Retropharyngeal Hematoma after Stellate Ganglion Block: Analysis of 27 Patients Reported in the Literature

We searched MEDLINE for reports from 1966 to 2006, and Japana Centra Revuo Medicina for reports from 1983 to 2006 using the following terms and key words: stellate ganglion block , complication , hematoma , and retropharyngeal hematoma . These databases were last accessed on June 28, 2006. The retrieved articles were read, and relevant references of each article were also reviewed.

The following data in each patient were extracted: sex; age; disease for which SGB was performed; concurrent diseases; use of drugs that could affect hemostasis; results of bleeding and coagulation studies; characteristics of the neck; method by which SGB was conducted, including the results of a blood aspiration test before the injection of a local anesthetic; time of onset of the initial symptoms and signs; initial symptoms and signs; results of imaging studies of the neck and/or mediastinum; time of emergency airway management; method of airway management; and surgical findings on evacuation of the hematoma or autopsy findings.

Statistical analysis was performed with unpaired t  test or chi-square test with Yates correction. P < 0.05 was considered statistically significant.

In addition to the four patients reported on in the English-language literature,6–923 patients who developed RPH were found in Japanese-language journals,10–28a total of 27 patients in the past 40 yr.

Table 1shows the characteristics of the patients. The patients comprised 13 men and 14 women. The mean age of the patients was 54.5 ± 14.6 yr (mean ± SD; range, 26–76 yr). The diseases for which SGB was performed in these patients were diverse, and many patients had concurrent diseases; however, only 3 had diseases that might affect hemostasis: chronic renal failure on hemodialysis in 1; chronic renal failure in 1; and idiopathic thrombocytopenic purpura, which became apparent after SGB, in 1 patient.

Six patients were taking oral drugs that could affect hemostasis: aspirin and ticlopidine in 1, ticlopidine in 1, loxoprofen in 1, trapidil in 1, a nonsteroidal antiinflammatory drug (drug name was not stated) in 1, and aspirin in 1. Four patients were receiving intravenous drugs that could affect hemostasis: dextran in 2, dextran and urokinase in 1, and batroxobin in 1. Thus, a total of 10 patients were receiving drugs that could affect hemostasis. No patient was simultaneously taking oral medications and receiving intravenous drugs that could affect hemostasis. Another patient had been taking ticlopidine, but treatment had been discontinued 11 days before SGB. Two patients were not taking any drugs that could affect hemostasis. The medications in the remaining 14 patients were not stated.

Bleeding and coagulation profiles were studied around the onset of RPH after SGB in 17 patients. There were no abnormalities except for 2 patients who had a thrombotest of 56% (reference range, 70–130%) and a platelet count of 7,000/mm³due to idiopathic thrombocytopenic purpura, respectively. Among the 10 patients who were taking medications or receiving intravenous drugs that could affect hemostasis, the results of bleeding and coagulation studies were normal in 5, 1 had a thrombotest of 56%, and 1 had a platelet count of 7,000/mm³.

Stellate ganglion block was conducted on the right in 10 patients and on the left in 14. The laterality of SGB was not stated in the remaining 3 patients. SGB was performed aiming at the C6 tubercle in 9 patients and at the C7 tubercle in 8 patients. This information was not provided in the remaining 10 patients.

The result of an aspiration test for blood before injection of a local anesthetic at the first puncture was positive and the needle was redirected in 4 patients; the test result was negative in 15. The results of this test were not stated in the remaining 8 patients.

Table 2shows the initial symptoms and signs of RPH after SGB in each patient. Table 3summarizes the numbers of patients who later needed emergency airway management according to the initial symptoms and signs.

Neck pain and dyspnea were the most frequent symptoms (n = 10) of RPH after SGB, followed by neck swelling (n = 8), hoarseness (n = 5), and sore throat (n = 5). Although the initial symptoms and signs of RPH after SGB were diverse, they can be summarized as the pain in the head, neck, chest, and back, accompanied with upper airway symptoms and signs. Emergency airway management was needed in 21 patients (78%), and was not needed in 6 (22%) throughout the course of RPH after SGB. There were no statistically significant predictors of later emergency airway management. However, the patients having subcutaneous ecchymosis in the neck as one of the initial signs of RPH did not significantly need emergency airway management (P = 0.006).

Retropharyngeal hematoma was suspected by x-ray, computed tomography, and/or magnetic resonance imaging studies. They showed widening of the retrotracheal space with a ventral displacement of the trachea (table 1and fig. 1). The distances from the ventral line of the cervical spine to the retrotracheal wall on lateral x-ray studies were stated in three patients. They were 19, 36, and 48 mm, respectively.

Figure 2shows the times of onset of the initial symptoms and of emergency airway management of RPH after SGB, and the method of emergency airway management, in each patient. There was no statistically significant difference in the times of onset of the initial symptoms of RPH after SGB between patients who later needed emergency airway management and those who did not (3.2 ± 4.2 h [n = 20]vs.  1.1 ± 0.8 h [n = 6]; P = 0.25). The onset of the initial symptoms of RPH was 2 h or more after SGB in 14 patients (52%).

