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Case 2 Week 25
PC• 65 yo LBPHPC• 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 concerns in taking a hx for LBP:1. Is there evidence of systemic disease2. Is there evidence of neurologic compromise3. Is there social or psychological distress tUnderlying 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)
Trigger 2• No injury to back • No hx of back problems • No fever, urinary symptoms, or GIT symptoms
Q2 Detail your proposed examination
• 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
Trigger 3O/E• Back and abdo exam is normalTHEN• 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?
• 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
• Within 3 to 4 days, vesicular lesions become pustular or hemorrhagic
• 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
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)
• 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
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
• Q7 List 2 possible complications of this presentation