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

Immunocompromisedmultiple dermatomes/ visceral dissemination / cutaneous dissemination

ETIOPATHOGENESIS

•Neurogenicinflammation•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 dermoepidermal junction via cutaneous nerves

•Demyelination•Increase in the electrical

activity of peripheral nociceptors

Inflammation and tissue necrosis leading to rash

PERIPHERAL NERVESSKIN

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 –

3 w

eeks

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 seronegative 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 seronegativepatients who are exposed to chicken pox / herpes zoster

• Herpes zoster vaccination for adults

POST HERPETIC NEURALGIA

INTRODUCTION

• POST HERPETIC NEURALGIA : dermatomalpain 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 dermatomalpain

• 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