• Archives of Reconstructive Microsurgery
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• v.20 no.2
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• pp.102-107
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• 2011

Purpose: As clinical manifestations of thoracic outlet syndrome are vague pain or symptoms in upper extremity, the diagnosis of the disease is delayed or misdiagnosed as cervical HNP, shoulder pathologies, or peripheral neuropathies. In that reason, many patients spend time for unnecessary or ineffective treatments. We report the results of our thoracic outlet syndrome cases, which were treated by conservative care or surgical treatment. Materials & Methods: Twenty five cases, diagnosed as thoracic outlet syndrome since 1999, were reviewed retrospectively. Physical examinations including Adson's and reverse Adson's test, hyperabduction test, costoclavicular maneuver, and Roo's test, plain radiography of shoulder and cervical spine, MRI of neck or brachial plexus, and EMG were checked. If subjective symptoms were not improved after conservative treatments over three months, surgical treatment were performed. Nine patients were performed operative treatment and the others had conservative treatment in outpatient clinic. Postoperative improvement of symptoms and the follow up period, and the results of conservative care were reviewed. Results: Among five physical examinations, mean 1.75 tests were positive, and EMG has little diagnostic value. MRI were performed in twenty cases and compression of brachial plexus were found in 6 cases (30%). Ten patients out of 16 conservative treatment group had excellent improvement of symptoms, and 5 had good results. Eight patients out of 9 operative treatment group had excellent improvement with mean 5.1 months of follow-up period. Conclusion: Diagnosis of thoracic outlet syndrome is difficult due to bizarre and vague symptoms. However if the diagnosis is suspected by careful physical examinations, radiologic studies, or nerve conduction studies, conservative care should be done as initial treatment and at least after three months, reassess the patient's condition. If the results of conservative treatment is not satisfactory and still the thoracic outlet syndrome is suspected, surgical treatment should be considered. Conservative treatment and operative technique are the valuable for the treatment of this disease.

• The Journal of Korean Academy of Orthopedic Manual Physical Therapy
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• v.9 no.2
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• pp.5-11
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• 2003

Thoracic outlet syndrome is actually a collection of syndromes brought about by abnormal compression of the neurovascular bundle by bony, ligamentous or muscular obstacles between the cervical spine and the lower border of the axilla. First of all a syndrome is defined as a group of signs and symptoms that collectively characterize or indicate a particular disease or abnormal condition. The neurovascular bundle which can suffer compression consists of the brachial plexus plus the C8 and T1 nerve roots and the subclavian artery and vein. The brachial plexus is the network of motor and sensory nerves which innervate the arm, the hand, and the region of the shoulder girdle. The vascular component of the bundle, the subclavian artery and vein transport blood to and from the arm. the hand. the shoulder girdle and the regions of the neck and head. The bony, ligamentous, and muscular obstacles all define the cervicoaxillary canal or the thoracic outlet and its course from the base of the neck to the axilla or arm pit. Look at the scheme of this region and it all becomes more easily understood. Compression occurs when the size and shape of the thoracic outlet is altered. The outlet can be altered by exercise, trauma, pregnancy, a congenital anomaly, an exostosis, postural weakness or changes. Thoracic outlet syndrome has been described as occurring in a diverse population. It is most often the result of poor or strenuous posture but can also result from trauma or constant muscle tension in the shoulder girdle. The first step to beginning any treatment begins with a trip to the doctor. Make a list of all of the symptoms which seem to be present even if the sensations are vague. Make a note of what activities and positions produce or alleviate the symptoms and the time of day when symptoms are worst. Also, note when the symptoms first appeared. This list is important and should also include any questions one may have.

• The Korean Journal of Pain
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• v.13 no.1
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• pp.97-100
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• 2000

Thoracic outlet syndrome (TOS) is a combination of signs and symptoms caused by the compression of the vital neurovascular structure at the thoracic outlet region. It may stem from a number of abnormalities, including degenerative or bony disorders, trauma to cervical spine, fibromuscular bands, vascular abnormalities and spasm of the anterior scalene muscle. CPT (current perception threshold) is defined as the minimum amount of current applied transcutaneously that an individual consciously perceives. It enables quantification of the hyperesthesia that precedes progressive nerve impairment, as well as hypoesthetic conditions. We experienced a case of thoracic outlet syndrome caused by fibrosis of anterior scalene muscle. The patient was a 30 years old woman with a 3 years history of numbness on the ulnar side, progressive weakness and coldness of both hand, tiredness in the left arm, nocturnal pain in the left forearm, and pain in the left elbow, shoulder and neck. Conservative treatment, stellate ganglion block, cervical epidural block, anterior scalene block and previous operation, including both carpal tunnel release, provided no remarkable relief to the patient. A left scalenectomy and first rib resection were performed by transaxillary approach and left cervical root neurolysis was done. After surgery, we measured CPT using neurometer and found conditions worsening in the opposite arm. We performed the same procedure on right side, and followed by CPT measurement. This case suggests that CPT is a useful measurement of recovery and progression of TOS.

