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A flare is a return of symptoms of active inflammation of GCA or PMR. The symptoms can be the same as those experienced initially, or they can be new symptoms. The flare occurs when inflammation is not adequately suppressed by the amount of prednisone being administered. Blindness, aortic aneurysm formation and other serious and debilitating complications can occur during a flare. Descriptions follow of Pearl’s new symptoms that were not recognized (except for vision loss) as flares by her medical specialists as they were happening.
Legs claudication
The Rheumatologist continued to decrease prednisone even as sed rate was increasing though still in the normal range. After start of prednisone in Dec. ’98, sed rate reduced to 10 mm/hr or less and remained there through May, ’99. Sed rate rose to 23 in June – it decreased to 10 once again in July after the hospital administered a stress dose of > 100 mg of a corticosteroid to perform an arteriogram to evaluate her leg arteries. We learned over the years following that having a sed rate of 20 was an indicator for Pearl that GCA/PMR wasn’t being managed with enough prednisone. Sed rate values over 10 should have been reason to increase prednisone. The Rheumatologist said at one point early in her treatment that anything below 15 was normal. Had prednisone been increased when sed rate increased to 15 in March, 1999, Pearl’s leg arteries likely would have remained open. Sed rate eventually reached 50 a few months later, finally triggering an increase in prednisone by the Rheumatologist.
Decreased circulation in the feet became apparent in June, 1999, so Pearl was referred to a Vascular Surgeon to evaluate the legs. Within four days after the Vascular Surgeon did a doppler scan on the legs, circulation diminished to a point of being an emergency, prompting her to go the hospital for care. The hospital repeated the doppler scan and followed up with an arteriogram. Significant blockages and restrictions were found in most large arteries of both legs. Also, the blockages and restrictions were spasmodic, that is, opening and closing in a periodic manner – about an hour per cycle. A large dose of prednisone was administered for the arteriogram. That broke the spasms and restored circulation.
Despite the evidence of arteritis in the large leg arteries all doctors involved at this time regarded Pearl’s problem as atherosclerosis, not related to GCA. They assumed that all of Pearl’s arteries were atherosclerotic because of a probable genetic condition – this was erroneous. There was no history of atherosclerosis in Pearl or her siblings. She never smoked, had very low risk in lipids tests – high HDL, low LDL and total cholesterol. Her rheumatologist had never heard or read of GCA affecting a patient’s leg arteries. Because of this erroneous speculation the Rheumatologist continued to decrease Pearl’s prednisone dosage resulting in ulceration of the right heel.
A Cardiologist will be called upon who will make the correct diagnosis that the leg artery problems are due to GCA/PMR and not atherosclerosis. This will be discussed later, starting on 8/11/99
Allegra-D (the D component is pseudoephedrine – a vasoconstrictor) was started by Pearl in April, 1999. It was prescribed by her allergist to eliminate coughing. It was considered benign but I speculate it would have been better for her if it had not been started. Over the years I attempted to get Pearl off of it but she found it too helpful for the cough to give it up. I had no support from any of her physicians to help stop its use. They supported the belief that it had no effect on her leg arteries.
Pain behind Pearl’s left eye was reported on 4/23/99 but ignored – it felt similar to the pain behind her right eye at the beginning of her illness. This and headaches reported a month later were symptoms of GCA the Ophthalmologist and Rheumatologist failed to act upon. Both the headaches and the sed rate of 15 in March should have caused prednisone to be increased by the Rheumatologist but didn’t.
The following is a detailed chronology of events leading to the legs claudication and hospital emergency care on 7/10/99.
Chronological overview of legs claudication
3/24/99 – Blood test showed sed rate increased to 15; was 10 in earlier report. Dr reduced prednisone to 12.5 mg/day (was 15).
4/12/99 – FPP prescribed eight weeks of physical therapy.
4/19/99 – Started Allegra-D for coughing – the pseudoephedrine component is a vasoconstrictor.
4/23/99 – Pearl complained of headaches occurring once/wk behind left (good) eye – taking Darvocet for pain.
5/10/99 – Sed rate measured at 11, was 10 on 4/12/99.
5/21/99 – Darvocet doesn’t knock the headaches, just dulls them – reported to Ophthalmologist.
5/24/99 – Sed rate increased to 23; Rheumatologist decreased prednisone from 10 to 8 mg/day.
