Case Reports

Anterior-inferior and posterior-inferior labral tears are common injuries treated with arthroscopic surgery¹ typically performed with beach-chair^2,3 or lateral decubitus^1,2 positioning and variable headrest positioning. Iatrogenic nerve damage that occurs after arthroscopic shoulder surgery—including damage to the suprascapular, axillary, musculocutaneous, subscapular, and spinal accessory nerves—has recently been reported to be more common than previously recognized.^2,4

Although iatrogenic nerve injuries are in general being recognized,^1,2,4 reports of greater auricular nerve injuries are limited. The greater auricular nerve is a superficial cutaneous nerve that arises from the cervical plexus at the C2 and C3 spinal nerves, obliquely crosses the sternocleidomastoid muscle, and splits into anterior and posterior portions that innervate the skin over the mastoid process and parotid gland.^5,6 In particular, as illustrated by Ginsberg and Eicher⁶ (Figure 1), its superficial anatomy lies very near where a headrest is positioned during arthroscopic surgery, and increased pressure on the nerve throughout arthroscopic shoulder surgery may lead to neurapraxia.^6,7 In 2 case series, authors reported on a total of 5 patients who had greater auricular nerve palsy after uncomplicated shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 The authors attributed these palsies to the horseshoe headrest, which they believed was compressing the greater auricular nerve during the entire surgery.^7,8 However, standard universal headrests, which are thought to distribute pressures that would theoretically place the greater auricular nerve at risk for palsy, previously had not been described as contributing to palsy of the greater auricular nerve.

In this article, we report on a case of greater auricular nerve palsy that occurred after the patient’s anterior-inferior and posterior-inferior labral tear was arthroscopically repaired using beach-chair positioning and a standard universal headrest. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An 18-year-old right-hand–dominant high school American football player was referred for orthopedic evaluation of left chronic glenohumeral instability after 6 months of physical therapy. Physical examination revealed a positive apprehension test with the shoulder abducted and externally rotated at 90° and a positive relocation test. The patient complained of pain and instability when his arm was placed in a cross-chest adducted position and a posteroinferiorly directed axial load was applied. Magnetic resonance arthrogram showed an anterior-inferior labral Bankart tear with a small Hill-Sachs lesion to the humeral head but did not clearly reveal the posterior-inferior labral tear. Because of persistent left shoulder instability with most overhead activities and continued pain, the patient decided to undergo left shoulder arthroscopic Bankart repair with inferior capsular shift and posterior-inferior labral repair with capsulorraphy. He had no significant past medical history or known drug allergies.

The patient was placed in the standard beach-chair position: upright at 45° to the floor, hips flexed at 60°, knees flexed at 30°.¹ Pneumatic compression devices were placed on his lower extremities. His head was secured in neutral position to a standard universal headrest (model A-90026; Allen Medical Systems, Acton, Massachusetts) (Figures 2, 3). Care was taken to protect the deep neurovascular structures and bony prominences throughout. The patient was in this position for 122 minutes of the operation, from positioning and draping to wound closure and dressing application. Before draping, the anesthesiologist, head nurse, and circulating nurse ensured that head and neck were in neutral position. The anesthesiologist monitored positioning throughout the perioperative period to ensure head and neck were in neutral, and the head did not need to be repositioned during surgery. Standard preoperative intravenous antibiotics were given.

General anesthesia and postoperative interscalene block were used. Standard preparation and draping were performed. Three standard arthroscopic portal incisions were used: posterior, anterior, and anterosuperolateral. Findings included extensive labral pathology, small bony Hill-Sachs lesion to humeral head, small bony anterior glenoid deficiency, and deficient anterior-inferior and posterior-inferior labral remnant. These were repaired arthroscopically in a standard fashion using bioabsorbable suture anchors. There were no arthroscopic complications. After surgery, a standard well-fitted shoulder immobilizer was placed. The anesthesiologist provided interscalene regional analgesia (15 mL of bupivacaine 0.5%) in the recovery area after surgery.

Postoperative neurovascular examination in the recovery room revealed no discomfort. The patient was discharged the same day. At a scheduled 1-week follow-up, he complained of numbness and dysesthesia on the left side of the greater auricular nerve distribution. A diagnosis of greater auricular nerve palsy was made by physical examination; the symptoms were along the classic greater auricular nerve distribution affecting the lower face and ear (Figure 4). The patient had no pain, skin lesions, or soft-tissue swelling. Otolaryngology confirmed the diagnosis and recommended observation-only treatment of symptoms. Symptoms lessened over the next 3 months, and the altered sensation resolved without deficit by 6 months. In addition, by 6 months the patient had returned to full activities (including collision sports) pain-free and with normal left shoulder function. Because symptoms continued to improve, the patient was followed with clinical observation, and a formal work-up was not necessary.

Discussion

The most important finding in this case is the greater auricular nerve palsy that occurred after arthroscopic anterior-inferior and posterior-inferior labral repairs in beach-chair positioning. This greater auricular nerve palsy was the first encountered by Dr. Foad, who over 17 years in a primarily shoulder practice setting has used beach-chair positioning exclusively. Previous reports have described a palsy occurring after arthroscopic shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 Ng and Page⁷ discontinued and recommended against use of this headrest because of the complications of the palsy, and Park and Kim⁸ recommended a headrest redesign. We think the present case report is the first to describe a greater auricular nerve palsy that occurred after arthroscopic surgery using a standard universal headrest, which theoretically should prevent compression of the greater auricular nerve. Increased awareness of the possibility of greater auricular nerve palsy, even when proper precautions are taken,¹ is therefore warranted.

Based on the location of our patient’s palsy, we think his paralysis was most likely the result of nerve compression by the headrest during the shoulder surgery. Other factors, though unlikely, may have played a role. These include operative time (increases duration of nerve compression) and head positioning. However, 122 minutes is not unusually long for a patient’s head to be in this position during a procedure, and over the past 10 years the same anesthesiologist, head nurse, and circulating nurse have routinely used the same beach-chair positioning and headrest for Dr. Foad’s patients. Second, the postoperative interscalene block theoretically could have caused the palsy, but we think this is unlikely, as the block is placed lower on the neck, at the C6 level, and the greater auricular nerve branches off the C2–C3 spinal nerves. As described by Rains and colleagues,⁹ other authors have reported transient neuropathies to the brachial plexus, which originates in the C5–C8 region, but not to the greater auricular nerve. Last, it cannot be ruled out that a variant of the greater auricular nerve could have played a role, given the variation in the greater auricular nerve.^10,11 However, Brennan and colleagues¹⁰ reported that 2 of 25 neck dissections involved a variant in which the anterior division of the greater auricular nerve passed into the submandibular triangle and joined the mandibular region of the facial nerve. Stimulation of this nerve resulted in activity of the depressor of the lower lip, which was not the location of our patient’s palsy. In addition, our patient’s symptoms followed a classic nerve distribution of the greater auricular nerve (Figures 1, 4), which would seem to decrease the likelihood that a variant was the source of the palsy.

The superficial nature of the greater auricular nerve, which runs roughly parallel with the sternocleidomastoid muscle and innervates much of the superficial region of the skin over the mastoid, parotid gland, and mandible,^5-7 theoretically places the nerve at risk for compressive forces from the headrest during arthroscopic shoulder surgery. Skyhar and colleagues³ first described beach-chair positioning as an alternative to lateral decubitus positioning, which had been reported to result in neurologic injury in about 10% of surgical cases.⁹ The theoretical advantages of beach-chair positioning are lack of traction needed and ease of setup, which would therefore decrease the possibility of neuropathy.^1,3 However, as seen in this and other case reports,^7,8 greater auricular nerve neuropathy should still be considered a possible complication, even when using beach-chair positioning.

Besides neuropathy after arthroscopic shoulder surgery, as described in previous case reports^7,8 and in the present report, greater auricular nerve injury has been described as arising from other stimuli. Greater auricular nerve injury has arisen after perineural tumor metastasis,⁶ neuroma of greater auricular nerve after endolympathic shunt surgery,¹² internal fixation of mandibular condyle,¹³ and carotid endarterectomy.^14,15 Given the superficial nature of the greater auricular nerve, it may not be all that surprising that a palsy could also develop after headrest compression during arthroscopic shoulder surgery.

This case report brings to light a possible complication of greater auricular nerve palsy during arthroscopic shoulder surgery using beach-chair positioning and a standard universal headrest. Studies should now investigate whether greater auricular nerve palsy is more common than realized, especially with regard to specific headrests in beach-chair positioning. For now, though, Dr. Foad’s intention is not to change to a different headrest or discontinue beach-chair positioning but to draw attention to this rare complication. Additional attention should be given to the location of the headrest in relation to the greater auricular nerve, especially in cases in which operative time may be longer.

Conclusion

We have reported a greater auricular nerve palsy that occurred after arthroscopic shoulder surgery for an anterior-inferior and posterior-inferior labral tear. This is the first report of a greater auricular nerve palsy occurring with beach-chair positioning and a standard universal headrest. Symptoms resolved within 6 months. New studies should investigate the incidence of greater auricular nerve palsy after arthroscopic shoulder surgery.

Anterior-inferior and posterior-inferior labral tears are common injuries treated with arthroscopic surgery¹ typically performed with beach-chair^2,3 or lateral decubitus^1,2 positioning and variable headrest positioning. Iatrogenic nerve damage that occurs after arthroscopic shoulder surgery—including damage to the suprascapular, axillary, musculocutaneous, subscapular, and spinal accessory nerves—has recently been reported to be more common than previously recognized.^2,4

Although iatrogenic nerve injuries are in general being recognized,^1,2,4 reports of greater auricular nerve injuries are limited. The greater auricular nerve is a superficial cutaneous nerve that arises from the cervical plexus at the C2 and C3 spinal nerves, obliquely crosses the sternocleidomastoid muscle, and splits into anterior and posterior portions that innervate the skin over the mastoid process and parotid gland.^5,6 In particular, as illustrated by Ginsberg and Eicher⁶ (Figure 1), its superficial anatomy lies very near where a headrest is positioned during arthroscopic surgery, and increased pressure on the nerve throughout arthroscopic shoulder surgery may lead to neurapraxia.^6,7 In 2 case series, authors reported on a total of 5 patients who had greater auricular nerve palsy after uncomplicated shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 The authors attributed these palsies to the horseshoe headrest, which they believed was compressing the greater auricular nerve during the entire surgery.^7,8 However, standard universal headrests, which are thought to distribute pressures that would theoretically place the greater auricular nerve at risk for palsy, previously had not been described as contributing to palsy of the greater auricular nerve.

In this article, we report on a case of greater auricular nerve palsy that occurred after the patient’s anterior-inferior and posterior-inferior labral tear was arthroscopically repaired using beach-chair positioning and a standard universal headrest. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An 18-year-old right-hand–dominant high school American football player was referred for orthopedic evaluation of left chronic glenohumeral instability after 6 months of physical therapy. Physical examination revealed a positive apprehension test with the shoulder abducted and externally rotated at 90° and a positive relocation test. The patient complained of pain and instability when his arm was placed in a cross-chest adducted position and a posteroinferiorly directed axial load was applied. Magnetic resonance arthrogram showed an anterior-inferior labral Bankart tear with a small Hill-Sachs lesion to the humeral head but did not clearly reveal the posterior-inferior labral tear. Because of persistent left shoulder instability with most overhead activities and continued pain, the patient decided to undergo left shoulder arthroscopic Bankart repair with inferior capsular shift and posterior-inferior labral repair with capsulorraphy. He had no significant past medical history or known drug allergies.

The patient was placed in the standard beach-chair position: upright at 45° to the floor, hips flexed at 60°, knees flexed at 30°.¹ Pneumatic compression devices were placed on his lower extremities. His head was secured in neutral position to a standard universal headrest (model A-90026; Allen Medical Systems, Acton, Massachusetts) (Figures 2, 3). Care was taken to protect the deep neurovascular structures and bony prominences throughout. The patient was in this position for 122 minutes of the operation, from positioning and draping to wound closure and dressing application. Before draping, the anesthesiologist, head nurse, and circulating nurse ensured that head and neck were in neutral position. The anesthesiologist monitored positioning throughout the perioperative period to ensure head and neck were in neutral, and the head did not need to be repositioned during surgery. Standard preoperative intravenous antibiotics were given.

General anesthesia and postoperative interscalene block were used. Standard preparation and draping were performed. Three standard arthroscopic portal incisions were used: posterior, anterior, and anterosuperolateral. Findings included extensive labral pathology, small bony Hill-Sachs lesion to humeral head, small bony anterior glenoid deficiency, and deficient anterior-inferior and posterior-inferior labral remnant. These were repaired arthroscopically in a standard fashion using bioabsorbable suture anchors. There were no arthroscopic complications. After surgery, a standard well-fitted shoulder immobilizer was placed. The anesthesiologist provided interscalene regional analgesia (15 mL of bupivacaine 0.5%) in the recovery area after surgery.

Postoperative neurovascular examination in the recovery room revealed no discomfort. The patient was discharged the same day. At a scheduled 1-week follow-up, he complained of numbness and dysesthesia on the left side of the greater auricular nerve distribution. A diagnosis of greater auricular nerve palsy was made by physical examination; the symptoms were along the classic greater auricular nerve distribution affecting the lower face and ear (Figure 4). The patient had no pain, skin lesions, or soft-tissue swelling. Otolaryngology confirmed the diagnosis and recommended observation-only treatment of symptoms. Symptoms lessened over the next 3 months, and the altered sensation resolved without deficit by 6 months. In addition, by 6 months the patient had returned to full activities (including collision sports) pain-free and with normal left shoulder function. Because symptoms continued to improve, the patient was followed with clinical observation, and a formal work-up was not necessary.