• Journal of Chest Surgery
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• v.29 no.10
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• pp.1160-1165
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• 1996

We report a case of an angiosarcoma arising from the subclavian artery, a site not previously described. A 19-year-old girl, born with a rudimentary first rib, has been suffered from arterial thoracic outlet syndrome due to a complete occlusion of the third portion of the subclavian artery for 1 year. Partial claviculectomy, excision of completely occluded arterial segment, and reconstruction with great r saphenous vein graft were done. Histologic study for the subclavlan artery revealed mural type anglosarcoma. The histochemici1 staining for factor VIII related antigen was positive. The debilitating symptoms that did not allow her a normal daily life, almost subsided postoperatively. And she has remained well with no clinical evidence of disease for 4 months post-operation.

• The Korean Journal of Pain
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• v.19 no.2
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• pp.296-298
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• 2006

Droopy shoulder syndrome (DSS) is a rare disease, characterized by drooping shoulders, which stretches the brachial plexus, and causes pain, but without any signs of neurological impairment. These patients suffer from pain in the neck, shoulders, arms and hands, which result in long, graceful, swan necks, low-set shoulders, and horizontal or down sloping clavicles. No abnormalities in the vascular, neurological or electrical findings have also been known. The T1 and/or T2 bodies can be seen in the lateral view in a radiological study of the cervical spine. In the majority of cases, conservative treatments, such as postural correction and shoulder girdle strengthening exercise, are commonly recommended. However, DSS may be misdiagnosed as severe thoracic outlet syndrome or herniated cervical disc disease, leading to unnecessary and hazardous invasive treatments. The presented case was consistent with DSS, and was treated with stellate ganglion block, trigger point injection, and shoulder girdle strengthening exercise.

• Journal of Chest Surgery
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• v.40 no.6 s.275
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• pp.451-454
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• 2007

Subclavian vein thrombosis in thoracic outlet syndrome is an uncommon disease. Thrombolysis, venoplasty with a balloon and stent insertion are needed for treating this condition. Sometimes, trans-axillary first rib resection is also needed. We report here on a case of subclavian vein thrombosis that was successfully treated with the medial calviculectomy, internal jugular vein transposition and stent insertion.

• The Journal of Korean Medicine
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• v.28 no.3 s.71
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• pp.45-56
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• 2007

Objectives : We investigated the possibility of cervical spine misalignment caused by scalenus anticus syndrome to find out how it affects cervical spine misalignments. Methods : 28 patients with scalenus anticus syndrome (sample group), along with 21 participants without neck pain (control group), who attended the Dept. of Oriental Rehabilitation Medicine, College of Oriental Medicine, Dong-guk University from the 20th of June to the 30th of November, 2006 were investigated. After researching misalignments through neutrality, flexion and extension lateral x-ray examination views, we measured the difference of each length of cervical spine misalignment. We analyzed the relationships among the neutrality lateral, flexion lateral and extension lateral positions. Results : We found with statistical significance that there were differences in length of cervical spine misalignments between the sample and control groups. Furthermore, we found that C3 and C4 vertebra bodies were shown in lateral neutrality position, only C3 vertebra body in flexion lateral position, and C2, C3, and C4 vertebra bodies in extension lateral position. Conclusions : It is considered that scalenus anticus syndrome could increase cervical spine misalignment which could be a factor in causing cervical spine disease.

