Indian Dermatology Online Journal

LETTER TO THE EDITOR
Year
: 2018  |  Volume : 9  |  Issue : 4  |  Page : 278--279

Abdominal wall herniation after herpes zoster


Pragya A Nair, Kira Pariath 
 Department of Dermatology and Venereology, Pramukhswami Medical College, Karamsad, Gujarat, India

Correspondence Address:
Pragya A Nair
Department of Dermatology and Venereology, Pramukhswami Medical College, Karamsad, Gujarat
India




How to cite this article:
Nair PA, Pariath K. Abdominal wall herniation after herpes zoster.Indian Dermatol Online J 2018;9:278-279


How to cite this URL:
Nair PA, Pariath K. Abdominal wall herniation after herpes zoster. Indian Dermatol Online J [serial online] 2018 [cited 2021 Apr 10 ];9:278-279
Available from: https://www.idoj.in/text.asp?2018/9/4/278/235706


Full Text



Sir,

A 60-year-old male presented with a nonprogressive swelling on the left side of his lower abdomen since 20 days. The patient had a history of sudden appearance of vesicles over the swollen area 1 month back with shooting pain. These vesicles extended from the back to just below the umbilicus on the left side. He has been given treatment for herpes zoster (HZ) of which no medical records were available. The lesions healed in 3 weeks, leaving a scar in that area. The patient had no other comorbidities like diabetes mellitus, hypertension, pre-existing hernias, or past surgical intervention. Intense burning and hyperesthesia with sharp shooting pain was the symptom when he presented to us. He was given oral pregabalin and amitriptyline with partial relief.

One week later, he noticed an abnormal swelling on the left side of abdomen, in the hypochondriac and lumbar region with hyperesthesia. On examination, a prominent bulge of 15 × 10 cm size was present on the left side of the trunk, in the area of T9–T11 dermatomes [Figure 1] and [Figure 2] with hyperpigmented scars and scabs. The overlying skin was lax. The bulge increased on coughing, sneezing, defecating, and was reducible in lying down position. The swelling was skin colored, soft, non-tender, non-cystic, non-mobile, with well-defined sloping margins. Routine investigations were normal, and serology for HIV was negative. An ultrasonography was done which showed no obvious evidence of any focal defect in the anterolateral aspect of the abdominal wall on the left side. The neurologist consulted confirmed the diagnosis of HZ paresis by the absence of abdominal superficial reflexes on the side affected. Further, electromyography (EMG) of the abdominal muscles was considered unnecessary. The patient was labeled as a case of pseudohernia, post HZ infection.{Figure 1}{Figure 2}

HZ affects 10–20% of the general population.[1] It is primarily caused by reactivation of a latent varicella-zoster virus. Clinically, HZ is characterized by the appearance of grouped vesicular eruption on skin and mucous membranes in a dermatomal distribution. The virus mainly affects the posterior root ganglia, causing majority of neurological complications which are sensory in nature, rarely affecting motor component. It involves cranial nerves, mainly facial nerve, and nerves of extremities. Motor weakness of thoracic segments is a rare presentation with an estimated incidence of 1–5%, but can cause abdominal wall weakness presenting with abdominal or flank bulges mimicking abdominal-wall hernias.[2] The first case of motor weakness following HZ was reported in 1886 by Broadbent.[3]

In a study by Thomas et al.[4] with 1,210 patients of HZ, two cases of abdominal wall paralysis were seen out of the 277 cases having T8–T12 dermatomal involvement, i.e., only 0.7%, while the rate of paresis in cephalic zoster was 12%.

The segmental paresis is a rare postherpetic complication characterized by focal and asymmetrical neurogenic paresis that affects the myotome corresponding to the dermatomal distribution of the rash. Its pathogenesis is still controversial, but virus spreading from the dorsal root ganglion to the anterior horn cells, thereby resulting in medullary, root plexus, or peripheral nerve inflammation is the presumed cause.[5] Segmental zoster paresis can affect diaphragmatic and abdominal-wall muscles, face, upper and lower limb, bladder, urinary and gastrointestinal viscera resulting in urinary retention, cystitis, and colonic pseudo-obstruction. In our case, only abdominal-wall muscle paresis was present.

HZ paralysis has been described in middle-aged or elderly persons, patients with underlying hematological malignancies, and immunocompromised individuals.[6] The age of our patient was compatible with the epidemiology but there was no immunosuppression.

The symptoms of focal muscle paresis usually appear within 2–3 weeks of the appearance of the rash and shows reduced or absent segmental reflexes to confirm paralysis. A nerve conduction study can be done using an electroneuromyography.[7] EMG will reveal a denervation pattern of the paraspinal muscles at the affected levels, indicating that the nerve segment involved is proximal to the posterior rami, probably within the anterior horn itself. Magnetic resonance imaging (MRI) with gadolinium-DTPA (diethylenetriamine penta-acetic acid) can help to delineate the extent of the inflammation as it shows abnormal contrast enhancement of anterior and posterior nerve roots at the affected segment [8] and will also exclude the local entrapment of spinal nerve roots, known to be a predisposing factor of HZ. However, both these investigations are expensive and looking at the benign nature of the disease, we decided to consult a neurologist first. The neurologist confirmed the diagnosis of HZ paresis by the absence of abdominal superficial reflexes on the side affected and exclusion of other diseases. Further, EMG of the abdominal muscles was considered unnecessary.

The differential diagnosis includes diabetes, HZ, intercostal nerve lesions in surgical or other thoracic procedures, thoracic disk hernia, vertebral metastasis or trauma, appendicitis or colitis, and thoracic root alteration.[9] Zoster sine herpete is considered when a patient shows pain and neuropathy distributed in the area innervated by one cranial nerve or spinal root without typical vesicular eruptions. It can also lead to pseudohernia as a complication.

The prognosis for motor weakness in such cases is good, with complete recovery in 55–75% of patients within 6–12 months of the onset, but some patients remain with permanent weakness.[1],[8],[10] Apparently, there is no relationship between the degree of paralysis and complete recovery.

It is important to consider HZ as a cause of unilateral segmental paralysis of the abdominal muscles, which resembles an abdominal wall hernia and is important for making a correct diagnosis, so that unnecessary investigations and interventions can be avoided.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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3Broadbent WH. A case of herpetic eruption in the course of branches of the brachial plexus, followed by partial paralysis in corresponding motor nerves. Br Med J 1866;2:460.
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