Discussion

The most important finding in this case is the greater auricular nerve palsy that occurred after arthroscopic anterior-inferior and posterior-inferior labral repairs in beach-chair positioning. This greater auricular nerve palsy was the first encountered by Dr. Foad, who over 17 years in a primarily shoulder practice setting has used beach-chair positioning exclusively. Previous reports have described a palsy occurring after arthroscopic shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 Ng and Page⁷ discontinued and recommended against use of this headrest because of the complications of the palsy, and Park and Kim⁸ recommended a headrest redesign. We think the present case report is the first to describe a greater auricular nerve palsy that occurred after arthroscopic surgery using a standard universal headrest, which theoretically should prevent compression of the greater auricular nerve. Increased awareness of the possibility of greater auricular nerve palsy, even when proper precautions are taken,¹ is therefore warranted.

Based on the location of our patient’s palsy, we think his paralysis was most likely the result of nerve compression by the headrest during the shoulder surgery. Other factors, though unlikely, may have played a role. These include operative time (increases duration of nerve compression) and head positioning. However, 122 minutes is not unusually long for a patient’s head to be in this position during a procedure, and over the past 10 years the same anesthesiologist, head nurse, and circulating nurse have routinely used the same beach-chair positioning and headrest for Dr. Foad’s patients. Second, the postoperative interscalene block theoretically could have caused the palsy, but we think this is unlikely, as the block is placed lower on the neck, at the C6 level, and the greater auricular nerve branches off the C2–C3 spinal nerves. As described by Rains and colleagues,⁹ other authors have reported transient neuropathies to the brachial plexus, which originates in the C5–C8 region, but not to the greater auricular nerve. Last, it cannot be ruled out that a variant of the greater auricular nerve could have played a role, given the variation in the greater auricular nerve.^10,11 However, Brennan and colleagues¹⁰ reported that 2 of 25 neck dissections involved a variant in which the anterior division of the greater auricular nerve passed into the submandibular triangle and joined the mandibular region of the facial nerve. Stimulation of this nerve resulted in activity of the depressor of the lower lip, which was not the location of our patient’s palsy. In addition, our patient’s symptoms followed a classic nerve distribution of the greater auricular nerve (Figures 1, 4), which would seem to decrease the likelihood that a variant was the source of the palsy.

The superficial nature of the greater auricular nerve, which runs roughly parallel with the sternocleidomastoid muscle and innervates much of the superficial region of the skin over the mastoid, parotid gland, and mandible,^5-7 theoretically places the nerve at risk for compressive forces from the headrest during arthroscopic shoulder surgery. Skyhar and colleagues³ first described beach-chair positioning as an alternative to lateral decubitus positioning, which had been reported to result in neurologic injury in about 10% of surgical cases.⁹ The theoretical advantages of beach-chair positioning are lack of traction needed and ease of setup, which would therefore decrease the possibility of neuropathy.^1,3 However, as seen in this and other case reports,^7,8 greater auricular nerve neuropathy should still be considered a possible complication, even when using beach-chair positioning.

Besides neuropathy after arthroscopic shoulder surgery, as described in previous case reports^7,8 and in the present report, greater auricular nerve injury has been described as arising from other stimuli. Greater auricular nerve injury has arisen after perineural tumor metastasis,⁶ neuroma of greater auricular nerve after endolympathic shunt surgery,¹² internal fixation of mandibular condyle,¹³ and carotid endarterectomy.^14,15 Given the superficial nature of the greater auricular nerve, it may not be all that surprising that a palsy could also develop after headrest compression during arthroscopic shoulder surgery.

This case report brings to light a possible complication of greater auricular nerve palsy during arthroscopic shoulder surgery using beach-chair positioning and a standard universal headrest. Studies should now investigate whether greater auricular nerve palsy is more common than realized, especially with regard to specific headrests in beach-chair positioning. For now, though, Dr. Foad’s intention is not to change to a different headrest or discontinue beach-chair positioning but to draw attention to this rare complication. Additional attention should be given to the location of the headrest in relation to the greater auricular nerve, especially in cases in which operative time may be longer.

Conclusion

We have reported a greater auricular nerve palsy that occurred after arthroscopic shoulder surgery for an anterior-inferior and posterior-inferior labral tear. This is the first report of a greater auricular nerve palsy occurring with beach-chair positioning and a standard universal headrest. Symptoms resolved within 6 months. New studies should investigate the incidence of greater auricular nerve palsy after arthroscopic shoulder surgery.

Anterior-inferior and posterior-inferior labral tears are common injuries treated with arthroscopic surgery¹ typically performed with beach-chair^2,3 or lateral decubitus^1,2 positioning and variable headrest positioning. Iatrogenic nerve damage that occurs after arthroscopic shoulder surgery—including damage to the suprascapular, axillary, musculocutaneous, subscapular, and spinal accessory nerves—has recently been reported to be more common than previously recognized.^2,4

Although iatrogenic nerve injuries are in general being recognized,^1,2,4 reports of greater auricular nerve injuries are limited. The greater auricular nerve is a superficial cutaneous nerve that arises from the cervical plexus at the C2 and C3 spinal nerves, obliquely crosses the sternocleidomastoid muscle, and splits into anterior and posterior portions that innervate the skin over the mastoid process and parotid gland.^5,6 In particular, as illustrated by Ginsberg and Eicher⁶ (Figure 1), its superficial anatomy lies very near where a headrest is positioned during arthroscopic surgery, and increased pressure on the nerve throughout arthroscopic shoulder surgery may lead to neurapraxia.^6,7 In 2 case series, authors reported on a total of 5 patients who had greater auricular nerve palsy after uncomplicated shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 The authors attributed these palsies to the horseshoe headrest, which they believed was compressing the greater auricular nerve during the entire surgery.^7,8 However, standard universal headrests, which are thought to distribute pressures that would theoretically place the greater auricular nerve at risk for palsy, previously had not been described as contributing to palsy of the greater auricular nerve.

In this article, we report on a case of greater auricular nerve palsy that occurred after the patient’s anterior-inferior and posterior-inferior labral tear was arthroscopically repaired using beach-chair positioning and a standard universal headrest. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An 18-year-old right-hand–dominant high school American football player was referred for orthopedic evaluation of left chronic glenohumeral instability after 6 months of physical therapy. Physical examination revealed a positive apprehension test with the shoulder abducted and externally rotated at 90° and a positive relocation test. The patient complained of pain and instability when his arm was placed in a cross-chest adducted position and a posteroinferiorly directed axial load was applied. Magnetic resonance arthrogram showed an anterior-inferior labral Bankart tear with a small Hill-Sachs lesion to the humeral head but did not clearly reveal the posterior-inferior labral tear. Because of persistent left shoulder instability with most overhead activities and continued pain, the patient decided to undergo left shoulder arthroscopic Bankart repair with inferior capsular shift and posterior-inferior labral repair with capsulorraphy. He had no significant past medical history or known drug allergies.

The patient was placed in the standard beach-chair position: upright at 45° to the floor, hips flexed at 60°, knees flexed at 30°.¹ Pneumatic compression devices were placed on his lower extremities. His head was secured in neutral position to a standard universal headrest (model A-90026; Allen Medical Systems, Acton, Massachusetts) (Figures 2, 3). Care was taken to protect the deep neurovascular structures and bony prominences throughout. The patient was in this position for 122 minutes of the operation, from positioning and draping to wound closure and dressing application. Before draping, the anesthesiologist, head nurse, and circulating nurse ensured that head and neck were in neutral position. The anesthesiologist monitored positioning throughout the perioperative period to ensure head and neck were in neutral, and the head did not need to be repositioned during surgery. Standard preoperative intravenous antibiotics were given.

General anesthesia and postoperative interscalene block were used. Standard preparation and draping were performed. Three standard arthroscopic portal incisions were used: posterior, anterior, and anterosuperolateral. Findings included extensive labral pathology, small bony Hill-Sachs lesion to humeral head, small bony anterior glenoid deficiency, and deficient anterior-inferior and posterior-inferior labral remnant. These were repaired arthroscopically in a standard fashion using bioabsorbable suture anchors. There were no arthroscopic complications. After surgery, a standard well-fitted shoulder immobilizer was placed. The anesthesiologist provided interscalene regional analgesia (15 mL of bupivacaine 0.5%) in the recovery area after surgery.

Postoperative neurovascular examination in the recovery room revealed no discomfort. The patient was discharged the same day. At a scheduled 1-week follow-up, he complained of numbness and dysesthesia on the left side of the greater auricular nerve distribution. A diagnosis of greater auricular nerve palsy was made by physical examination; the symptoms were along the classic greater auricular nerve distribution affecting the lower face and ear (Figure 4). The patient had no pain, skin lesions, or soft-tissue swelling. Otolaryngology confirmed the diagnosis and recommended observation-only treatment of symptoms. Symptoms lessened over the next 3 months, and the altered sensation resolved without deficit by 6 months. In addition, by 6 months the patient had returned to full activities (including collision sports) pain-free and with normal left shoulder function. Because symptoms continued to improve, the patient was followed with clinical observation, and a formal work-up was not necessary.

Discussion

The most important finding in this case is the greater auricular nerve palsy that occurred after arthroscopic anterior-inferior and posterior-inferior labral repairs in beach-chair positioning. This greater auricular nerve palsy was the first encountered by Dr. Foad, who over 17 years in a primarily shoulder practice setting has used beach-chair positioning exclusively. Previous reports have described a palsy occurring after arthroscopic shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 Ng and Page⁷ discontinued and recommended against use of this headrest because of the complications of the palsy, and Park and Kim⁸ recommended a headrest redesign. We think the present case report is the first to describe a greater auricular nerve palsy that occurred after arthroscopic surgery using a standard universal headrest, which theoretically should prevent compression of the greater auricular nerve. Increased awareness of the possibility of greater auricular nerve palsy, even when proper precautions are taken,¹ is therefore warranted.

Based on the location of our patient’s palsy, we think his paralysis was most likely the result of nerve compression by the headrest during the shoulder surgery. Other factors, though unlikely, may have played a role. These include operative time (increases duration of nerve compression) and head positioning. However, 122 minutes is not unusually long for a patient’s head to be in this position during a procedure, and over the past 10 years the same anesthesiologist, head nurse, and circulating nurse have routinely used the same beach-chair positioning and headrest for Dr. Foad’s patients. Second, the postoperative interscalene block theoretically could have caused the palsy, but we think this is unlikely, as the block is placed lower on the neck, at the C6 level, and the greater auricular nerve branches off the C2–C3 spinal nerves. As described by Rains and colleagues,⁹ other authors have reported transient neuropathies to the brachial plexus, which originates in the C5–C8 region, but not to the greater auricular nerve. Last, it cannot be ruled out that a variant of the greater auricular nerve could have played a role, given the variation in the greater auricular nerve.^10,11 However, Brennan and colleagues¹⁰ reported that 2 of 25 neck dissections involved a variant in which the anterior division of the greater auricular nerve passed into the submandibular triangle and joined the mandibular region of the facial nerve. Stimulation of this nerve resulted in activity of the depressor of the lower lip, which was not the location of our patient’s palsy. In addition, our patient’s symptoms followed a classic nerve distribution of the greater auricular nerve (Figures 1, 4), which would seem to decrease the likelihood that a variant was the source of the palsy.

The superficial nature of the greater auricular nerve, which runs roughly parallel with the sternocleidomastoid muscle and innervates much of the superficial region of the skin over the mastoid, parotid gland, and mandible,^5-7 theoretically places the nerve at risk for compressive forces from the headrest during arthroscopic shoulder surgery. Skyhar and colleagues³ first described beach-chair positioning as an alternative to lateral decubitus positioning, which had been reported to result in neurologic injury in about 10% of surgical cases.⁹ The theoretical advantages of beach-chair positioning are lack of traction needed and ease of setup, which would therefore decrease the possibility of neuropathy.^1,3 However, as seen in this and other case reports,^7,8 greater auricular nerve neuropathy should still be considered a possible complication, even when using beach-chair positioning.

Besides neuropathy after arthroscopic shoulder surgery, as described in previous case reports^7,8 and in the present report, greater auricular nerve injury has been described as arising from other stimuli. Greater auricular nerve injury has arisen after perineural tumor metastasis,⁶ neuroma of greater auricular nerve after endolympathic shunt surgery,¹² internal fixation of mandibular condyle,¹³ and carotid endarterectomy.^14,15 Given the superficial nature of the greater auricular nerve, it may not be all that surprising that a palsy could also develop after headrest compression during arthroscopic shoulder surgery.

This case report brings to light a possible complication of greater auricular nerve palsy during arthroscopic shoulder surgery using beach-chair positioning and a standard universal headrest. Studies should now investigate whether greater auricular nerve palsy is more common than realized, especially with regard to specific headrests in beach-chair positioning. For now, though, Dr. Foad’s intention is not to change to a different headrest or discontinue beach-chair positioning but to draw attention to this rare complication. Additional attention should be given to the location of the headrest in relation to the greater auricular nerve, especially in cases in which operative time may be longer.

Conclusion

We have reported a greater auricular nerve palsy that occurred after arthroscopic shoulder surgery for an anterior-inferior and posterior-inferior labral tear. This is the first report of a greater auricular nerve palsy occurring with beach-chair positioning and a standard universal headrest. Symptoms resolved within 6 months. New studies should investigate the incidence of greater auricular nerve palsy after arthroscopic shoulder surgery.

THE CASE

A 31-year-old man came to an internal medicine clinic because he’d been losing weight over the past 2 years and hadn’t been able to regain any weight despite eating properly. Our patient was born in Ethiopia, but had been living in Canada for 6 years. He reported a remote history of 2 episodes of diarrhea.

His physical exam was normal and laboratory results revealed mild eosinophilia of 0.6 × 10⁹/L (normal range, <0.45 × 10⁹/L). Additional tests (including complete blood count, electrolytes, liver panel, thyrotropin, and blood smear) revealed no apparent metabolic causes of the patient’s weight loss. Stool analysis (3 exams) was negative for ova and parasites.

THE DIAGNOSIS

Because our patient was born in Ethiopia, we did serologic testing for Strongyloides, which was positive (enzyme-linked immunosorbent assay for immunoglobulin G antibodies [IgG-ELISA] was 2.9; positive is >2.1). We diagnosed strongyloidiasis in this patient.

