Current guidelines recommend four weeks of stress ulcer prophylaxis following traumatic spinal cord injury.

Assess the current literature on the incidence, timing, and risk factors for gastrointestinal bleeding/clinically important gastrointestinal bleeding in the acute setting following a traumatic spinal cord injury and whether the use of stress ulcer prophylaxis has been shown to reduce the rates of gastrointestinal bleeding.

A systematic review was performed in PubMed, Embase, Web of Science, and Cochrane Library following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines.

A total of 24 articles met the inclusion/exclusion criteria. The average rate of gastrointestinal bleeding among all studies was 5.5% (95% CI = 5.4-5.6%; n = 26,576). The average rate of clinically important gastrointestinal bleeding was 1.8% (95% CI = 1.79-1.82%; n = 3,857). The mean time since injury to when gastrointestinal bleeding occurred ranged from 5 to 22.5 days. For clinically important gastrointestinal bleeding the average time was 16 days or less. Those with cervical injuries had a higher incidence of clinically important gastrointestinal bleeding compared to those with non-cervical injuries (2.7% vs. 0.7%). No study found any difference in the use of stress ulcer prophylaxis in participants with or without gastrointestinal bleeding.

The overall incidence of clinically important gastrointestinal bleeding among studies was found to be low. Individuals with non-cervical injury were not found to be at high risk of clinically important gastrointestinal bleeding. There was also insufficient evidence to indicate that use of stress ulcer prophylaxis reduces the rate of gastrointestinal bleeding in those with traumatic spinal cord injury.

Spinal Cord Injury (SCI) disrupts critical autonomic pathways responsible for the regulation of the immune function. Consequently, individuals with SCI often exhibit a spectrum of immune dysfunctions ranging from the development of damaging pro-inflammatory responses to severe immunosuppression. Thus, it is imperative to gain a more comprehensive understanding of the extent and mechanisms through which SCI-induced autonomic dysfunction influences the immune response. In this review, we provide an overview of the anatomical organization and physiology of the autonomic nervous system (ANS), elucidating how SCI impacts its function, with a particular focus on lymphoid organs and immune activity. We highlight recent advances in understanding how intraspinal plasticity that follows SCI may contribute to aberrant autonomic activity in lymphoid organs. Additionally, we discuss how sympathetic mediators released by these neuron terminals affect immune cell function. Finally, we discuss emerging innovative technologies and potential clinical interventions targeting the ANS as a strategy to restore the normal regulation of the immune response in individuals with SCI.

Spinal cord injury (SCI) damages multiple structures at the lesion site, including ascending, descending, and propriospinal axons; interrupting the conduction of information up and down the spinal cord. Additionally, axons associated with the autonomic nervous system that control involuntary physiological functions course through the spinal cord. Moreover, sympathetic, and parasympathetic preganglionic neurons reside in the spinal cord. Thus, depending on the level of an SCI, autonomic function can be greatly impacted by the trauma resulting in dysfunction of various organs. For example, SCI can lead to dysregulation of a variety of organs, such as the pineal gland, the heart and vasculature, lungs, spleen, kidneys, and bladder. Indeed, it is becoming more apparent that many disorders that negatively affect quality-of-life for SCI individuals have a basis in dysregulation of the sympathetic nervous system. Here, we will review how SCI impacts the sympathetic nervous system and how that negatively impacts target organs that receive sympathetic innervation. A deeper understanding of this may offer potential therapeutic insight into how to improve health and quality-of-life for those living with SCI.

Individuals with chronic traumatic spinal cord injury (SCI) develop progressive multi-system health problems that result in clinical illness and disability. Systemic inflammation is associated with many of the common medical complications and acquired diseases that accompany chronic SCI, suggesting that it contributes to a number of comorbid pathological conditions. However, many of the mechanisms that promote persistent systemic inflammation and its consequences remain ill-defined. This review describes the significant biological factors that contribute to systemic inflammation, major organ systems affected, health risks, and the potential treatment strategies. We aim to highlight the need for a better understanding of inflammatory processes, and to establish appropriate strategies to address inflammation in SCI.

Traumatic brain injury (TBI) is a major cause of long-term physical and psychological disability and death. In patients with TBI, undernutrition is associated with an increased mortality rate, more infectious complications, and worse neurologic outcomes. Therefore, timely and effective nutritional therapy is particularly crucial in the management of TBI to improve patients' prognoses. This narrative review summarizes the issues encountered in clinical practice for patients with neurotrauma who receive acute and post-acute in-patient rehabilitation services, and it comprehensively incorporates a wide range of studies, including recent clinical practice guidelines (CPGs), with the aim of better understanding the current evidence for optimal nutritional therapy focused on TBI patients. Recent CPGs were reviewed for 6 topics: 1) hypermetabolism and variation in energy expenditure in patients with TBI, 2) delayed gastric emptying and intolerance to enteral nutrition, 3) decision-making on the route and timing of access in patients with TBI who are unable to maintain volitional intake (enteral nutrition versus parenteral nutrition), 4) decision-making on the enteral formula (standard or immune-modulating formulas), 5) glycemic control, and 6) protein support. We also identified areas that need further research in the future.