6/9/99 – FPP prescribed another four weeks of physical therapy after first session ends tomorrow.
6/24/99 – Pearl has lower leg aches when walking around the block. Rheumatologist notes that blood pressure in ankles is lower than it should be – referred her to a Vascular Surgeon. Sed rate is 20 on 6/28.
7/7/99 - Doppler scan by Vascular Surgeon; pulse is minimal in lower left leg.
7/10/99 - Pain & paleness in right leg caused visit to hospital ER. Hourly cycles of pain/discoloration.
7/11/99 - Sed rate 20. Doppler scan in hospital of both legs. No increase in prednisone.
7/12/99 - Arteriogram done on both legs – left has two of three arteries completely blocked; shunt surgery recommended for the right leg. Large dose of steroids for the arteriogram. Color came back. Discharged; legs sore when Pearl stands on them, discomfort goes away when seated or lying down.
7/20/99 - Vascular Surgeon visit – arteriogram findings. Left leg – 40% blockage at mid-thigh of main artery; 100% blockage behind the knee, two of three lower leg arteries completely blocked – all toes have pulse. Right leg – 100% blockage of artery behind knee, one of three lower leg arteries completely blocked – all toes have pulse. Right leg has better flow than left leg. His diagnosis: atherosclerosis, probably hereditary. He doesn’t think there’s a tie-in with GCA/PMR.
7/22/99 - Rheumatologist visit – legs coloring looks good but they pain when walking short distances, mainly the right leg. He reduced prednisone to 7 mg because sed rate was 20 in the hospital and prednisone increases atherosclerosis.
Details of events and Drs’ visits from 3/24/99 thru 7/22/99 are provided in Appendix 2.
Right heel ulcer
Despite sed rate being in excess of the limit of 15 mm/hr that the Rheumatologist told me on 1/26/99 was problematic, he continued to decrease prednisone. The sudden loss of circulation to the legs didn’t raise a flag of caution or concern. Increased pain, after being pain-free when prednisone was started at diagnosis of GCA/PMR, was not a concern to him. The pain was addressed by prescribing pain medication instead of increasing prednisone to see if it might have a favorable impact on both legs circulation and increasing pain in the head and other places in her body.
Prednisone was not to be increased until the sed rate made a spectacular jump to 50 on 9/23/99, two months after legs circulation was significantly impaired. By that time an ulcer had formed on her right heel requiring the care of a Podiatrist, a Cardiologist, a Dermatologist and the Wound Care Clinic’s hyperbaric oxygen (HBO) chamber, in addition to the Vascular Surgeon already involved.
Prednisone was finally increased from 6 mg/day to 15 – two weeks later she could walk around the block whereas she could hardly walk 20 feet earlier. The episode of legs claudication and subsequent ulcer led to my doing some serious research of medical articles to learn more about GCA inflammation. I found that GCA can be present in any large artery – it isn’t confined to the cranium or the aorta. Sharing these articles with her doctors seemed to have little impact on her treatment or their view of her conditions.
After discovering so much information published about GCA inflammation affecting arteries anywhere it is difficult to understand how tenacious the doctors were in holding to their convictions that GCA wasn’t involved in these arterial blockages. Only the Cardiologist identified the diminished circulation as being caused by GCA.
The cycle of undertreatment continued resulting in the same heel ulcer condition occurring months later on the left foot in the same location. This and left arm claudication will be discussed later with events starting on 10/20/99.
The following chronology describes visits and activities leading to diagnosis and treatment of the first right heel ulcer with events starting on 8/11/99.
Chronological overview of right heel ulcer
8/11/99 – FPP recommends shunt surgery for knee blockages. Sed rate is 10. Bruise on right ankle.8/12/99 – Podiatrist x-rayed right ankle bruise – no damage to bone evident.
8/19/99 – Skin crack formed at site of ankle bruise (wasn’t a bruise) – Podiatrist applied topical ointment.
8/20/99 – Open sore found on inside of right foot small toe by Rheumatologist – see Vascular Surgeon. Reduce prednisone to 6 mg/day since sed rate is 10.
8/26/99 – Vascular Surgeon and Podiatrist agreed that hyperbaric oxygen treatment is needed to heal open wounds on right foot. Referred Pearl to the Hospital Wound Care dept. Also Dr. prescribed Pletal to open arteries and improve blood flow – takes two weeks to become effective. Need cardiologist for HBO.
