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The reawakening of a sleeping little giant
  1. R Goddard
  1. Correspondence to:
 Dr Robert Goddard
 General Surgery, Queen Elizabeth and Queen Mary Hospitals, East Kent Hospitals NHS Trust;


This case report and literature review highlights the classical signs and symptoms of herpes zoster infection involving the trigeminal nerve. Incorrect diagnosis leads to delay in providing effective treatment and could result in failure to identify potentially hazardous ocular complications and to prevent chronic post-herpetic pain.

  • herpes zoster
  • zoster immunisation
  • zoster morbidity
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It is likely that herpes zoster will become more prevalent as the population ages. It is therefore important that all physicians, regardless of their specialty, be aware of this “classical” disease. It is advisable that all physicians examine the patients with anatomy in mind. In this case, intra-oral examination clinched the diagnosed. The oral cavity should not be considered as the sole domain of dentists.

Herpes zoster is rarely seen in the acute setting of the accident and emergency department, especially when it involves the trigeminal nerve. Varicella-zoster virus causes chickenpox (varicella). This is followed by a period of latency in cranial nerve and dorsal root ganglia. It can reactivate many years later to produce shingles (zoster) and post-herpetic neuralgia. It is therefore a disease that is familiar to those specialist clinicians (paediatricians and geriatricians) who encounter the disease as chicken pox in childhood and shingles in the elderly. Other clinicians familiar with this virus include those who deal directly with its complications, such as dentists, oral physicians, and ophthalmologists. A re-emergence of the disease demands revision by generalist medical and surgical clinicians.


A general practitioner was called to make a home visit to an 89 year old man who developed facial swelling that caused him to “take to his bed.” The GP diagnosed a facial infection involving the lower eyelid. Admission was sought at the local hospital on the grounds that facial cellulitis was present requiring intravenous antibiotics. The GP was encouraged to transfer the patient to a hospital where maxillo-facial services were available, but this option was declined as the patient’s spouse was elderly and would find it difficult to visit. The patient was thus admitted to his nearest hospital under the care of the surgical team, despite the lack of maxillo-facial services.

On presentation to the A&E department, the patient complained of headache, difficulty in swallowing, and facial/eye swelling. He reported that he had been well up to three days before, when he noticed the presence of mouth ulcers. Pain ensued soon afterwards. This was sharp and constant in nature, sited in the medial aspect of his left cheek and radiating to the left supraorbital region. He complained of brown-yellowish slime in his mouth. He also developed rhinorrhoea and ulcerative lesions on the left cheek.

The patient had a past medical history typical for a man of his age, with a previous myocardial infarct and a cerebrovascular accident. He was a non-smoker and had no overt immunodeficiency disorder.

Significant examination findings were confined to the maxillo-facial region. He had an erythematous left cheek with what appeared to be multiple herpetiform crusted lesions. There was a thick white mucus discharge from the left eye. Intraoral examination showed a greyish slough covering only the left primary and secondary palate (fig 1). The patient was edentulous. His respiratory system was free of clinical signs. He had a normal white cell count and was apyrexial on admission and throughout his hospital course.

Figure 1

 The appearance of the mouth and palate in the patient.

Herpes-zoster infection of the trigeminal nerve was diagnosed and the patient was transferred to the care of general physicians for further management. At this point the possibility of a dental abscess or mumps was considered by junior staff on the medical firm. He was started on a course of oral flucloxacillin, metronidazole mouthwash, and intravenous benzyl penicillin. Aciclovir was not started until the following day. The antibacterial agents were discontinued after three days. The patient’s recovery was somewhat delayed owing to poor mobility and the development of a short bout of diarrhoea and vomiting. After five days in hospital he was discharged home with no further prescription for aciclovir.


This case appeared to present in a classical way yet still raised diagnostic difficulties in the unwary physician, leading to delayed implementation of appropriate treatment. Physicians need to be mindful of the key diagnostic features of the re-emerging dormant disease.

Herpes-zoster is very common, especially in the elderly. The annual incidence of latent herpes-zoster, which is approximately 1/1000 before the age of 20, increases five to 10-fold (to 4.5 to 11/1000) after 80. Among adults over the age of 70 with acute herpes-zoster, treatment reduces the incidence of persisting pain to an estimated 50%, compared with up to 70% without treatment. Approximately half the patients over 70 with herpes-zoster report pain lasting more than one year.1 The lifetime risk of shingles is estimated at 20% and the risk of a second attack is less than 5%.2

Herpes-zoster affects the sexes equally and its commonest symptom is pain. Patients often get a feeling of helplessness and depression and may have flu-like symptoms. A prodromal phase may include itching and paraesthesiae. Other symptoms include insomnia, limitation of movement, and post-herpetic neuralgia (pain after the cessation of the rash). The most commonly affected dermatomes are the thoracic (45%), cervical (23%), and trigeminal (15%). It may affect one or more dermatomes at a time. Secondary bacterial infection may occur but rarely causes intraoral pus in an edentulous mouth.

