The purpose of this study was to evaluate the incidence of neuropathy in a consecutive cohort of patients with major burn injuries and investigate the clinical correlates for both mononeuropathy and generalized peripheral polyneuropathy. Of 572 patients examined, 64 (11%) patients had clinical evidence of mononeuropathy or peripheral neuropathy or both. Associations of mononeuropathy and peripheral neuropathy with potential risk factors were identified using logistic regression analyses. Electrical cause (odds ratio [OR] = 4.1022, P < .01), history of alcohol abuse (OR = 2.2893, P <.05), and number of days in intensive care (OR = 1.0457, P < .001) were significantly associated with mononeuropathy. The number of days in intensive care (OR = 1.0740, P < .001) and patient age (OR = 1.0543, P < .01) were significantly associated with peripheral neuropathy. This study demonstrates that neuropathy is a common complication of severe burn injury in patients who are older, critically ill, have an electrical cause, or history of alcohol abuse.
Peripheral neuropathy is a well-known disabling complication after major burn injury. The incidence varies based on the methodology of each individual study. When patients with neurologic symptoms are evaluated, more than 50% have electrodiagnostic findings of neuropathy. When the determination of neuropathy is made by retrospective chart review, the incidence is 2%. Exact quantification of true incidence of neuropathy is difficult because it requires electrodiagnostic testing, which is time consuming, expensive, and may be uncomfortable for the patient. Determining the underlying cause is also difficult because of the complex metabolic nature of burn injury, the high incidence of sepsis and subsequent use of neurotoxic antibiotics, and the numerous iatrogenic causes of neuropathy. Previous studies have shown that the presence of neuropathy correlates with percent burn, percent full-thickness burn, and other measures of severe illness.
The incidence of neuropathy after burn injury was first well described by Henderson et al in 1971. 1 In that study electrodiagnostic testing was performed on 249 hospitalized burn patients. Forty-four patients had conduction slowing in two or more nerves. Follow-up testing showed persistent abnormalities in 36 cases for an incidence of 15%. Burn size ranged from 14 to 85% with 10 to 77% full-thickness skin loss. Mean age was 41 years. All 36 patients with persistent neuropathic changes had laboratory evidence of metabolic imbalance, including elevated blood glucose, renal failure, or hepatic dysfunction. No single medication was common to all cases, although all received antibiotics with potentially neurotoxic side effects.
In 1977 Helm et al 2 found neuropathy in 24 of 66 patients with weakness (incidence of 37%). When five patients with a history of alcoholism were eliminated, the incidence was 29%. Twenty-one of the 24 patients with neuropathy had a TBSA > 20%. An additional 28 patients had spontaneous activity on electromyogram (EMG), with 22 having myopathic potentials in the proximal muscles. This finding was attributed to injections but may actually have been caused by critical illness myopathy. In 1985 Helm et al 3 evaluated 88 burn patients referred for electrodiagnostic testing. Of these, 74 patients had diagnosable neuromuscular problems, with 46 (52%) having peripheral polyneuropathy. Nineteen had “deltoid injury,” and the remainder had mononeuropathies.
Carver and Logan in 1989 4 described a single case of severe sensorimotor neuropathy after burn injury in a patient with renal failure. This description is consistent with a case of severe critical illness neuropathy. The mononeuropathy multiplex pattern was described by Dagum et al in 1993. 5 In a retrospective chart review 9 of 121 burn patients were found to have severe peripheral neuropathy. Burn size ranged from 40 to 75% with 20 to 60% full thickness. All had a prolonged hospital course with a mean length of stay of 112 days (range, 44–182). The number of nerves involved ranged from 3 to 7 (mean, 4.9). Seven patients had prolonged sepsis. Multisystem organ failure was seen in nine. Six patients had uremia with associated sepsis. All patients had burns over the involved nerves.
In 1993 Marquez et al 6 performed a retrospective review of 800 burn patients and found neuropathy in 19, for an incidence of 2%. Sixty-nine percent had a TBSA > 20% with a range of 10 to 75%. The mean full-thickness burn was 28%. Of the 19 patients identified, 69% had the mononeuropathy multiplex pattern. Eleven patients had sepsis and 5 had renal failure. The length of hospitalization (range, 25–150 days; mean, 71) and the severity of burns correlated with the number of nerves involved. In 1995 Margherita et al 7 found neuropathic changes with electrodiagnostic testing in 7 of 17 (41%) consecutive patients with major burns. Twenty-seven percent (3/11) had persistent changes at 6 weeks.
A review of the literature demonstrates the broad range of findings seen when evaluating burn patients for neuropathy. The incidence is as low as 2% or as high as 84% depending on inclusion criteria of the study. The purpose of this study was to evaluate the incidence of neuropathy in a large prospective database and to investigate the clinical correlates for both mononeuropathy and generalized peripheral polyneuropathy.
From the University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Reprint Requests: K. Kowalske, MD, Department of Physical Medicine and Rehabilitation, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9055.
Supported by grant #H133A970023 from The National Institute on Disability and Rehabilitation Research, Department of Education, Washington, D.C.
Presented at the meeting of the American Burn Association, Las Vegas, Nevada, March 14 to 17, 2000.