Among the 21 patients who needed emergency airway management, orotracheal intubation was attempted first in 17 patients, nasotracheal intubation with a bronchofiberscope in 1, and tracheostomy in 3. Among the 17 patients in whom orotracheal intubation was attempted first, it was successful in 12, but was extremely difficult in 5.12,14,19,24,27Tracheal tubes as small as 6.0, 6.5, and 7.0 mm were successfully managed to be inserted in 3 patients.12,14,24The remaining 5 patients in whom orotracheal intubation failed, despite multiple attempts, received emergency tracheostomy. One patient died because the airway could not be secured promptly at the time of respiratory arrest.6There were 5 patients who had inspiratory dyspnea/stridors immediately before they developed airway obstruction and needed emergency airway management.18,19,22,23,26 

There was marked swelling of the soft palate,12pharynx,14,19hypopharynx,21epiglottis,19,24and vocal cords11,18,24in patients in whom tracheal intubation was extremely difficult or impossible. Marked swelling of the pharyngolarynx distorted the normal anatomy, making direct visualization of the vocal cords extremely difficult by laryngoscopy.12,14,19,21,24 

The speed with which airway compromise worsened was unpredictable and varied greatly among patients. One patient developed dyspnea and neck swelling 1 h 35 min after SGB, followed by a rapid development of airway obstruction and respiratory arrest 10 min later.24Another patient noted a feeling of suffocation and chest oppression 3 h after SGB. These symptoms were stable over the ensuing 22 h; however, dyspnea, hoarseness, and stridors suddenly developed at that time.13Both patients needed emergency tracheal intubation.

Hematoma was evacuated in five patients,9,13,14,22and autopsy was performed in one patient.6The autopsy revealed blood in the retropharyngeal space and a small hemorrhage in the soft tissue in front of the C7 transverse process; however, no apparent trauma to the carotid or vertebral artery was noted.6At operation, one patient was found to have blood in the retropharyngeal space and a bleeding arteriole in front of the longus colli muscle. The vertebral artery did not appear in the operative field.22In the remaining four patients who received hematoma evacuation, the bleeding arteries could not be identified.9,13,14 

Retropharyngeal hematoma after SGB occurred even in patients who did not have abnormal hemostasis and who had a negative aspiration test for blood. Common initial symptoms and signs of RPH after SGB were pain in the head, neck, and chest; dyspnea; neck swelling; and abnormal sensations in the upper airway. Initial symptoms of RPH occurred 2 h or more after SGB in almost half of the patients. Many patients needed emergency airway management, and orotracheal intubation was extremely difficult in some patients. There was one patient who died because of failed airway management. Therefore, RPH is a potentially fatal complication of SGB.

Retropharyngeal space is a distensible space in the neck. The ventral border of the retropharyngeal space is the buccopharyngeal fascia, the lateral borders are the carotid sheaths, and the dorsal border is the prevertebral fascia. The retropharyngeal space extends from the base of the skull to the posterior mediastinum, which ends at the level of the second to sixth thoracic vertebrae.29,30Blood accumulation in this space causes RPH. RPH is rare, but various conditions can cause RPH, e.g. , anticoagulation, cervical spine fracture, thyroid surgery, trauma to the vertebral artery, carotid endarterectomy, inadvertent carotid artery puncture, and carotid angiography.2,31,32We found reports on 27 patients who developed RPH after SGB in the past 40 yr. The frequency of RPH after SGB was reported to be 1 in 100,000 SGBs.18 

The symptoms and signs of RPH after trauma are hoarseness, inspiratory stridor, and dysphagia,2and the three primary signs of RPH are superior mediastinal obstruction, ventral displacement of the trachea, and subcutaneous ecchymosis over the neck and anterior chest wall.33However, these symptoms and signs are those of established RPH. Early symptoms of RPH after SGB are important for early detection and prompt treatment but have not yet been clarified. Our analyses revealed that the early symptoms of RPH after SGB were pain in the head, neck, and chest and abnormal sensations in the upper airway. If these symptoms occur after SGB, RPH should be suspected. In addition, these symptoms occurred 2 h or more after SGB in approximately half of the patients. Therefore, because many patients would be out of the hospital at the time of onset of airway compromise due to RPH, prompt airway management would not be feasible. Patients who receive SGB should be warned of the possibility of delayed onset of RPH and should be told that if the symptoms of RPH occur, prompt contact, as early as possible, should be made with medical staff.