DISCUSSION

Strongyloidiasis is an infection caused by the parasite Strongyloides stercoralis.¹ It affects an estimated 30 to 100 million people worldwide, mainly in Africa, Southeast Asia, Central America, and South America, but it also can occur in temperate climates.²Strongyloides is a soil-transmitted helminth (parasitic worm). The prevalence of Strongyloides infection among refugee groups in the United States is 1% to 4.3%.^3-5

Although patients with strongyloidiasis are often asymptomatic, they can present with a wide range of nonspecific symptoms. In the acute stage, patients may develop signs and symptoms including cough, wheeze, abdominal pain, weight loss, diarrhea, pruritus ani, and larva currens.² Respiratory symptoms, including tracheal irritation and a dry cough, are often confused with asthma. In the generally asymptomatic chronic stage, patients may develop gastrointestinal complaints, such as epigastric pain and heartburn.⁶

Hyperinfection syndrome can occur when patients with subclinical infection receive high doses of corticosteroids for asthma or chronic obstructive pulmonary disease exacerbations. Risk of hyperinfection is increased among immunocompromised patients with human T lymphotropic virus type-1 (HTLV-1),⁷ as well as in patients with malignancies, malnutrition, and alcohol use disorder. Eosinophilia is often absent in patients with hyperinfection, and stool examination results are almost always positive.⁸

Who to screen, how to make the diagnosis

Suspect strongyloidiasis infection in immigrants, refugees, and travelers from endemic regions who have eosinophilia. The presence of eosinophilia in immigrants, refugees, and travelers from endemic regions should alert clinicians to the possibility of an underlying helminth infection. However, because eosinophilia occurs intermittently in response to tissue invasion, absence of eosinophilia does not exclude strongyloidiasis.

The Canadian Collaboration for Immigrants and Refugee Health (CCIRH) recommends using serologic testing to screen for Strongyloides in all newly arrived refugees from low-income countries in Southeast Asia and Africa.⁹ The CCIRH also advises that while data on the burden of strongyloidiasis in non-refugee immigrant populations is limited, you should consider screening foreign-born individuals who have lived in endemic areas, have symptoms and/or signs of Strongyloides infection, and/or have evidence of eosinophilia.⁹ Because the risk of hyperinfection is increased in immunocompromised individuals, screening should be done to detect Strongyloides infection before starting chemotherapy and before initiating corticosteroids in patients from endemic areas.¹⁰

Diagnostic methods. Stool examination⁶ and IgG-ELISA² are the main methods used to diagnose strongyloidiasis. However, traditional stool examinations have low sensitivity, and it may require up to 7 stool exams to reach a sensitivity of 100%,⁶ which could explain why our patient’s stool analysis was negative for parasites. In our experience, a positive serology result should always be assumed to indicate an active infection unless there is a well documented history of prior therapy. (In such cases, a positive serology result could represent persistent antibodies following therapy.)

First-line therapy and alternative treatment

All patients with strongyloidiasis, regardless of whether they are symptomatic, must be treated to prevent possible late-onset disseminated disease and hyperinfection.⁹ The Centers for Disease Control and Prevention recommends one to 2 doses of ivermectin 200 mcg/kg as first-line therapy or albendazole 400 mg twice daily for 3 days as an alternative treatment (TABLE).¹¹ Ivermectin cures more than 95% of cases.¹² Albendazole has lower efficacy (78%).¹³ Some experts recommend administering the 2 doses of ivermectin 2 weeks apart to allow enough time for the parasite to migrate to the gut.⁴

Consider referral to an infectious disease specialist for patients coinfected with HTLV-1, as well as those who are immunocompromised. Coinfection with HTLV-1 (which is endemic in areas where Strongyloides also is
endemic) modifies patients’ immune response and can complicate treatment.⁹ Clinicians should screen strongyloidiasis patients for HTLV-1 if they come from high-prevalence areas and/or have persistent strongyloidiasis that responds poorly to antiparasitic treatment.⁹

Consider referral to an infectious disease specialist for patients coinfected with
HTLV-1, as well as those who are immunocompromised. Such referral also may be appropriate for patients from countries where loa loa is endemic, because encephalopathy has occurred in patients coinfected with loa loa who were treated with ivermectin.¹⁰

Our patient was treated with 2 doses of ivermectin 200 mcg/kg, 2 weeks apart. Four months later, his eosinophilia had resolved, his IgG-ELISA dropped to 0.37, and he had gained 2.5 pounds.

THE TAKEAWAY

Strongyloidiasis is an infection caused by the parasitic worm Strongyloides stercoralis that is most common in tropical or subtropical areas. It can be asymptomatic or present with a wide range of nonspecific signs and symptoms, such as eosinophilia, cough, wheeze, abdominal pain, weight loss, diarrhea, pruritus ani, and larva currens. It is diagnosed by stool examination and serologic testing. Ivermectin is first-line therapy; albendazole is an alternative.

THE CASE

A 31-year-old man came to an internal medicine clinic because he’d been losing weight over the past 2 years and hadn’t been able to regain any weight despite eating properly. Our patient was born in Ethiopia, but had been living in Canada for 6 years. He reported a remote history of 2 episodes of diarrhea.

His physical exam was normal and laboratory results revealed mild eosinophilia of 0.6 × 10⁹/L (normal range, <0.45 × 10⁹/L). Additional tests (including complete blood count, electrolytes, liver panel, thyrotropin, and blood smear) revealed no apparent metabolic causes of the patient’s weight loss. Stool analysis (3 exams) was negative for ova and parasites.

THE DIAGNOSIS

Because our patient was born in Ethiopia, we did serologic testing for Strongyloides, which was positive (enzyme-linked immunosorbent assay for immunoglobulin G antibodies [IgG-ELISA] was 2.9; positive is >2.1). We diagnosed strongyloidiasis in this patient.

DISCUSSION

Strongyloidiasis is an infection caused by the parasite Strongyloides stercoralis.¹ It affects an estimated 30 to 100 million people worldwide, mainly in Africa, Southeast Asia, Central America, and South America, but it also can occur in temperate climates.²Strongyloides is a soil-transmitted helminth (parasitic worm). The prevalence of Strongyloides infection among refugee groups in the United States is 1% to 4.3%.^3-5

Although patients with strongyloidiasis are often asymptomatic, they can present with a wide range of nonspecific symptoms. In the acute stage, patients may develop signs and symptoms including cough, wheeze, abdominal pain, weight loss, diarrhea, pruritus ani, and larva currens.² Respiratory symptoms, including tracheal irritation and a dry cough, are often confused with asthma. In the generally asymptomatic chronic stage, patients may develop gastrointestinal complaints, such as epigastric pain and heartburn.⁶

Hyperinfection syndrome can occur when patients with subclinical infection receive high doses of corticosteroids for asthma or chronic obstructive pulmonary disease exacerbations. Risk of hyperinfection is increased among immunocompromised patients with human T lymphotropic virus type-1 (HTLV-1),⁷ as well as in patients with malignancies, malnutrition, and alcohol use disorder. Eosinophilia is often absent in patients with hyperinfection, and stool examination results are almost always positive.⁸

Who to screen, how to make the diagnosis

Suspect strongyloidiasis infection in immigrants, refugees, and travelers from endemic regions who have eosinophilia. The presence of eosinophilia in immigrants, refugees, and travelers from endemic regions should alert clinicians to the possibility of an underlying helminth infection. However, because eosinophilia occurs intermittently in response to tissue invasion, absence of eosinophilia does not exclude strongyloidiasis.

The Canadian Collaboration for Immigrants and Refugee Health (CCIRH) recommends using serologic testing to screen for Strongyloides in all newly arrived refugees from low-income countries in Southeast Asia and Africa.⁹ The CCIRH also advises that while data on the burden of strongyloidiasis in non-refugee immigrant populations is limited, you should consider screening foreign-born individuals who have lived in endemic areas, have symptoms and/or signs of Strongyloides infection, and/or have evidence of eosinophilia.⁹ Because the risk of hyperinfection is increased in immunocompromised individuals, screening should be done to detect Strongyloides infection before starting chemotherapy and before initiating corticosteroids in patients from endemic areas.¹⁰

Diagnostic methods. Stool examination⁶ and IgG-ELISA² are the main methods used to diagnose strongyloidiasis. However, traditional stool examinations have low sensitivity, and it may require up to 7 stool exams to reach a sensitivity of 100%,⁶ which could explain why our patient’s stool analysis was negative for parasites. In our experience, a positive serology result should always be assumed to indicate an active infection unless there is a well documented history of prior therapy. (In such cases, a positive serology result could represent persistent antibodies following therapy.)

First-line therapy and alternative treatment

All patients with strongyloidiasis, regardless of whether they are symptomatic, must be treated to prevent possible late-onset disseminated disease and hyperinfection.⁹ The Centers for Disease Control and Prevention recommends one to 2 doses of ivermectin 200 mcg/kg as first-line therapy or albendazole 400 mg twice daily for 3 days as an alternative treatment (TABLE).¹¹ Ivermectin cures more than 95% of cases.¹² Albendazole has lower efficacy (78%).¹³ Some experts recommend administering the 2 doses of ivermectin 2 weeks apart to allow enough time for the parasite to migrate to the gut.⁴

Consider referral to an infectious disease specialist for patients coinfected with HTLV-1, as well as those who are immunocompromised. Coinfection with HTLV-1 (which is endemic in areas where Strongyloides also is
endemic) modifies patients’ immune response and can complicate treatment.⁹ Clinicians should screen strongyloidiasis patients for HTLV-1 if they come from high-prevalence areas and/or have persistent strongyloidiasis that responds poorly to antiparasitic treatment.⁹

Consider referral to an infectious disease specialist for patients coinfected with
HTLV-1, as well as those who are immunocompromised. Such referral also may be appropriate for patients from countries where loa loa is endemic, because encephalopathy has occurred in patients coinfected with loa loa who were treated with ivermectin.¹⁰

Our patient was treated with 2 doses of ivermectin 200 mcg/kg, 2 weeks apart. Four months later, his eosinophilia had resolved, his IgG-ELISA dropped to 0.37, and he had gained 2.5 pounds.

THE TAKEAWAY

Strongyloidiasis is an infection caused by the parasitic worm Strongyloides stercoralis that is most common in tropical or subtropical areas. It can be asymptomatic or present with a wide range of nonspecific signs and symptoms, such as eosinophilia, cough, wheeze, abdominal pain, weight loss, diarrhea, pruritus ani, and larva currens. It is diagnosed by stool examination and serologic testing. Ivermectin is first-line therapy; albendazole is an alternative.

THE CASE

A 31-year-old man came to an internal medicine clinic because he’d been losing weight over the past 2 years and hadn’t been able to regain any weight despite eating properly. Our patient was born in Ethiopia, but had been living in Canada for 6 years. He reported a remote history of 2 episodes of diarrhea.

His physical exam was normal and laboratory results revealed mild eosinophilia of 0.6 × 10⁹/L (normal range, <0.45 × 10⁹/L). Additional tests (including complete blood count, electrolytes, liver panel, thyrotropin, and blood smear) revealed no apparent metabolic causes of the patient’s weight loss. Stool analysis (3 exams) was negative for ova and parasites.

THE DIAGNOSIS

Because our patient was born in Ethiopia, we did serologic testing for Strongyloides, which was positive (enzyme-linked immunosorbent assay for immunoglobulin G antibodies [IgG-ELISA] was 2.9; positive is >2.1). We diagnosed strongyloidiasis in this patient.

DISCUSSION

Strongyloidiasis is an infection caused by the parasite Strongyloides stercoralis.¹ It affects an estimated 30 to 100 million people worldwide, mainly in Africa, Southeast Asia, Central America, and South America, but it also can occur in temperate climates.²Strongyloides is a soil-transmitted helminth (parasitic worm). The prevalence of Strongyloides infection among refugee groups in the United States is 1% to 4.3%.^3-5

Although patients with strongyloidiasis are often asymptomatic, they can present with a wide range of nonspecific symptoms. In the acute stage, patients may develop signs and symptoms including cough, wheeze, abdominal pain, weight loss, diarrhea, pruritus ani, and larva currens.² Respiratory symptoms, including tracheal irritation and a dry cough, are often confused with asthma. In the generally asymptomatic chronic stage, patients may develop gastrointestinal complaints, such as epigastric pain and heartburn.⁶

Hyperinfection syndrome can occur when patients with subclinical infection receive high doses of corticosteroids for asthma or chronic obstructive pulmonary disease exacerbations. Risk of hyperinfection is increased among immunocompromised patients with human T lymphotropic virus type-1 (HTLV-1),⁷ as well as in patients with malignancies, malnutrition, and alcohol use disorder. Eosinophilia is often absent in patients with hyperinfection, and stool examination results are almost always positive.⁸

Who to screen, how to make the diagnosis

Suspect strongyloidiasis infection in immigrants, refugees, and travelers from endemic regions who have eosinophilia. The presence of eosinophilia in immigrants, refugees, and travelers from endemic regions should alert clinicians to the possibility of an underlying helminth infection. However, because eosinophilia occurs intermittently in response to tissue invasion, absence of eosinophilia does not exclude strongyloidiasis.

The Canadian Collaboration for Immigrants and Refugee Health (CCIRH) recommends using serologic testing to screen for Strongyloides in all newly arrived refugees from low-income countries in Southeast Asia and Africa.⁹ The CCIRH also advises that while data on the burden of strongyloidiasis in non-refugee immigrant populations is limited, you should consider screening foreign-born individuals who have lived in endemic areas, have symptoms and/or signs of Strongyloides infection, and/or have evidence of eosinophilia.⁹ Because the risk of hyperinfection is increased in immunocompromised individuals, screening should be done to detect Strongyloides infection before starting chemotherapy and before initiating corticosteroids in patients from endemic areas.¹⁰

Diagnostic methods. Stool examination⁶ and IgG-ELISA² are the main methods used to diagnose strongyloidiasis. However, traditional stool examinations have low sensitivity, and it may require up to 7 stool exams to reach a sensitivity of 100%,⁶ which could explain why our patient’s stool analysis was negative for parasites. In our experience, a positive serology result should always be assumed to indicate an active infection unless there is a well documented history of prior therapy. (In such cases, a positive serology result could represent persistent antibodies following therapy.)

