Mrs. A. is a 74-year-old housewife who for years has volunteered at the local hospital. She’s seldom ill. Beginning in midsummer, about 2 months after a normal physical, she started complaining of a multitude of problems, including vertex headache, weakness, night sweats, anorexia and a 1.4 kg weight loss.
On examination, she had left costovertebral angle and left upper quadrant tenderness. The presumptive diagnosis was possible left pyelonephritis or diverticulosis; white blood count was 14,200, ALT 95. She was sent for abdominal and pelvic ultrasound for pyrexia of unknown origin.
Ultrasound showed multiple gallstones, already known, and a hypoechoic 1.8cm mass in the left kidney, possibly a proteinaceous cyst. A computerized tomography intravenous pyelogram (CT IVP) was suggested. Pelvic ultrasound showed nonspecific trace fluid in the endometrial cavity; possible adhesion, possible neoplastic cause. CT of the abdomen and pelvis showed diverticulosis but no inflammation. Skull x-ray was normal.
She continued to lose weight (1 kg) and complained of bilateral swelling in the temples. She also suffered from bites on both ankles and feared she might have Lyme disease. On examination, there was tenderness and swelling in the posterior cervical muscles but none in the temples. Blood pressure was normal, as were kidney and urine tests, including urine cultures.
At the next visit 2 weeks later, she no longer complained of temple pain and swelling but she mentioned having puffy eyes. Blood work showed a sedimentation rate of 67, platelets 627,000, white blood count 13,400 and liver function tests mildly elevated with AST 54, ALT 82, and Alk Phos 221. Presumptive diagnoses were unidentified left kidney mass (a cyst?), mild hepatitis, jaw joint arthritis, thrombocytosis, and gallstone cholecystitis (but without pain).
Inflammatory markers rising
One week later, on the brink of departing for a holiday in Nova Scotia, she said she was feeling better, and was free of pain. But now the sed rate was 100, platelets 660,000, HGB 114 and WBC 16,100. I postponed her holiday and told her to go to emergency. I thought at the time she might have myeloma. The internist believed she must have some infection that hadn’t been found, and at least deserved blood cultures. Endocarditis was a possibility. Mrs. A. said she was sleeping 14 hours a day. She had low-grade fever.
She was admitted to hospital — but why?
Mrs. A. was admitted with a diagnosis of possible temporal arteritis. In retrospect, I was glad I’d postponed her holiday as she might have suffered visual loss.
Biopsy of temporal artery was initially negative, but when repeated was positive. She was started on steroids. Sed rate 3 months later is 7.
Temporal arteritis, also known as giant cell arteritis, is inflammation plus damage to blood vessels that supply the head area, particularly the medium to large arteries that branch from the neck. It occurs fairly commonly and can also be systemic, affecting medium to large-sized arteries throughout.
The cause is unknown but thought to be an effect of immune response. The disorder has been associated with large doses of antibiotics and severe infections. It may develop alongside polymyalgia rheumatica; usually seen in those over 50, it can sometimes run in families.
These may include excessive sweating, fever, malaise, jaw pain (intermittent or when chewing), loss of appetite, myalgia, throbbing headache on one side of the head or back, scalp sensitivity, vision difficulties (blurred, double, or lost vision), and weight loss (more than 5%). Additional possible symptoms are bleeding gums, face pain, hearing loss, joint pain/stiffness, and mouth sores. Some people (40%) will have other symptoms like dry cough or persistent fever as the only symptom.
Examination and tests
Look for a thick tender temporal artery with weak pulse or no pulse. Blood tests may show high sedimentation rate, elevated C-reactive protein, low hemoglobin, elevated alkaline phosphatase or other liver function markers. Biopsy is the only diagnostic test.
The goal is to reduce tissue damage from lack of blood flow. Steroids are usually prescribed and can continue for 1-2 years. Sometimes aspirin is used; occasionally, immune suppressants like methotrexate.
Most people make a full recovery, but the condition may return later on. Possible complications include blindness or muscle weakness, TIA or stroke.
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