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| CASE REPORT |
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| Year : 2016 | Volume
: 17
| Issue : 2 | Page : 52-54 |
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Takayasu's arteritis: An anesthetic challenge
Geetanjali S Verma
Department of Anesthesia, St. Martha's Hospital, Bengaluru, Karnataka, India
| Date of Submission | 24-May-2016 |
| Date of Acceptance | 09-Sep-2016 |
| Date of Web Publication | 16-Dec-2016 |
Correspondence Address:
Dr. Geetanjali S Verma
Active Acres Tower 3B, Flat 9 G, 54/10, D C Dey Road, Kolkata - 700 015, West Bengal
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0973-0311.194266
Takayasu's arteritis (TA) is found commonly in young women presenting for cesarean section. A 24-year-old woman with a history of cerebrovascular disease and known case of Type I TA was managed successfully without perioperative complications under general anesthesia.
Keywords: Anesthesia, cesarean, monitoring, Takayasu
How to cite this article:
Verma GS. Takayasu's arteritis: An anesthetic challenge. Indian Anaesth Forum 2016;17:52-4 |
| Introduction | |  |
Takayasu arteritis (TA) (pulseless disease) is a granulomatous vasculitis of unknown etiology. An anesthesiologist most commonly comes across this condition in women presenting for cesarean section, as young women are the most vulnerable group. The knowledge of this disease is, therefore, important for all anesthesiologists working in the Asian subcontinent due to its high incidence in this part of the world compared to the other regions.
| Case Report | | |
A full-term 24-year-old (weight 71 kg, height 155 cm) gravida 2 para 1 living 1 with a history of previous cesarean section was admitted to the labor ward for elective cesarean section.
History revealed cerebrovascular accident in 2009, manifested as right-sided hemiplegia from which she gradually recovered. She was diagnosed with Takayasu's disease in 2012 for which she had received steroids for 6 months. Magnetic resonance imaging (MRI) of the brain done at that time revealed subarachnoid hemorrhage with edema in the left temporo-parietal and cerebellar region, significant long segment stenosis/occlusion of cervical proximal intracranial portion of the left internal carotid and left common carotid artery (LCCA) with a significant stenosis of 70%-80%. She underwent cesarean section 3 years back under spinal anesthesia, 4 h after which she had an epileptic episode (details not known). MRI of the brain revealed medium-sized arteries with the left basal ganglia and chronic deep watershed territory infarcts, suggestive of Takayasu's disease. MRI of the brain was repeated in 2014 that showed chronic infarcts in the left posterior putamen, anterior communicating artery-middle communicating artery watershed territory, and motor cortex. There was an irregular narrowing of bilateral subclavian, right common carotid artery with nonvisualization of LCCA, left internal carotid artery, and proximal segment of the left vertebral artery. For the above issues, she was receiving phenytoin 100 mg per oral tds, levipril 500 mg per oral bd, and ecosprin 150 mg per oral od (which was changed to enoxaparin 40 mg subcutaneous od 6 days prior to the planned date of surgery).
On examination, the pulse rate was 92/min, blood pressure was 120/80 mmHg (right arm), and respiratory rate was 14/min. The patient was afebrile and oxygen saturation was 99% (right hand).
The right-sided pulses (radial, brachial, and dorsalis pedis) were normal whereas the left radial could not be felt, left brachial was feeble, and dorsalis pedis was normal on palpation. General examination also revealed presence of bilateral pedal edema. There were no signs of anemia, cyanosis, clubbing, icterus, or lymphadenopathy. Systemic examination revealed no abnormalities. Airway and spine examination was normal.
Preoperative investigations were within normal limits (hemoglobin: 13, PCV: 38, erythrocyte sedimentation rate: 89 mm/h, platelet count: 2.76 lakhs/mm3 , prothrombin time: 12.3, aPTT: 43.5, INR 1.1, creatinine: 0.7 mg/dl, urea: 12, random blood sugar: 101, thyroid-stimulating hormone: 1.97, blood group: O positive, and serology negative).