First-line therapy and alternative treatment

All patients with strongyloidiasis, regardless of whether they are symptomatic, must be treated to prevent possible late-onset disseminated disease and hyperinfection.⁹ The Centers for Disease Control and Prevention recommends one to 2 doses of ivermectin 200 mcg/kg as first-line therapy or albendazole 400 mg twice daily for 3 days as an alternative treatment (TABLE).¹¹ Ivermectin cures more than 95% of cases.¹² Albendazole has lower efficacy (78%).¹³ Some experts recommend administering the 2 doses of ivermectin 2 weeks apart to allow enough time for the parasite to migrate to the gut.⁴

Consider referral to an infectious disease specialist for patients coinfected with HTLV-1, as well as those who are immunocompromised. Coinfection with HTLV-1 (which is endemic in areas where Strongyloides also is
endemic) modifies patients’ immune response and can complicate treatment.⁹ Clinicians should screen strongyloidiasis patients for HTLV-1 if they come from high-prevalence areas and/or have persistent strongyloidiasis that responds poorly to antiparasitic treatment.⁹

Consider referral to an infectious disease specialist for patients coinfected with
HTLV-1, as well as those who are immunocompromised. Such referral also may be appropriate for patients from countries where loa loa is endemic, because encephalopathy has occurred in patients coinfected with loa loa who were treated with ivermectin.¹⁰

Our patient was treated with 2 doses of ivermectin 200 mcg/kg, 2 weeks apart. Four months later, his eosinophilia had resolved, his IgG-ELISA dropped to 0.37, and he had gained 2.5 pounds.

THE TAKEAWAY

Strongyloidiasis is an infection caused by the parasitic worm Strongyloides stercoralis that is most common in tropical or subtropical areas. It can be asymptomatic or present with a wide range of nonspecific signs and symptoms, such as eosinophilia, cough, wheeze, abdominal pain, weight loss, diarrhea, pruritus ani, and larva currens. It is diagnosed by stool examination and serologic testing. Ivermectin is first-line therapy; albendazole is an alternative.

Case

A previously healthy 10-month-old girl was brought to the ED by her mother, who noted that the child had been excessively drowsy throughout the day. She reported that her husband had dropped an unknown amount of his morphine sulfate extended-release 60-mg tablets and oxycodone 10-mg/acetaminophen 325-mg tablets on the floor 5 days earlier. Although unsure of how many tablets he had dropped, the father believed he had located all of them. The mother, however, found some of the tablets around the crib in their daughter’s room.

When the child arrived to the ED, her vital signs were: blood pressure, 95/60 mm Hg; heart rate, 102 beats/minute; respiratory rate (RR), 18 breaths/minute; and temperature, 98.4°F. Oxygen saturation was 98% on room air. On physical examination, the child was lethargic, her pupils were less than 1 mm in diameter, and her bowel sounds were absent. After the administration of intravenous (IV) naloxone 0.4 mg, the patient became less drowsy and her RR normalized. Approximately 1 hour later, though, the child again became lethargic; she was given a repeat dose of IV naloxone 0.4 mg, and a naloxone infusion was initiated at 0.3 mg/h. Over approximately 20 hours, the infusion was tapered and discontinued. Three hours after the infusion was stopped, the child’s vital signs and behavior were both normal. After a social worker and representative from the Administration for Children’s Services reviewed the patient’s case, she was discharged home with her parents.

Less than 1 hour later, however, the mother returned to the ED with the child, who was again unresponsive. Although the girl’s RR was normal, she had pinpoint pupils. After she was given IV naloxone 0.4 mg, the child awoke and remained responsive for 20 minutes before returning to a somnolent state. Another IV dose of naloxone 0.4 mg was administered, which showed partial improvement in responsiveness. A naloxone infusion was then initiated and titrated up to 1 mg/h to maintain wakefulness and ventilation. In the pediatric intensive care unit, the child required titration of the naloxone infusion to 2 mg/h to which she responded well. Over the next 12 hours, the infusion was tapered off and the child was discharged home with her parents.

Blood samples from both the initial visit and the return visit were sent for toxicologic analysis by gas chromatography-mass spectrometry (GC-MS). Serum from the first visit contained morphine at a concentration of 3,000 ng/mL; serum from the second visit contained morphine at 420 ng/mL. Both samples were negative for oxycodone or any of the other substances checked on the extended GC-MS screen.

What is the toxicologic differential?

Although this patient’s extreme somnolence was suspected to be opioid-induced, and was confirmed by an appropriate response to naloxone, children may present to the ED somnolent for a variety of unknown reasons. Even with a fairly clear history, the clinician should also consider metabolic, neurological, infectious, traumatic, and psychiatric causes of altered mental status.¹ The toxicologic causes of altered mental status are expansive and include the effects of many medications used therapeutically or in overdose. Opioids, benzodiazepines, barbiturates, α-2 agonists (eg, clonidine), sleep aids (eg, zolpidem, diphenhydramine), and ethanol are common causes of induced an altered mental status. When taking a toxicologic history, it is important to inquire not only about the patient’s medications but also the medications of other members of the household to which the patient may have access. This includes not only prescription medications but also over-the-counter, complementary, and herbal preparations.

Why did this child have delayed recurrent opioid toxicity?

When used as directed, opioids cause analgesia and euphoria. Analgesia is mediated by agonism at the μ- , κ-, and δ-opioid receptors throughout the brain and spinal cord. The majority of morphine’s analgesic activity comes from activation of the μ-opioid receptors.² In overdose, opioids classically cause a toxidrome characterized by miosis, coma, decreased bowel sounds, and respiratory depression. These signs can give clues to a patient’s exposure.

Supportive care is the cornerstone of treatment for patients with opioid toxicity, and maintaining the airway and monitoring the respiratory status are extremely important. When ventilation decreases due to the actions of opioids (typically denoted by a RR of <12 breaths/minute in adults, but may be marked by a reduction in depth of breathing as well), the use of an opioid antagonist is appropriate.⁴ The most commonly used antagonist is naloxone, an antidote with antagonism at all opioid receptor subtypes.⁵

In patients who are not dependent on opioids, IV naloxone 0.4 mg is an appropriate initial dose—regardless of patient size or specifics of the exposure. Patients with opioid dependency (eg, patients taking opioids for chronic pain or palliative care, or in those with suspected or confirmed opioid abuse), should receive smaller initial doses of naloxone (eg, 0.04 mg); the dose should be titrated up to effect to avoid precipitating acute opioid withdrawal. The goal of opioid antagonism is to allow the patient to breathe spontaneously and at an appropriate rate and depth without precipitating withdrawal. The duration of action of naloxone is 20 to 90 minutes in adults.

Patients presenting with heroin overdose should be monitored for at least 2 hours after naloxone administration (some suggest 3 hours) to determine whether or not additional dosing will be necessary. After oral opioid exposures, particularly with extended-release or long-acting formulations, longer periods of observation are required (this is unrelated to the naloxone pharmacokinetics, but rather to the slow rise in blood levels from some of these formulations). If repeated opioid toxicity occurs in adults, a naloxone infusion may be helpful to reduce the need for repetitive re-dosing. Initially, an hourly infusion equal to two-thirds of the dose of naloxone that reversed the patient’s respiratory depression is suggested⁶

Naloxone is eliminated by conjugation with glucuronic acid before is it excreted from the body. Due to decreased hepatic conjugation and prolonged metabolization of drugs in pediatric patients, naloxone may have a longer half-life in children—especially neonates and infants⁷; in children, the half-life of naloxone may extend up to three times that of adults.⁸ This extended half-life can lead to a false sense of assurance that a child is free of opioid effects 120 minutes after receiving naloxone—the time by which an adult patient would likely be without significant systemic effects of naloxone—when in fact the effect of naloxone has not yet sufficiently waned. This in turn may prompt discharge before sufficient time has passed to exclude recrudescence of opioid toxicity: The presence of persistent opioid agonist concentrations in the blood, even at consequential amounts, remains masked by the persistent presence of naloxone.

The goal of opioid antagonism is to allow the patient to breathe spontaneously and at an appropriate rate and depth without precipitating withdrawal. In this patient, it is not surprising that the the ingestion of an extended-relief form of morphine should produce a prolonged opioid effect. At therapeutic concentrations in children (~10 ng/mL), the half-life of morphine is slightly longer than in adults (~3 hours vs 2 hours) and is likely even longer with very high serum concentrations. It is metabolized to morphine 6-glucuronide, which is active and longer lasting than the parent compound. This may account for additional clinical effects beyond the time that the serum morphine concentration falls, and is particularly relevant following immediate-release morphine overdose.

In this case it is also important to consider whether or not the patient was re-exposed to an opioid between the first and second ED visit. The dramatically elevated initial serum morphine concentrations and the relatively appropriate fall in magnitude of the second sample suggest that the recurrence of respiratory depression was not the result of re-exposure. The patient’s recurrent effects, even a day out from exposure, can be explained by the immediate-release morphine exposure and the discharge prior to waning of the naloxone. In children with opioid toxicity, another potential option, though not directly studied, is to administer the long-acting opioid antagonist naltrexone to the patient prior to discharge.

Case Conclusion

When used appropriately and under the correct circumstances, naloxone is safe and effective for the reversal of opioid toxicity. As with any antidote, patients must be appropriately monitored for any adverse effects or recurrence of toxicity. Moreover, the clinician should be mindful of the pharmacokinetic differences between adults and young children and the possibility of a later-than-expected recurrence of opioid toxicity in pediatric patients.

This case is a reminder of the importance of safe medication storage. Infants and young children who are crawling and exploring their environment are especially vulnerable to toxicity from medications found on the floor. Regardless of age, quick recognition of opioid-induced respiratory depression and appropriate use of naloxone can help to decrease the morbidity associated with excessive opioid exposures in all patients.

Dr Berman is a senior medical toxicology fellow at North Shore-Long Island Jewish Medical Center, New York. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board. Dr Majlesi is the director of medical toxicology at Staten Island University Hospital, New York.

Case

A previously healthy 10-month-old girl was brought to the ED by her mother, who noted that the child had been excessively drowsy throughout the day. She reported that her husband had dropped an unknown amount of his morphine sulfate extended-release 60-mg tablets and oxycodone 10-mg/acetaminophen 325-mg tablets on the floor 5 days earlier. Although unsure of how many tablets he had dropped, the father believed he had located all of them. The mother, however, found some of the tablets around the crib in their daughter’s room.

When the child arrived to the ED, her vital signs were: blood pressure, 95/60 mm Hg; heart rate, 102 beats/minute; respiratory rate (RR), 18 breaths/minute; and temperature, 98.4°F. Oxygen saturation was 98% on room air. On physical examination, the child was lethargic, her pupils were less than 1 mm in diameter, and her bowel sounds were absent. After the administration of intravenous (IV) naloxone 0.4 mg, the patient became less drowsy and her RR normalized. Approximately 1 hour later, though, the child again became lethargic; she was given a repeat dose of IV naloxone 0.4 mg, and a naloxone infusion was initiated at 0.3 mg/h. Over approximately 20 hours, the infusion was tapered and discontinued. Three hours after the infusion was stopped, the child’s vital signs and behavior were both normal. After a social worker and representative from the Administration for Children’s Services reviewed the patient’s case, she was discharged home with her parents.

Less than 1 hour later, however, the mother returned to the ED with the child, who was again unresponsive. Although the girl’s RR was normal, she had pinpoint pupils. After she was given IV naloxone 0.4 mg, the child awoke and remained responsive for 20 minutes before returning to a somnolent state. Another IV dose of naloxone 0.4 mg was administered, which showed partial improvement in responsiveness. A naloxone infusion was then initiated and titrated up to 1 mg/h to maintain wakefulness and ventilation. In the pediatric intensive care unit, the child required titration of the naloxone infusion to 2 mg/h to which she responded well. Over the next 12 hours, the infusion was tapered off and the child was discharged home with her parents.

Blood samples from both the initial visit and the return visit were sent for toxicologic analysis by gas chromatography-mass spectrometry (GC-MS). Serum from the first visit contained morphine at a concentration of 3,000 ng/mL; serum from the second visit contained morphine at 420 ng/mL. Both samples were negative for oxycodone or any of the other substances checked on the extended GC-MS screen.

What is the toxicologic differential?

Although this patient’s extreme somnolence was suspected to be opioid-induced, and was confirmed by an appropriate response to naloxone, children may present to the ED somnolent for a variety of unknown reasons. Even with a fairly clear history, the clinician should also consider metabolic, neurological, infectious, traumatic, and psychiatric causes of altered mental status.¹ The toxicologic causes of altered mental status are expansive and include the effects of many medications used therapeutically or in overdose. Opioids, benzodiazepines, barbiturates, α-2 agonists (eg, clonidine), sleep aids (eg, zolpidem, diphenhydramine), and ethanol are common causes of induced an altered mental status. When taking a toxicologic history, it is important to inquire not only about the patient’s medications but also the medications of other members of the household to which the patient may have access. This includes not only prescription medications but also over-the-counter, complementary, and herbal preparations.

Why did this child have delayed recurrent opioid toxicity?

When used as directed, opioids cause analgesia and euphoria. Analgesia is mediated by agonism at the μ- , κ-, and δ-opioid receptors throughout the brain and spinal cord. The majority of morphine’s analgesic activity comes from activation of the μ-opioid receptors.² In overdose, opioids classically cause a toxidrome characterized by miosis, coma, decreased bowel sounds, and respiratory depression. These signs can give clues to a patient’s exposure.

Supportive care is the cornerstone of treatment for patients with opioid toxicity, and maintaining the airway and monitoring the respiratory status are extremely important. When ventilation decreases due to the actions of opioids (typically denoted by a RR of <12 breaths/minute in adults, but may be marked by a reduction in depth of breathing as well), the use of an opioid antagonist is appropriate.⁴ The most commonly used antagonist is naloxone, an antidote with antagonism at all opioid receptor subtypes.⁵

In patients who are not dependent on opioids, IV naloxone 0.4 mg is an appropriate initial dose—regardless of patient size or specifics of the exposure. Patients with opioid dependency (eg, patients taking opioids for chronic pain or palliative care, or in those with suspected or confirmed opioid abuse), should receive smaller initial doses of naloxone (eg, 0.04 mg); the dose should be titrated up to effect to avoid precipitating acute opioid withdrawal. The goal of opioid antagonism is to allow the patient to breathe spontaneously and at an appropriate rate and depth without precipitating withdrawal. The duration of action of naloxone is 20 to 90 minutes in adults.

