Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Robert Wang, OD, FAAO Giant Cell Arteritis? Second Chances... Abstract: Sixty four year old white male arriving in clinic with signs of giant cell arteritis refusing advanced care and then lost to follow up. Patient returns to clinic with signs of recalcitrant giant cell arteritis. I. Case History Patient demographics 64 year old white male. Chief complaints Reporting to eye clinic with CC of not being able to see out of left eye, onset 4-5 days prior. Patient notes “flashes of light and big blobs or stuff moving” in his vision, then finally vision is completely dark. Ocular, medical history No significant prior ocular history. Intervertebral disc disorder, Tobacco use disorder, constipation, chronic low back pain, muscle weakness, anemia, malnutrition of mild degree, chronic obstructive pulmonary disease, essential hypertension, peptic ulcer, shoulder pain. Medications Hydrocodone/acetaminophen tab, epi-pen, amlodipine besylate, Lisinopril, ranitidine, albuterol, aldendronate, calcium/vitamin D Other salient information None II. Pertinent findings Clinical 2/4/13 VA 20/30 ph 20/25+2 right, NLP PH NI left APD left, confrontation fields fill right, restricted 360 left IOPs 10mmHg right and 11mmHg left Anterior segment unremarkable Posterior segment .2/.2 right, no cup, swollen nerve with flame hemorrhage just inf/temp left OCT: notes optic nerve head drusen, but also a triangular separation of fluid/edema characteristic of optic nerve head edema Physical Laboratory studies CRP 30.7 ESR 49 Radiology studies Ct: no abnormalities Others III. Differential diagnoses Primary/leading Giant cell arteritis Non-arteritic ischemic optic neuropathy Others IV. Diagnosis and discussion Elaborate on the condition Giant cell arteritis is a chronic vasculitis of medium and large size arteries and appears to favor the smaller branches of the external carotid artery. This eventually leads to endovascular damage, vessel stenosis and occlusion which then leads to tissue necrosis (Smetana). In the presence of a swollen nerve in an age group over 50, clinicians should always consider Giant cell arteritis. Most commonly patients will complain of headaches in 56%, followed by anorexia/weight loss in 52%, and jaw claudication in 48% (Hayreh). Studies have shown that a useful criteria for normal ESR is <30 mm/hr in men and <35mm/hr in women with a sensitivity and specificity of 92%. (Hayreh), however notes that a normal ESR does not rule out the possibility of GCA. CRP appears to be more reliable test as sensitivity in detecting GCA was noted 100% and the specificity noted at 7983% (Hayreh). Vision loss of varying severity was reported in 92% in a case series (Hayreh). Visual acuity varies from 20/40 or better to no light perception. The gold standard for GCA arteritis is a temporal artery biopsy, however even these biopsy’s can be subject to skip lesions where normal tissue can be found even with GCA. Given this possibility of skip lesions, studies have emerged on using MRI to specifically search for inflamed portions of the temporal arteries to direct temporal artery biopsies (Bley). Expound on the unique features Patients over 50 with temporal headache and jaw claudication with a swollen nerve are considered to have giant cell arteritis until proven otherwise. V. Treatment, management Treatment and response to treatment Treatment can precede diagnosis given the threat of further irreversible vision loss. Hayreh suggests treatment with systemic corticosteroids, starting with a megadose of intravenous steroids as a loading dose, followed by oral Prednisone. Hayreh also recommends altering the steroid dosage based on the ESR and CPR reading rather than systemic conditions. Patients should be warned that usually there is no useful recovery of vision in the effected eye, and that the goal of treatment is to save the vision in the opposing eye. Many of these patients will be on steroid therapy for long term treatment. Recently evidence that MRI with sufficient resolution and an auto injector maybe able to point areas that are most effected by giant cell arteritis and be markers for possible sites for biopsy. In our case our patient was walked to the Emergency department in preparation to be admitted to the hospital for intravenous steroids. Somehow the patient was never admitted, and instead was given a regiment of oral steroids for treatment. The following temporal artery biopsy was negative. Patient was lost to follow up until... 4/11/14 Patient returning to eye clinic with eye pain once a week for 2 months. Patient denies temporal scalp tenderness/pain or jaw claudication. Va 20/20-3 right, LP without directionality left APD left IOPs 14mmHG right and 12mmHg left @ 3:45p Unremarkable anterior segment Posterior segment .2r right, .2r left with diffuse pallor, noted optic nerve head drusen both No clinical signs of giant cell arteritis at this visit, but given history of persistent headache ordered ESR and CRP. CRP > 55mg/L and ESR 67mmHR. Spoke to ED after hours and make call to patient regarding lab findings. Patient noted that they still had oral steroids from the ED as they never finished the treatment. Patient could not return to the hospital that night, and instead began 80mg steroid PO each day until he could return to the hospital. 4/14/14 Patient arrived in ED, while being on oral steroids 40mg bid po. Patient did not want to have a temporal biopsy, refused IV steroids and consult to rheumatology. A compromise of sorts was made with tapering to 60mg for 7 days oral then to 40mg for 30 days and to re-evaluate following this dosing. ESR 4mg/L, CRP 14.30mmHR. Labs to be done every month or ESR, CRP and A1C. Monthly optometry visits as well as Primary care visits. Of interesting note, patient had a longstanding history of shoulder and lower back pain for which he was on hydrocodone. Also noted was that he had mild malnutrition. The oral steroids had an astonishing effect on both of these problems. Patient likely had polymyalgia rheumatic as this occurs in 40-50 percent of giant cell patients. This pain was largely relieved by the oral steroids to the point that the patient noted that he no longer needed his hydrocodone as much. In addition because of the steroids the patient was able to put on some weight. Patient is currently being followed monthly by primary care provider and Optometry, current goal of treatment is to taper oral steroids as much as possible. Recent Rheumatology consult noted that they will be pursuing a neuro eval and MRI of the head to eliminate other possible causes. If no other causes are found they will consider addition of immunosuppressives to possibly allow the taper of Prednisolone. Refer to research where appropriate. Bibliography, literature review encouraged Bley Thorsten, Oliver Wieben, Markus Uhl, Jens Thiel, Dieter Schmidt, and Mathias Langer. "High Resolution MRI in Giant Cell Arteritis: Imaging of the Wall of the Superficial Temporal Artery." American Journal of Roentgenology 184 (2005): 283. Hayreh, Sohan Singh. "Giant Cell Arteritis." . The University of Iowa. N.p., n.d. Web. 12 Nov. 2013. <http://webeye.ophth.uiowa.edu/dept/GCA/GCA.htm>. Smetana, Gerald, and Robert Shmerling. "Does this patient have temporal arteritis?." Journal of the American Medical Association 287 (2002): 92. VI. Conclusion Clinical pearls, take away points if indicated While there are few true optometric emergencies, giant cell can be fairly common, and should be a differential in all patients with sudden loss of vision over 50. While our patient did not have the hallmark signs of giant cell (jaw claudication etc), lab testing and other symptoms painted a clear picture of giant cell arteritis, with an extremely high risk for complete blindness.