The patient was brought to the operation room with fasting status of 8 h. A 20-gauge intravenous access was established in the right arm, and Ringer's lactate infusion was started. Monitors were connected; the noninvasive blood pressure was 90/60 mm Hg in the left arm and 140/80 mmHg in the right arm, the rhythm was sinus, heart rate was 100/min, and the saturation was 99% on room air on the right hand. General anesthesia (GA) was planned and she was induced with thiopentone (250 mg intravenous) and intubated using succinylcholine (100 mg intravenous) after adequate preoxygenation with size 7 cuffed endotracheal tube. After confirmation of bilateral air entry, the tube was secured and the surgery was started. After delivery of the child, midazolam 1 mg, fentanyl 100 mcg, and atracurium 30 mg were given intravenously. An infusion of 10 units of oxytocin was started simultaneously. Anesthesia was maintained using subanesthetic minimum alveolar concentration isoflurane (<1), nitrous oxide, and oxygen. The vital parameters remained s throughout the surgery. After completion of the surgery, the neuromuscular blockade was reversed with intravenous neostigmine and glycopyrrolate, and the patient was extubated after complete reversal. The oxytocin infusion was continued postoperatively, and she was shifted to the Intensive Care Unit for monitoring. No neurological deficits or events were noted postoperatively.
| Discussion | | |
Takayasu's disease was first described by two Japanese ophthalmologists (Takayasu and Onishi) in 1908, who observed retinopathy with the absence of limb pulses. It is a rare granulomatous vasculitis (2-3 per million)[1] of the aorta and the pulmonary arteries.[2],[3] It is more common in women than men (8:1), and the peak incidence is in the second and third decades, although a substantial minority, including this patient, present in their teens.[4] It is found to be more common in the Asian ethnic origin although it has a worldwide occurrence[ 2 ] (Japan - 1 in 3000 persons[5] and America - 2.6 new cases/million/year[6] ). The incidence in India is not known. The cause is unknown, but it may have an autoimmune basis. Since it is more prevalent in women of childbearing age, sex hormones may be involved in the pathogenesis.[7] Genetic predisposition for TA in families, linked to the presence of human leukocyte antigen-Bw52 and MIC-A gene, has been suggested.[4],[8]
TA results from infiltration of the intima, by lymphocyte and other inflammatory cells, causing arteritis. The resultant loss of elastic tissue and its replacement by fibrous tissue leads to progressive thickening and deformity of the arterial wall, causing occlusion, stenosis, dilation, or aneurysm formation.[ 4]
In the initial active phase, nearly 60% of patients present with constitutional symptoms. The disease is characterized classically by a triphasic course, commencing with an initial active phase of constitutional symptoms such as malaise, weight loss, fever, myalgias, and arthralgias, and it is associated with an increase in acute phase reactants. This progresses to a second stage with symptoms of cerebral, visceral, or extremity ischemia before resulting in a final "burned-out" quiescent phase of fibrosis. Progression of the disease results in systemic involvement and symptoms, with or without associated complications such as dizziness, vertigo, visual disturbance, angina, cardiac failure, renal failure, and intermittent claudication, resulting from cerebral, visceral, and extremity ischemia due to stenosis/occlusion of vessels.[4] The presence of retinopathy, aortic regurgitation, and aneurysm formation signals a poor prognosis. Five-year mortality varies from 3% to 35%, with heart failure, myocardial infarction, and stroke being the most common cause of death.[4],[9] Biopsy of the vessel wall is the gold standard for diagnosis. Treatment of TA involves the use of corticosteroids and/or immunosuppressants such as methotrexate and azathioprine, which are given over a period of time, depending on the presentation of the patient. The course of the disease is unaltered in pregnancy; however, peripartum complications such as hypertension, multiple organ dysfunction, hampered regional blood flow, and intrauterine growth restriction are known to occur.[10]
There are four types of TA depending on the level of aortic involvement.[2],[11] Type I involves the aortic arch and its main branches. Type II is restricted to descending thoracic aorta and abdominal aorta. Type III shows features of Type I and II. Type IV shows additional involvement of pulmonary artery. Based on this classification, our patient belonged to Type I with the involvement of the aortic arch and its branches. In such cases, any change in blood pressure-a rise or fall-may be detrimental to the patient. Hypertension may result in neurological injury whereas hypotension may worsen the preexisting ischemia.
