To treat the necrotic and inflammatory soft tissue swelling, debridement and decompression were performed under general anesthesia. A 30 × 25 cm sized soft tissue defects remained, and greater trochanter, lesser trochanter, and neck of femur were exposed (Fig. 4). Frequent dressing changes were administered on the remaining soft tissue defects and the patient underwent psychiatric treatment with concomitant physical therapy.
After 6 months of frequent dressing changes and serial debridement, the pressure ulcer exhibited moderate improvement. Soft tissue defects decreased in size from 30 × 25 to 25 x 15 cm and healed with granulation tissue (Fig. 5A, B). Although a gait disorder was still present as a sequela of sciatic neuropathy, the patient's motor function recovered to some extent with MRC grade 2 of 5. However, valproic acid, which was administered as a psychiatric medication while the patient was admitted to the hospital, caused toxic hepatitis. The patient was transferred to the department of gastroenterology for the treatment of toxic hepatitis.
The patient provided informed consent for the publication of her clinical and radiological data. This study was approved by the Institutional Review Board of Chonnam National University Hospital (Gwangju, Korea) and was conducted in accordance with the principles of the Helsinki Declaration II.
The sciatic nerve runs through the lower extremity and is the largest and longest nerve in the human body. The sciatic nerve divides into the tibial nerve and common peroneal nerve branches, and runs to the feet. It is susceptible to injury due to its long length, and sciatic neuropathy can occur due to several causes, including fracture, dislocation, hematoma, and hip replacement surgery,[1–6] leading to neurological deficits. Sciatic neuropathy is diagnosed based on nerve conduction studies, electromyography (EMG), and MRI. One of the most common symptoms of sciatic neuropathy is foot drop; other symptoms include weakened knee flexion, pain and sensory loss in the foot, and decreased ankle jerk.[1,2] It is important to determine the exact cause of sciatic neuropathy before treatment. For example, if a patient has piriformis syndrome, the first-line therapy should be conservative therapy or botulinum toxin injection, and tricyclic antidepressants or anticonvulsants should be administered to control neuropathic pain. In contrast, surgery is the treatment of choice if it is accompanied by compartment syndrome.[1,4] In this study, debridement and decompression were combined with rehabilitation to treat a decubitus ulcer that was accompanied by inflammation and edema, which caused sciatic neuropathy.
Electrodiagnosis is a very useful method for diagnosing sciatic neuropathy. The following electrodiagnostic findings are characteristic of sciatic neuropathy. Motor nerve conduction studies demonstrate typically decreased amplitudes of compound muscle action potentials in the peroneal and tibial nerves. The F latency of the peroneal and tibial nerves is absent or prolonged, and sensory nerve conduction studies reveal decreased amplitudes of the superficial peroneal sensory and sural sensory nerve action potential.[1,2] In addition, a needle EMG, in addition to a nerve conduction study, is necessary to distinguish between sciatic neuropathy and peroneal mononeuropathy. However, needle EMG was not performed in this case because of the high risk of infection from the soft tissue defects in the right buttock.
MRI is the optimal medical imaging technique for evaluating pathologies of the sciatic nerve. Depending on the severity of the injury, the nerve exhibits high signal intensity on T2-weighted MRI[9–11]; moreover, MRI can detect the extent of the lesion and identify inflammatory etiology. In this case, we confirmed inflammatory soft tissue swelling using MRI, which was helpful in diagnosing sciatic neuropathy and identifying its cause.
The currently known complications of pressure ulcers include cellulitis, osteomyelitis, bacteremia, endocarditis, meningitis, septic arthritis, abscesses, and squamous cell skin cancer, among others. The present findings suggest that neuropathy can also occur as a complication of pressure ulcers.
Khaykin et al noted that patients with schizophrenia have an increased risk of adverse events including decubitus ulcer and it may be related to medication resulting in oversedation and decreased mobility. Gefen  noted that pressure ulcers in subdermal tissues under bony prominences very likely occur approximately between the first hour and 4 to 6 hours after sustained loading. In our case, the patient overdosed on the schizophrenia medication and was bedridden for 2 days in a coma. It is sufficient to cause the pressure ulcer.
This patient ultimately should have undergone flap surgery to cover the soft tissue defects. However, in general, if a patient's risk factors remained, operative reconstruction must be delayed. Furthermore, if there is a high possibility of a surgery failing or ulcer recurrence, chronic wound care is more effective. In the case study presented here, because of uncontrolled moods or refusal of psychiatric treatment, we anticipated her poor cooperation and prolonged care postoperatively. Moreover, toxic hepatitis occurred during psychopharmacological treatment. The patient was susceptible to hepatic failure, and liver transplantation was a possibility. As a result, we could not perform flap surgery under general anesthesia; instead, the patient received conservative treatment while her general condition improved. Some examples of conservative treatment include debridement, frequent dressing changes, and irrigation of deep areas of the ulcer.[12,15,16]
There are several limitations to our study. First, follow-up nerve conduction studies after 6 months do not exist. Those data provide a better idea of the treatment method and the expected duration of treatment. Second, EMG is helpful to distinguish between sciatic neuropathy and peroneal mononeuropathy, but we could not perform needle EMG because of the high risk of infection. And third, further studies and long-term data are needed to confirm our finding due to small sample size.
Because pressure ulcers most commonly occur in patients with paraplegia or quadriplegia, physicians are generally less interested in sensory and motor disorders in the lower extremity caused by pressure ulcers. However, as this case reveals, the possibility of sciatic neuropathy occurring due to a pressure ulcer should be considered when treating pressure ulcer patients who do not have paraplegia or quadriplegia. Sciatic neuropathy should be prevented by aggressive pressure ulcer treatment and, if neurological symptoms occur, an accurate diagnosis of sciatic neuropathy should be made based on a physical examination, nerve conduction studies, and imaging studies to provide the appropriate treatment.
Conceptualization: Jae Ha Hwang.
Data curation: Dong Wan Kim.
Formal analysis: Dong Wan Kim.
Resources: Jae Ha Hwang.
Supervision: Kwang Seog Kim, Sam Yong Lee.
Writing – original draft: Jae Ha Hwang.
Writing – review & editing: Jae Ha Hwang.
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. Liu LQ, Moody J, Traynor M, et al. A systematic review of electrical stimulation for pressure ulcer prevention and treatment in people with spinal cord injuries. J Spinal Cord Med 2014;37:703–18.
. Khaykin E, Ford DE, Pronovost PJ, et al. National estimates of adverse events during nonpsychiatric hospitalizations for persons with schizophrenia. Gen Hosp Psychiatry 2010;32:419–25.
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Keywords:Copyright © 2018 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.
pressure sore; sciatic nerve; sciatic neuropathy