The diagnosis of RPH is made by x-ray, computed tomography, and magnetic resonance imaging. Lateral neck x-ray examination is a simple and useful method for detecting the possible presence of RPH. The maximum distance from the anterior cervical vertebral line to the retrotracheal wall in adults without retropharyngeal diseases is 22 mm at C5, 20 mm at C6, and 21 mm at C7.34These distances do not change with neck positions (i.e. , flexed, neutral, and extended positions).34When the distance from the anterior cervical line to the retrotracheal wall is greater than the above values after SGB, RPH should be suspected. Computed tomography and magnetic resonance imaging can be used to make a definite diagnosis of RPH.9,29,35,36 

The most serious complication of RPH is airway obstruction, which can result in respiratory arrest and death3,5; however, it is difficult to predict the occurrence and onset of airway obstruction leading to respiratory arrest at the outset.2,37Our analyses revealed that there was no statistically significant difference in the onset times of the initial symptoms and signs of RPH after SGB between patients who later needed emergency airway management and those who did not, and that there were no statistically significant predictors of the initial symptoms or signs for later emergency airway management. These findings indicate that respiratory obstruction cannot be predicted in the early stages of RPH after SGB. When RPH occurs after SGB, it is essential to have emergency airway management tools at hand, and the patency of the airway should be continuously evaluated.

Airway obstruction in RPH is not caused by mechanical compression of the rigid trachea, but rather by swelling of the pharyngolarynx because of venous and lymphatic congestion.38,39When the vocal cords become more edematous than the critical level, inspiratory stridors develop. Further worsening of edema of the vocal cords, even if it is slight, can give rise to a rapid worsening of airway obstruction, leading to respiratory arrest, because negative pressure in the trachea on inspiration can close the swollen vocal cords.38The airway should be urgently secured when inspiratory stridors occur in patients with RPH.38There were five patients with RPH after SGB who developed inspiratory stridors/dyspnea immediately before they needed emergency airway management.

The patients having subcutaneous ecchymosis in the neck, as one of the initial signs of RPH after SGB, did not significantly need emergency airway management. Because the cervical subcutaneous space connects with the retropharyngeal space via  the parapharyngeal space,30early presence of subcutaneous ecchymosis in the neck would indicate that the blood flowed out from the retropharyngeal space, resulting in decompression of the retropharyngeal space. This may improve the venous and lymphatic congestion of the pharyngolarynx, with a resultant improvement of the edema of the vocal cords.

Massive swelling of the pharyngolarynx in RPH distorts the normal anatomy and makes direct visualization of the vocal cords difficult or even impossible, resulting in tracheal intubation becoming extremely difficult, even for experienced anesthesiologists.38Even when the trachea could be intubated, only tracheal tubes that were smaller than usual ones could be inserted in some patients with RPH.40,41Among the patients with RPH after SGB, there were three patients whose tracheas were able to be intubated only with 7.0-mm or smaller tracheal tubes. Recent reports have shown that transtracheal jet ventilation of the lungs via  the cricothyroid ligament with a large bore needle was a simple and effective way to oxygenate and ventilate patients with airway obstruction due to swelling of the upper airway.42,43Positive pressure in the trachea achieved by jet ventilation opened the swollen vocal cords on inspiration, and the escape of gas under high pressure made identification of the vocal cords and tracheal intubation easier.42,43 

Emergency reintubation was often needed in patients with RPH who still had pharyngolaryngeal edema at the time of extubation, and reintubation of the trachea in such patients was extremely difficult.44It is essential to confirm resolution of pharyngolaryngeal edema by fiberscopy before extubation of the trachea to avoid emergency reintubation.45 

The vertebral artery usually runs ventrally to the seventh cervical transverse process and enters the foramen transversarium of the sixth cervical vertebra. However, it enters the foramen transversarium of the fifth cervical vertebra or higher in some people. In addition, tortuous vertebral arteries are more frequent on the left.46These anatomical characteristics of the vertebral artery lead to speculate that SGB using the anterior paratracheal approach is more likely to puncture the vertebral artery, especially on the left.47However, our analyses revealed that patients who developed RPH after SGB showed no laterality or any apparent difference between SGBs aiming at C6 and those aiming at C7. Many patients developed RPH after SGB despite having a negative aspiration test for blood before SGB. In addition, surgical and autopsy findings in the patients with RPH after SGB showed that there was no injury to the vertebral artery, but rather bleeding from arterioles.6,22These findings, in combination with the anatomical information that the inferior thyroid artery runs ventrally to the C6 or C7 vertebral level,48cannot rule out the possibility that the cause of RPH after SGB is severing of a smaller artery, e.g. , the inferior thyroid artery or its branch, rather than puncture of a larger artery, e.g. , the vertebral artery, with the block needle.

In conclusion, RPH after stellate ganglion block is rare but a potentially fatal complication due to respiratory obstruction. The initial symptoms of retropharyngeal hematoma after SGB include pain in the neck, throat, chest, and back, and upper airway symptoms. Physicians who perform SGB should be aware of RPH and be prepared for emergency airway management if RPH develops.

The authors thank Yasuhisa Okuda, M.D. (Professor, Department of Anesthesiology, Koshigaya Hospital, Dokkyo University School of Medicine, Koshigaya, Japan), for his valuable comments and Sachiko Fujii (Secretary, Department of Anesthesiology, Fukuoka University, Fukuoka, Japan) for her help with making figures and tables.