Both GA and regional anesthesia (RA) have been administered for cesarean section in patients with TA. Administration of anesthesia may increase morbidity and mortality by reducing the organ perfusion and thus worsening the existing ischemia. Rapid sequence intubation and a light plane of GA maintained till childbirth may trigger a severe hypertensive response and result in neurological injury,[12] while regional anesthesia resulting in sympathetic blockade may compromise regional blood flow due to stenosed vessels.[4] The only advantage that regional anesthesia provides in such patients is that it allows monitoring of brain perfusion through the patient's level of consciousness, which is lost in GA,[13] and neurologic monitoring is important while providing GA in patients with TA and common carotid artery involvement.[14]
Keeping the above considerations in mind for a patient with Type I TA, we planned to administer GA as the hemodynamic fluctuations can be controlled better under GA. We chose noninvasive monitoring for blood pressure as the radial artery pulsations were normal on the right hand which provided as a good guide for management as has been reported previously.[15]
Case reports and observational studies found spinal anesthesia in cases of TA to be safe with 7.5 mg bupivacaine.[16],[17] Another case report in 2012 documented the safe use of low dose of spinal anesthesia for Type I cases but suggested that the anesthetic plan to be tailored according to patient presentation.[18]
TA in pregnancy has a favorable outcome, and any technique of anesthesia that minimizes the risk of complication should be implemented based on the condition of the patient. Special attention should be given to maintain the blood pressure and fluid status of the patient.[19] Maintaining the vital parameters within normal limits (within 10% of baseline/preoperative values) guided by monitoring tools is the basic key to successful management of such cases.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Matsumura A, Moriwaki R, Numano F. Pregnancy in Takayasu arteritis from the view of internal medicine. Heart Vessels Suppl 1992;7:120-4.  |
| 2. | Kerr GS, Hallahan CW, Giordano J, Leavitt RY, Fauci AS, Rottem M, et al. Takayasu arteritis. Ann Intern Med 1994;120:919-29. |
| 3. | Kerr GS. Takayasu′s arteritis. Rheum Dis Clin North Am 1995;21:1041-58. |
| 4. | Henderson K, Fludder P. Epidural anaesthesia for caesarean section in a patient with severe Takayasu′s disease. Br J Anaesth 1999;83:956-9. |
| 5. | Nasu T. Takayasu′s truncoarteritis in Japan. A statistical observation of 76 autopsy cases. Pathol Microbiol (Basel) 1975;43:140-6. |
| 6. | Hall S, Barr W, Lie JT, Stanson AW, Kazmier FJ, Hunder GG. Takayasu arteritis. A study of 32 North American patients. Medicine (Baltimore) 1985;64:89-99. |
| 7. | Leal Pda C, Silveira FF, Sadatsune EJ, Clivatti J, Yamashita AM. Takayasu′s arteritis in pregnancy. Case report and literature review. Rev Bras Anestesiol 2011;61:479-85. |
| 8. | Johnston SL, Lock RJ, Gompels MM. Takayasu arteritis: A review. J Clin Pathol 2002;55:481-6. |
| 9. | Morales E, Pineda C, Martínez-Lavín M. Takayasu′s arteritis in children. J Rheumatol 1991;18:1081-4. |
| 10. | Hauth JC, Cunningham FG, Young BK. Takayasu′s syndrome in pregnancy. Obstet Gynecol 1977;50:373-5. |
| 11. | Stoelting RK, Dierdorf SF. Anaesthesia and Co-existing Disease. 4 th ed. New York: Churchill Livingstone; 2002. |
| 12. | Kathirvel S, Chavan S, Arya VK, Rehman I, Babu V, Malhotra N, et al. Anesthetic management of patients with Takayasu′s arteritis: A case series and review. Anesth Analg 2001;93:60-5. |
| 13. | Ramanathan S, Gupta U, Chalon J, Turndorf H. Anesthetic considerations in Takayasu arteritis. Anesth Analg 1979; 58: 247-9. |
| 14. | Winn HN, Setaro JF, Mazor M, Reece EA, Black HR, Hobbins JC. Severe Takayasu′s arteritis in pregnancy: The role of central hemodynamic monitoring. Am J Obstet Gynecol 1988;159:1135-6. |
| 15. | Meikle A, Milne B. Extreme arterial blood pressure differentials in a patient with Takayasu′s arteritis. Can J Anaesth 1997;44:868-71. |
| 16. | Khan AM, Kapoor MC, Puri A. Cesarean section under spinal anesthesia in a patient of Takayasu′s arteritis. J Obstet Anaesth Crit Care 2015;5:90-2.  |
| 17. | Hauth JC, Cunningham FG, Young BK. Takayasu′s syndrome in pregnancy. Obstet Gynecol 1997;50:373-5. |
| 18. | Kiran S. Anesthetic management in a parturient with Takayasu arteritis. Egypt J Anesth 2012;28:287-9. |
| 19. | Poonam SG, Kalpana DH. Anesthetic considerations in a patient with Takayasu′s arteritis for cesarean section. Ain-Shams J Anesthesiol 2015;8:681-2. |
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