Sacral Decubitus After Cervical Spine Injury: A Case Report and Suggestions for Avoiding Such Wounds

Sacral decubitus ulcers after cervical spine injuries are particularly debilitating wounds. An illustrative case is presented here and strategies are proposed that may help reduce the incidence of this type of wound. These include early involvement in the patient’s care by a wound prevention specialist and the incorporation of a cholera cot design into the spinal transport board with a hole to completely offload the sacral tissue and permit the drainage of stool. Because intermittent visual inspection of skin is probably inadequate to detect the first sign of impending complications, there is a need for technology to objectively assess the status of skin’s integrity so a computer program could automatically adjust the pressure on the patient’s skin and alert the doctor. Sophisticated equipment that measures mattress pressure on skin is now widely available; sensors of this type could be situated on top of a quilt of miniature air bags (ie, smart cubes) so that individual computer-controlled areas of the quilt could be deflated to offload pressure as required. In the future, probes capable of measuring CO2 production, electrical resistance, or even polarization spectroscopy might be interspersed among the cubes so that ongoing skin viability and integrity could also be monitored. Finally, if the middle model, which proposes that pressure damage starts deep in the middle of the tissue overlying the sacrum before spreading to the skin, proves to be correct and the ground zero for some decubitus really is in the sacral fat, then even more advanced monitoring will be required such as implantable biosensors, and treatment plans might require hyperbaric oxygen or even preemptive liposuction of necrotic fat.

  The development of a sacral decubitus ulcer following a cervical spine injury is an especially pernicious wound because of its intractable nature and the frequency with which it leads to complications such as osteomyelitis and sepsis. This type of wound truly provides, in Lady Macbeth’s words, an “access and passage to remorse,” and tragically still occurs in 30% to 50% of patients with cervical spine injuries.¹

  In order to reduce the incidence of this type of wound, wound care specialists need to communicate a sense of urgency to neurosurgical and critical care colleagues to ensure a wound prevention consult be obtained as soon as the patient arrives in the emergency room. While life- saving measures are appropriately focused on the front of the patient, damage to that critical small triangle of tissue over the sacrum has long-term consequences. Its close proximity to the anus means that when a decubitus ulcer does develop, dressing changes are both embarrassing for the patient and depressingly malodorous. Additionally, the wound is easily infected and reinfected. Hence, it cannot be overemphasized that the patient’s first week in the intensive care unit must be a time of hypervigilance for risk of pressure ulcer development.²

  Salcido et al³ points out that there is still a need to determine the relative contribution of duration of pressure, magnitude of pressure, and tissue perfusion to the development of pressure ulcers. Some authorities maintain that sacral decubitus ulcers may be started by ischemic reperfusion events at pressures as low as 45 mm Hg⁴ and by immobilization for 6 hours.⁵ Even the perception that pressures below 32 mm Hg are safe has been questioned, and when neo-synephrine is used to combat shock it also adversely impacts skin perfusion.² Whether the anatomy of the pelvis and its inclination angle, the weight of the patient, or the thickness of the sacral skin are factors is not known. There is no consensus on what the most important risk factors are for pressure ulcers in critically ill patients, and thus, no risk assessment scale exclusively for this patient population.²

   Moreover, since the majority of critical care physicians reported poor knowledge concerning pressure ulcer prevention,⁶ the causative ischemic injury can occur early, either on the unyielding surfaces in the emergency room or x-ray department,7 on the operating table, or even prior to the patient’s arrival at the facility, while they are trapped in a car or being transported while strapped to a spinal board.

  The sacral tissue damage will not be immediately apparent and more effective technology to objectively assess the status of the sacral skin and underlying tissue is needed; it is the author’s experience that the human eye alone is probably inadequate to detect subtle early warning signs of skin damage while therapeutic intervention is still possible, particularly when the skin is pigmented. This has important medico-legal consequences, as the time when the damage manifests itself is considerably later than the time of the precipitating pressure trauma and the personnel discovering the decubitus often get blamed for its occurrence.

