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Case Reports |
RK Shields, PT, PhD, is Associate Professor, Graduate Program in Physical Therapy and Physical Rehabilitation Science, Roy J and Lucille A Carver College of Medicine, The University of Iowa, 1-252 MEB, Iowa City, IA, 52242 (USA) (richard-shields{at}uiowa.edu).
S Dudley-Javoroski, PT, is Research Assistant, Graduate Program in Physical Therapy and Physical Rehabilitation Science, The University of Iowa, and Physical Therapist, University of Iowa Hospitals and Clinics, Iowa City, Iowa
Address all correspondence to Dr Shields
Submitted August 15, 2002;
Accepted October 10, 2002
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Key Words: Decubitus ulcers Hemicorporectomy Secondary complications Spinal cord injury
| Introduction |
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Hemicorporectomy was first proposed by Kredel in 1951 after he demonstrated its feasibility in a cadaver study.4 Kennedy and colleagues7 attempted the first HCP in 1960, but the patient died on the 11th postoperative day due to pulmonary edema. During blood transfusions, this individual received fluid volumes that were standard for an individual with normal body mass and blood volume, leading to a fluid load appropriate for a person twice his weight.2 The first successful HCP was performed in 1961 on a man with spina bifida and with squamous cell carcinoma in a sacral decubitus ulcer. This patient underwent rehabilitation, was employed, and survived until 1980 when he apparently became overhydrated while being resuscitated for heat stroke.2
Since its introduction as a viable surgical technique, at least 44 cases of HCP have been reported in the medical literature, although speculation exists that many more cases remain unreported.8 Narrow criteria exist for determining appropriate candidates for an HCP, such as: (1) an expected normal life span after removal of the diseased structures, (2) sufficient emotional and psychological maturity to cope with the physical and functional aspects of a translumbar amputation, and (3) sufficient determination and physical strength to undergo the intensive rehabilitation required to attain at least 95% of independence in activities of daily living.3 As Weaver and Flynn1 stated, only patients with a "fierce determination to survive" should be considered for an HCP.
Due to the rarity of this procedure, few physical therapists will encounter a client with a spinal cord injury who has undergone an HCP. Those who do, however, must understand the issues associated with the long-term management of a client with an HCP. Few articles are available that describe the chronology of the long-term rehabilitation of a client with an HCP. Four articles5,911 from 1969 to 1972 described early prosthetic innovations and attempts at ambulation and driving after an HCP. One of these articles10 focused on an upper-extremity strengthening program over 36 months following an HCP. A report published in 199212 described the 3-year history after an HCP as a result of tumor resection and not secondary problems from spinal cord injury. The reported client had limited wheelchair experience (1
years) and had intractable pain prior to the HCP. Thus, the rehabilitation emphasis was not similar to that for someone with a complete spinal cord injury. One report13 presented a case of HCP as a result of spinal cord injury and pressure ulcers; however, the report began immediately before the HCP and followed the patient for just 1 month after the procedure. No previous report provides a long-term longitudinal chronology of the events preceding and following an HCP necessitated by pressure ulcers in an individual with spinal cord injury.
The purposes of this case report are: (1) to describe the 25-year history (12+ years before HCP and 12+ years after HCP) of an individual with spinal cord injury and decubitus ulcers that ultimately led to an HCP, (2) to present factors that may have contributed to the individual's documented musculoskeletal deterioration, and (3) to present the rehabilitation and prosthetic interventions as documented following the HCP. Although it is beyond the scope of this case report to provide a comprehensive review of wound care management or spinal cord injury rehabilitation philosophies, we anticipate that practitioners will find this patient's chronology of events instructive and perhaps an educational resource for future clients about the potential implications of pressure ulcers after spinal cord injury.
| Case Description |
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thoraco-lumbar-sacral orthosis was fabricated for him, and he was discharged to a rehabilitation facility 1 month later. His rehabilitation progress was limited by the restrictive orthosis, which he was required to wear for 6 months. After 1 month of rehabilitation, he tolerated only 1 hour of sitting, twice a day, and he had developed phlebitis in the lower extremities; this limited his participation in physical therapy to supine upper-extremity exercise with hand-held weights. Following the resolution of the phlebitis, Mr P learned wheelchair mobility and transfer skills. No other information was documented about Mr P's rehabilitation program at that time.