Patients presenting with heroin overdose should be monitored for at least 2 hours after naloxone administration (some suggest 3 hours) to determine whether or not additional dosing will be necessary. After oral opioid exposures, particularly with extended-release or long-acting formulations, longer periods of observation are required (this is unrelated to the naloxone pharmacokinetics, but rather to the slow rise in blood levels from some of these formulations). If repeated opioid toxicity occurs in adults, a naloxone infusion may be helpful to reduce the need for repetitive re-dosing. Initially, an hourly infusion equal to two-thirds of the dose of naloxone that reversed the patient’s respiratory depression is suggested⁶

Naloxone is eliminated by conjugation with glucuronic acid before is it excreted from the body. Due to decreased hepatic conjugation and prolonged metabolization of drugs in pediatric patients, naloxone may have a longer half-life in children—especially neonates and infants⁷; in children, the half-life of naloxone may extend up to three times that of adults.⁸ This extended half-life can lead to a false sense of assurance that a child is free of opioid effects 120 minutes after receiving naloxone—the time by which an adult patient would likely be without significant systemic effects of naloxone—when in fact the effect of naloxone has not yet sufficiently waned. This in turn may prompt discharge before sufficient time has passed to exclude recrudescence of opioid toxicity: The presence of persistent opioid agonist concentrations in the blood, even at consequential amounts, remains masked by the persistent presence of naloxone.

The goal of opioid antagonism is to allow the patient to breathe spontaneously and at an appropriate rate and depth without precipitating withdrawal. In this patient, it is not surprising that the the ingestion of an extended-relief form of morphine should produce a prolonged opioid effect. At therapeutic concentrations in children (~10 ng/mL), the half-life of morphine is slightly longer than in adults (~3 hours vs 2 hours) and is likely even longer with very high serum concentrations. It is metabolized to morphine 6-glucuronide, which is active and longer lasting than the parent compound. This may account for additional clinical effects beyond the time that the serum morphine concentration falls, and is particularly relevant following immediate-release morphine overdose.

In this case it is also important to consider whether or not the patient was re-exposed to an opioid between the first and second ED visit. The dramatically elevated initial serum morphine concentrations and the relatively appropriate fall in magnitude of the second sample suggest that the recurrence of respiratory depression was not the result of re-exposure. The patient’s recurrent effects, even a day out from exposure, can be explained by the immediate-release morphine exposure and the discharge prior to waning of the naloxone. In children with opioid toxicity, another potential option, though not directly studied, is to administer the long-acting opioid antagonist naltrexone to the patient prior to discharge.

Case Conclusion

When used appropriately and under the correct circumstances, naloxone is safe and effective for the reversal of opioid toxicity. As with any antidote, patients must be appropriately monitored for any adverse effects or recurrence of toxicity. Moreover, the clinician should be mindful of the pharmacokinetic differences between adults and young children and the possibility of a later-than-expected recurrence of opioid toxicity in pediatric patients.

This case is a reminder of the importance of safe medication storage. Infants and young children who are crawling and exploring their environment are especially vulnerable to toxicity from medications found on the floor. Regardless of age, quick recognition of opioid-induced respiratory depression and appropriate use of naloxone can help to decrease the morbidity associated with excessive opioid exposures in all patients.

Dr Berman is a senior medical toxicology fellow at North Shore-Long Island Jewish Medical Center, New York. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board. Dr Majlesi is the director of medical toxicology at Staten Island University Hospital, New York.

Case

A previously healthy 10-month-old girl was brought to the ED by her mother, who noted that the child had been excessively drowsy throughout the day. She reported that her husband had dropped an unknown amount of his morphine sulfate extended-release 60-mg tablets and oxycodone 10-mg/acetaminophen 325-mg tablets on the floor 5 days earlier. Although unsure of how many tablets he had dropped, the father believed he had located all of them. The mother, however, found some of the tablets around the crib in their daughter’s room.

When the child arrived to the ED, her vital signs were: blood pressure, 95/60 mm Hg; heart rate, 102 beats/minute; respiratory rate (RR), 18 breaths/minute; and temperature, 98.4°F. Oxygen saturation was 98% on room air. On physical examination, the child was lethargic, her pupils were less than 1 mm in diameter, and her bowel sounds were absent. After the administration of intravenous (IV) naloxone 0.4 mg, the patient became less drowsy and her RR normalized. Approximately 1 hour later, though, the child again became lethargic; she was given a repeat dose of IV naloxone 0.4 mg, and a naloxone infusion was initiated at 0.3 mg/h. Over approximately 20 hours, the infusion was tapered and discontinued. Three hours after the infusion was stopped, the child’s vital signs and behavior were both normal. After a social worker and representative from the Administration for Children’s Services reviewed the patient’s case, she was discharged home with her parents.

Less than 1 hour later, however, the mother returned to the ED with the child, who was again unresponsive. Although the girl’s RR was normal, she had pinpoint pupils. After she was given IV naloxone 0.4 mg, the child awoke and remained responsive for 20 minutes before returning to a somnolent state. Another IV dose of naloxone 0.4 mg was administered, which showed partial improvement in responsiveness. A naloxone infusion was then initiated and titrated up to 1 mg/h to maintain wakefulness and ventilation. In the pediatric intensive care unit, the child required titration of the naloxone infusion to 2 mg/h to which she responded well. Over the next 12 hours, the infusion was tapered off and the child was discharged home with her parents.

Blood samples from both the initial visit and the return visit were sent for toxicologic analysis by gas chromatography-mass spectrometry (GC-MS). Serum from the first visit contained morphine at a concentration of 3,000 ng/mL; serum from the second visit contained morphine at 420 ng/mL. Both samples were negative for oxycodone or any of the other substances checked on the extended GC-MS screen.

What is the toxicologic differential?

Although this patient’s extreme somnolence was suspected to be opioid-induced, and was confirmed by an appropriate response to naloxone, children may present to the ED somnolent for a variety of unknown reasons. Even with a fairly clear history, the clinician should also consider metabolic, neurological, infectious, traumatic, and psychiatric causes of altered mental status.¹ The toxicologic causes of altered mental status are expansive and include the effects of many medications used therapeutically or in overdose. Opioids, benzodiazepines, barbiturates, α-2 agonists (eg, clonidine), sleep aids (eg, zolpidem, diphenhydramine), and ethanol are common causes of induced an altered mental status. When taking a toxicologic history, it is important to inquire not only about the patient’s medications but also the medications of other members of the household to which the patient may have access. This includes not only prescription medications but also over-the-counter, complementary, and herbal preparations.

Why did this child have delayed recurrent opioid toxicity?

When used as directed, opioids cause analgesia and euphoria. Analgesia is mediated by agonism at the μ- , κ-, and δ-opioid receptors throughout the brain and spinal cord. The majority of morphine’s analgesic activity comes from activation of the μ-opioid receptors.² In overdose, opioids classically cause a toxidrome characterized by miosis, coma, decreased bowel sounds, and respiratory depression. These signs can give clues to a patient’s exposure.

Supportive care is the cornerstone of treatment for patients with opioid toxicity, and maintaining the airway and monitoring the respiratory status are extremely important. When ventilation decreases due to the actions of opioids (typically denoted by a RR of <12 breaths/minute in adults, but may be marked by a reduction in depth of breathing as well), the use of an opioid antagonist is appropriate.⁴ The most commonly used antagonist is naloxone, an antidote with antagonism at all opioid receptor subtypes.⁵

In patients who are not dependent on opioids, IV naloxone 0.4 mg is an appropriate initial dose—regardless of patient size or specifics of the exposure. Patients with opioid dependency (eg, patients taking opioids for chronic pain or palliative care, or in those with suspected or confirmed opioid abuse), should receive smaller initial doses of naloxone (eg, 0.04 mg); the dose should be titrated up to effect to avoid precipitating acute opioid withdrawal. The goal of opioid antagonism is to allow the patient to breathe spontaneously and at an appropriate rate and depth without precipitating withdrawal. The duration of action of naloxone is 20 to 90 minutes in adults.

Patients presenting with heroin overdose should be monitored for at least 2 hours after naloxone administration (some suggest 3 hours) to determine whether or not additional dosing will be necessary. After oral opioid exposures, particularly with extended-release or long-acting formulations, longer periods of observation are required (this is unrelated to the naloxone pharmacokinetics, but rather to the slow rise in blood levels from some of these formulations). If repeated opioid toxicity occurs in adults, a naloxone infusion may be helpful to reduce the need for repetitive re-dosing. Initially, an hourly infusion equal to two-thirds of the dose of naloxone that reversed the patient’s respiratory depression is suggested⁶

Naloxone is eliminated by conjugation with glucuronic acid before is it excreted from the body. Due to decreased hepatic conjugation and prolonged metabolization of drugs in pediatric patients, naloxone may have a longer half-life in children—especially neonates and infants⁷; in children, the half-life of naloxone may extend up to three times that of adults.⁸ This extended half-life can lead to a false sense of assurance that a child is free of opioid effects 120 minutes after receiving naloxone—the time by which an adult patient would likely be without significant systemic effects of naloxone—when in fact the effect of naloxone has not yet sufficiently waned. This in turn may prompt discharge before sufficient time has passed to exclude recrudescence of opioid toxicity: The presence of persistent opioid agonist concentrations in the blood, even at consequential amounts, remains masked by the persistent presence of naloxone.

The goal of opioid antagonism is to allow the patient to breathe spontaneously and at an appropriate rate and depth without precipitating withdrawal. In this patient, it is not surprising that the the ingestion of an extended-relief form of morphine should produce a prolonged opioid effect. At therapeutic concentrations in children (~10 ng/mL), the half-life of morphine is slightly longer than in adults (~3 hours vs 2 hours) and is likely even longer with very high serum concentrations. It is metabolized to morphine 6-glucuronide, which is active and longer lasting than the parent compound. This may account for additional clinical effects beyond the time that the serum morphine concentration falls, and is particularly relevant following immediate-release morphine overdose.

In this case it is also important to consider whether or not the patient was re-exposed to an opioid between the first and second ED visit. The dramatically elevated initial serum morphine concentrations and the relatively appropriate fall in magnitude of the second sample suggest that the recurrence of respiratory depression was not the result of re-exposure. The patient’s recurrent effects, even a day out from exposure, can be explained by the immediate-release morphine exposure and the discharge prior to waning of the naloxone. In children with opioid toxicity, another potential option, though not directly studied, is to administer the long-acting opioid antagonist naltrexone to the patient prior to discharge.

Case Conclusion

When used appropriately and under the correct circumstances, naloxone is safe and effective for the reversal of opioid toxicity. As with any antidote, patients must be appropriately monitored for any adverse effects or recurrence of toxicity. Moreover, the clinician should be mindful of the pharmacokinetic differences between adults and young children and the possibility of a later-than-expected recurrence of opioid toxicity in pediatric patients.

This case is a reminder of the importance of safe medication storage. Infants and young children who are crawling and exploring their environment are especially vulnerable to toxicity from medications found on the floor. Regardless of age, quick recognition of opioid-induced respiratory depression and appropriate use of naloxone can help to decrease the morbidity associated with excessive opioid exposures in all patients.

Dr Berman is a senior medical toxicology fellow at North Shore-Long Island Jewish Medical Center, New York. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board. Dr Majlesi is the director of medical toxicology at Staten Island University Hospital, New York.

Fracture of the tibial shaft below an ipsilateral total knee arthroplasty (TKA) is an infrequently occurring injury pattern that presents a unique treatment scenario. The high predilection for open wounds associated with these diaphyseal fractures further complicates the treatment algorithm.^1,2 The standard principles of treatment for open tibial shaft fractures entail open fracture débridement followed by adequate fracture reduction and stable skeletal fixation in a manner that limits adverse complications of this injury, which include nonunion, malunion, infection, soft-tissue compromise, and reoperation.^3,4

Antegrade intramedullary (IM) tibial nailing has become standard treatment for tibial shaft fractures.^5-7 This minimally invasive method of fixation limits damage to the soft-tissue envelope, provides superior neutralization of the mechanical forces to provide a template for biologic fracture healing, and allows the best options for revision procedures in the event of inadequate healing. This case report examines treatment options for an open tibial shaft fracture of an ipsilateral TKA, complicating the standard treatment of antegrade tibial nailing. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 66-year-old woman became light-headed and fell down a flight of stairs at her home. She was taken to the local emergency room where she presented with left leg pain, deformity, and a skin wound. The wound was dressed with sterile gauze and the extremity immobilized in a temporary plaster splint after which the patient was transferred to our level I trauma center. The accident occurred shortly after dawn, and she received definitive evaluation at the level I trauma center before noon the same day, making the time from injury to evaluation less than 6 hours.

The patient’s medical history was significant for depressive and anxiety disorders, fibromyalgia, hypertension, peripheral vascular disease, and lymphedema. Her surgical history was significant for a remote left TKA and remote open reduction with internal fixation of a left lateral malleolus fracture. She was prescribed antidepressant and anti-anxiolytic medications, narcotic medication, and antihypertensive therapy. She smoked 1 pack of cigarettes per day for approximately 20 years and denied alcohol consumption or illicit drug use. Her body mass index was 37.5, and she ambulated independently in the community.

Upon presentation at our hospital, the patient was hemodynamically stable with no discernable systemic compromise from the extremity injury. An examination of the left lower extremity showed a large longitudinal skin wound over the anteromedial surface of the lower leg measuring roughly 10 cm in length with obvious periosteal stripping and protrusion of the proximal fracture segment. Neurologic motor and sensory function was intact in the lower extremities and pulses were strong. Lower leg compartments were soft. Radiographic imaging confirmed a short oblique fracture of the distal third of the tibial diaphysis. The left TKA was intact with no signs of component loosening or periprosthetic fracture (Figures 1A, 1B).

