202 741 2921

E-mail address: apourmand@mfa.gwu.edu http://dx.doi.org/10.1016/j.ajem.2015.11.052

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    Fig. 2. Right and left shoulder fracture dislocations.