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HERPES ZOSTER & P.H.N
Dr. Ravi Shankar Sharma
DARADIA
INTRODUCTION
• Viral infection caused by the reactivation of the
varicella-zoster virus (VZV).
• Primary varicella infection - chicken pox.
• Neuronal destruction and inflammation pain
interference with daily activities
• Does not cross midline
• Immunocompetent  single dermatome affected
Immunocompromised  multiple dermatomes/
visceral dissemination / cutaneous dissemination
ETIOPATHOGENESIS
•Neurogenic
inflammation
•Haemorrhagic
necrosis
•Neuronal loss
& scarring
Primary VZV infection ( chicken pox )
virus remains dormant in DRG & cranial N nuclei
CMI for VZV decreases with age
VIRAL REPLICATION in DRG
Anti dromic conduction of virus to dermo
epidermal junction via cutaneous nerves
•Demyelination
•Increase in the electrical
activity of peripheral
nociceptors
Inflammation and tissue
necrosis leading to rash
PERIPHERAL NERVES
SKIN
Pathophysiology PHN
PHASES
• Prodrome
• Rash
• Pain
PRODROME
• Precedes the appearance of rash by 3 – 7
days
• Result of viral replication and inflammation
• Flu like symptoms malaise, fatigue,
headache, fever, neck stiffness
• U/L dermatomal pain / altered sensation /
pruritis
RASH
Maculopapular rash
7
days
2–3weeks
PAIN
• It can precede or accompany the rash
• Burning / throbbing / stabbing / electric shock
like pain which may be constant or intermitent
• Associated with hyperaesthesia and allodynia
• Interfere with sleep, physical and emotional
functioning
DERMATOMAL DISTRIBUTION
• Thoracic – upto 50%
• Cranial – 10 – 20 %
• Cervical -- 10 – 20 %
• Lumbar – 10 – 20 %
• Sacral – 2 – 8 %
• Generalised - < 1 %
CLINICAL VARIANTS
• Herpes zoster ophthalmicus – ophthalmic
division of trigeminal nerve
• Herpes zoster oticus – VII cranial nerve
• Zoster sine herpete – dermatomal pain
without rash
LAB DIAGNOSIS
• VIRAL CULTURE: (1 to 2 weeks)
• DIRECT IMMUNOFLOUROSCENCE : ( 3 hours)
• VIRAL DNA TESTING(PCR): ( 1 day )
100 %sensitivity in old crusted lesions
• BIOPSY: reserved for difficult to diagnose cases.
- ballooning degeneration
- acantholysis of keratinocytes
- leukoclastocytic vasculitis
DIFFERENTIAL DIAGNOSIS
• Coronary artery disease,
• Pleurodynia
• Costochondritis (Tietze’s syndrome)
• Pericarditis,
• Cholecystitis
• Acute abdominal diseases.
• Disc diseases.
• Nerve diseases and Myofascial pain.
TREATMENT
Objectives :
• Reduction of severity and duration of the pain.
• To limit viral replication.
• Recovery of epidermal defects and prevention
of secondary infections.
• Reduction or prevention of PHN.
