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An 86‐year‐old man was presented to the emergency department with an acute‐onset severe, throbbing headache and vision changes. He reported intermittent pain in the left scalp for the past two days in the temporal region and new‐onset blurry vision without the occurrence of preceding head trauma. He was prescribed with oral analgesics, but the medications were found to be ineffective. He reported a fever of 38.7°C. There were no features of inflammatory arthritis, morning stiffness, myalgias, jaw claudication or limb claudication.
Which of the following method should be adopted?
High dose corticosteroids
Performing a lumbar puncture
Assessment of peripheral blood cultures
All of these
Herpes zoster opthalmicus (HZO) is a common infection caused by reactivation of varicella-zoster virus (VZV) in the ophthalmic division of the trigeminal nerve. The incidence of HZO is 104.6 per 100 000 person‐years.
The patient reported a history of seropositive rheumatoid arthritis (RA) on longstanding sulfasalazine. He had not pursued any age‐appropriate vaccinations due to nausea secondary to the influenza vaccination many years prior.
The patient was haemodynamically stable, alert and oriented on physical examination. There was no incidence of temporal artery beading or pulsations. Erythema was reported over his left eye and tenderness and rubor to the left scalp. The left temporal artery was not palpable. Ophthalmological examination revealed painless eye movements, normal visual acuity, and normal fundi. Jolt accentuation testing showed negative results, and there was no nuchal rigidity. Neurological examination and routine blood work, including a complete blood count, was unremarkable. C‐reactive protein levels and erythrocyte sedimentation rate (ESR) were elevated at 21.8 mg/L and 90 mm/h, respectively. Computed tomography of his head showed no evidence of cerebral vascular disease or any acute changes. The infectious aetiology was unlikely given his physical examination findings and investigations. Lumbar puncture was not pursued, and blood cultures were negative.
The absence of jolt accentuation of the headache excludes the possibility of meningitis. The patient was predisposed to central nervous system infections due to the patient's age, history of RA, and being on a disease‐modifying antirheumatic drug (DMARD). Therefore it is essential to perform a neurological infectious work‐up with a lumbar puncture and drawing peripheral blood cultures. The patient was elderly and presented with scalp tenderness, unilateral temporal headache and blurred vision. Differential diagnosis of large vessel vasculitis such as giant cell arteritis (GCA) was made, and high‐dose steroids (the equivalent of 1 mg/kg prednisone daily) were initiated for three days to prevent vision loss while awaiting temporal artery biopsy. He was further referred to ophthalmology one week after symptom onset for assessment and temporal artery biopsy. Visual acuity/ field testing was unremarkable, and there were no findings suggestive of GCA on fundoscopy, including the absence of disc oedema, pallor, and nerve fiber layer infarction. No afferent pupillary defect was observed. Optic nerve cup-to-disc ratio and intraocular pressures were bilaterally within normal limits. The dermatological examination indicated new vesicular lesions over his scalp since his initial presentation to the emergency room. The patient vesicular lesions over the ophthalmic branch of the trigeminal nerve are classical for HZO. The temporal artery biopsy was cancelled due to the risk of infectious spread.
The patient was prescribed with a 2‐week course of oral valacyclovir. Inflammation and symptoms resolved, and his high‐dose prednisone was tapered given that the HZO infection provided an adequate explanation for his symptoms and signs.
The present case highlighted the differential diagnosis of HZO distinguished from GCA. The patient was presented with features of GCA initially, a medical emergency requiring prompt treatment with high-dose steroids to avoid permanent vision loss. However, the physician should consider infectious differentials, especially in the immunocompromised patient population. The comorbidities developed due to the utility of DMARD and lack of appropriate vaccinations predisposed the patients to infectious causes of headache, which in this case was HZO, but could be extended to other central nervous system infections.
The primary prevention of HZO and HZ lies in vaccination. RA patients have a 2.4 times greater risk of developing HZ. Currently, two vaccines have been approved; one is a live attenuated vaccine, and other is a newer adjuvant recombinant subunit vaccine. It is best to undergo VZV vaccination for patients with RA aged ≥50 years before initiating biologic therapy or tofacitinib, according to the guidelines. The use of live attenuated vaccines is safe in population on DMARDs, excluding biologic treatment. The adjuvant recombinant subunit vaccine is superior and more reliable than the live attenuated vaccine in preventing HZ, but there are currently no formal guidelines about the RA or immunocompromised patient population. Furthermore, many non-specific symptoms such as nausea post-vaccination do not necessarily reflect a true allergy rather than the side effect to a vaccine after which subsequent vaccines can be safely administered.
Patients with inflammatory rheumatic diseases are often immunosuppressed and predisposed to severe infections such as HZO. The vaccination rates for these patients are low. One of the strongest predictors for a vaccine acceptance is a rheumatologist's recommendation. Therefore, rheumatologists can make a significant impact in preventing potentially devastating infections in patients by recommending evidence‐based vaccinations.
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Headache and vision changes in an elderly man with rheumatoid arthritis
Timothy S.H. Kwok et al.
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