• Journal of Chest Surgery
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• v.12 no.3
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• pp.281-288
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• 1979

For years, physicians and anatomists have been interested in the heart that has one functioning ventricle. Various terms have been suggested for this entity including single ventricle, common ventricle, double-inlet left ventricle, cor biatriatum triloculare, and primitive ventricle. In this report, the term "single ventricle" is utilized as suggested by Van Praagh, and is defined as that congenital cardiac anomaly in which a common or separate atrioventricular valves open into a ventricular chamber from which both great arterial trunks emerge. An outlet chamber, or infundibulum, may or may not be present and give rise to the origin of either of the great arteries. This definition excludes the entity of mitral and tricuspid atresia. An 11 year old cyanotic boy was admitted chief complaints of exertional dyspnea and frequent upper respiratory infection since 2 weeks after birth. He was diagnosed as inoperable cyanotic congenital heart disease, and remained without any corrective treatment up to his age of 11 year when he suffered from aggravation of symptoms and signs of congestive heart failure for 2 months before this admission. On 22nd of May 1979, he was admitted for total corrective operation under the impression of tricuspid atresia suggested by a pediatrician. Physical check revealed deep cyanosis with finger and toe clubbing, and grade V systolic ejection murmur with single second heart sound was audible at the left 3rd intercostal space. Development was moderate in height [135 cm] and weight[28Kg]. Routine lab findings were normal except increased hemoglobin [21.1gm%], hematocrit [64 %], and left axis deviation with left ventricular hypertrophy on EKG. Cardiac catheterization and angiography revealed 1-transposition of aorta, pulmonic valvular stenosis, double inlet of a single ventricle with d-loop, and normal atriovisceral relationship [Type III C solitus according to the classification of Van Praagh]. At operation, longitudinal incision at the outflow tract of right ventricle in between the right coronary artery and its branch [LAD from RCA] revealed high far anterior aortic valve which had fibrous continuity with mitral annulus, and pulmonic valve was stenotic up to 4 mm in diameter positioned posterolaterally to the aorta. Ventricular septum was totally defective, and one markedly hypertrophied moderator band originated from crista supraventricularis was connected down to the imaginary septum of the ventricular cavity as a pseudoseptum of the ventricle. Size of the defect was 3X3 cm2 in total. Patch closure of the defect with a Teflon felt of 3.5 x 4 cm2 was done with interrupted multiple sutures after cut off of the moderator band, which was resutured to the artificial septum after reconstruction of the ventricular septum. Pulmonic valvotomy was done from 4 mm to 11 mm in diameter thru another pulmonary arteriotomy incision, and right ventriculotomy wound was closed reconstructing the right ventricular outflow tract with pericardial autograft of 3 x 4 cm2. Atrial septal defect of 2 cm in diameter was closed with 3-0 Erdeck suture, and atrial wall was sutured also when rectal temperature reached from 24`C to 35.5`C. Complete A-V block was managed with temporary external pacemaker with a pacing rate of 110/min. thru myocardial wire, and arterial blood pressure of 80/50 mmHg was maintained with Isuprel or Dopamine dripping under the CVP of 25-cm saline. Consciousness was recovered one hour after the operation when his blood pressure reached 100 /70 mmHg, but vital signs were not stable, and bleeding from the pericardial drainage and complete anuria were persisted until his heart could not capture the pacemaker impulse, and patient died of low output syndrome 320 min after the operation.

• Journal of Chest Surgery
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• v.12 no.3
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• pp.289-296
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• 1979