TREATMENT – ACUTE HERPES ZOSTER
CONSERVATIVE MANAGEMENT
• Patient education
- avoid contact with individuals who are sero
negative for VZV
- keep rash clean and free of adhesive
dressings to prevent secondary infections
ANTI VIRAL THERAPY:
- Inhibit viral DNA polymerase and hence its
replication
- must be given to all herpes zoster patients
- beneficial when given within 72 hrs of onset of
rash
Those who benefit even > 72 hrs :
- ophthalmic zoster
- immunocompromised
- neurological damage
Benefits of antiviral therapy
• Inhibition of viral replication
• Reduce duration of viral shedding
• Hastens rash healing
• Decrease the degree of neural damage
• Decrease the severity and duration of acute pain
• Decrease duration of PHN
• Decrease incidence of PHN
CONSERVATIVE MANAGEMENT contd
• ANALGESICS:
- mild pain – NSAIDS / acetaminophen / weak
opioids
- moderate pain – strong opioids ( effective in
reducing pain )
• CO ANALGESICS: gabapentin , pregabalin , TCA’S may
be used
CONSERVATIVE MANAGEMENT contd
• CORTICOSTEROIDS:
- reduce inflammatory features of acute zoster
- possibly prevent injury to affected neurons
- effective when used in combination with antivirals
- no effect on the healing of rash
- no effect on the occurrence of PHN
INTERVENTIONS
• Single shot epidural with local anaesthetic + STEROID
(level B evidence)
• Continuous epidural with LA
• Paravertebral blocks
• Sympathetic blocks
• SCS
PREVENTION
• VZV vaccination for children
• VZIG – for immunocompromised seronegative
patients who are exposed to chicken pox /
herpes zoster
• Herpes zoster vaccination for adults
POST HERPETIC NEURALGIA
INTRODUCTION
• POST HERPETIC NEURALGIA : dermatomal
pain persistent > 120 days after the onset of
rash
• PHN risk factors:
- age > 50 yrs
- painful prodrome
- severe acute pain / rash
PATHOPHYSIOLOGY
VIRAL REPLICATION 
NEURAL DAMAGE AND
INFLAMMATION
(GANGLIONITIS)
SENSITIZATION
PERIPHERAL C FIBRES
 burning,
hyperalgesia, allodynia
CENTRAL  involves
NMDA R & Glutamate
R / EPHAPTIC
conduction
DEAFFERENTIATION
Loss of large and small
diameter fibers
Ectopic discharges
Collateral sproutings
CLINICAL FEATURES
• sharp shooting, electric shock like pain
- continuous burning / throbbing pain
• tactile allodynia ( most deblitating )
- hyperalgesia
• Musculoskeletal pain
• Sensory abnormalities :
- hypoaesthesia, altered temperature sensation,
paraesthesia, dysaesthesia, chronic pruritis
DIAGNOSIS OF PHN
• h/o rash f/b dermatological pain
• h/o rash  12 months pain free  dermatomal
pain
• Lab diagnosis :
- quantitative sensory testing
- skin biopsy
- NCV
TREATMENT
OBJECTIVES :
• To alleviate pain
• To Improve quality of life
CONSERVATIVE MANAGEMENT
• ANTICONVULSANTS:
- Gabapentin : alpha 2 delta L type voltage gated
Ca++ channel blocker
- start with 300mg / day (max dose upto 3600mg /
day )
- Pregabalin : alpha 2 delta L type voltage gated
Ca++ channel blocker
- start with 150 mg / day ( max upto 600 mg/day)
- better tolerated
CONSERVATIVE MANAGEMENT contd
• ANTI DEPRESSANTS:
- TCA’s : amitryptyline / nortryptyline
• Provides moderate to excellent pain relief .
(used esp in those suffering with insomnia)
desipramine – less sedating
- SNRI’s : not FDA approved
duloxetine is still used
CONSERVATIVE MANAGEMENT contd
• OPIOIDS: Tramadol & Oxycodone useful
CLINICAL RECOMMENDATIONS:
• Use lowest effective dose
• Initiate with short acting opioids
• Convert to long acting
• Proactively combat nausea and constipation
INTERVENTIONAL MANAGEMENT
• SYMPATHETIC NERVE BLOCKS :
- Good evidence
- it reduces sympathetically mediated neuronalinflammation
• SPINAL CORD STIMULATION : good evidence
• POOR EVIDENCE :
- Continuous epidural for one week
- intercostal N block
- transforaminal DRG
- intra thecal opioids
• PRF leisoning
• Narrow band UVB
PREVENTION OF PHN
• Vaccination
• Anti viral therapy
• Pharmacotherapy – alleviate pain
• Sympathetic blocks
PREVENTION OF PHN
• Vaccination
• Early antiviral therapy
• Early treatment of neuropathic pain
Thank YOU

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Herpes zoster and phn (1)

  • 1. HERPES ZOSTER & P.H.N Dr. Ravi Shankar Sharma DARADIA
  • 2. INTRODUCTION • Viral infection caused by the reactivation of the varicella-zoster virus (VZV). • Primary varicella infection - chicken pox. • Neuronal destruction and inflammation pain interference with daily activities • Does not cross midline • Immunocompetent  single dermatome affected Immunocompromised  multiple dermatomes/ visceral dissemination / cutaneous dissemination
  • 3.
