University for development studies

School of allied and health science

Department of nursing

Assignment topic: herpes zoster by group four members

Date: 20th November 2018
Course:
Course code:
Name of group members
Name(s) Id number(s)
Boahen Emmanuel Nu/0075/16
Ntsiako ewusi Kenneth Nu/0121/16
Ahmed naziru Nu/0044/16
Ngiye dennicia n-kitibe Nu/0120/16
Abdul lateef o. lateefat Nu/0027/16
Mills asiaw theophilus Nu/0108/16
Akarikiya paulina Nu/0225/16
Yakubu muruana Nu/0146/16
Akenkagte clement Nu/0046/16
Naabo salifu abdul aziz Nu/0115/16
Shani m. saviour Nu/0139/16
Mantowura askanda abass Nu/0024/16
Dadzie edu Elizabeth Nu/0077/16
Munroh Anthony kojo Nu/0143/17
Yelka Christopher nyaaba Nu/1609/15
Saka elham maltiti Nu/o131/16
Outline
Definition of herpes zoster
Causes
Risk factors
Pathophysiology
Diagnosis
Clinical manifestations
Managements/treatment
Possible complications
Nursing management

Definition of herpes zoster

Herpes zoster, also known as shingles, is a viral diseases characterized by a painful skin rash
with blisters in localized area. Typically, the rash occurs in a single, wide stripe either on the left
or right side of the body or face.
Causes
It is caused by varicella zoster virus. After a primary varicella zoster(VZU) infection termed as
“varicella” or “chickenpox” the virus establishes latency in dorsal root and cranial nerve ganglia,
herpes zoster also known as shingles arise from the reactivation of VZU and it spreads from a
single ganglion to the neural tissue of the affected segment and the corresponding cutaneous
dermatome.
However, the causes for this reactivation is unknown.
Risk factors
The following are risk factors that trigger reactivation of the virus
Old age
Poor immune function
Having had chickenpox
Immunosuppressive therapy
Anti-tumor necrosis factor agent(TNF-α)
Immune reconstitution inflammatory syndrome
Pathophysiology
Varicella zoster infection gives rise to two 2 distinct syndromes. The primary infection,
chickenpox, is a contagious and usually benign febrile illness. After this infection resolves, viral
particles remain in the dorsal root or other sensory ganglia, where they lay dormant for years to
decades.
In this latent period, host immunologic mechanisms suppress replication of the virus but VZU
reactivates when the host mechanisms fail to contain the virus. Such failure may result from wide
spectrum of conditions ranging from stress to severe immunosuppression; it follows chest
trauma, VZU viremia occurs frequently with chickenpox but also may arise with herpes zoster.
Once VZU is activated at the spinal root or cranial nerve neurons, an inflammatory response
occurs that also encompasses the leptomeninges; both plasma cells and lymphocytes are noted.
This inflammation in the dorsal root ganglion can be accompanied by hemorrhagic necrosis of
nerve cells. The result is neuronal loss and fibrosis.
The frequency of dermatologic involvement is correlated with the centripetal distribution of the
initial varicella lesions. This pattern suggest that the latency may arise from contagious spread of
the virus during varicella from infected skin cells to sensory nerve endings, with subsequent
ascent to the ganglia. Alternatively, the ganglia may become infected hematogenously during the
viremic phase of varicella, and the frequency of the dermatome involvement in herpes zoster
may reflect the ganglia most often exposed to reactivating stimuli.
The appearance of the cutaneous rash due to herpes zoster coincides with a profound VZU-
specific T cell proliferation. In immunocompetent patient’s specific antibodies
(immunoglobulins G, A and M) appear more rapidly and reach higher titers during reactivation
than during infection.
The anatomical location of the involved dermatome often determines the specific manifestations.
Mode of transmission
It is contagious to people with no previous immunity to varicella zoster virus. However, herpes
zoster is estimated to be only one third a contagious as primary varicella. It is transmitted either
via direct contact with lesions or via the respiratory route.
Manifestations
The clinical manifestations of herpes zoster can be divided into the following three phases
The pre-eruptive phase
The acute eruptive phase
The chronic eruptive phase (PHN)
Some of the clinical manifestations includes;
Headaches
Fever
Malaise
Note; the above may result in incorrect diagnosis.
Sensations of the burning pain
Itching
Hyperesthesia (over sensitivity)
Paresthesia (abnormal skin sensations as tingling, tickling, itching or burning)
Pain rating from mild from extreme in the affected dermatome.
Skin rashes (commonly at torso and other areas of the body such as face and eyes), these rashes
first appear as hive later vesicular, it then forms a small blisters filled with a serous exudate.
Note
shingles in children are often painless.
Diagnosis
Family history
Physical examination
Lab studies for VZU
Direct fluorescent antibody (DFA) of vesicular fluid
Polymerase chain reaction(PCR) testing of vesicular fluid
Tzanck smear
Differential diagnosis
Shingles can be confused with herpes simplex, dermatitis herpetiformis and impetigo and skin
reactions caused by contact dermatitis, candidiasis, certain drugs and insect bites.
Management
Treatment aims are to limit the severity and duration of pain, shorten the duration of shingles
episodes and reduce complications.
The following can be use
Analgesics
Antivirals
Anticonvulsant agent
Steroids
The use of steroids treatment is controversial. Typically, a substantial dose of 40mg-60mg oral of
prednisone is administered every morning as early as possible in the course of the diseases and is
continued for 1 week, followed by a rapid taper over 1-2 weeks.
Complications
The complications of herpes zoster can be group into acute and chronic
Acute complications
cutaneous and mucocutaneous sites
Cellulitis
Zoster gangrenosum
Septicemia
Cutaneous VZU dissemination
Neurological
Cranial nerve palsies
Aseptic meningitis
Meningo- encephalitis
Ocular
Conjunctivitis
Uveitis
Loss of cornea sensation
Optic neurophaty
Acute retinal necrosis
Visceral
Neural extension of VZU infection
Bronchitis
Pneumonia
Chronic complications
Ocular
Keratitis
Chorioretinitis
Neurological
Sensory loss
Deafness
Tranveerse and ascending myelitis
Cerebral angitis
Nursing care
Patient education
Patient should be informed about the natural progression of herpes zoster and it potential
complications
Patient should be educated on the need to take medications.
Patients should be educated that treatment must be started within 72 hours of onset.
Patient should be educated on the side effect of the drugs.
Patients must be told not to scratch the lesions; doing so may predispose them to secondary
infections
Nursing interventions
Wet dressings with 5% aluminum acetate(barium solution), applied for 30 – 60 minutes 4 – 6
times daily.
Application of lotions to prevent itching eg. Calamine
Administration of prescribed drugs
References
Zekayi k et al. Journal Of The Turkish Academy Of Dermatology, Complications Of Herpes
Zoster:2004.
en.m.wikipedia.org/wiki/shingles.
David W. Judith B. Herpes Zoster, British Medical Journal: 2007.
https://www.researchgate.net/publication/6281278