L OWER BACK PAIN Pete, Andy and Jackie

P RESENTATION 65 y.o. man with lower back pain 3 day history, pain comes and goes Sharp, burning pain. Like “electric shock”. Can be severe Left side only Radiates to flank, sometimes to abdomen Unrelated to activity Q1 What further history do you require ?

S EEMS NEURAL. S HINGLES ? I MPINGEMENT ? Previous back pain? Neural review Neck stiffness, vision, hearing, balance, tingling/numbness, tics, tremors, weakness, bowel and bladder changes Systems review Fever, sweats, weight changes, cough, dysphagia, palpitations, SOB, chest pain PMHx Chicken pox when young Cancers (also FHx) Recent illness, fever PSHx Surgery or trauma to back, neck, or head Meds Painkillers Corticosteroids Social Hx Occupation, hobbies, exercise, stress Change in sleeping conditions? New mattress? Other changes? New shoes? New car?

M ORE H ISTORY No injury to his back No history of back problems Denies fever Denies urinary symptoms Denies gastrointestinal symptoms. Q2 Detail your proposed examination.

E XAMINATION Body temp Gross neural Gait, hand strength, pupils, fundoscopy, mental state At level of pain: Which dermatome/s Skin changes – rash, scar, swelling, color, temperature Palpation – spinous processes, laminae, musculature Sensation – touch, pain, vibration Lower limb neural exam

T RIGGER 3 Examination is normal Prescribe NSAIDs Patient returns complaining of an allergic reaction to meds – rash Rash – located in area where pain was, eruption consisting of patches of erythema with clusters of vesicles extending a dermatomal distribution from left lower back to midline of abdomen What is your diagnosis? And what is the cause of the rash?

SHINGLES!!! Caused by varicella-zoster virus

W HAT IS THE MECHANISM FOR THE DERMATOMAL DISTRIBUTION OF THE RASH ? Varicella-zoster virus (VZV) lies dormant in the spinal dorsal root ganglia until a decrease in cellular immunity triggers the reactivation of the virus VZV reactivation causes inflammation in the dorsal root ganglion, accompanied by hemorrhagic necrosis of nerve cells. The result is neuronal loss and fibrosis. The distribution of the rash corresponds to the sensory fields of the infected neurons within a specific ganglion. The anatomic location of the involved dermatome often determines the specific manifestation

D ISCUSS A GENERAL MANAGEMENT PLAN FOR THIS PATIENT. Rash usually resolves within days Prognosis good for young and otherwise healthy patients Elderly patients have a significantly higher risk of complications including postherpetic neuralgia, bacterial infections and scarring TREATMENT Antiviral treatment should be commenced in any patient within 72 hours of the onset of vesicles, all patients with herpes zoster ophthalmicus and in immunocompromised patients Famciclovir Valaciclovir Aciclovir For 7 days, or 10 for immunocompromised. Early therapy has been shown to reduce both early and late- onset pain, especially in patients over 65 (reduces pain by 10 days and risk of post-herpetic neuralgia by 8%)

L IST TWO ( OR 3) POSSIBLE COMPLICATIONS OF THIS PRESENTATION. Postherpetic neuralgia pain that persists for longer than 1 month following resolution of the vesicular rash. incidence increases dramatically with age (ie, 3-4% in those aged y; 34% in those >80 y) Treated with analgesics, TCA, gabapentin, possibly opioids or topical lignocaine Herpes zoster ophthalmicus (occurs in 10-25% of shingles cases) Results from reactivation of HZV in trigeminal gangli, can lead to: Chronic ocular inflammation Visual loss Debilitating pain Ramsay Hunt syndrome Also known as herpes zoster oticus, geniculate neuralgia, or herpes zoster auricularis, Caused by VZV reactivation involving the facial and auditory nerves Vesicular eruptions may manifest on the pinna, tragus, or tympanic membrane or in the auditory canal, as well as anywhere in the facial nerve distribution. The patient may experience hearing impairment nystagmus vertigo or facial nerve palsy (mimicking Bell palsy). Patients may lose taste sensation in the anterior two thirds of the tongue.