History of Decubitus Ulcers and Potential Contributing Factors
The patient's first decubitus ulcers were documented 9 weeks after his spinal cord injury. He developed lesions over both anterior superior iliac spines (ASISs) and over the buttocks, presumably due to pressure from the Plastazote orthosis. Mr P was discharged from the rehabilitation center and moved to a nursing facility until he could continue rehabilitation without the orthosis. His wounds were treated with heat lamps and GelFoam powder
. He was instructed to perform wheelchair push-ups every 10 minutes while sitting. Mr P was independent in wheelchair transfers and propulsion at that time, but he required assistance for dressing. He began to independently self-catheterize 4 months after his injury. Mr P was readmitted to the original major tertiary care facility 2 months later for care of his decubitus ulcers. Intervention at that time consisted of 0.25% acetic acid soaks. He received a referral for physical therapy for strengthening and for ambulation with long leg braces. Mr P's wounds stabilized sufficiently to allow him to be discharged, but he was again admitted 9 months after his injury for care of his ulcers and for a urinary tract infection. Again his wounds were treated with acetic acid soaks. Mr P developed bladder stones and underwent transurethral cystolithotripsy 2 years after injury. At that point, the left ASIS lesion was 3 cm in diameter and the buttock and right ASIS wounds had closed.
During the early years of his spinal cord injury, Mr P developed spinal deformity. His posture was so lordotic that he bore weight on his pubic ramus, and his anterior superior iliac spines (ASISs) opposed his femurs in the seated position. Mr P's seating system did not correct this position, as it consisted of a standard wheelchair, sling seat and backrest, and standard foam cushion. Three years after injury he had a 23-degree lumbar lordosis and a compensatory right upper thoracic kyphoscoliosis.
Mr P was treated for a large suprapubic abscess that extended into the urethra 2
years after injury. Surgeons removed a necrotic left testis and placed a suprapubic catheter. However, the left ASIS wound continued to worsen, and he was admitted for left hip septic arthritis 5 months later. He underwent excision of a sinus tract from the wound and excision of the head and neck of the left femur at that time. Physical therapy during this admission was limited by the surgeon's orders for supine activities, which included range of motion to address 10-degree plantar-flexion contractures, range of motion to increase knee flexion beyond 100 degrees, and upper-extremity strengthening (bench press and weighted pulleys). When he was again allowed to sit in his wheelchair, he continued to sit with markedly increased lumbar lordosis. During physical therapy sessions, his therapist temporarily placed a transfer board behind his back and secured Mr P to the board with the seatbelt on his wheelchair, which corrected the hyperlordosis. His physical therapist later used a sacral insert and a custom-made lumbar support pillow to attenuate the hyperlordotic posture. However, these interventions appeared to have been only temporarily successful because future therapists continued to note Mr P's hyperlordotic seated posture in subsequent treatment sessions. At that time (1978), no adjustable seat and backrest systems were commercially available for active individuals with spinal cord injury.
During this stage in his life (late 1970s and early 1980s), Mr P lived alone and was employed part-time in clerical positions. He matriculated as an undergraduate at a university, but his chronic decubitus wounds were a major obstacle in his educational process. His social worker noted that Mr P missed numerous days of class when he became ill and that these illnesses caused "tremendous fluctuation in [Mr P's] emotional response level and ability to concentrate and goal set." Despite these challenges, Mr P earned a bachelor's degree in the mid-1980s.
Despite interventions by physical therapists and repeated hospitalizations for care of his ulcers, Mr P's condition continued to deteriorate. Factors that may have impeded his progress were reports of tobacco abuse, poor nutritional status, and chronic poor adherence to wound care and pressure relief recommendations. A nurse's notation a year after Mr P's injury reported that he did not follow recommendations to avoid lying supine on his wounds, even after repeated requests. A physician noted that in the early years following his spinal cord injury, Mr P's attitude toward decubitus ulcers was "you're always going to have a few." Such statements reflect the fact that Mr P most likely was never without pressure ulcers from 9 weeks after his spinal cord injury and probably believed that pressure ulcers were a standard part of having a spinal cord injury.