The patient urgently received broad-spectrum antibiotics with intravenous (IV) cefazolin and IV gentamicin as well as tetanus vaccination. Her fracture was temporarily stabilized in a long-leg splint before she was transported to the operating room. Based upon the characteristics of the patient and the open fracture, we had an extensive discussion with the patient regarding the severity of her injury and treatment options, including nonoperative treatment, operative irrigation and débridement with skeletal stabilization, or below-knee amputation. The patient was adamant that limb salvage be attempted despite adequate understanding that she was exposing herself to risk of multiple reoperations from potential complications, as well as systemic medical compromise. Thus, we considered possible techniques for internal fixation of the tibial shaft fracture and treatment of the open wound.

Two primary technical concerns were addressed in the preoperative planning phase: the first was the need for primary closure of the open wound. This patient had a large wound over the anteromedial surface of the distal third of the tibia with scant soft-tissue coverage. Consequently, skin graft alone would not be adequate. While a muscle flap is another option, it would be prone to failure because of the patient’s age and comorbidities, including hypertension, peripheral vascular disease, lymphedema, and tobacco use. Therefore, we hoped to achieve primary closure. Our second major concern was that the method of fixation must be biomechanically sound without impeding our first goal of primary wound closure. In the setting of an ipsilateral TKA, standard antegrade IM nail fixation would not be possible. While we considered plate fixation, it is biomechanically less stable than an IM nail, and we had great concerns about wound complications. External fixation—uniplanar and mutliplanar (eg, Ilizarov)—was limited by issues of long-term fracture stability and risk of pin-site infection. Both methods appeared less desirable compared with IM nail fixation. Thus, we devised an innovative technique to implant an IM nail into the tibial canal. 

The operative procedure first entailed standard open fracture care comprising débridement of nonviable soft tissue from the traumatic anteromedial tibial wound, curettage of the fractured bone ends, and irrigation with pulse-jet lavage. Then, we turned to reduction and internal fixation of the bony injury. The large traumatic wound was not extended and was used as the primary surgical approach to permit introduction of the IM nail into the canal. Through the traumatic wound, we performed limited reaming of the proximal and distal fracture segments. Using a cannulated technique over guide wires, we reamed to 11 mm (Figure 2). The tourniquet was not used during the IM reaming. We determined the maximum nail length (approximately 22 cm) by measuring the distance from the fracture to the bone interface with the tibial component. We used a 10×200-mm femoral retrograde Synthes nail (Synthes, Inc, West Chester, Pennsylvania) for the procedure, although we considered an IM humerus nail. Through the traumatic wound, the nail was advanced in its entirety into the proximal tibial segment (Figure 3). The fracture was reduced anatomically and held with a bone tenaculum (Figures 4A, 4B). A medial cortical window proximal to the proximal extent of the IM nail was created through which the Synthes IM reduction tool (aluminum femoral finger) was advanced to impact the IM nail antegrade through the fracture site into the distal segment (Figure 5). After placement of the nail was complete, the excised fragment of bone was reinserted into the cortical window. The Synthes IM reduction tool was chosen for its diameter, length, and, most important, its relative flexibility. While maintaining reduction of the fracture, cross-locking of the nail was performed at the distal and proximal ends with perfect circle technique through stab incisions. Length, alignment, and rotation of the affected tibia were deemed symmetric to the contralateral side based on preoperative clinical measurements. Final fluoroscopic images showed appropriate alignment and proper implant placement.

Following open reduction and internal fixation of the fracture, the traumatic and surgical wounds were closed in a layered fashion. A subcutaneous drain and an incisional vacuum-assisted closure (VAC) device were applied to the closed traumatic wound, and a second subcutaneous drain was placed at the site of the cortical window. The patient tolerated the procedure well without perioperative complications.

In the acute period after surgery, the patient’s neurologic and vascular status remained stable. Her muscular compartments remained soft and compressible on physical examination, and her pain was well controlled. The incisional VAC and the 2 Hemovac drains were removed within a few days of the operation. Intravenous cefazolin was continued through her hospital stay and she was transitioned to oral cephalexin at discharge as recommended by our infectious disease colleagues to complete a 10-day course of antibiotic therapy.

At the time of discharge—within 1 week of her initial injury—the patient’s wounds were dry and she was ambulatory with a walker. She was instructed to remain non-weight-bearing and to keep her wounds clean and dry with follow-up in 2 weeks. Over 6 to 8 weeks after surgery, the patient’s weight-bearing status was gradually advanced to full weight-bearing, and she achieved union of the fracture and uneventful healing of the traumatic wound (Figures 6A, 6B, 7). 

Discussion

We have presented a case of an open distal-third tibial shaft fracture in a 66-year-old obese woman with an ipsilateral TKA. Open fracture of the tibial shaft is potentially limb-threatening because of the challenging management of the bone and soft-tissue injury. The presence of an ipsilateral TKA adds a degree of complexity. From a biomechanical standpoint, the lower interdigitation of cortical bone, coupled with weight-bearing of the lower extremity, subjects the tibia diaphysis to issues of rotation, length, and angular control.⁸ Due to the diaphyseal nature of the fracture, consisting of cortical bone with comparably lower vascularity and a small soft-tissue envelope, these fractures heal very slowly and often take as many as 6 to 9 months to achieve union.^9,10 Furthermore, as was the case here, short oblique fractures of the tibial shaft often occur under bending stresses that also cause significant damage to the tibial soft-tissue envelope and periosteum, as indicated by the open wound. This disruption deprives the fracture and soft tissues of important vascular supply that is critical to healing and to avoiding infection and soft-tissue necrosis.^11-13 The effects of treatment may magnify these biomechanical and biologic consequences. Ideal fixation serves to minimize potential complications by neutralizing the biomechanical forces to permit fracture healing while also limiting the amount of soft-tissue trauma and tension. Because the challenges associated with treatment of open tibial shaft fractures make it a limb-threatening injury in a patient with poor peripheral circulation, it is appropriate to consider primary amputation.¹⁴

If circumstances warrant an attempt at limb salvage, IM nailing with static interlocking screws would typically be the standard of care for treatment of an open fracture of the tibia shaft. This provides stable internal fixation that controls tibial alignment in 6° of freedom and neutralizes bending forces with less strain on the implant because of the IM position.^15,16 In addition to superior neutralization of the biomechanical forces, IM nailing is also a minimally invasive approach that limits further trauma to the periosteum and soft-tissue envelope surrounding the fracture site. This optimizes biologic fracture healing and minimizes complications of malunion, infection, and nonunion.^17-19 Moreover, by limiting further damage to the surrounding soft tissue, there is a diminished need for a plastic surgery procedure to reestablish soft-tissue integrity overlying the fracture site. This is particularly advantageous in patients with medical comorbidities that make skin grafts and muscle flaps less likely to succeed. For these reasons, IM nailing was our preferred method of fixation in our patient; however, the presence of an ipsilateral TKA made this standard treatment through an antegrade approach impossible. 

Consequently, we considered other methods of fixation, including internal fixation with plate application or external fixation with a multiplanar construct, such as an Ilizarov frame. Some orthopedists consider plate application a superior technique for achieving fracture union because it results in interfragmentary compression, which promotes primary healing. Interestingly, some would argue that the absolute stability provided by the plate may be too rigid a construct to enable optimal fracture healing biology if compression is not achieved.²⁰ However, to allow primary healing to complete fracture union, absolute stability with rigid and strong fixation must be provided. In the tibial shaft, with large bending forces and rotational moments, this is difficult to achieve with plate fixation alone.⁸ Furthermore, plate application often requires relatively extensive soft-tissue dissection and may impede biologic factors in healing of the bone and soft tissue, increasing the likelihood of infection.²¹ Finally, adequate plate fixation would significantly increase the soft-tissue volume at this location, further compromising the soft tissues and impeding our goal of primary wound closure.

A uniplanar or mutliplanar external fixator would be an appealing option for definitive fixation because of minimal additional soft-tissue damage that is created during its application. However, it is difficult to achieve adequate stability to encourage either primary, or more commonly, secondary healing in the adult or elderly population.²² An Ilizarov frame is a multiplanar external construct, which allows reconstructive applications because of multiple points of fixation in bone.²³ However, the multiple fixation points result in burdensome size of the implant for the patient and requires patient compliance to minimize risk of pin-site infection, which is magnified in a patient with multiple medical comorbid conditions. Furthermore, when comparing treatment options that aim to minimize additional soft-tissue trauma at the site of injury, there is little evidence to show a lower risk of infection at the open fracture site compared with IM nailing.^24,25 Thus, in our patient, customary treatment of an open tibial shaft fracture using antegrade IM nailing was not possible, while plate application and external fixation, though potential treatment options, would be relatively contraindicated due to a higher likelihood of failure. 

Consequently, primary amputation may be the most appropriate treatment option in a patient with multiple comorbid medical conditions, including peripheral vascular disease. Primary amputation prevents morbidity and mortality associated with complications related to the aforementioned treatment options, as well as limiting risks associated with multiple re­operations.^14,25 Studies illustrate that patient functional outcomes after primary amputation are equal to and, in some cases, superior to those patients undergoing limb salvage procedures for open tibial shaft fractures.^26-28

Despite the appropriateness of primary amputation in this case, the patient requested limb salvage. Therefore, other innovative treatment options were explored to achieve our goals of primary wound closure and stable internal fixation. Previous case reports have examined retrograde IM nailing as a means of rigidly fixing tibial shaft fractures in the setting of poor soft tissues or ipsilateral knee arthroplasty.^29-31 However, the retrograde approach to IM nailing requires passage of reamers through the subtalar and ankle joints, leading to associated arthritis in these joints or, more commonly, rigidity because the final nail position often crosses these joints in addition to the fracture site. Therefore, a novel approach for IM nailing was performed using the large open-fracture wound. Through the traumatic wound, open-fracture débridement was first performed, followed by placement of a nail into the medullary canal with little additional disruption of the surrounding periosteum or soft tissue.

Possible complications of this novel method for IM nail passage warrant discussion. First, potentially unfavorable aspects associated with IM reaming include impairment of endosteal blood circulation in the subacute postoperative period.^32-34 If the patient develops complications, such as deep infection, nonunion, hardware failure, or periprosthetic fracture, treatment options that require removal of the nail would be very difficult to execute because this nail was passed “intragrade,” or through the fracture site, not from the knee or the calcaneus. However, unique to this case of intragrade nailing, complications associated with the proximal cortical window may occur. In particular, unintended cortical fracture may happen during impaction of the nail into the distal segment of the fracture after reduction. However, this complication may be avoided with the use of a 1-cm wide and 2-cm long window and the use of the malleable aluminum femoral finger (Synthes). Furthermore, use of a femoral nail is recommended because the Herzog curve of a tibial nail cannot be inserted in the proximal tibial segment using an “intragrade” nailing technique. However, fracture may occur intraoperatively or during rehabilitation after surgery because the cortical window creates a region of high stress distal to the tibial arthroplasty component. Likewise, the area of bone between the proximal extent of the IM nail and tibial component of the TKA represents an area of high stress susceptible to periprosthetic fracture.

Conclusion

We have presented a case of a high-energy open distal tibial diaphyseal fracture in a 66-year-old woman with medical comorbidities and treatment complicated by the presence of an ipsilateral TKA. Intramedullary nailing has become the standard of care for open fractures of the tibial diaphysis because of the high rate of union with little additional soft-tissue damage at the fracture site. Despite these advantages, the ipsilateral TKA complicated the placement of an antegrade tibial nail. An alternative treatment, such as an external fixation using an Ilizarov frame, would present equally challenging treatment aspects, including patient compliance, with little proven benefit over an IM nail. Application of a plate would be less desirable because of increased risk of infection at the fracture site, soft-tissue and periosteum disruption, and muscle necrosis compared with other treatment options. Primary amputation was an appropriate consideration for this patient given her comorbid medical circumstances, but the patient refused this treatment option. Therefore, we created a novel approach to place an IM nail, using the traumatic wound to achieve access to the medullary canal proximally and distally.

Fracture of the tibial shaft below an ipsilateral total knee arthroplasty (TKA) is an infrequently occurring injury pattern that presents a unique treatment scenario. The high predilection for open wounds associated with these diaphyseal fractures further complicates the treatment algorithm.^1,2 The standard principles of treatment for open tibial shaft fractures entail open fracture débridement followed by adequate fracture reduction and stable skeletal fixation in a manner that limits adverse complications of this injury, which include nonunion, malunion, infection, soft-tissue compromise, and reoperation.^3,4

Antegrade intramedullary (IM) tibial nailing has become standard treatment for tibial shaft fractures.^5-7 This minimally invasive method of fixation limits damage to the soft-tissue envelope, provides superior neutralization of the mechanical forces to provide a template for biologic fracture healing, and allows the best options for revision procedures in the event of inadequate healing. This case report examines treatment options for an open tibial shaft fracture of an ipsilateral TKA, complicating the standard treatment of antegrade tibial nailing. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 66-year-old woman became light-headed and fell down a flight of stairs at her home. She was taken to the local emergency room where she presented with left leg pain, deformity, and a skin wound. The wound was dressed with sterile gauze and the extremity immobilized in a temporary plaster splint after which the patient was transferred to our level I trauma center. The accident occurred shortly after dawn, and she received definitive evaluation at the level I trauma center before noon the same day, making the time from injury to evaluation less than 6 hours.

The patient’s medical history was significant for depressive and anxiety disorders, fibromyalgia, hypertension, peripheral vascular disease, and lymphedema. Her surgical history was significant for a remote left TKA and remote open reduction with internal fixation of a left lateral malleolus fracture. She was prescribed antidepressant and anti-anxiolytic medications, narcotic medication, and antihypertensive therapy. She smoked 1 pack of cigarettes per day for approximately 20 years and denied alcohol consumption or illicit drug use. Her body mass index was 37.5, and she ambulated independently in the community.

