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Dysphagia, Hoarseness, and a Hypopharyngeal Mass

England, Michael R. MD; Schwartz, Marissa A. MD; Flis, Daniel MD; Kelly, Brian DO; Wein, Richard O. MD

doi: 10.1213/XAA.0000000000000084
Case Reports: Case Report
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We describe a patient who developed a hypopharyngeal mass (in the setting of a cervical osteophyte) while taking clopidogrel and aspirin for coronary artery disease. He had a 2-month history of progressive dysphagia and hoarseness. Physical examination and computed tomography scan revealed a soft tissue retropharyngeal mass of unclear etiology yet with a stable airway. He was admitted to the intensive care unit for a 48-hour clopidogrel washout followed by surgery. A hematoma and cervical osteophyte were removed with scant bleeding. This case report emphasizes the need to consider the medication history of a patient when assessing the cause of an otherwise unexpected finding.

From the *Department of Anesthesiology, Tufts Medical Center, Tufts University School of Medicine, Boston, Massachusetts; Otolaryngology Resident, University of Connecticut School of Medicine, Farmington, Connecticut; and Department of Otolarngology, Tufts Medical Center, Tufts University School of Medicine, Boston, Massachusetts.

Accepted for publication April 5, 2014.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Michael R. England, MD, Department of Anesthesiology, Tufts Medical Center, Box 298, 800 Washington St., Boston, MA 02111. Address e-mail to Drmengland@yahoo.com.

Clopidogrel has become the second most prescribed drug worldwide.1 It is an antiplatelet drug (often in combination with acetylsalicylic acid), and its indications include (but are not limited to) the prevention of stent thrombosis in those with coronary or peripheral vascular disease, thrombosis prevention after placement of a mechanical heart valve, and stroke prevention after a transient ischemic attack.2 Upon cessation of either drug, return of normal platelet function may take as long as 7 days, the life span of an inhibited platelet.3,4 Emergency surgery during this time period in a patient taking clopidogrel may increase the risk from surgical bleeding and complicate recovery4 and has to be balanced with the risk of possible thromboembolism.3 In a recent meta-analysis evaluating whether continuing dual antiplatelet therapy before cardiac surgery (requiring cardiopulmonary bypass) influenced the need for reexploration, the authors noted that “continuing antiplatelet therapy may be acceptable in patients at high risk of thrombosis as it is associated with a low risk of increased need for reexploration.”5 In this case report, we describe the use of clopidogrel in a man with an unrecognized cervical osteophyte. He presented with a retropharyngeal soft tissue mass of unclear etiology in the setting of potential airway compromise. We will discuss the differential diagnosis of the retropharyngeal mass and the appropriate timing of surgery to reduce the risk of intraoperative bleeding.

The patient gave verbal and written consent to have this case report published.

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CASE DESCRIPTION

A 67-year-old man with a medical history of coronary and peripheral vascular disease, 30 pack-years of smoking, and modest daily alcohol intake presented with a 2-month history of progressive dysphagia, shortness of breath, and hoarseness. He denied recent trauma or upper respiratory illness. Initially, he was unable to swallow solids and transitioned himself to a liquid diet. Upon first medical evaluation for cough and worsening dysphagia, he was treated with oral steroids and azithromycin with some initial improvement in symptoms.

In the remote past, he had a left carotid endarterectomy, an aortobifemoral bypass, and a percutaneous coronary drug eluting stent (8 years) for which he was taking clopidogrel and aspirin. At the time of his aortic surgery, it was noted that tracheal intubation may be difficult and a fiberoptic intubation was performed. A retropharyngeal mass was noted but was neither defined further nor evaluated afterward.

On examination in the ear–nose–throat clinic late in the afternoon, he was noted to have an altered vocal quality with a distortion of vowel production (also known as “hot potato voice”) without stridor or inability to swallow secretions. Endoscopically, a right submucosal hypopharyngeal mass compressing the epiglottis was noted, and computed tomography (CT) sagittal view imaging of the neck showed a 2.5 cm × 2.1 cm × 4.4 cm low-density (predominantly submucosal) lesion at the level of the hypopharynx (Fig. 1). It was to the right of midline anteriorly and partially effacing the hypopharyngeal airway, leading to airway compromise at the level of the hyoid bone. A cervical osteophyte was noted abutting the lesion (Fig. 1). In Figure 2, a CT scan (coronal view) shows the relationship of the hematoma and osteophyte causing airway narrowing.