Although statements such as these in Mr P's medical record suggest that his health care providers attributed his wounds to nonadherence, his first wounds appeared within 2 months of his injury, at a time when he adhered to recommendations to wear a Plastazote shell. Other factors may have contributed to the chronic nature of his decubitus ulcers. For example, the standard treatment for his wounds during the 1970s (both during hospitalizations and during home care) was acetic acid soaks, a technique that is generally no longer used due to its deleterious effect on granulation tissue.15 Similarly, Mr P's standing program, because of his hip flexion contractures, may have contributed to his later postural problems. While wearing long leg braces, Mr P stood in parallel bars and was asked to repetitively lean back as far as possible in order to stretch his contracted hip flexor muscles. Because his Harrington rods extended only to L1 and not to the pelvis, it seems plausible that the lower lumbar spine became hypermobile during forceful attempts at hip extension. The marked lumbar lordosis during wheelchair sitting caused the pubic ramus to become the primary site for loading on the pelvis, which likely contributed to the necrotic testis and suprapubic abscess that eventually opened into the urethra. Excessive stretch of the anterior spinal ligaments may have eliminated Mr P's passive anatomical restraint against excessive lordosis, which in the absence of functioning abdominal muscles, may have contributed to his exaggerated lordotic seating posture.
Because of Mr P's chronic decubitus ulcers and poor seated posture, physical therapists tried several pressure-relief devices in Mr P's wheelchair. Mr P used a "bucket seat" and a succession of 3 Roho cushions
and one Stryker pad|| in 4 years prior to 1981 (6 years after injury), with no improvement in his wounds. The bucket seat was made of high-density foam and was contoured from a cast taken from the patient's buttocks. It appeared that Mr P only sporadically used these pressure-relief seating surfaces, which may have contributed to the chronic nature of his wounds. One entry in the medical record noted that Mr P did not use a cushion in his car, yet he drove for several hours almost daily to and from social engagements and to and from his job as a convenience store clerk. Nurses and therapists reported that he did not perform wheelchair push-ups for pressure relief on a routine basis.
In 1981, a physical therapist attempted to fit Mr P for another contoured foam seating system, but continued progression of his wounds and repeated hospitalizations prevented completion of this system. A punch graft was attempted for the left buttock wound, but this intervention failed due to infection of the graft. During a hospitalization for care of his ulcers 7 years after his injury, one of the authors (RKS) met Mr P and evaluated the chronology of his seating and pressure ulcer problems. It was noted that Mr P's seated posture was unusual and his hyperlordosis was opposite the more typical kyphoscoliosis usually seen for individuals with chronic spinal cord injury. Problems included lumbar hyperlordosis, pelvic obliquity, right thoracic C-curve scoliosis, and decreased ankle dorsiflexion. His wheelchair armrests were too low, the sling seat offered an inadequate base of support for the Roho cushion, he sat with increased thigh-trunk angle, and his backrest was too low. The patient began rectus femoris muscle and Achilles tendon stretching while hospitalized. The physical therapist adjusted the backrest, replaced the sling seat with a solid plywood insert, raised the footrests, added a lumbar support, provided an ischial pad to compensate for the pelvic obliquity, and provided the patient with an abdominal binder to improve thoracic column rigidity and stability and to support his abdominal contents. The therapist inserted a 5.08-cm to 0-cm (2-in to 0-in) foam wedge (with the thicker portion placed anteriorly) under the Roho cushion to decrease the thigh-trunk angle to 95 degrees, as suggested by Zacharkow.16 In principle, the wedge was inserted to decrease the client's forward shear in the wheelchair and so that the client could maximally use the backrest.16 The patient reported an improved posture and noted increased comfort with these wheelchair modifications; however, none of the modifications were sufficient to allow complete healing of his extensive wounds.