Upon presentation at our hospital, the patient was hemodynamically stable with no discernable systemic compromise from the extremity injury. An examination of the left lower extremity showed a large longitudinal skin wound over the anteromedial surface of the lower leg measuring roughly 10 cm in length with obvious periosteal stripping and protrusion of the proximal fracture segment. Neurologic motor and sensory function was intact in the lower extremities and pulses were strong. Lower leg compartments were soft. Radiographic imaging confirmed a short oblique fracture of the distal third of the tibial diaphysis. The left TKA was intact with no signs of component loosening or periprosthetic fracture (Figures 1A, 1B).

The patient urgently received broad-spectrum antibiotics with intravenous (IV) cefazolin and IV gentamicin as well as tetanus vaccination. Her fracture was temporarily stabilized in a long-leg splint before she was transported to the operating room. Based upon the characteristics of the patient and the open fracture, we had an extensive discussion with the patient regarding the severity of her injury and treatment options, including nonoperative treatment, operative irrigation and débridement with skeletal stabilization, or below-knee amputation. The patient was adamant that limb salvage be attempted despite adequate understanding that she was exposing herself to risk of multiple reoperations from potential complications, as well as systemic medical compromise. Thus, we considered possible techniques for internal fixation of the tibial shaft fracture and treatment of the open wound.

Two primary technical concerns were addressed in the preoperative planning phase: the first was the need for primary closure of the open wound. This patient had a large wound over the anteromedial surface of the distal third of the tibia with scant soft-tissue coverage. Consequently, skin graft alone would not be adequate. While a muscle flap is another option, it would be prone to failure because of the patient’s age and comorbidities, including hypertension, peripheral vascular disease, lymphedema, and tobacco use. Therefore, we hoped to achieve primary closure. Our second major concern was that the method of fixation must be biomechanically sound without impeding our first goal of primary wound closure. In the setting of an ipsilateral TKA, standard antegrade IM nail fixation would not be possible. While we considered plate fixation, it is biomechanically less stable than an IM nail, and we had great concerns about wound complications. External fixation—uniplanar and mutliplanar (eg, Ilizarov)—was limited by issues of long-term fracture stability and risk of pin-site infection. Both methods appeared less desirable compared with IM nail fixation. Thus, we devised an innovative technique to implant an IM nail into the tibial canal. 

The operative procedure first entailed standard open fracture care comprising débridement of nonviable soft tissue from the traumatic anteromedial tibial wound, curettage of the fractured bone ends, and irrigation with pulse-jet lavage. Then, we turned to reduction and internal fixation of the bony injury. The large traumatic wound was not extended and was used as the primary surgical approach to permit introduction of the IM nail into the canal. Through the traumatic wound, we performed limited reaming of the proximal and distal fracture segments. Using a cannulated technique over guide wires, we reamed to 11 mm (Figure 2). The tourniquet was not used during the IM reaming. We determined the maximum nail length (approximately 22 cm) by measuring the distance from the fracture to the bone interface with the tibial component. We used a 10×200-mm femoral retrograde Synthes nail (Synthes, Inc, West Chester, Pennsylvania) for the procedure, although we considered an IM humerus nail. Through the traumatic wound, the nail was advanced in its entirety into the proximal tibial segment (Figure 3). The fracture was reduced anatomically and held with a bone tenaculum (Figures 4A, 4B). A medial cortical window proximal to the proximal extent of the IM nail was created through which the Synthes IM reduction tool (aluminum femoral finger) was advanced to impact the IM nail antegrade through the fracture site into the distal segment (Figure 5). After placement of the nail was complete, the excised fragment of bone was reinserted into the cortical window. The Synthes IM reduction tool was chosen for its diameter, length, and, most important, its relative flexibility. While maintaining reduction of the fracture, cross-locking of the nail was performed at the distal and proximal ends with perfect circle technique through stab incisions. Length, alignment, and rotation of the affected tibia were deemed symmetric to the contralateral side based on preoperative clinical measurements. Final fluoroscopic images showed appropriate alignment and proper implant placement.

Following open reduction and internal fixation of the fracture, the traumatic and surgical wounds were closed in a layered fashion. A subcutaneous drain and an incisional vacuum-assisted closure (VAC) device were applied to the closed traumatic wound, and a second subcutaneous drain was placed at the site of the cortical window. The patient tolerated the procedure well without perioperative complications.

In the acute period after surgery, the patient’s neurologic and vascular status remained stable. Her muscular compartments remained soft and compressible on physical examination, and her pain was well controlled. The incisional VAC and the 2 Hemovac drains were removed within a few days of the operation. Intravenous cefazolin was continued through her hospital stay and she was transitioned to oral cephalexin at discharge as recommended by our infectious disease colleagues to complete a 10-day course of antibiotic therapy.

At the time of discharge—within 1 week of her initial injury—the patient’s wounds were dry and she was ambulatory with a walker. She was instructed to remain non-weight-bearing and to keep her wounds clean and dry with follow-up in 2 weeks. Over 6 to 8 weeks after surgery, the patient’s weight-bearing status was gradually advanced to full weight-bearing, and she achieved union of the fracture and uneventful healing of the traumatic wound (Figures 6A, 6B, 7). 

Discussion

We have presented a case of an open distal-third tibial shaft fracture in a 66-year-old obese woman with an ipsilateral TKA. Open fracture of the tibial shaft is potentially limb-threatening because of the challenging management of the bone and soft-tissue injury. The presence of an ipsilateral TKA adds a degree of complexity. From a biomechanical standpoint, the lower interdigitation of cortical bone, coupled with weight-bearing of the lower extremity, subjects the tibia diaphysis to issues of rotation, length, and angular control.⁸ Due to the diaphyseal nature of the fracture, consisting of cortical bone with comparably lower vascularity and a small soft-tissue envelope, these fractures heal very slowly and often take as many as 6 to 9 months to achieve union.^9,10 Furthermore, as was the case here, short oblique fractures of the tibial shaft often occur under bending stresses that also cause significant damage to the tibial soft-tissue envelope and periosteum, as indicated by the open wound. This disruption deprives the fracture and soft tissues of important vascular supply that is critical to healing and to avoiding infection and soft-tissue necrosis.^11-13 The effects of treatment may magnify these biomechanical and biologic consequences. Ideal fixation serves to minimize potential complications by neutralizing the biomechanical forces to permit fracture healing while also limiting the amount of soft-tissue trauma and tension. Because the challenges associated with treatment of open tibial shaft fractures make it a limb-threatening injury in a patient with poor peripheral circulation, it is appropriate to consider primary amputation.¹⁴

If circumstances warrant an attempt at limb salvage, IM nailing with static interlocking screws would typically be the standard of care for treatment of an open fracture of the tibia shaft. This provides stable internal fixation that controls tibial alignment in 6° of freedom and neutralizes bending forces with less strain on the implant because of the IM position.^15,16 In addition to superior neutralization of the biomechanical forces, IM nailing is also a minimally invasive approach that limits further trauma to the periosteum and soft-tissue envelope surrounding the fracture site. This optimizes biologic fracture healing and minimizes complications of malunion, infection, and nonunion.^17-19 Moreover, by limiting further damage to the surrounding soft tissue, there is a diminished need for a plastic surgery procedure to reestablish soft-tissue integrity overlying the fracture site. This is particularly advantageous in patients with medical comorbidities that make skin grafts and muscle flaps less likely to succeed. For these reasons, IM nailing was our preferred method of fixation in our patient; however, the presence of an ipsilateral TKA made this standard treatment through an antegrade approach impossible. 

Consequently, we considered other methods of fixation, including internal fixation with plate application or external fixation with a multiplanar construct, such as an Ilizarov frame. Some orthopedists consider plate application a superior technique for achieving fracture union because it results in interfragmentary compression, which promotes primary healing. Interestingly, some would argue that the absolute stability provided by the plate may be too rigid a construct to enable optimal fracture healing biology if compression is not achieved.²⁰ However, to allow primary healing to complete fracture union, absolute stability with rigid and strong fixation must be provided. In the tibial shaft, with large bending forces and rotational moments, this is difficult to achieve with plate fixation alone.⁸ Furthermore, plate application often requires relatively extensive soft-tissue dissection and may impede biologic factors in healing of the bone and soft tissue, increasing the likelihood of infection.²¹ Finally, adequate plate fixation would significantly increase the soft-tissue volume at this location, further compromising the soft tissues and impeding our goal of primary wound closure.

A uniplanar or mutliplanar external fixator would be an appealing option for definitive fixation because of minimal additional soft-tissue damage that is created during its application. However, it is difficult to achieve adequate stability to encourage either primary, or more commonly, secondary healing in the adult or elderly population.²² An Ilizarov frame is a multiplanar external construct, which allows reconstructive applications because of multiple points of fixation in bone.²³ However, the multiple fixation points result in burdensome size of the implant for the patient and requires patient compliance to minimize risk of pin-site infection, which is magnified in a patient with multiple medical comorbid conditions. Furthermore, when comparing treatment options that aim to minimize additional soft-tissue trauma at the site of injury, there is little evidence to show a lower risk of infection at the open fracture site compared with IM nailing.^24,25 Thus, in our patient, customary treatment of an open tibial shaft fracture using antegrade IM nailing was not possible, while plate application and external fixation, though potential treatment options, would be relatively contraindicated due to a higher likelihood of failure. 

Consequently, primary amputation may be the most appropriate treatment option in a patient with multiple comorbid medical conditions, including peripheral vascular disease. Primary amputation prevents morbidity and mortality associated with complications related to the aforementioned treatment options, as well as limiting risks associated with multiple re­operations.^14,25 Studies illustrate that patient functional outcomes after primary amputation are equal to and, in some cases, superior to those patients undergoing limb salvage procedures for open tibial shaft fractures.^26-28

Despite the appropriateness of primary amputation in this case, the patient requested limb salvage. Therefore, other innovative treatment options were explored to achieve our goals of primary wound closure and stable internal fixation. Previous case reports have examined retrograde IM nailing as a means of rigidly fixing tibial shaft fractures in the setting of poor soft tissues or ipsilateral knee arthroplasty.^29-31 However, the retrograde approach to IM nailing requires passage of reamers through the subtalar and ankle joints, leading to associated arthritis in these joints or, more commonly, rigidity because the final nail position often crosses these joints in addition to the fracture site. Therefore, a novel approach for IM nailing was performed using the large open-fracture wound. Through the traumatic wound, open-fracture débridement was first performed, followed by placement of a nail into the medullary canal with little additional disruption of the surrounding periosteum or soft tissue.

Possible complications of this novel method for IM nail passage warrant discussion. First, potentially unfavorable aspects associated with IM reaming include impairment of endosteal blood circulation in the subacute postoperative period.^32-34 If the patient develops complications, such as deep infection, nonunion, hardware failure, or periprosthetic fracture, treatment options that require removal of the nail would be very difficult to execute because this nail was passed “intragrade,” or through the fracture site, not from the knee or the calcaneus. However, unique to this case of intragrade nailing, complications associated with the proximal cortical window may occur. In particular, unintended cortical fracture may happen during impaction of the nail into the distal segment of the fracture after reduction. However, this complication may be avoided with the use of a 1-cm wide and 2-cm long window and the use of the malleable aluminum femoral finger (Synthes). Furthermore, use of a femoral nail is recommended because the Herzog curve of a tibial nail cannot be inserted in the proximal tibial segment using an “intragrade” nailing technique. However, fracture may occur intraoperatively or during rehabilitation after surgery because the cortical window creates a region of high stress distal to the tibial arthroplasty component. Likewise, the area of bone between the proximal extent of the IM nail and tibial component of the TKA represents an area of high stress susceptible to periprosthetic fracture.

Conclusion

We have presented a case of a high-energy open distal tibial diaphyseal fracture in a 66-year-old woman with medical comorbidities and treatment complicated by the presence of an ipsilateral TKA. Intramedullary nailing has become the standard of care for open fractures of the tibial diaphysis because of the high rate of union with little additional soft-tissue damage at the fracture site. Despite these advantages, the ipsilateral TKA complicated the placement of an antegrade tibial nail. An alternative treatment, such as an external fixation using an Ilizarov frame, would present equally challenging treatment aspects, including patient compliance, with little proven benefit over an IM nail. Application of a plate would be less desirable because of increased risk of infection at the fracture site, soft-tissue and periosteum disruption, and muscle necrosis compared with other treatment options. Primary amputation was an appropriate consideration for this patient given her comorbid medical circumstances, but the patient refused this treatment option. Therefore, we created a novel approach to place an IM nail, using the traumatic wound to achieve access to the medullary canal proximally and distally.

Fracture of the tibial shaft below an ipsilateral total knee arthroplasty (TKA) is an infrequently occurring injury pattern that presents a unique treatment scenario. The high predilection for open wounds associated with these diaphyseal fractures further complicates the treatment algorithm.^1,2 The standard principles of treatment for open tibial shaft fractures entail open fracture débridement followed by adequate fracture reduction and stable skeletal fixation in a manner that limits adverse complications of this injury, which include nonunion, malunion, infection, soft-tissue compromise, and reoperation.^3,4

Antegrade intramedullary (IM) tibial nailing has become standard treatment for tibial shaft fractures.^5-7 This minimally invasive method of fixation limits damage to the soft-tissue envelope, provides superior neutralization of the mechanical forces to provide a template for biologic fracture healing, and allows the best options for revision procedures in the event of inadequate healing. This case report examines treatment options for an open tibial shaft fracture of an ipsilateral TKA, complicating the standard treatment of antegrade tibial nailing. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 66-year-old woman became light-headed and fell down a flight of stairs at her home. She was taken to the local emergency room where she presented with left leg pain, deformity, and a skin wound. The wound was dressed with sterile gauze and the extremity immobilized in a temporary plaster splint after which the patient was transferred to our level I trauma center. The accident occurred shortly after dawn, and she received definitive evaluation at the level I trauma center before noon the same day, making the time from injury to evaluation less than 6 hours.