8/30/99 – Fax to Rheumatologist: Can she increase prednisone? She has had a headache above her right eye (forehead), and complained that she feels like she is reverting back to the discomfort she had before starting the prednisone. Rheumatologist advised Pearl can increase prednisone from 6 to 7 mg/day if symptoms of GCA/PMR are being experienced.
9/2/99 - First visit with the Cardiologist. Ran EKG. Advised that leg artery problems are due to GCA since she has none of typical risk factors for atherosclerosis. Stress test to be done 9/3/99.
9/7/99 - Pearl was cleared for HBO; first of 10 treatments started today.
9/17/99 – Blood specimen was drawn for Berkeley Heart Panel Test – ten days for results.
9/22/99 - Final HBO therapy was done today – wounds on right foot are closed; no further treatments.
9/23/99 - Pearl told Rheumatologist that she had two instances of low diastolic pressure at 123/47 lasting a few hours each time. He didn’t think it was arteritis returning. He was surprised Vascular Surgeon hasn’t recommended arterial shunt surgery for her right leg. Sed rate checked – found to be high at 50. Increased prednisone from 6 to 15 mg/day on 9/24/99.
10/11/99 – Pearl can walk a block now before cramps/numbness set in. I found several medical publications that describe GCA inflammation found in leg and other medium/large arteries in the body.
10/20/99 – Sed rate is now 7 – prednisone reduced to 10 mg/day. Berkeley Heart Panel report distributed.
Details of events and Drs’ visits from 8/11/99 thru 10/20/99 are provided in Appendix 3.
Left arm claudication
Reductions in prednisone likely vary from one physician to another – some literature recommend guidelines for taper. One indicated a 50% increase upon flare indication, followed by gradual decreases back to a controlling level. Another advised 2.5 mg reductions every two weeks between 20 and 10 mg/day, then 1 mg decrease per month below 10 mg. It would seem prudent to make small changes once evidence of active inflammation is present, such as leg arteries stenosis and ischemia, and finding a significant increase in sed rate. Pearl’s doctor reduced prednisone from 15 to 10 – a 33% decrease – a month after an elevated sed rate of 50.
The subclavian artery, located in the shoulder, is a focal point for GCA inflammation according to literature. Pain and arm numbness developed in this area in Pearl after the sed rate had increased to 50. Like the leg arteries, this also went unrecognized as a GCA symptom. A few years later poor circulation to her left shoulder would result in rotator cuff tendonitis and bursitis (both symptoms of PMR) and necrosis and fracture of her shoulder blade.
A Berkeley Heart Panel Test was done by the Cardiologist. A blood specimen was sent to the U of California at Berkeley where it was subjected to a profile of tests. Pearl’s indicated low risk of heart disease, no hypertension and no atherosclerosis – confirming the Cardiologist’s view that Pearl’s leg problems were arteritis rather than atherosclerosis. But that was his opinion – others retained their original judgment despite this new information.
The left shoulder/neck pain was followed about two weeks later by flu-like symptoms which likely were manifestations of smoldering GCA – coughing, earache, runny nose, pain throughout her body and a slight fever. Two courses of antibiotics didn’t help. Sed rate was found to have increased once again - this time to 34. Prednisone was at 10 mg/day. Dr increased it by 2.5 mg. A few weeks later her right eye socket became inflamed and bulged out about 2 mm. An MRI showed nothing. The next sed rate measurement was still elevated at 24 but Dr wouldn’t increase the prednisone. His rationale was he wants to wean Pearl off of prednisone as soon as possible – long-term effects are bad so the sooner we can reduce/stop the better. However, all through her treatment this prevailing attitude meant that she continued to have "smoldering GCA" which continued to take its’ toll. He wasn’t treating the disease he was continually focussed on fear of secondary effects of prednisone.
I found literature recommending the use of C-rP in managing GCA. I asked the Rheumatologist why C-rP isn’t being measured. He advised that it isn’t necessary to monitor both sed rate and C-rP; since he’s been tracking sed rate he’ll continue with that. This attitude and lack of recognition of GCA symptoms when they occurred led me to seek a second opinion – this will be described later.
The following chronology describes visits and activities leading to diagnosis and treatment of left arm claudication with events starting on 10/20/99.