Mr P underwent a left ischiectomy (partial resection of the ischial tuberosity) for continued osteomyelitis in 1982. He received physical therapy interventions, including range of motion exercises to correct plantar-flexion contractures and to increase knee flexion, as well as upper-extremity strengthening with pulleys and hand-held weights. At the time of discharge following this surgery, the patient's wounds were beginning to slowly close for the first time. A prosthetist was consulted to construct a cushion integrating the above-mentioned modifications (ischial pad and underlying wedge) into a permanent seating system. Mr P alternated between this custom-made cushion and a Roho cushion with underlying foam wedge because it was unclear which system offered the best pressure relief. He did not require hospitalization again for 2 years, when his suprapubic catheter site was found to be continuous (via a fistula) with his extensive decubitus ulcers, which necessitated placement of an ileal conduit.
Although Mr P lived independently and had developed exceptional upper-extremity force-generating capacity due to upper-extremity compensation for paraplegia, his endurance for functional tasks began to decline by 1984 (9 years after injury). He was constantly febrile due to chronic infections of his extensive decubitus ulcers. He felt ill most of the time due to the infection, and he gradually became unable to propel his manual wheelchair independently. Mr P lived by himself throughout the late 1980s and received care from visiting nurses for his wounds. He began to use an electric wheelchair 10 years after injury so that he could be independently mobile as a student on a college campus. He was referred for physical therapy the following year for endurance training, and he was instructed in a program of biceps muscle curls, triceps muscle extensions, lateral raises, pectoral muscle pulls, and latissimus dorsi muscle pull-downs. He also received instruction in an arm ergometer progression for endurance training. The patient performed these activities outside of the clinic, but he chose not to return to his manual wheelchair. In 1987 (12 years after injury), he underwent a right proximal femur excision due to continued osteomyelitis. At that time, his thoracic scoliosis had progressed to over 40 degrees.
Post-hemicorporectomy History: Prosthetic and Rehabilitation Interventions
Mr P was admitted for sepsis in August 1987 and then was readmitted in September after an episode of purulent discharge from his previously healed suprapubic catheter site. Two months later, he was diagnosed with a large suprapenile cavity with no definite tract site. A computed tomography scan also showed a parasacral abscess with destruction of portions of the L5 body and evidence of extension into the vertebral canal, as well as osteomyelitis of the right iliac wing with formation of abscesses over the external surface of the wing. It became clear that Mr P's condition was life-threatening, requiring removal of the infected body segments. He had no other systemic condition (such as metastatic tumors) that would reduce his survivability after an HCP; therefore, Mr P was offered an HCP as a life-saving measure. According to the social worker's notes, Mr P had an appropriately strong emotional reaction to this option, but decided he would rather try to extend his life expectancy by this surgical procedure than to face continued dressing changes and progressive illness from infection.
Although Mr P had interacted with social workers and clinical psychologists at various times after his spinal cord injury, this interaction intensified as he tried to prepare emotionally for his HCP. In the past, social workers documented that Mr P faced physical and emotional isolation because of his extensive wounds. He was diagnosed with depression and resisted hospitalization because, in the words of his social worker, "he had been here [hospitalized] so much and so often that...[hospitalization] was beginning to resemble more of an incarceration than a hospitalization." As Mr P faced the decision to undergo an HCP, it appeared that he had good family support (from siblings, in particular) that enabled him to prepare for the changes the surgery would produce.
In preparation for the HCP, Mr P underwent a cystectomy, revision of his ileal conduit, a colostomy, and left leg amputation in January 1988. Two weeks later, he underwent an HCP at the level of the L45 disk space. The amputated specimen included the body of L5, spinous process of L5, portions of the L45 facet joint, the right iliac wing and remaining bony pelvis, and the right leg. The distal ends of the psoas major and minor muscles and the adjacent soft tissues were brought medially over the exposed body of L4 and thecal sac to allow some degree of cushioning over the stump and body of L4. Skin flaps preserved from the posterior thighs were brought forward to close the HCP wound (Fig. 1). Due to the patient's history of delayed healing and history of pressure sore problems, physical therapists urged that he not be allowed to sit for 6 weeks, until his prosthesis could be fabricated and his skin flaps could adequately heal.