For years, physicians and anatomists have been interested in the heart that has one functioning ventricle. Various terms have been suggested for this entity including single ventricle, common ventricle, double-inlet left ventricle, cor biatriatum triloculare, and primitive ventricle. In this report, the term "single ventricle" is utilized as suggested by Van Praagh, and is defined as that congenital cardiac anomaly in which a common or separate atrioventricular valves open into a ventricular chamber from which both great arterial trunks emerge. An outlet chamber, or infundibulum, may or may not be present and give rise to the origin of either of the great arteries. This definition excludes the entity of mitral and tricuspid atresia. An 11 year old cyanotic boy was admitted chief complaints of exertional dyspnea and frequent upper respiratory infection since 2 weeks after birth. He was diagnosed as inoperable cyanotic congenital heart disease, and remained without any corrective treatment up to his age of 11 year when he suffered from aggravation of symptoms and signs of congestive heart failure for 2 months before this admission. On 22nd of May 1979, he was admitted for total corrective operation under the impression of tricuspid atresia suggested by a pediatrician. Physical check revealed deep cyanosis with finger and toe clubbing, and grade V systolic ejection murmur with single second heart sound was audible at the left 3rd intercostal space. Development was moderate in height [135 cm] and weight[28Kg]. Routine lab findings were normal except increased hemoglobin [21.1gm%], hematocrit [64 %], and left axis deviation with left ventricular hypertrophy on EKG. Cardiac catheterization and angiography revealed 1-transposition of aorta, pulmonic valvular stenosis, double inlet of a single ventricle with d-loop, and normal atriovisceral relationship [Type III C solitus according to the classification of Van Praagh]. At operation, longitudinal incision at the outflow tract of right ventricle in between the right coronary artery and its branch [LAD from RCA] revealed high far anterior aortic valve which had fibrous continuity with mitral annulus, and pulmonic valve was stenotic up to 4 mm in diameter positioned posterolaterally to the aorta. Ventricular septum was totally defective, and one markedly hypertrophied moderator band originated from crista supraventricularis was connected down to the imaginary septum of the ventricular cavity as a pseudoseptum of the ventricle. Size of the defect was 3X3 cm2 in total. Patch closure of the defect with a Teflon felt of 3.5 x 4 cm2 was done with interrupted multiple sutures after cut off of the moderator band, which was resutured to the artificial septum after reconstruction of the ventricular septum. Pulmonic valvotomy was done from 4 mm to 11 mm in diameter thru another pulmonary arteriotomy incision, and right ventriculotomy wound was closed reconstructing the right ventricular outflow tract with pericardial autograft of 3 x 4 cm2. Atrial septal defect of 2 cm in diameter was closed with 3-0 Erdeck suture, and atrial wall was sutured also when rectal temperature reached from 24`C to 35.5`C. Complete A-V block was managed with temporary external pacemaker with a pacing rate of 110/min. thru myocardial wire, and arterial blood pressure of 80/50 mmHg was maintained with Isuprel or Dopamine dripping under the CVP of 25-cm saline. Consciousness was recovered one hour after the operation when his blood pressure reached 100 /70 mmHg, but vital signs were not stable, and bleeding from the pericardial drainage and complete anuria were persisted until his heart could not capture the pacemaker impulse, and patient died of low output syndrome 320 min after the operation.

• Journal of Chest Surgery
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• v.37 no.6
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• pp.504-510
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• 2004

Background: Vasodilatory shock after cardiac surgery may result from the vasopressin deficiency following cardio-pulmonary bypass and sepsis, which did not respond to usual intravenous inotropes. In contrast to the adult patients, the effectiveness of vasopressin for vasodilatory shock in children has not been known well and so we reviewed our experience of vasopressin therapy in the small babies with a cardiac disease. Material and Method: Between February and August 2003, intravenous vasopressin was administrated in 6 patients for vasodilatory shock despite being supported on intravenous inotropes after cardiac surgery. Median age at operation was 25 days old (ranges; 2∼41 days) and median body weight was 2,870 grams (ranges; 900∼3,530 grams). Preoperative diag-noses were complete transposition of the great arteries in 2 patients, hypoplastic left heart syndrome in 1, Fallot type double-outlet right ventricle in 1, aortic coarctation with severe atrioventricular valve regurgitation in 1, and total anomalous pulmonary venous return in 1. Total repair and palliative repair were undertaken in each 3 patient. Result: Most patients showed vasodilatory shock not responding to the inotropes and required the vasopressin therapy within 24 hours after cardiac surgery and its readministration for septic shock. The dosing range for vasopressin was 0.0002∼0.008 unit/kg/minute with a median total time of its administration of 59 hours (ranges; 26∼140 hours). Systolic blood pressure before, 1 hour, and 6 hours after its administration were 42.7$\pm$7.4 mmHg, 53.7$\pm$11.4 mmHg, and 56.3$\pm$13.4 mmHg, respectively, which shows a significant increase in systolic blood pressure (systolic pressure 1hour and 6 hours after the administration compared to before the administration; p=0.042 in all). Inotropic indexes before, 6 hour, and 12 hours after its administration were 32.3$\pm$7.2, 21.0$\pm$8.4, and 21.2$\pm$8.9, respectively, which reveals a significant decrease in inotropic index (inotropic indexes 6 hour and 12 hours after the administration compared to before the administration; p=0.027 in all). Significant metabolic acidosis and decreased urine output related to systemic hypoperfusion were not found after vasopressin admin- istration. Conclusion: In young children suffering from vasodilatory shock not responding to common inotropes despite normal ventricular contractility, intravenous vasopressin reveals to be an effective vasoconstrictor to increase systolic blood pressure and to mitigate the complications related to higher doses of inotropes.