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Spinal Cord Perfusion Pressure Correlates with Anal Sphincter Function in a Cohort of Patients with Acute, Severe Traumatic Spinal Cord Injuries
BACKGROUND: Acute, severe traumatic spinal cord injury often causes fecal incontinence. Currently, there are no treatments to improve anal function after traumatic spinal cord injury. Our study aims to determine whether, after traumatic spinal cord injury, anal function can be improved by interventi...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8692299/ https://www.ncbi.nlm.nih.gov/pubmed/34100181 http://dx.doi.org/10.1007/s12028-021-01232-1 |
Sumario: | BACKGROUND: Acute, severe traumatic spinal cord injury often causes fecal incontinence. Currently, there are no treatments to improve anal function after traumatic spinal cord injury. Our study aims to determine whether, after traumatic spinal cord injury, anal function can be improved by interventions in the neuro-intensive care unit to alter the spinal cord perfusion pressure at the injury site. METHODS: We recruited a cohort of patients with acute, severe traumatic spinal cord injuries (American Spinal Injury Association Impairment Scale grades A–C). They underwent surgical fixation within 72 h of the injury and insertion of an intrathecal pressure probe at the injury site to monitor intraspinal pressure and compute spinal cord perfusion pressure as mean arterial pressure minus intraspinal pressure. Injury-site monitoring was performed at the neuro-intensive care unit for up to a week after injury. During monitoring, anorectal manometry was also conducted over a range of spinal cord perfusion pressures. RESULTS: Data were collected from 14 patients with consecutive traumatic spinal cord injury aged 22–67 years. The mean resting anal pressure was 44 cmH(2)O, which is considerably lower than the average for healthy patients, previously reported at 99 cmH(2)O. Mean resting anal pressure versus spinal cord perfusion pressure had an inverted U-shaped relation (Ȓ(2) = 0.82), with the highest resting anal pressures being at a spinal cord perfusion pressure of approximately 100 mmHg. The recto-anal inhibitory reflex (transient relaxation of the internal anal sphincter during rectal distension), which is important for maintaining fecal continence, was present in 90% of attempts at high (90 mmHg) spinal cord perfusion pressure versus 70% of attempts at low (60 mmHg) spinal cord perfusion pressure (P < 0.05). During cough, the rise in anal pressure from baseline was 51 cmH(2)O at high (86 mmHg) spinal cord perfusion pressure versus 37 cmH(2)O at low (62 mmHg) spinal cord perfusion pressure (P < 0.0001). During anal squeeze, higher spinal cord perfusion pressure was associated with longer endurance time and spinal cord perfusion pressure of 70–90 mmHg was associated with stronger squeeze. There were no complications associated with anorectal manometry. CONCLUSIONS: Our data indicate that spinal cord injury causes severe disruption of anal sphincter function. Several key components of anal continence (resting anal pressure, recto-anal inhibitory reflex, and anal pressure during cough and squeeze) markedly improve at higher spinal cord perfusion pressure. Maintaining too high of spinal cord perfusion pressure may worsen anal continence. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12028-021-01232-1. |
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