An unusual differential for a pulseless trauma patient.

Hemorrhagic shock is the most common reason to explain the inability to feel pulse in a trauma patient. However, clinicians should always suspect atypical causes for differential pulses in this population and Takayasu's arteritis (TA) is one such example. We report a case of aorto-arteritis in a patient who presented with trauma and was later diagnosed with TA. She had blood pressure discrepancy between upper and lower limbs noted upon her initial trauma evaluation.

INTRODUCTION

Takayasu's arteritis (TA) is a chronic idiopathic occlusive inflammation of aorta and its major branches predominantly affecting females in over 85% of cases.[1] The major clinical finding is loss of palpable pulses in the upper limbs and neck. The unsuspected ischemia of vital regional vascular beds may render these patients at risk for inappropriate management. This case report describes the management of a trauma patient in whom the diagnosis of TA was established by specific investigations done for the same. The role of meticulous monitoring and importance of anticipation of such disease for prompt diagnosis and management is emphasized.

CASE HISTORY

A 26-year-old female was brought to the emergency room (ER) with history of motor vehicle accident. On initial evaluation she was conscious and responsive with Glasgow Coma Scale Score of 15. Her physical examination revealed unrecordable upper limb peripheral pulses and blood pressure, although lower limb pulses were easily palpated. The radiological investigations revealed multiple left-sided rib fractures with bilateral pleural collections and small lung contusions. After infusion of two liters of Lactated Ringer's solution, her blood pressure (BP measured in right upper limb) increased to 80/50 mmHg and heart rate (HR) was 140/min. BP in left upper limb was 92/54 mmHg. She also had shaft and inter-trochanteric femur fractures on the right and left side, respectively. Focused assessment sonography in trauma (FAST) was negative and X-ray of the pelvis was normal. Hematological and biochemical investigations were within normal limits. Bilateral chest tubes were inserted and the patient was transferred to the intensive care unit (ICU) with ongoing resuscitation with fluids, blood products and dopamine infusion (7 μg/kg/min). Fluid resuscitation was continued to maintain a central venous pressure (CVP) of around 10 mmHg. Invasive arterial blood pressure monitoring was established via the right femoral artery and the BP recorded was 140/90 mmHg. Dopamine infusion was then discontinued and thereafter the patient was subjected to arterial Doppler and computed tomography (CT) angiography studies to rule out traumatic aortic rupture as a differential diagnosis. CT angiography revealed narrowing of bilateral subclavian artery just distal to ostium. Arterial Doppler showed low-velocity monophasic flow in bilateral axillary, brachial and ulnar arteries. Right radial artery at the level of wrist could not be visualized. Diagnosis of TA was established on the basis of above findings. There were no signs of active disease. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normal. Electrocardiography (ECG), 2D Echocardiography (2D Echo) and funduscopy were normal. There was no carotid bruit on auscultation. Thoracic epidural catheter was inserted for pain relief with continuous infusion of 0.125% bupivacaine and fentanyl (2 mcg/ml). Epidural catheter was removed on 5th day of hospitalization and patient was moved to the ward in a stable condition with advice for regular follow-up and advised to check BP measurements in the lower limb if ever required.

DISCUSSION

The occlusive thromboaortopathy (TA) is a group of diseases in which there is no or feeble pulses in upper half of body. TA is a chronic inflammatory arteriopathy of unknown origin. The site of occurrence is aorta or its main branches or both. The majority of the cases are idiopathic. The natural course of disease often gives rise to four main complications: Takayasu's hypertensive ischemic retinopathy, secondary hypertension, aortic regurgitation and aortic or arterial aneurysm.[23] The estimated worldwide incidence of TA is 2.6 cases per million per year. Most patients with TA present during their child-bearing age, and a high index of suspicion is required to make an early diagnosis.[4] Patient may be entirely asymptomatic and the incidental finding of unequal pulse and blood pressure in upper and lower limb, bruit and hypertension may prompt further evaluation. Conversely, presentation may be dramatic and disastrous. Stroke, congestive heart failure, and rarely ruptured aneurysm may be the heralding events.[4]

Hemorrhagic shock is the commonest type of shock in trauma patients. Any hypotensive trauma patient is presumed to be hypovolemic and resuscitative attempts are made with fluid infusion as was with our patient. There was no contributory past history of symptoms or signs suggestive of TA in our patient. A CVP of around 10 mmHg suggested a normovolemia status unlike the impression got by the low blood pressure (as recorded in upper limbs). The presence of tachycardia in our patient could be attributed to pain and anxiety associated with trauma. FAST was done to rule out pericardial fluid, intraperitoneal fluid and pelvic collection. There was no fall in hematocrit from the baseline (perhaps due to hemo-concentration). Dopamine infusion was started in our patient in an attempt to maintain perfusion and restore blood pressure but was discontinued when invasive monitoring revealed a normal BP. Normal value of ESR and C-reactive protein suggested that the disease was not active at that moment. Our patient was perhaps asymptomatic for the disease and was incidentally diagnosed during workup after trauma. But TA as a differential diagnosis of exclusion may be considered for a pulseless trauma patient.

No laboratory test is specific for diagnosis of TA.[4] Laboratory parameters may indicate active inflammation. Normocytic normochromic anemia, hyper-gammaglobulin, and elevated ESR may occur, but are not pathognomonic.[45] ESR is most often used as a tool to assess disease activity in TA.[4] Angiography remains the gold standard investigation for detecting diseased vessels in TA. The extent and nature of vessel involvement are well visualized via this imaging study. A full aortography is strongly recommended in the initial evaluation of TA.[4] Medical treatment includes corticosteroids, anticoagulants and symptomatic therapy for which anti-hypertensive agents, digitalis and antibiotics are frequently used.[3] Follow-up in cases of TA includes monitoring for disease activity and its complications like hypertension, organ failure, seizures etc. Long-term complications of corticosteroid use are also to be considered in the follow-up. Anesthesiologists may encounter these patients in operation theater for anesthesia[6] or in ICUs or emergency units after trauma or after one of its complications like a ruptured aneurysm.

CONCLUSION

TAs may be considered as a differential diagnosis in trauma patients, if examination reveals hypotension or unequal peripheral pulses in upper and lower limb in a young adult, provided hypovolemic shock is excluded. A thorough detailed physical examination with palpation of all the peripheral pulses as stressed in ATLS guidelines is reemphasized. Following the basic ATLS guidelines would assist clinicians in picking up this discrepancy as part of their routine evaluation for all trauma patients. Then, the clinician may suspect an atypical cause for hypotension if a blood pressure cuff on an upper extremity is reading a hypotensive measurement but the patient has strong, 2+ pulses in the lower extremities. These patients may be issued a special identification card containing the details of the disease and treatment course for future reference.