  To further complicate the picture, the middle model proposes that pressure damage starts in the middle of the tissue overlying the sacrum,⁴ then the effects of this damage spread both to the deeper and more superficial tissues including the skin. This would certainly explain the initial presentation of some sacral decubitus lesions as large cavities bordered by what appears to be preexisting necrotic fat. In turn, this means surveillance of the fatty tissue between the skin and the sacral bone is extremely important, which calls for new technology.

  A 40-year-old white male who was involved in a motor vehicle accident in December 2010 sustained a C6-C7 fracture with subluxation and paraplegia. He was transferred to a tertiary care center where he remained in neurogenic shock on vasopressor drips for 10 days; subsequently, he underwent an anterior discectomy and plating. He required a tracheostomy for prolonged respiratory failure; he then developed a tracheitis caused by Serratia marcescens and a pneumothorax, as well as a urinary tract infection with Enterococcus. Antibiotic therapy resulted in Clostridium difficile colitis and large volume diarrhea.

  Three weeks after his admission a foul odor was noted and the family requested an investigation. On turning the patient for the first time, he was found to have a large sacral decubitus full of stool. Antibotics were started to treat a series of infections of the decubitus, including Pseudomonas, Enterococcus, and methicillin resistant Staphylococcus aureus but eventually bone was exposed and the patient developed osteomyelitis of the sacrum.

  In September 2011 the patient had a consultation at Sandhills Regional Medical Center, Hamlet, NC. At the time the dimensions of the ulcer were 6 cm x 4.5 cm x 2 cm, and required debridement prior to treatment with Dakin’s solution and vancomycin for Proteus infection. A bone scan was also positive for osteomyelitis of the sacrum. Diarrhea continued to be a problem so the patient underwent a colostomy in October 2011. Following the procedure he was able to resume negative pressure therapy (V.A.C. GranuFoam, KCI, San Antonio, TX). This therapy had been initiated at the tertiary care hospital but had to be stopped because of the diarrhea problem. Hyperbaric oxygen treatment was contraindicated in this patient because of his history of bilateral pneumothorax.

   By January 2012, a 3-phase bone scan to check for possible persistent osteomyelitis was negative, but the decubitus persisted. Over the next 28 months (until March 2014), the patient required a series of different antibiotics to treat a succession of infections. Different dressings have included the empirical use of collagenase, Leptospermum honey, a collagen/oxidized regenerated cellulose dressing, a hydrophilic polyurethane membrane containing F 68 surfactant, and a textile substrate containing a controlled-release silver ion antimicrobial. The dimensions of the decubitus are currently much reduced to 1.2 cm x 1.3 cm x 1.7 cm, but nevertheless, more than 40 months after the patient’s accident, it was still present (Figure 1).

  Unfortunately, the case presented here is a familiar narrative with the sacral decubitus persisting long after the tracheostomy and the colostomy and the spinal surgery scars have healed. Since there are about 11,000 new spinal cord injuries per year,8 this amounts to a huge wound care burden, especially since about 40% of sacral decubitus wounds resulting from spinal cord injuries never heal.9

  Two different processes appear to be important in monitoring the sacral tissue. First, the pressure experienced by the skin and its effect on blood perfusion are interrelated and should be checked and adjusted every 15 minutes, taking into considerations the works of Clark,10 Thomas,7 and Wing,1 who all argue adjustments need to be made frequently. The optimal interval is not known and should be left to the discretion of the wound prevention consultant.

  Second, and far more important, is the continued health and integrity of the sacral skin and underlying tissue, which is not necessarily related to blood perfusion alone; this should be checked every 4 hours so that if a problem is detected, and additional offloading is not adequate to resolve the issue, other urgent interventions might be tried. The choice of 4 hours is based on the standard model for studying deep tissue injury, 3 hours of ischemia followed by 1 hour of reperfusion injury,11 but again, this time can be adjusted at the discretion of the wound prevention consultant.