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After sufficient healing of his HCP wound (about 6 weeks), Mr P began wearing the prosthesis for 1 hour at a time, as recommended by his prosthetist. He gradually increased wearing time according to his tolerance, based on his comfort and on the ability of his skin to resist redness and breakdown. He donned a custom-fitted stockinette while lying supine in bed and then fitted his torso and abdomen into the prosthesis. He then rose to a sitting position and transferred over into his wheelchair. Because of his long history of paraplegia, Mr P had developed exceptional upper-extremity force-production capacity and coordination, although these improvements were typically undermined by his constant fever and illness due to his massive infection. Removal of the diseased lower extremities eliminated the source of his chronic illness, which facilitated rapid return of his upper-extremity force-production capacity. Loss of roughly one half of his body weight also made independent transfers easier. Mr P required minimal guidance and instruction from physical therapists to master mobility skills, and he did not want to participate in any formal strengthening program. (For a detailed description of a physical therapy program after HCP, consult the article by Porter-Romatowski and Deckert13). Just 2 weeks after being released from bed rest (approximately 8 weeks total after surgery), Mr P was able to independently don and doff his prosthesis, come to a sitting position, independently transfer to his wheelchair, and transfer from the wheelchair to the floor and back. Mr P was advised not to hand walk given his previous history of pressure ulcers.
With the resolution of his chronic infection and subsequent resolution of his constant febrile state, Mr P's endurance improved, and he was able to switch from his power wheelchair to a manual wheelchair by the time he was discharged from the hospital, 109 days after the HCP. He propelled his manual wheelchair independently and was able to perform a wheelchair push-up to rotate the base of his prosthesis when he wanted to turn to either side (Fig. 2). His sitting time during this period was limited to 1-hour intervals with frequent checks of skin for the next several weeks. Eventually, Mr P's sitting time was extended to 6 hours a day.
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The major difficulty Mr P encountered while using his prosthesis (particularly between 5 and 6 years after the HCP) was recurrent prolapse of his colostomy. As his diaphragm migrated caudally during inspiration, the rigid prosthesis restricted abdominal wall expansion and created increased intra-abdominal pressure, forcing the stoma to prolapse through the aperture in the prosthesis. Mr P attempted to open a woodworking venture during this time, but found that he could not lift uncut lumber into place on his table saw because the increased abdominal pressure required for lifting caused problems with prolapse of his colostomy.
To reduce external pressure on Mr P's abdomen, prosthetists tried several innovative strategies, including using heat to deform and expand the prosthesis material distal to the stoma aperture, increasing the size of the stoma aperture, and increasing the volume of the abdominal section of the prosthesis. These measures were insufficient to prevent continued prolapse. The next strategy was to entirely cut away the abdominal portion of the prosthesis, then to cover this site with a 0.3-cm (
-in) silicone gel sheet as a retainer for abdominal tissue. Ports were then cut into the gel to accommodate the ileostomy and colostomy. It soon became apparent that this approach caused Mr P to migrate downward into his prosthesis. A foam pad placed around two thirds of the internal circumference of the thoracic portion of the prosthesis (capturing the costal margins) prevented migration, but caused areas of increased pressure about the patient's scoliotic curve. This strategy did not satisfactorily prevent prolapse of Mr P's colostomy site. The final and most successful approach to this problem was to attach "trapdoors" above the colostomy aperture, which could be swung into place and affixed with Velcro straps.# The trapdoor was an approximately 5- x 7.6-cm (3- x 2-in) piece of oval plastic, which prosthetists riveted to the prosthesis next to the colostomy aperture. Mr P attached a colostomy bag to his skin with adhesive strips, leaving the bag outside the prosthesis. He then swung the trapdoor downward over the opening, thus partially occluding the aperture for the colostomy. This external pressure restricted protrusion of Mr P's large intestine and prevented continued prolapse of the colostomy site. When Mr P developed a prolapsed ureter 11 years after the HCP, the "trapdoor" strategy was again successful for preventing progression of this problem.