  • 4.
  • 5. ETIOPATHOGENESIS •Neurogenic inflammation •Haemorrhagic necrosis •Neuronal loss & scarring Primary VZV infection ( chicken pox ) virus remains dormant in DRG & cranial N nuclei CMI for VZV decreases with age VIRAL REPLICATION in DRG
  • 6. Anti dromic conduction of virus to dermo epidermal junction via cutaneous nerves •Demyelination •Increase in the electrical activity of peripheral nociceptors Inflammation and tissue necrosis leading to rash PERIPHERAL NERVES SKIN
  • 9. PRODROME • Precedes the appearance of rash by 3 – 7 days • Result of viral replication and inflammation • Flu like symptoms malaise, fatigue, headache, fever, neck stiffness • U/L dermatomal pain / altered sensation / pruritis
  • 11. PAIN • It can precede or accompany the rash • Burning / throbbing / stabbing / electric shock like pain which may be constant or intermitent • Associated with hyperaesthesia and allodynia • Interfere with sleep, physical and emotional functioning
  • 12. DERMATOMAL DISTRIBUTION • Thoracic – upto 50% • Cranial – 10 – 20 % • Cervical -- 10 – 20 % • Lumbar – 10 – 20 % • Sacral – 2 – 8 % • Generalised - < 1 %
  • 13. CLINICAL VARIANTS • Herpes zoster ophthalmicus – ophthalmic division of trigeminal nerve • Herpes zoster oticus – VII cranial nerve • Zoster sine herpete – dermatomal pain without rash
  • 14. LAB DIAGNOSIS • VIRAL CULTURE: (1 to 2 weeks) • DIRECT IMMUNOFLOUROSCENCE : ( 3 hours) • VIRAL DNA TESTING(PCR): ( 1 day ) 100 %sensitivity in old crusted lesions • BIOPSY: reserved for difficult to diagnose cases. - ballooning degeneration - acantholysis of keratinocytes - leukoclastocytic vasculitis
  • 15. DIFFERENTIAL DIAGNOSIS • Coronary artery disease, • Pleurodynia • Costochondritis (Tietze’s syndrome) • Pericarditis, • Cholecystitis • Acute abdominal diseases. • Disc diseases. • Nerve diseases and Myofascial pain.
  • 16. TREATMENT Objectives : • Reduction of severity and duration of the pain. • To limit viral replication. • Recovery of epidermal defects and prevention of secondary infections. • Reduction or prevention of PHN.
  • 17. TREATMENT – ACUTE HERPES ZOSTER CONSERVATIVE MANAGEMENT • Patient education - avoid contact with individuals who are sero negative for VZV - keep rash clean and free of adhesive dressings to prevent secondary infections
  • 18. ANTI VIRAL THERAPY: - Inhibit viral DNA polymerase and hence its replication - must be given to all herpes zoster patients - beneficial when given within 72 hrs of onset of rash Those who benefit even > 72 hrs : - ophthalmic zoster - immunocompromised - neurological damage
  • 19. Benefits of antiviral therapy • Inhibition of viral replication • Reduce duration of viral shedding • Hastens rash healing • Decrease the degree of neural damage • Decrease the severity and duration of acute pain • Decrease duration of PHN • Decrease incidence of PHN
  • 20.