  This calls for 2 different technological breakthroughs. First, a computer-controlled system for offloading that takes human error out of the loop. This system should be based on continuous pulse oximetry measurements that regulate the pressure exerted on the skin to ensure adequate perfusion, essentially mimicking the function of a normal nervous system where, in response to a sensation of pain or discomfort, involuntary muscle movement results in offloading; but until it is possible to objectively quantitate pain, we as clinicians will have to be satisfied with proxy measurements such as perfusion and local pressure. Second, a technique needs to be developed that will detect and document the first sign of a problem that could lead to the breakdown of the integrity of the skin and sacral tissue. This is, technically, a far more difficult problem.

   Based on these considerations, there are a number of suggestions for improving the care of sacral skin after cervical spine injury. Early involvement of a wound prevention specialist should be utilized to maintain an awareness of the importance of avoiding pressure damage and to institute early nutritional support, including total parenteral nutrition. Additionally, modification of the spinal board used to transport the patient from the scene of the accident should be made to incorporate a large hole similar to the one in a cholera cot (Figure 2).12 This would completely offload the sacral tissue and permit drainage of body waste, thus preventing the bilge effect wherein the sacral area is immersed in stool for extended periods of time. This would also avoid the need for indwelling rectal tubes (Figure 3). The modified backboard should stay on the patient like a protective carapace during the remainder of his hospitalization, especially during visits to the x-ray department and the operating room.

   From T12 downwards, the surface of the spinal board should be covered with a pressure-sensing quilt of computer-controlled smart cubes (Figures 4 and 5). The dimensions of the individual cubes should be about 6 cm x 6 cm x 6 cm, and each cube should be inflated automatically by a computer-controlled program, similar to a miniature automobile air bag. Input to the program would come from pressure receptors on the top surface of the cube at the interface with the patient’s skin in much the same way Pompeo13 described; the computer would then adjust the inflation pressure appropriately, as programmed by the wound prevention consultant, and as previously described by Larson.14 In the future, continuous measurements of pulse oximetry by sensory probes could also be incorporated in the data going to the computer. This would enable periodic pressure adjustments to ensure adequate blood perfusion, rather than an assumption that the patient’s skin was safe below a certain pressure (Figure 5). Channels between the cubes would permit fluid drainage; the effectiveness of this process could readily be monitored by a system similar to that used to detect enuresis problems.15 Every 15 minutes a wave-like ripple of reduced pressure would traverse the entire quilt as a substitute for the medico- legally fraught and controversial 2-hour turning schedule, which may also be dangerous for a patient with a cervical spine injury, and quite impossible to perform on a patient on a ventilator and in shock.

  While these are relatively straightforward concepts, it is more difficult to conceive of the innovative technology required to continuously monitor ongoing skin health. One could envisage spring-loaded sensory probes interspersed among the cubes that would intermittently contact the skin, garner information in real time, and input it to the computer (Figure 5). It remains to be determined which technology would be both technically and economically feasible. Pulse oximetry measurements should not be too difficult. Possibly the measurement of CO2 production would provide an early warning of potential problems since reduced metabolism would herald impending ischemia.16 This alert would result in a computer-controlled reduction of cube pressure in the corresponding area. As an alternative to measuring CO2 production, the measurement of changes in the electrical resistance of a given area of skin could provide a simple and relatively inexpensive method of forestalling problems in a timely fashion.17

  The gold standard technique for monitoring ongoing probems with skin viability will probably prove to be based on polarization spectroscopy.18 However, it is mere speculation at this point as to whether the appropriate miniature probes could be developed, let alone mass produced.