Chronological overview of left arm claudication
10/20/99 – Started blood pressure medication; upper target limit is now 130 due to recent cardiology findings, not 160 as had been the earlier publicized limit. Sed rate went to 7, was 50 on 9/23; reduce prednisone from 15 to 10.10/27/99 – Pearl went to the hospital ER at 11:00 pm to check out pain in neck, left shoulder and numbness in left hand. The dull pain had been present for several hours. EKG good. ER advised it was a muscle spasm and anxiety; take more Darvocet. Spasm continued at home but was tolerable.
11/9/99 – Visit with Cardiologist. Left hand gets numb at times; she is shaky, nauseous daily, loss of appetite. Dr advised Berkeley Heart Panel Test indicates Pearl doesn’t have atherosclerosis – vasculitis is due to GCA. All readings are good – she has good genes. She is at low risk for heart disease and doesn’t have hypertension.
11/14/99 – Visit walk-in clinic due to flu-like symptoms (coughing, earache, runny nose, pain throughout body, slight fever). Prescribed Z-Pack and Protuss with Codeine for cough and pain.
11/29/99 – Repeated Z-Pack but still having difficulty with coughing through the day and night. Rheumatologist’s nurse called to say sed rate is 34 (was 7); increase prednisone from 10 to 12.5 mg/day.
12/8/99 – Legs seem to be doing OK – hasn’t had calf cramps recently, only "shin splints" after walking a block or so.
12/16/99 – Visited an Internist with the view of changing from FPP for general care.
12/21/99 – Visited Ophthalmologist on emergency basis to check out swollen and inflamed right eye socket. The eye was bulging out about 2 mm compared with left eye. MRI prescribed – done 12/27/99.
12/29/99 – Reported to Rheumatologist that Pearl is feeling the best she has during this past year – no vascular problems evident, no red blotches on her feet. Only problems are stamina, stomach aches and headache. Sed rate still high at 24; no change in prednisone.
1/10/00 – Hematologist felt liver – good, not hard; no swollen lymph nodes, good.
1/24/00 – Asked Rheumatologist why C-rP isn’t being measured – he advised that it isn’t necessary to monitor both sed rate and C-rP; since he’s been tracking sed rate he’ll continue with that. He wants to wean Pearl off of prednisone as soon as possible – long-term effects are bad so sooner we can reduce/stop the better. Sed rate is 15; reduce prednisone to 10 mg/day.
Details of events and Drs’ visits from 10/20/99 thru 1/24/00 are provided in Appendix 4.
Left heel ulcer
Pearl seemed to be stable and management was becoming routine. I took this occasion to initiate a change from the FPP to an Internist – this took place during 2000. I was disappointed in the FPP for several reasons – failure to diagnose GCA/PMR initially, his micromanagement of non-essentials (limiting Pearl on size of triamcinolone container in prescription; balking at writing mail order prescriptions), and lack of aggressiveness in coordinating activities of the many specialists involved in her care. I felt that I was the coordinator informing him of what he should have been doing for us. We needed a stronger medical professional on the team. I would go through several internists before finding one several years later who could make a significant contribution to Pearl’s care.
An ominous sign of impaired circulation began in both legs and feet four months after the right heel ulcer episode concluded favorably. Both Pletal and Trental had been in use since that time – Trental was stopped because circulation had improved but Pearl restarted it when circulation appeared to diminish once again. An ulcer began to form on her left heel, mirroring that on her right heel seven months before. A doppler scan confirmed degradation in the leg arteries. Sed rate increased from 15 to 19. We wanted to increase prednisone which had been at 10 mg/day, as did the Vascular Surgeon, but the Rheumatologist said no. Pearl increased the prednisone to 12 ½ mg on her own. The Dermatologist recommended the prednisone be increased to 15 mg – the Rheumatologist relented and accepted the Dermatologist’s recommendation. Pearl felt circulation increase in her legs during the night she started 15 mg.
We proposed visiting a remote reputable Clinic for a second opinion about Arteritis therapy, Vasculitis cause, and Sinusitis therapy. The report of an MRI of a swollen eye socket performed during this period mentioned chronic sinusitis. Her specialists welcomed this potential new input. The visit will be discussed later in the section on expanding management tools.
The Rheumatologist continued to insist that Pearl’s leg problems were due to atherosclerosis – he added that arteritis only affects temporal arteries. He wanted Pearl to have angioplasty on an urgent basis to avoid the need for shunt surgery in her legs. Increasing prednisone up to 20 mg corrected the left heel ulcer problem. Wound Care found that the skin area around the ulcer was getting good oxygenation so it would heal without HBO. It was almost completely healed at the last visit to Wound Care in mid-June. Again, the evidence for an arteritic problem in her legs rather than atherosclerosis was demonstrated by a favorable reaction to increased prednisone.