Figure 1

Figure 1

Figure 2

Figure 2

Because of the uncertain cause of the mass and the history of recent (last dose unclear) clopidogrel ingestion, rather than performing surgery emergently and during the off hours as originally envisioned, a discussion involving radiologists, otolaryngologists, cardiologists, and anesthesiologists as to the proper timing for surgery was held. The issue of clopidogrel inhibiting platelet function and potentially placing him at risk for excessive intraoral bleeding (without a clear diagnosis of either tumor, infection, or hematoma) during tracheal intubation or surgery (and the potential need for rapid surgical airway or blood, blood products, or platelets) was balanced with the concern for progressive loss of airway patency and possible stent thrombosis. However, since the condition of the airway appeared stable, he was admitted to the intensive care unit for observation, steroid administration, and a clopidogrel washout. Because of the issue of possible stent thrombosis, he was seen by the cardiology service for their assessment of this risk. Given the 8-year interval since placement of the drug-eluting stent, his excellent exercise capacity, and the low- to intermediate-risk surgical procedure, they felt it acceptable to withhold clopidogrel for a “short” period of time. After 48 hours (an admitted arbitrary decision made by the otolaryngology team, 5–7 days is suggested),4 he was brought to the operating room, and after awake fiberoptic tracheal intubation (using dexmedetomidine for sedation and aerosolized lidocaine for topical anesthesia followed by propofol, rocuronium, fentanyl, and sevoflurane) surgery (approached through a submandibular incision) revealed a 4 cm × 4 cm firm organized hematoma in the retropharyngeal space. This was evacuated, and a large osteophyte directly underneath the hematoma was removed with rongeurs. Bleeding was minimal and easily controlled, and after tracheal extubation the following day, complete resolution of his dysphonia and dysphagia had occurred.

He was discharged home on the second postoperative day and resumed taking aspirin and clopidogrel.

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DISCUSSION

Spontaneous retropharyngeal hematomas are a rare cause of upper airway compression. Patients may present with the classic triad described as tracheal and esophageal compressive symptoms, ventral tracheal displacement detected on lateral cervical radiograph, and bruising in the anterior neck and upper chest regions.6 The most common cause of acute retropharyngeal hematoma is cervical trauma7 and is frequently associated with cervical spine fracture. However, retropharyngeal hematomas may also follow infection, cervical spine surgery, injury to the great vessels, traumatic endoscopy, and foreign body ingestion.8 Additionally, factors such as anticoagulation or an intrinsic bleeding disorder may increase the likelihood of a retropharyngeal hematoma.8

The most common complication associated with oral anticoagulants is untoward bleeding, with the upper aerodigestive tract being an uncommon site of involvement.9 Nine cases of warfarin-associated retropharyngeal hematoma have been documented, with 3 of these cases progressing to airway compromise requiring urgent tracheotomy.10

The retropharyngeal space is located between the middle and deep layers of the deep cervical fascia that extends from the skull base to the upper mediastinum.11 The differential diagnosis of a retropharyngeal mass identified by CT imaging includes reactive adenopathy, nodal metastasis from head and neck cancers (melanoma, thyroid carcinoma), lymphoma, leukemia, direct invasion of squamous cell carcinoma, benign tumors (lipoma or hemangioma), retropharyngeal abscess, cellulitis, and edema.11

Management of retropharyngeal hematoma depends on the severity and cause of the symptoms. Some studies suggest early airway intervention, while others advocate close observation of patients in the intensive care unit with airway intervention only if necessary. However, there appears to be no consensus regarding passive management versus aggressive early airway intervention.12–14

In addition, because upper airway hematomas may be due to localized infection,15 some suggest a role for antibiotics in the treatment of retropharyngeal hematomas.16

Since spontaneous retropharyngeal hematomas are a rare cause of upper airway obstruction, patients at risk for hemorrhage (secondary to a preexisting medical condition or medication) with preexisting cervical spine pathology should be viewed with greater concern and may require emergent intervention to secure the airway. In the setting of altered hemostasis, waiting for in vitro laboratory tests to return to normal (either through the use of reversal agents/blood products) must be balanced with the constant possibility of acute airway compromise. In the face of recent clopidogrel ingestion, waiting for the ideal time to operate may be a challenge even though there are commercially available tests of the P2Y12 receptor blockade. These include VerifyNow® (Accriva Diagnostics, Piscataway, NJ), or thromboelastography/thromboelastometry (TEG®, Hema scope, Skokie, IL), or ROTEM (Tem International GmbH, Munich, Germany). However, acceptance of these testing modalities demonstrating return of normal platelet aggregation function has not gained enough widespread popularity to represent “standard of practice” to assist in clinical decision making. Therefore, 5 to 7 days are needed for new platelets to be formed and properly function (this timeframe may need to be extended if the patient had ingested ticlopidine)3; if clinical circumstances dictate the need for earlier surgery with a low risk of thrombosis, the waiting period may, as was the case with our patient, be shortened. The risk of coronary artery stent thrombosis is greatest within the first year of stent placement especially for a drug-eluting stent. Treatment with dual antiplatelet therapy decreases this risk. If such a patient is to undergo a procedure where there is a high risk of bleeding, bridging therapy may need to be considered.3 Ideally, patients receiving clopidogrel will have their platelet function tested perioperatively4 to reduce the risk of procedural (neuraxial) and intraoperative bleeding. This may assist in minimizing the exposure time for stent closure due to thrombosis and determine normal platelet activity to obviate the unnecessary exposure to allogenic platelets (and the risks associated with such transfusions) in the treatment of intraoperative bleeding.

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ACKNOWLEDGMENTS

The authors thank Dr. Roman Schumann for his thoughtful comments during manuscript preparation.

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