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