One day in June, 2000, Pearl spent several hours walking and standing while shopping, climbed stairs in two model homes and had no unusual pain in her legs or leg muscles. But that would change as prednisone was tapered too low repeatedly during treatment of her illness.
The following chronology describes visits and activities leading to diagnosis and treatment of left heel ulceration with events starting on 2/1/00.
Chronological overview of left heel ulcer
2/1/00 – Pearl restarted Trental after Rheumatologist stopped it on 1/24/00 – she thinks circulation is reducing in her legs/feet.
2/10/00 – Called Rheumatologist to advise that left heel is showing discoloration similar to that seen on right heel in July, 1999, which resulted in an ulcer and HBO treatments. Should Pearl increase prednisone? Ans: No.
2/14/00 – Doppler scan done by Vascular Surgeon. Results showed decline since Hospital scan in July, 1999 – flow in toes has diminished significantly. Purpura on the left heel; the right heel is clear at this time and has been since HBO was completed in 9/99. The left heel is not ulcerated yet (did ulcerate on 2/25/00). Dr suspects both arteritis and atherosclerosis are present. Dr checked sed rate and said if it has increased he would encourage the Rheumatologist to increase prednisone. It increased from 15 to 19. Advised Rheumatologist and again asked if Pearl should increase prednisone from 10. Ans: No. I sent a follow-up letter asking him to converse with the Vascular Surgeon.
2/18/00 – Increased prednisone to 12.5 mg/day to try to gain improvement of deteriorating left heel skin discoloration. On 2/25/00 the skin cracked producing an open wound, as the right heel did last summer.
2/29/00 – Dermatologist viewed left heel wound. Advised he would like to see Pearl at 15 mg/day of prednisone instead of 12.5 if Rheumatologist would agree to that. Contacted Rheumatologist and was advised to increase to 15 if that’s what the Dermatologist wants. During the night after starting 15 mg Pearl felt improved circulation in her legs.
3/6/00 – Discussed opinions of other doctors about Pearl’s vasculitis and heel ulcer with the Rheumatologist. He still thinks it is atherosclerosis because arteritis affects only temporal type arteries. He recommends angioplasty be done at once before shunt surgery becomes necessary. I requested 20 mg of prednisone for a month since 15 hasn’t had an effect on the heel ulcer yet. Dr agreed thinking that would show us if the problem is immune in nature or atherosclerosis. We discussed remote Clinic options for second opinions.
3/7/00 – Dermatologist recommended continuing prednisone at 15 mg for another week, then 17 ½ mg for a week followed by 20 mg for a week if improvement isn’t noticed at 15 mg.
3/10/00 – Advised Ophthalmologist of intent to visit a remote Clinic because of three uncertainties: Arteritis therapy; Vasculitis cause; and Sinusitis therapy – MRI of swollen eye suggested chronic sinusitis.
3/13/00 – Vascular Surgeon recommended no surgery for Pearl since her leg blockages may be arteritic – if so, surgery would only aggravate her vasculitis and might not be successful.
3/28/00 – Wound Care was consulted about left heel ulcer – they tested the skin around the wound and found good oxygenation so HBO isn’t necessary. It finally healed, being almost closed at the 5/11/00 visit with Wound Care. On 6/8/00 Pearl spent several hours walking and standing while shopping, climbed stairs in two model homes – had no unusual pain in legs or leg muscles.
Details of events and Drs’ visits from 2/1/00 thru 3/28/00 are provided in Appendix 5.
Rotator cuff tendonitis and bursitis, both shoulders and momentary loss of all vision
The obsession with prednisone reduction continued over the years of treatment. The Clinic Rheumatologist who was seen twice up to this point for a second opinion about several issues resulted in two significant changes in treatment. C-rP was recommended along with sed rate and clinical symptoms in managing GCA. Pearl’s rheumatologist accepted this advice. In the second visit the Clinic Rheumatologist advised GCA should have run its’ course because Pearl had GCA for over three years at that time. His advice in October, 2002, was to taper off of prednisone without monitoring sed rate and CrP any longer. This advice clearly contradicted all literature I’d read about managing GCA. Her rheumatologist agreed with this approach – I did also but insisted on measuring sed rate and CrP just for information.
