1. Case 2 Week 25

2. PC 65 yo  LBP HPC Lower back pain for past 3 days Sharp burning pain Left lower back, radiates to the flank and all the way around to his abdomen Pain comes and goes, like ‘electric shock’ Unrelated to activity Can be severe Q1 What further history do you require at this point?

3. 3 concerns in taking a hx for LBP: 1.Is there evidence of systemic disease 2.Is there evidence of neurologic compromise 3.Is there social or psychological distress t Underlying systemic diagnosis History of Ca Age over 50 yrs Unexplained weight loss Duration of pain greater than 1 mth  not in this case Nighttime pain Pain not relieved by lying down  can be because of cancer or infection Injection drug use, skin infection, UTI, or recent fever  spinal infection Is there sciatica? Incontinence Pain with walking (psedoclaudication)  sign of spinal stenosis (not in this case)

4. Trigger 2 No injury to back No hx of back problems No fever, urinary symptoms, or GIT symptoms Q2 Detail your proposed examination

5. Inspection of back and posture and abdo exam Palpation of spine  any tenderness sensitive but not specific for spinal infection Range of motion Femoral nerve stretch If any leg symptoms: -Straight leg raising  for radiculopathy -Lower limb neuro esp at L5 – S1 nerve root as 98% disc herniation occur at L4-5 and L5-S1 L5 motor: ankle and toe dorsiflexion L5 sensory damage: numbness in medial foot S1: plantar flexion, ankle reflexes, sensation at posterior calf and lateral foot If suggestion of systemic disease/malignancy (not in this case): examine prostate, lymph node exam

6. Trigger 3 O/E Back and abdo exam is normal THEN Prescribed NSAID for the pain Next day return saying that has allergic reaction to medication because developed rash Rash in area where he had the pain (left lower back, radiates to the flank, and abdominal) On exam now: Eruption consisting of patches of erythema with clusters of vesicles extending in dermatomal distribution from left lower back to midline of abdomen Q3 What is your diagnosis?

7. Shingles/Herpes Zoster (reactivation of endogenous latent VZV (Varizella Zoster Virus) within sensory ganglia) The clinical form of this disease is characterised by painful, unilateral vesicular eruption, occur in restricted dermatomal distribution Rash starts as erythematous papules  evolve to grouped vesicles or bullae

9. Within 3 to 4 days, vesicular lesions become pustular or hemorrhagic

10. If hosts immunocompetent  7-10 days lesion crust and no longer infectious. Therefore if there is new lesion after 1 week  ? Immunodeficiency Thoracic and lumbar dermatomes  most commonly involved sites of herpes zoster Acute neuritis  75% of pt have prodromal pain in dermatome where rash subsequently appears – Can precede by days to weeks – Deep ‘burning’, ‘throbbing’, ‘stabbing’ sensation

11. Complications: postherpetic neuralgia  increases as getting older Ocular (uveitis and keratitis), neurologic, bacterial superinfection of skin Herpes zoster ophthalmicus (VZV reactivation in trigeminal ganglion) Acute retinal necrosis Aseptic meningitis Affecting motor neurons in spinal cord and brainstem  motor neuropathies Herpes zoster oticus (Ramsay Hunt)  triad of ipsilateral facial paralysis, ear pain, and vesicles in auditory canal and auricle. Also taste perception, hearing (tinnitus, hyperacusis) and lacrimation Transverse myelitis Encephalitis Guillain Barre Syndrome Stroke syndromes (when vessels affected)

12. Q4 What is the cause of this rash Primary infection  chicken pox Virus then remains dormant in dorsal root ganglion When reactivated (eg. Due to immunosuppressant, getting old, etc)  virus replicates in nerve cells  virions are shed from cells and carried by axons to the skin served by that ganglion  in the skin, virus causes local inflammation and blisters Q5 What is mechanism for dermatomal distribution of the rash

13. Q6 Discuss general management plan for this patient Acyclovir (nucleoside analogue, converted to acyclovir monophosphate then to acyclovir triphosphate by virally encoded thymidine kinase, acyclovir triphosphate then inhibits viral DNA polymerase) Valacyclovir(converted to acyclovir) Famciclovir (prodrug to penciclovir  also converted to triphosphate) Analgesia for acute neuritis Routine use of corticosteroid not recommended

14. Q7 List 2 possible complications of this presentation