Despite routine adjustments to the fit of his prosthesis, Mr P continued to have difficulty with breakdown over his lower lumbar vertebrae. Figure 4 shows the large bony prominence over his L4 spinous process, the area most troublesome for him. In retrospect, it may have been prudent for the spinous process and lamina of L4 to have been removed during the HCP procedure, as was suggested in an article published 2 years after Mr P's HCP.3
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years after his HCP. Two more admissions followed for these same ulcers, eventually requiring a flap closure 4
years after his HCP. For 4 years he had no further admissions for care of ulcers. However, during this time, he had 3 revisions of his colostomy and several extracorporeal shock-wave lithotripsy treatments for renal stones. In 1996, the patient again began to have difficulty with breakdown over his lower lumbar area. He developed a staph infection in a stage IV ulcer (full-thickness destruction of dermal and subcutaneous tissues, with exposure of underlying muscle and bone) over the L4 spinous process. He developed endocarditis, necessitating hospitalization. After returning home, visiting nurses began to discover bone fragments during dressing changes to his lumbar wound, and radiographs confirmed that the L4 body had been destroyed by osteomyelitis. The L3 vertebral body also was badly affected by osteomyelitis. In 1997, 9 years after the HCP, the patient underwent a partial L3 vertebrectomy, shortening of the vertebral stump, debridement of chronic ulcers, a duroplasty, and skin flap reconstruction. He was referred for physical therapy for upper-extremity strengthening during this hospital stay, but he declined to participate in therapeutic activities. He remained on bed rest for 6 weeks, and new bucket prosthesis was fabricated for his return home.
Mr P successfully maintained his skin integrity after this procedure and required no further hospitalizations for the remaining 2
years of his life. He married, enrolled in law school, and routinely served as a guest lecturer at the University of Iowa Graduate Program in Physical Therapy during the late 1990s. He was involved in disabled rights activism through several local agencies and was active in local politics. He worked part-time as a cashier while in school, and he enjoyed photography and writing in his leisure time. He switched from law school to the social services curricula, and while working on a master's degree in social work, he died suddenly on January 31, 2000. Paramedics found Mr P unresponsive in his wheelchair outside his home, and he did not respond to resuscitation attempts at the emergency treatment center. An autopsy revealed that the immediate cause of death was a subarachnoid hemorrhage, but the precipitating cause of this event could not be conclusively determined.
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Staring at the night I see the slate is not as blank as I thought. Before the night my old mental self stands face to face with my new physical self. The physical was no longer the death I feared but a future I embrace. I moved my hand downward from my chest across my belly button and my abdomen to my back, never lifting my hand. Stunned, I raised the sheets from my body and my head from the pillow. I cannot see the end of my body. My arm reaches out at an expanse of whitemy mind is blank. There are no words to describe the loss. I drop the covers and my head in tears. My physical self is no longer the problem ...
Without a doubt, Mr P faced an enormous adjustment in perception of body image after his HCP. The question of psychological adjustment to HCP and the ethical issues surrounding the procedure concerned the surgeons who pioneered this technique.7,19 After the procedure became technically feasible, questions persisted regarding whether the procedure was humane and appropriate,7 partly because no data existed regarding quality of life after HCP. In subsequent years, success or failure of HCP has typically been quantified by how long patients survive after HCP. In the case of Mr P, hospital records not only document length of survival, but also indicate of the impact of HCP on Mr P's health.