Pearl experienced a sharp pain in her right upper arm as she reclined on the couch on 7/21/03. Her prednisone was at 4 mg, being decreased at 1 mg/wk. The Rheumatologist advised that she not increase prednisone for this trauma. An Orthopedist suggested that x-rays indicated rotator cuff tendonitis or bursitis – these are symptoms of PMR but he didn’t think that PMR was the cause. Sed rate increased to 56 and CrP was elevated at 2.4 mg/dl on 8/4/03. I sent an Email to the Clinic Rheumatologist for advice and received no response. Two weeks later the Rheumatologist advised Pearl to increase prednisone to 4 mg (it was 3 mg by that time, on a reducing schedule). He was alarmed at the sudden increase of sed rate from 6 on 5/21/03. Oddly he still wasn’t attuned to the value of CrP in managing GCA – it was .6 mg/dl (normal) on 5/1/03 but was significantly elevated at 2.32 mg/dl on 5/21/03. Only sed rate continued to be important to him. Finally on 8/20/03 when sed rate and CrP remained elevated he increased prednisone to 10 mg. This attempt at tapering off of prednisone was to be the last.
Pearl made an emergency visit to the Ophthalmologist after losing sight momentarily in her left (good) eye while shopping on 12/12/03. He increased Prednisone to 60 mg/day of prednisone for 3 days, then tapered. CrP was 2.1 mg/dl and sed rate was 26 – both indicating flare. MRI showed no problem in the left eye but the right optic nerve was inflamed which became a curiosity item without conclusion. Both eyes appeared to be healthy based on photos with dye taken of the retinas.
Two weeks later a large welt appeared on Pearl’s upper right arm a couple of hours after rolling out pumpkin pie shells on Christmas Eve. This led to stopping use of Plavix which promotes circulation by making platelets "slippery". A month later the Orthopedist prescribed light physical therapy for Pearl’s upper arms which had been painful to move for much of the past year. Sed rate and CrP continued to be elevated much of the time with prednisone cycling continuing. After 9 sessions of therapy didn’t make a difference he prescribed more intense therapy for another round of 10 sessions. MRIs taken after showed both rotator cuffs were completely torn. An Orthopedic Surgeon advised that both were not repairable surgically. Pearl could only raise arms to shoulder height. Bones in both shoulders were badly degenerated and dislocated. The left shoulder blade was necrotic and fractured. She received several injections of corticosteroids by various doctors for pain relief. Injections are limited to three per year to avoid bone disintegration.
The shoulder problems were not attributed to GCA by the specialists involved. Since they have characteristic symptoms associated with PMR in literature, along with vision loss, while sed rate and CrP were elevated convinces me that they are a result of the on-going partially controlled GCA condition.
I began to suspect at this point that even 10 mg/day is not enough to maintain control of Pearl’s GCA.
The following chronology describes visits and activities leading to diagnosis and treatment of rotator cuff tendonitis and bursitis in both shoulders and momentary loss of all vision with events starting on 5/1/03.
Chronological overview of rotator cuff tendonitis and bursitis, both shoulders and momentary loss of all vision
5/1/03 – Sed rate 15; CrP .6 mg/dl (normal if < 1.0 mg/dl). Decrease prednisone from 10 to 8 mg/day.
5/15/03 – Rheumatologist observed Pearl’s left ankle has good pulse – no soreness, though redness remains at spot of earlier ulcer. Reduce prednisone at rate of 1 mg/month.
5/21/03 – Hematologist did blood test – sed rate is 6; C-rP is 2.32 mg/dl (high).
7/14/03 – Hydrocortisone replaced prednisone for tapering – prednisone is 4 times stronger. Hydrocortisone dosage is 20 mg/day, had been 25 mg (equivalent of 6 mg of prednisone). Attempting to reduce by 5 mg every two weeks.
7/22/03 – Sharp pain in right upper arm last evening as Pearl was reclining on couch – half hour later noticed minor swelling where pain occurred. Internist referred her to an Orthopedist. Rheumatologist in response to my E-mail advising of Pearl’s pain said to not increase hydrocortisone for this trauma.
7/23/03 – Orthopedist took x-ray and advised right shoulder has rotator cuff tendonitis. Injected lidocaine (anesthetic) and Medrol (cortisone) in the shoulder joint.