There are a many serious complications3 which can affect the central nervous system (for example, myelitis, large and small vessel encephalitis, ventriculitis) and the peripheral nervous system (Guillain–Barré syndrome/postinfectious polyneuritis). Non-neurological complications may result from neuronal or haematological spread, especially in immunocompromised individuals, such as the elderly. These include visceral spread causing hepatitis, pneumonitis, and ophthalmic shingles. Approximately 50% of patients with herpes-zoster involving the first division of the trigeminal nerve will have ocular complications, some of which may threaten the sight. The morbidity and mortality resulting from this disease are also reflected in increased rates of hospital admission, case fatality ratios, and the incidence of cases of post-herpetic neuralgia. All these have been shown to increase markedly with the age of the patient. In a study done in Tayside it was found that most admissions resulted from involvement of the trigeminal nerve.4 The duration of hospital admission ranged from 1 to 70 days, with a median stay of 11 days. It has been estimated that it costs £47.6 m annually to treat herpes-zoster. There is an estimated loss of 20 000 quality of life years annually in England and Wales from this disease. There is therefore a very high human as well as financial cost of neglecting its prevention and treatment.

Potential strategies for the management of herpes-zoster are based, as for any other disease, on prevention (including vaccination), treatment, and follow up.


Edmunds et al suggest that varicella vaccination is a “double edged sword”.5 They concluded that vaccination of the elderly is expected to be cost–effective under most situations. On the other hand, in further paper from the same group6 it was suggested that, although vaccination results in high initial protection, full protection is lost relatively rapidly (3% per year). It was also stated that once total protection has waned, there is a high probability of developing breakthrough infection if exposed to varicella (73% of the probability in the unvaccinated susceptible individuals).

The varicella-zoster virus Oka strain vaccine is currently recommended by the Advisory Committee on Immunisation Practices for universal childhood vaccination in the USA.6,7 This vaccine increases cytotoxic lymphocyte responses specific for varicella-zoster virus in seropositive elderly people.8 There is doubt whether vaccine induced immune enhancement will reduce the incidence or severity of herpes zoster in the elderly. It appears evident that we have a hung jury on whether mass vaccination of the elderly is indicated at present.


Early diagnosis and prompt treatment of the disease in the prodromal phase by the use of antiviral agents should probably be the mainstay of its management. The aim of this treatment is to accelerate healing, limit the severity and duration of acute and subsequent chronic pain, and reduce complications. The adjunctive use of corticosteroids should be considered, especially in the elderly, as many studies have shown accelerated rates of cutaneous healing and alleviation of acute pain. Torrens et al9 showed that there was a wide variation in both preadmission and inpatient treatment. They reported that 53.3% did not receive any anti-viral therapy before admission. It was found that general practitioners prescribed 5% idoxuridine topically in 15% of the cases despite multiple sources agreeing that there is no role for the use of topical antiviral drugs in the management of herpes zoster. Goh and Khoo10 confirmed that only 9% of affected patients consulted their GP during the prodrome or on the day of skin eruptions. They concluded there was a need for patient education to identify prodrome and skin eruptions of herpes zoster so that early antiviral therapy can be given at the optimal time.

Follow up

These patients need following up in the community, and there should be continuing audit of the disease to try to minimise further morbidity. This is particularly important with respect to post-herpetic neuralgia and ocular complications. Review of the patient after four to six weeks, or earlier if the pain is poorly controlled, allows prompt treatment with neurotropic agents4 (for example, gabapentin, carbamazepine, or amitriptyline). Acute retinal necrosis can occur in immunocompetent patients. Visual changes begin weeks or months after the resolution of herpes-zoster as a result of haematogenous spread. Herpes-zoster affecting any dermatome could therefore lead to ocular damage, and this could be minimised by early ophthalmic review and the use of oral corticosteroids.11 Review of the patient could also help to ensure that cutaneous lesions are kept clean and dry, to reduce the risk of bacterial superinfection.

In summary, failure of early diagnosis by junior staff in this case led to delayed implementation of antiviral therapy in a patient with herpes zoster affecting the trigeminal nerve. There was no supporting evidence to suggest bacterial superinfection yet the patient received multiple antibiotics. It is questionable whether steroid therapy or an alternative antiviral agent to aciclovir could also have been useful in speeding the patient’s recovery. A mucus discharge was noted from the left eye but no other signs of involvement of the ophthalmic branch of trigeminal nerve. As a precautionary measure, and in the light of what is known about ocular spread, it might have been prudent to have sought an ophthalmic review at some stage.


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