An analysis of Mr P's number of days hospitalized demonstrates that despite his chronic troubles with decubitus ulcers even after his HCP, this procedure had a positive impact on his overall health and function. Hemicorporectomy reduced the time he spent hospitalized (Fig. 5). He spent 820 days hospitalized in the 2,740 days (about 12 years) between his spinal cord injury and his HCP, which constitutes 29.9% of the time before his HCP. Even when subtracting his acute care hospital and rehabilitation stays to compensate for reduced acute and subacute care hospital stays during the past decade, he was hospitalized 749 days for complications of his spinal cord injury, or 27.3% of the time before his HCP. Even when not hospitalized, Mr P was chronically febrile and generally ill due to his infection. In the roughly 12 years between his HCP and his death (2,555 days), he was hospitalized only 299 days, which constitutes 11.6% of the time after his HCP. He spent 109 days hospitalized for the HCP procedure, leaving only 190 days (7.4%) during which he was hospitalized for complications after his HCP. A conservative estimate of the costs associated with this case is in excess of $1 million, based on the billing records of Mr P's primary care hospital. The psychological stress, human suffering, and lost quality of life are difficult to quantify, but should not be underestimated.
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Although Mr P's caregivers used standard practice guidelines of the time, modern wound care products and knowledge may have limited the scope of his wounds or even allowed healing, if they had been available in the early years of his spinal cord injury. Applying current knowledge of the deleterious effect of acetic acid soaks, for example, may have steered Mr P's health care providers toward other treatment alternatives,15 such as the use of hydrogels, hydrocolloids, alginates, semipermeable film dressings, wound vacuum pumps, and enzymatic debridement agents. Mr P also may have benefited from the services of multidisciplinary wound care teams that are becoming common in tertiary medical facilities today. These teams typically provide enhanced follow-up for patients with wounds, as well as expert care and management of wounds.
Physical therapists applying current knowledge also may have had opportunities to alter the course of Mr P's musculoskeletal deterioration. Although Mr P's record indicates that therapists attempted to address his hip flexion contractures on numerous occasions, his excessive lumbar hyperlordosis may not have occurred if hyperlordosis had been avoided during his early standing program. Methods such as prone positioning may have offered an appropriate degree of stretch with less risk of excessive movement at the lumbar spine. It appears that other interventions by physical therapists, in particular his wheelchair cushions and postural aids, would have been more successful if the client had adhered more fully to using these devices. Prosthetists appeared to have the most success in dealing with their component of Mr P's care; the innovations they devised to prevent ostomy prolapse were highly effective, as were the modifications that allowed control over sagittal- and frontal-plane tilt.
Based on this patient's medical records and available billing records, hospital and physician charges for Mr P's care were over $1 million over a 25-year period. This does not include the cost of prostheses, visiting nurses, wheelchairs, 2 decades of wound care supplies, or care at other medical facilities. The expense of a sound rehabilitation management plan, which in the acute phase appears costly, is minimal compared with the spiraling costs associated with the musculoskeletal deterioration discussed in this case report.
We highlight the importance of preventing early secondary complications after spinal cord injury. As rehabilitation specialists, we must educate clients about the role that pressure ulcers play in the development of further disability, and we must do everything possible to arrest the development of secondary complications in individuals with spinal cord injury.
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| Footnotes |
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This report was supported, in part, by National Institutes of Health grant R01HD39445.
* Merck & Co Inc, West Point, PA 19486. ![]()
Bakelite Xylonite Ltd, London, England, distributed by Alimed Inc, 297 High St, Dedham, MA 02026. ![]()
Pharmacia & Upjohn, 7000 Portage Rd, Kalamazoo, MI 49001. ![]()
The Roho Group Inc, 100 N Florida Ave, Belleville, IL 62221. ![]()
|| Stryker Medical, 6300 S Sprinkle Rd, Kalamazoo, MI 49001. ![]()
# Velcro USA Inc, 406 Brown Ave, Manchester, NH 03103. ![]()
| References |
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R. K. Shields, S. Dudley-Javoroski, and A. E. Littmann Postfatigue potentiation of the paralyzed soleus muscle: evidence for adaptation with long-term electrical stimulation training J Appl Physiol, August 1, 2006; 101(2): 556 - 565. [Abstract] [Full Text] [PDF] |
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R. K. Shields and S. Dudley-Javoroski Musculoskeletal Plasticity After Acute Spinal Cord Injury: Effects of Long-Term Neuromuscular Electrical Stimulation Training J Neurophysiol, April 1, 2006; 95(4): 2380 - 2390. [Abstract] [Full Text] [PDF] |
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