7/30/03 – Shoulder continues to hurt but not as bad – could be bursitis; was dismissed by Orthopedist.
8/4/03 – Blood test showed sed rate 56, CrP 2.4 mg/dl – both indicative of flare. Hydrocortisone at 15.
8/5/03 – Email message sent to Clinic Rheumatologist who advised Pearl last October she should taper off of prednisone, ignoring sed rate and CrP even if sed rate exceeds 80 mm/hr. No response.
8/6/03 – Rheumatologist advised Pearl to increase hydrocortisone to 20 (equivalent of 4 mg of prednisone).
8/14/03 – In visit Rheumatologist expressed his alarm at sudden increase in sed rate from 6 on 5/21/03 to 56 on 8/4/03.
8/19/03 – New Internist prescribed physical therapy for Pearl’s right shoulder. We didn’t do therapy.
8/20/03 – Blood test – sed rate 52, down from 56; CrP remains at 2.4 mg/dl – both indicating flare. Rheumatologist increased prednisone to 10 mg/day from 4 mg (20 mg of hydrocortisone). Pearl decided to wait on physical therapy until seeing the effect of increased prednisone in case the problem is PMR.
9/9/03 – Sed rate 21, CrP 12 – both still indicating flare. Rheumatologist reduced prednisone to 8 from 10 mg.
10/1/03 – Sed rate 37, CrP 2.4 mg/dl. Rheumatologist increased prednisone to 10 mg.
11/30/03 – Dosage analysis by James indicates 8 mg/day is needed to keep C-rP and sed rate normal. Now at 7 ½ mg.
12/13/03 – Emergency visit to Ophthalmologist after Pearl lost sight momentarily in left (good) eye while shopping. Increase to 60 mg/day of prednisone if sed rate and CrP indicate flare. CrP is 2.1 mg/dl; sed rate is 26 – both indicating flare. Prednisone increased to 60 for 3 days, 40 for 3 days, then 20 for 3 days. She will drop to 15, 12 ½ for a week at each level, then to 10 mg for a month. Rheumatologist agreed.
12/18/03 – Left orbital MRI done at Ophthalmologist’s request. Contrast IV fed in right hand – large bruise developed covering most of hand. Report results on 12/30/03 showed left eye good, right optic nerve inflamed.
12/24/03 – Visit to Hospital ER for a large red welt on upper right arm. Formed within a couple of hours of Pearl rolling out pumpkin pie shells. Appeared like a sack of blood, area raised about ¼ inch. The arm remained swollen similar to the appearance it had on 7/22/03 when the initial pain was encountered. During the night the sharp edge of the heating pad ripped a 1 ½ inch long gash in the bottom of the welt.
1/21/04 - Orthopedist prescribed light physical therapy after viewing my list of PMR problems Pearl’s
had with her arms and shoulders over the past few years – therapy will start 1/27/04; both upper arms are bothering Pearl on 1/27/04.
2/5/04 – Sed rate 22, was 16 on 1/6/04; CrP elevated at 1.5 mg/dl (was negative 1/6/04). Increased prednisone to 11.5 mg, was 10 mg.
2/10/04 – leg cramps occurred in both calves this afternoon – first time in several years. Increased prednisone to 15 mg and restarted Plavix – but only every other day. Stopped Plavix on 2/23/03 due to bleeding and easy bruising under the skin.
2/11/04 – Orthopedist gave a prescription for more intense physical therapy since initial course of seven sessions to date of nine hasn’t made a difference.
4/7/04 – MRI of left shoulder shows significant degeneration, very similar to right shoulder MRI of 3/4/04. Physical therapy appears to have caused complete rotator cuff tears in both shoulders. Can’t raise arms above shoulder.
4/12/04 – Evaluation by an Orthopedic Surgeon showed both shoulders equally bad and non-repairable.
4/22/04 – Persistent cough, unaffected by two courses of antibiotics, and Pearl’s low grade fever are symptomatic of GCA so I recommended increasing prednisone. Sed rate is 36, CrP is 1.4 mg/dl. Rheumatologist suggested increasing to 12 mg based on sed rate and CrP; I opted for 15 after notifying Dr of her symptoms.
4/27/04 – Coughing stopped and fever dissipated ending flare so reduced prednisone to 13 ½ mg.
Details of events and Drs’ visits from 5/1/03 thru 4/27/04 are provided in Appendix 6.