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 • Nighttimepain • 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 neuroesp 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 dermatomaldistribution • 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: • postherpeticneuralgia 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 • GuillainBarre 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 thymidinekinase, 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