  • 21. CONSERVATIVE MANAGEMENT contd • ANALGESICS: - mild pain – NSAIDS / acetaminophen / weak opioids - moderate pain – strong opioids ( effective in reducing pain ) • CO ANALGESICS: gabapentin , pregabalin , TCA’S may be used
  • 22. CONSERVATIVE MANAGEMENT contd • CORTICOSTEROIDS: - reduce inflammatory features of acute zoster - possibly prevent injury to affected neurons - effective when used in combination with antivirals - no effect on the healing of rash - no effect on the occurrence of PHN
  • 23. INTERVENTIONS • Single shot epidural with local anaesthetic + STEROID (level B evidence) • Continuous epidural with LA • Paravertebral blocks • Sympathetic blocks • SCS
  • 24.
  • 25. PREVENTION • VZV vaccination for children • VZIG – for immunocompromised seronegative patients who are exposed to chicken pox / herpes zoster • Herpes zoster vaccination for adults
  • 27. INTRODUCTION • POST HERPETIC NEURALGIA : dermatomal pain persistent > 120 days after the onset of rash • PHN risk factors: - age > 50 yrs - painful prodrome - severe acute pain / rash
  • 28. PATHOPHYSIOLOGY VIRAL REPLICATION  NEURAL DAMAGE AND INFLAMMATION (GANGLIONITIS) SENSITIZATION PERIPHERAL C FIBRES  burning, hyperalgesia, allodynia CENTRAL  involves NMDA R & Glutamate R / EPHAPTIC conduction DEAFFERENTIATION Loss of large and small diameter fibers Ectopic discharges Collateral sproutings
  • 29. CLINICAL FEATURES • sharp shooting, electric shock like pain - continuous burning / throbbing pain • tactile allodynia ( most deblitating ) - hyperalgesia • Musculoskeletal pain • Sensory abnormalities : - hypoaesthesia, altered temperature sensation, paraesthesia, dysaesthesia, chronic pruritis
  • 30.
  • 31. DIAGNOSIS OF PHN • h/o rash f/b dermatological pain • h/o rash  12 months pain free  dermatomal pain • Lab diagnosis : - quantitative sensory testing - skin biopsy - NCV
  • 32. TREATMENT OBJECTIVES : • To alleviate pain • To Improve quality of life
  • 33. CONSERVATIVE MANAGEMENT • ANTICONVULSANTS: - Gabapentin : alpha 2 delta L type voltage gated Ca++ channel blocker - start with 300mg / day (max dose upto 3600mg / day ) - Pregabalin : alpha 2 delta L type voltage gated Ca++ channel blocker - start with 150 mg / day ( max upto 600 mg/day) - better tolerated
  • 34. CONSERVATIVE MANAGEMENT contd • ANTI DEPRESSANTS: - TCA’s : amitryptyline / nortryptyline • Provides moderate to excellent pain relief . (used esp in those suffering with insomnia) desipramine – less sedating - SNRI’s : not FDA approved duloxetine is still used
  • 35. CONSERVATIVE MANAGEMENT contd • OPIOIDS: Tramadol & Oxycodone useful CLINICAL RECOMMENDATIONS: • Use lowest effective dose • Initiate with short acting opioids • Convert to long acting • Proactively combat nausea and constipation
  • 36.
  • 37. INTERVENTIONAL MANAGEMENT • SYMPATHETIC NERVE BLOCKS : - Good evidence - it reduces sympathetically mediated neuronalinflammation • SPINAL CORD STIMULATION : good evidence • POOR EVIDENCE : - Continuous epidural for one week - intercostal N block - transforaminal DRG - intra thecal opioids • PRF leisoning • Narrow band UVB
  • 38. PREVENTION OF PHN • Vaccination • Anti viral therapy • Pharmacotherapy – alleviate pain • Sympathetic blocks
  • 39. PREVENTION OF PHN • Vaccination • Early antiviral therapy • Early treatment of neuropathic pain

Editor's Notes

  1. Acy-60 days,valc-40 days