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A Medical Emergency
On December 10th, 1998, at age 65 a severe migraine-type headache and permanent loss of vision in Pearl’s right eye occurred while preparing for bed. I administered an injection of Imitrex and a second injection an hour later when the first didn’t help. This was the prescribed protocol for migraine headaches which we had done often before over the years. I learned later that Imitrex is a vasoconstrictor – producing the opposite effect of what Pearl needed in this crisis. GCA reduces the flow area in the arteries so a vasoconstrictor would contribute to further reduction of flow to the optic nerve if it weren’t already completely closed. Permanent blindness occurs in less than four hours if the optic nerve is starved of blood.
In the morning sight hadn’t returned in her right eye so a Family Practice Physician (FPP) advised that she go to the hospital ER. There we heard Giant Cell Arteritis mentioned for the first time – they sent us to see an Ophthalmologist on an emergency basis. He examined Pearl upon arrival at his office and confirmed the GCA diagnosis and the permanent loss of vision. He prescribed 120 mg/day of oral prednisone.
The hospital did a blood test before Pearl was taken to the Ophthalmologist’s office. The Ophthalmologist received a copy of the results during our visit and became irate because the Erythrocyte Sedimentation Rate (sed rate) was 124 mm/hr – he called the FPP to question why he didn’t diagnose her condition earlier, noting the highly elevated sed rate. The FPP pointed out that the sed rate was normal at 19 when he tested it a month earlier on November 9, 1998. Some data indicates that sed rate is considered "normal" if it is less than 40 mm/hr for an average elderly woman. Sed rate varies for individuals and circumstances. I learned later that Pearl’s normal sed rate is 10 mm/hr or less based on readings taken when high prednisone was administered early in the first few months of her illness. So it was elevated in November but not recognized to be. Another fact not recognized then was that sed rate might not be elevated in all cases of GCA/PMR inflammation so symptoms are very important also.
We returned to the FPP for referrals to several other specialists who Pearl would need to confirm and manage this new illness. These included a Rheumatologist, Hematologist, and Gastroenterologist.
The Rheumatologist we learned would provide the prednisone management after the immediate vision crisis passed. The Ophthalmologist monitored closely the dosage and tapering prescribed by the Rheumatologist until 20 mg/day was reached. By that time he was confident she would retain vision in the good eye with the dosage needed to control the GCA inflammation.
The Hematologist was needed because the platelets were highly elevated at 751 (normal range 140-440). While this provides evidence of GCA it could reflect lupus if platelets exceeded 1,000 in the coming days.
The Gastroenterologist was solicited by the FPP to advise him of why alkaline phosphatase (alk phos) had been elevated in the November 9th, 1998, blood test. The elevated alk phos was a marker for GCA that the FPP didn’t recognize. He should have determined in November why it was elevated.
The temporal artery biopsy on the right side was done by the Ophthalmologist on December 16, 1998, and being positive confirmed the diagnosis of GCA.
Our immediate task at home was to search the internet and medical reference books for what we could learn about GCA. We weren’t aware yet of polymyalgia rheumatica, the companion illness.