“Medic 77, please respond with BLS 1281 to a residential home for an elderly male not alert, 26C1.”
The paramedic responds to the scene with the BLS crew. They arrive at a well-kept Victorian home in the village five minutes after dispatch and are greeted by a number of concerned family members. The patient, Mr. H, is found seated in a lift chair in the living room of the house, which has been converted to his bedroom. His eyes are closed, but he responds appropriately to questions.
He’s maintaining his airway and doesn’t appear to be in distress. Family members report he’s become increasingly weak over the past few days; he’s normally able to use his lift chair and ambulate to the bathroom down the hall with the assistance of his wheeled walker, but it now takes three people to assist him to the bathroom. They’re very concerned about his safety.
Baseline vitals are obtained that show a pulse of 70 irregularly irregular by palpation, respiratory rate of 14 and easy, room air pulse oximetry of 94% and manual blood pressure of 150/80. He’s found to have a low-grade fever with a temperature of 37.5 degrees C. Pupils are equal and reactive bilaterally. Oral mucosa is dry. Lung sounds are clear and equal bilaterally and heart assessment shows irregularly irregular rhythm without murmur, rub or gallop. Abdomen is soft and non-tender. Trace pedal edema is noted in both lower extremities, as are skin changes consistent with venous stasis. Peripheral pulses are intact in all four extremities. Skin is warm and dry without rash. Cranial nerve exam is grossly intact. Grip strength in both upper extremities is weak but equal. No facial asymmetry is noted. Speech is fluid.
Mr. H is assisted to a standing position by two crew members and is able to pivot to sit onto the gurney. He’s secured and moved to the ambulance for transport.
Cardiac monitoring is initiated in the ambulance. Initial rhythm is atrial fibrillation. A 12-lead ECG is obtained, which shows atrial fibrillation with a rate of 66 and an occasional premature ventricular contraction (PVC). IV access is obtained with a 20-gauge IV inserted in the left forearm. Blood glucose is determined to be 172 mm/Hg. Mr. H then indicates he needs to urinate. A small amount of dark yellow concentrated urine is produced.
Due to the combination of dark, concentrated urine, dry oral mucosa and weakness, fluid challenge with 500 ccs of normal saline is initiated with good response as Mr. H becomes more conversant.
During transport, additional history is obtained. Mr. H reports he’s been feeling weak for the past several weeks, but it became more pronounced about five days ago. He also reports recent treatment for herpes zoster (shingles) after he developed a painful facial rash. The rash has resolved, but he now notes a persistent headache, averaging 3–4/10. He reports he had a follow-up visit with his physician and was told the headache was post-herpetic neuralgia. He was placed on Neurontin (gabapentin), which he feels hasn’t helped. He states that this morning he noted his vision seemed “off.” He’s had an intermittent “flashing light” in his right field of vision.
Transport to the hospital is uneventful. Past medical history and medications are reviewed during transport. The paramedic has a good rapport with the hospital staff and gives report to both the bedside nurse and the physician assistant (PA) who will be caring for the patient. The urine sample is given to the hospital staff to be sent for urinalysis and urine culture if indicated.
Urinary tract infection is ruled out as are other infectious causes when white blood cell count is normal. Red blood cell count is normal as well, ruling out anemia as a cause of weakness. Head CT is negative for stroke. The ED PA checks an erythrocyte sedimentation rate (ESR)—a nonspecific measure of inflammation— which is markedly elevated at 96. Mr. H is admitted to the hospital for further evaluation. Due to the headache and elevated ESR, the hospital team orders a cranial ultrasound that shows a halo sign consistent with giant cell (temporal) arteritis (GCA). His weakness s primarily in the hip and shoulder girdle, so a concomitant diagnosis of polymyalgia rheumatica (PMR) is made. Mr. H is started on oral prednisone with rapid improvement of his symptoms of weakness, headache and visual disturbance.
Temporal artery biopsy is eventually performed. It’s indeterminate, but given the patient’s improvement on prednisone, the team feels confident the diagnosis and treatment were appropriate. Mr. H is evaluated by physical and occupational therapy staff and is pleased to be discharged back to his home.
PMR is the second most common inflammatory autoimmune rheumatic disease.1 The cause is unknown. Symptoms can include stiffness, pain, synovitis, bursitis, joint swelling, muscle tenderness, weakness, decreased range of motion, malaise, fatigue, weight loss and low-grade fever.2 Patients are often more symptomatic in the morning hours. Peak incidence occurs between the ages of 70 and 80. It’s more common in females, with women accounting for 65–75% of cases.3
GCA is an inflammation of the medium to large arteries and can lead to luminal occlusion with ischemic complications such as ischemic optic neuropathy. This can cause vision loss in 10–15% of patients. Estimates vary, but up to 50% of patients with GCA are also diagnosed with PMR. The incidence is highest in whites of Northern European descent.4
Diagnosis of GCA and PMR is challenging since objective findings are often absent. It’s primarily made on clinical grounds using laboratory testing, imaging studies and exclusion of other diagnoses. Table 1, above, illustrates one possible set of diagnostic criteria for PMR. Table 2, above, illustrates diagnostic criteria for temporal arteritis. Interestingly, temporal artery ultrasound is easily performed and is included in the list of diagnostic testing for GCA. This medical condition can be investigated more as prehospital ultrasounds become more readily available.
Treatment of both PMR and GCA consists of prompt initiation of glucocorticoid therapy, with higher doses needed for GCA.3 Disease flares are common and tapering of glucocorticoid therapy is often very slow and difficult.
Taking an accurate history, performing a thorough physical exam and formulating a differential diagnosis are essential to good patient care. Weakness is a common complaint in the elderly.
Table 3 illustrates a differential diagnosis of weakness in the geriatric population. It includes many of the common diagnoses that we see on a regular basis, but it also includes some of the uncommon ones. An old medical adage says, “When you hear hoof beats, think horses, not zebras.” The zebras should still be on the differential diagnosis, just farther down the list.
Sometimes, however, those hoof beats really are zebras. By forming a differential diagnosis and having good communication with hospital staff, EMS providers can have great impact on the outcome of patient evaluations in the ED and throughout a patient’s hospital stay.
1. Crowson CS, Matteson EL, Myasoedova E, et al. The lifetime risk of adult-onset rheumatoid arthritis and other inflammatory autoimmune rheumatic diseases. Arthritis Rheum. 2011;63(3):633–639.
2. Nesher G. Polymyalgia rheumatica-diagnosis and classification. J Autoimmun. 2014;48–49:76–78.
3. Weyand CM, Goronzy JJ. Giant-cell arteritis and polymyalgia rheumatica. N Engl J Med. 2014;371(1):50–57.
4. Ameer F, McNeil J. Polymyalgia rheumatica: Clinical update. Aust Fam Physician. 2014;43(6):373–376.