The patient’s medical history was significant for depressive and anxiety disorders, fibromyalgia, hypertension, peripheral vascular disease, and lymphedema. Her surgical history was significant for a remote left TKA and remote open reduction with internal fixation of a left lateral malleolus fracture. She was prescribed antidepressant and anti-anxiolytic medications, narcotic medication, and antihypertensive therapy. She smoked 1 pack of cigarettes per day for approximately 20 years and denied alcohol consumption or illicit drug use. Her body mass index was 37.5, and she ambulated independently in the community.

Upon presentation at our hospital, the patient was hemodynamically stable with no discernable systemic compromise from the extremity injury. An examination of the left lower extremity showed a large longitudinal skin wound over the anteromedial surface of the lower leg measuring roughly 10 cm in length with obvious periosteal stripping and protrusion of the proximal fracture segment. Neurologic motor and sensory function was intact in the lower extremities and pulses were strong. Lower leg compartments were soft. Radiographic imaging confirmed a short oblique fracture of the distal third of the tibial diaphysis. The left TKA was intact with no signs of component loosening or periprosthetic fracture (Figures 1A, 1B).

The patient urgently received broad-spectrum antibiotics with intravenous (IV) cefazolin and IV gentamicin as well as tetanus vaccination. Her fracture was temporarily stabilized in a long-leg splint before she was transported to the operating room. Based upon the characteristics of the patient and the open fracture, we had an extensive discussion with the patient regarding the severity of her injury and treatment options, including nonoperative treatment, operative irrigation and débridement with skeletal stabilization, or below-knee amputation. The patient was adamant that limb salvage be attempted despite adequate understanding that she was exposing herself to risk of multiple reoperations from potential complications, as well as systemic medical compromise. Thus, we considered possible techniques for internal fixation of the tibial shaft fracture and treatment of the open wound.

Two primary technical concerns were addressed in the preoperative planning phase: the first was the need for primary closure of the open wound. This patient had a large wound over the anteromedial surface of the distal third of the tibia with scant soft-tissue coverage. Consequently, skin graft alone would not be adequate. While a muscle flap is another option, it would be prone to failure because of the patient’s age and comorbidities, including hypertension, peripheral vascular disease, lymphedema, and tobacco use. Therefore, we hoped to achieve primary closure. Our second major concern was that the method of fixation must be biomechanically sound without impeding our first goal of primary wound closure. In the setting of an ipsilateral TKA, standard antegrade IM nail fixation would not be possible. While we considered plate fixation, it is biomechanically less stable than an IM nail, and we had great concerns about wound complications. External fixation—uniplanar and mutliplanar (eg, Ilizarov)—was limited by issues of long-term fracture stability and risk of pin-site infection. Both methods appeared less desirable compared with IM nail fixation. Thus, we devised an innovative technique to implant an IM nail into the tibial canal. 

The operative procedure first entailed standard open fracture care comprising débridement of nonviable soft tissue from the traumatic anteromedial tibial wound, curettage of the fractured bone ends, and irrigation with pulse-jet lavage. Then, we turned to reduction and internal fixation of the bony injury. The large traumatic wound was not extended and was used as the primary surgical approach to permit introduction of the IM nail into the canal. Through the traumatic wound, we performed limited reaming of the proximal and distal fracture segments. Using a cannulated technique over guide wires, we reamed to 11 mm (Figure 2). The tourniquet was not used during the IM reaming. We determined the maximum nail length (approximately 22 cm) by measuring the distance from the fracture to the bone interface with the tibial component. We used a 10×200-mm femoral retrograde Synthes nail (Synthes, Inc, West Chester, Pennsylvania) for the procedure, although we considered an IM humerus nail. Through the traumatic wound, the nail was advanced in its entirety into the proximal tibial segment (Figure 3). The fracture was reduced anatomically and held with a bone tenaculum (Figures 4A, 4B). A medial cortical window proximal to the proximal extent of the IM nail was created through which the Synthes IM reduction tool (aluminum femoral finger) was advanced to impact the IM nail antegrade through the fracture site into the distal segment (Figure 5). After placement of the nail was complete, the excised fragment of bone was reinserted into the cortical window. The Synthes IM reduction tool was chosen for its diameter, length, and, most important, its relative flexibility. While maintaining reduction of the fracture, cross-locking of the nail was performed at the distal and proximal ends with perfect circle technique through stab incisions. Length, alignment, and rotation of the affected tibia were deemed symmetric to the contralateral side based on preoperative clinical measurements. Final fluoroscopic images showed appropriate alignment and proper implant placement.

Following open reduction and internal fixation of the fracture, the traumatic and surgical wounds were closed in a layered fashion. A subcutaneous drain and an incisional vacuum-assisted closure (VAC) device were applied to the closed traumatic wound, and a second subcutaneous drain was placed at the site of the cortical window. The patient tolerated the procedure well without perioperative complications.

In the acute period after surgery, the patient’s neurologic and vascular status remained stable. Her muscular compartments remained soft and compressible on physical examination, and her pain was well controlled. The incisional VAC and the 2 Hemovac drains were removed within a few days of the operation. Intravenous cefazolin was continued through her hospital stay and she was transitioned to oral cephalexin at discharge as recommended by our infectious disease colleagues to complete a 10-day course of antibiotic therapy.

At the time of discharge—within 1 week of her initial injury—the patient’s wounds were dry and she was ambulatory with a walker. She was instructed to remain non-weight-bearing and to keep her wounds clean and dry with follow-up in 2 weeks. Over 6 to 8 weeks after surgery, the patient’s weight-bearing status was gradually advanced to full weight-bearing, and she achieved union of the fracture and uneventful healing of the traumatic wound (Figures 6A, 6B, 7). 

Discussion

We have presented a case of an open distal-third tibial shaft fracture in a 66-year-old obese woman with an ipsilateral TKA. Open fracture of the tibial shaft is potentially limb-threatening because of the challenging management of the bone and soft-tissue injury. The presence of an ipsilateral TKA adds a degree of complexity. From a biomechanical standpoint, the lower interdigitation of cortical bone, coupled with weight-bearing of the lower extremity, subjects the tibia diaphysis to issues of rotation, length, and angular control.⁸ Due to the diaphyseal nature of the fracture, consisting of cortical bone with comparably lower vascularity and a small soft-tissue envelope, these fractures heal very slowly and often take as many as 6 to 9 months to achieve union.^9,10 Furthermore, as was the case here, short oblique fractures of the tibial shaft often occur under bending stresses that also cause significant damage to the tibial soft-tissue envelope and periosteum, as indicated by the open wound. This disruption deprives the fracture and soft tissues of important vascular supply that is critical to healing and to avoiding infection and soft-tissue necrosis.^11-13 The effects of treatment may magnify these biomechanical and biologic consequences. Ideal fixation serves to minimize potential complications by neutralizing the biomechanical forces to permit fracture healing while also limiting the amount of soft-tissue trauma and tension. Because the challenges associated with treatment of open tibial shaft fractures make it a limb-threatening injury in a patient with poor peripheral circulation, it is appropriate to consider primary amputation.¹⁴

If circumstances warrant an attempt at limb salvage, IM nailing with static interlocking screws would typically be the standard of care for treatment of an open fracture of the tibia shaft. This provides stable internal fixation that controls tibial alignment in 6° of freedom and neutralizes bending forces with less strain on the implant because of the IM position.^15,16 In addition to superior neutralization of the biomechanical forces, IM nailing is also a minimally invasive approach that limits further trauma to the periosteum and soft-tissue envelope surrounding the fracture site. This optimizes biologic fracture healing and minimizes complications of malunion, infection, and nonunion.^17-19 Moreover, by limiting further damage to the surrounding soft tissue, there is a diminished need for a plastic surgery procedure to reestablish soft-tissue integrity overlying the fracture site. This is particularly advantageous in patients with medical comorbidities that make skin grafts and muscle flaps less likely to succeed. For these reasons, IM nailing was our preferred method of fixation in our patient; however, the presence of an ipsilateral TKA made this standard treatment through an antegrade approach impossible. 

Consequently, we considered other methods of fixation, including internal fixation with plate application or external fixation with a multiplanar construct, such as an Ilizarov frame. Some orthopedists consider plate application a superior technique for achieving fracture union because it results in interfragmentary compression, which promotes primary healing. Interestingly, some would argue that the absolute stability provided by the plate may be too rigid a construct to enable optimal fracture healing biology if compression is not achieved.²⁰ However, to allow primary healing to complete fracture union, absolute stability with rigid and strong fixation must be provided. In the tibial shaft, with large bending forces and rotational moments, this is difficult to achieve with plate fixation alone.⁸ Furthermore, plate application often requires relatively extensive soft-tissue dissection and may impede biologic factors in healing of the bone and soft tissue, increasing the likelihood of infection.²¹ Finally, adequate plate fixation would significantly increase the soft-tissue volume at this location, further compromising the soft tissues and impeding our goal of primary wound closure.

A uniplanar or mutliplanar external fixator would be an appealing option for definitive fixation because of minimal additional soft-tissue damage that is created during its application. However, it is difficult to achieve adequate stability to encourage either primary, or more commonly, secondary healing in the adult or elderly population.²² An Ilizarov frame is a multiplanar external construct, which allows reconstructive applications because of multiple points of fixation in bone.²³ However, the multiple fixation points result in burdensome size of the implant for the patient and requires patient compliance to minimize risk of pin-site infection, which is magnified in a patient with multiple medical comorbid conditions. Furthermore, when comparing treatment options that aim to minimize additional soft-tissue trauma at the site of injury, there is little evidence to show a lower risk of infection at the open fracture site compared with IM nailing.^24,25 Thus, in our patient, customary treatment of an open tibial shaft fracture using antegrade IM nailing was not possible, while plate application and external fixation, though potential treatment options, would be relatively contraindicated due to a higher likelihood of failure. 

Consequently, primary amputation may be the most appropriate treatment option in a patient with multiple comorbid medical conditions, including peripheral vascular disease. Primary amputation prevents morbidity and mortality associated with complications related to the aforementioned treatment options, as well as limiting risks associated with multiple re­operations.^14,25 Studies illustrate that patient functional outcomes after primary amputation are equal to and, in some cases, superior to those patients undergoing limb salvage procedures for open tibial shaft fractures.^26-28

Despite the appropriateness of primary amputation in this case, the patient requested limb salvage. Therefore, other innovative treatment options were explored to achieve our goals of primary wound closure and stable internal fixation. Previous case reports have examined retrograde IM nailing as a means of rigidly fixing tibial shaft fractures in the setting of poor soft tissues or ipsilateral knee arthroplasty.^29-31 However, the retrograde approach to IM nailing requires passage of reamers through the subtalar and ankle joints, leading to associated arthritis in these joints or, more commonly, rigidity because the final nail position often crosses these joints in addition to the fracture site. Therefore, a novel approach for IM nailing was performed using the large open-fracture wound. Through the traumatic wound, open-fracture débridement was first performed, followed by placement of a nail into the medullary canal with little additional disruption of the surrounding periosteum or soft tissue.

Possible complications of this novel method for IM nail passage warrant discussion. First, potentially unfavorable aspects associated with IM reaming include impairment of endosteal blood circulation in the subacute postoperative period.^32-34 If the patient develops complications, such as deep infection, nonunion, hardware failure, or periprosthetic fracture, treatment options that require removal of the nail would be very difficult to execute because this nail was passed “intragrade,” or through the fracture site, not from the knee or the calcaneus. However, unique to this case of intragrade nailing, complications associated with the proximal cortical window may occur. In particular, unintended cortical fracture may happen during impaction of the nail into the distal segment of the fracture after reduction. However, this complication may be avoided with the use of a 1-cm wide and 2-cm long window and the use of the malleable aluminum femoral finger (Synthes). Furthermore, use of a femoral nail is recommended because the Herzog curve of a tibial nail cannot be inserted in the proximal tibial segment using an “intragrade” nailing technique. However, fracture may occur intraoperatively or during rehabilitation after surgery because the cortical window creates a region of high stress distal to the tibial arthroplasty component. Likewise, the area of bone between the proximal extent of the IM nail and tibial component of the TKA represents an area of high stress susceptible to periprosthetic fracture.

Conclusion

We have presented a case of a high-energy open distal tibial diaphyseal fracture in a 66-year-old woman with medical comorbidities and treatment complicated by the presence of an ipsilateral TKA. Intramedullary nailing has become the standard of care for open fractures of the tibial diaphysis because of the high rate of union with little additional soft-tissue damage at the fracture site. Despite these advantages, the ipsilateral TKA complicated the placement of an antegrade tibial nail. An alternative treatment, such as an external fixation using an Ilizarov frame, would present equally challenging treatment aspects, including patient compliance, with little proven benefit over an IM nail. Application of a plate would be less desirable because of increased risk of infection at the fracture site, soft-tissue and periosteum disruption, and muscle necrosis compared with other treatment options. Primary amputation was an appropriate consideration for this patient given her comorbid medical circumstances, but the patient refused this treatment option. Therefore, we created a novel approach to place an IM nail, using the traumatic wound to achieve access to the medullary canal proximally and distally.

Complications with the use of anchor screws in shoulder surgery have been well-documented^1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.

Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.^3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.³ However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.

Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.

Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.

A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.

After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.

The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.

Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.

After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).

Discussion

Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.^3,4 Zuckerman and Matsen⁴ divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.⁵ In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.

Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues⁵ performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.

The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.

This case has shown the importance of obtaining post­operative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.¹

Conclusion

Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.^1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.

Complications with the use of anchor screws in shoulder surgery have been well-documented^1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.

Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.^3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.³ However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.

Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.

Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.

A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.

After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.

The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.

Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.

After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).

Discussion

Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.^3,4 Zuckerman and Matsen⁴ divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.⁵ In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.

Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues⁵ performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.

The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.

This case has shown the importance of obtaining post­operative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.¹

Conclusion

Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.^1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.

Complications with the use of anchor screws in shoulder surgery have been well-documented^1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.

Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.^3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.³ However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.

Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.

Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.

A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.

After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.

The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.

Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.

After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).

Discussion

Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.^3,4 Zuckerman and Matsen⁴ divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.⁵ In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.

Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues⁵ performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.

The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.

This case has shown the importance of obtaining post­operative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.¹

Conclusion

Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.^1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.