  An approach that holds promise for the future is the use of implantable biosensors.19 Already widely used to monitor glucose levels, these sensors could be adapted to detect adipocyte cell membrane damage by detecting the release of glycerol-3-phosphate dehydrogenase.20 A biosensor implanted in the middle area, the fat deep to the sacral skin, where some decubitus are thought to have their origins, could respond to interrogation by the computer, in the same way pacemakers respond to programming devices, and indicate the need for intervention by the wound prevention consultant. The microchip biosensor should be inserted using laparoscopic techniques from the lateral aspect of the pelvis. Hyperbaric treatment might be the only way to reverse ischemia in this middle area. If this failed, then consideration could be given to preemptive liposuction to remove dead and dying fat tissue before it caused skin breakdown. Deep to the middle area is denervated bone. A recent review of the pathogenesis of the Charcot foot21 points to another area that needs to be examined: the role of neuropeptides in the prevention and possible treatment of sacral decubitus ulcers.22 Investigation of the molecular biology of the toxic conflation of the receptor activator of nuclear factor kappa-B ligand pathway and the calcitonin gene-related peptide as it relates to the denervated sacral bone and overlying denervated tissue could be very rewarding. If it could be determined that there was indeed, a molecular biology component to the origin of the decubitus, this would pave the way for therapeutic intervention. Perhaps in the future prophylactic depot injections of critical neuropeptides could prevent the onset of what otherwise amounts to tissue corrosion in the sacral area.

  Finally, if offloading alone proved inadequate to resolve impending skin problems then use of iontophoretic technology to introduce topical vasodilators such as nitroglycerine into the troubled area and, perhaps, stimulating factors such as epidermal growth factor, transforming growth factor beta, and keratinocyte growth factor could also be introduced as needed, along with nerve-derived substance P.

  Sacral decubitus ulcers after cervical spine injuries are particularly tenacious and debilitating wounds. An illustrative case, in which the patient’s wound had not completely healed after 40 months of treatment, is presented here. Strategies to try and reduce the incidence of this type of wound include early involvement in the patient’s care by a wound prevention specialist and the incorporation of a cholera cot design into the spinal stabilization transport board, with a hole to enable complete offloading of the sacral tissue and permit the drainage of stool. This modified board should remain on the patient as a protective carapace, especially in high-risk areas such as the emergency room and in the diagnostic imaging department.

  Intermittent visual inspection of skin is probably inadequate to detect the first signs of impending trouble. There is, however, a need for technology to objectively assess the status of skin integrity. In this way, a computer program could interpret this information and automatically adjust the pressure on the patient’s skin while alerting the wound prevention specialist if the adjustment did not resolve the problem.

  Sophisticated equipment that measures mattress pressure on skin is now widely available; as a first step, sensors of this type could be situated on top of a quilt of miniature air bags, (ie, smart cubes) so that individual areas of the quilt could be deflated to offload pressure as required. If it were possible for these smart cubes to also measure pulse oximetry this would be an even more meaningful parameter to track, as computer-controlled offloading would then help ensure adequate perfusion. The technology would essentially attempt to replicate normal function, wherein pain triggers movement to offload and relieve pressure. A regular wave of reduced pressure rippling across the quilt would replace the tedium of the recommended 2-hour turn schedule.

  In the future, spring loaded probes capable of measuring CO2 production, electrical resistance, or even polarization spectroscopy might be interspersed among the cubes so that ongoing skin viability and integrity could be monitored in addition to perfusion. Iontophoretic therapy with vasodilators and skin growth factors could be implemented if offloading alone did not prove therapeutic.

  Finally, if the middle model proves correct and the ground zero for some decubitus is in the sacral fat, even more complex monitoring will be required, such as implantable biosensors, and treatment plans might require hyperbaric oxygen or preemptive liposuction of necrotic fat. An investigation of the disruption of the normal molecular biology milieu as it relates to denervation, particularly of bone tissue, may prove to be very rewarding as it would pave the way to therapeutic intervention at the earliest stages of the disease process.

The author is from the Hamlet PPM, LLC, Sandhills Surgical, Hamlet, North Carolina.

Address correspondence to:
Alan Coulson, MD, PhD
108 Endo Lane
Hamlet, NC 28345
alan.coulson@hma.com

Disclosure: The authors disclose no financial or other conflicts of interest.