Gastrointestinal (GI) complications and their clinical implications are poorly characterized in dogs treated surgically for acute thoracolumbar intervertebral disc extrusion (TL-IVDE). The objective of this retrospective study was to characterize GI signs (including vomiting, diarrhea, melena, and hematochezia) in dogs undergoing hemilaminectomy for acute TL-IVDE. One-hundred and sixteen dogs were included. Frequency, type and severity of GI signs during hospitalization, duration of hospitalization and outcome were obtained from the medical record. Potential risk factors for the development of GI signs were explored using univariable and multivariable analyses. Gastrointestinal signs occurred in 55/116 dogs (47%); 22/55 dogs (40%) had one episode and 21/55 (38%) had ≥5 episodes. Diarrhea was the most common (40/55, 73%) while melena was rare (1/55, 2%). GI signs developed in 8/11 dogs (73%) treated perioperatively with both non-steroidal anti-inflammatories and corticosteroids with or without a washout period and in 25/52 dogs (48%) treated prophylactically with proton pump inhibitors. Median hospitalization was 7 days (4-15 days) vs. 5 days (4-11 days) in dogs with or without GI signs, respectively. Duration of hospitalization was associated with development of any GI signs, diarrhea and more severe GI signs (p = 0.001, 0.005, 0.021, respectively). Pre-operative paraplegia with absent pain perception was identified on univariable analysis (p = 0.005) and longer anesthetic duration on multivariable analysis to be associated with development of more severe GI signs (p = 0.047). In dogs undergoing surgery for acute TL-IVDE, GI signs were common and associated with duration of hospitalization and anesthesia. The influence of specific medications and neurologic severity on development of GI signs requires further investigation.

Bowel dysfunction after chronic spinal cord injury (SCI) is a common source of morbidity and rehospitalization. Typical complications include constipation, fecal impaction, incontinence, abdominal distention, autonomic dysreflexia, and the necessity of interventions (i.e., suppositories, digital stimulation) to defecate. Numerous surveys have confirmed that the remediation of bowel complications is more highly valued for quality of life than improvements in walking. Much of what is known about bowel function after SCI for diagnosis and research in humans has been gained using anorectal manometry (ARM) procedures. However, ARM has been underutilized in pre-clinical animal work. Therefore, a novel combination of outcome measures was examined in the current study that incorporates functional output of the bowel (weekly fecal measurements), weight gain (pre-injury to terminal weight), and terminal ARM measurement with external anal sphincter electromyography under urethane anesthesia. The results indicate higher fecal output after contusion during the sub-acute period (4-7 days) post-injury, changes in the composition of the feces, and functionally obstructive responses in a specific section of the rectum (increased baseline pressure, increased frequency of contraction, and reduced ability to trigger a giant contraction to a distension stimulus). These results demonstrate significant bowel dysfunction in the rodent SCI contusion model that is consistent with data from human research. Thus, the combined measurement protocol enables the detection of changes and can be used, with minimal cost, to assess effectiveness of therapeutic interventions on bowel complications.

Superior mesenteric artery syndrome (SMAS) is rare cause of small bowel obstruction and is characterized by an extrinsic vascular compression of the duodenum. The most common cause of SMAS is known as rapid and significant weight loss.

A 61-year-old man who was diagnosed with amyotrophic lateral sclerosis and maintained a stable diet before admission. When the patient re-started feeding by gastrostomy tube after 5 days of therapeutic fasting due to gastric ulcer caused by gastrostomy tube irritation, he presented postprandial vomiting, abdominal distention, and tachycardia. Since fasting, his weight has been reduced by about 3 kg.

Based on clinical symptoms and radiological findings, diagnose of SMAS was finally made. Abdomen computed tomography confirmed decreased aortomesenteric distance and tubography confirmed gastric and proximal duodenum distension above the compressed part.

We performed jejunal tube insertion and the amount of feeding through the jejunal tube was gradually increased while maintaining parenteral nutrition.

The presenting symptoms of the patient gradually improved. Follow-up abdomen computed tomography and tubography showed improvement in duodenal narrowing and stomach distension.

SMAS should be considered when there is an abrupt observation of symptom of gastrointestinal obstruction in patients with predisposing condition such as a low body weight, even if the weight loss is relatively small.

Gastrointestinal (GI) dysfunction is observed clinically after spinal cord injury (SCI) and contributes to the diminished long-term quality of life. Our study examined the acute and chronic GI vascular changes that occur following SCI. We demonstrated that the GI vascular tract in SCI mice becomes compromised during the acute phase of injury and persists into the chronic phase of injury.

Gastrointestinal vasculature permeability was measured using dynamic contrast-enhanced magnetic resonance imaging (DCE MRI) at 48 hours, and 2 and 4 weeks following contusion spinal cord injury. Angiopoietin-1, a vascular stabilizing protein, was administered intravenously following injury. Intestinal contractile activity assessments were performed following the last imaging session.

Our results indicated that a single administration of Ang-1 reduced vascular permeability at 48 hours but the effect was only transient. However, when the treatment paradigm was changed from a single administration to multiple administrations of Ang-1 following contusion injury, our DCE MRI data indicated a significant decrease in GI vascular permeability 4 weeks after injury compared with vehicle control treated animals. This improved GI vascular permeability was associated with improved sustained intestinal contractile activity. We also demonstrated that Ang-1 reduced the expression of sICAM-1 in the ileum compared with the saline-treated group.

We show that the GI vasculature is compromised in the acute and chronic phase of injury following spinal contusion. Our results also indicate that multiple administrations of Ang-1 can attenuate GI vascular permeability, possibly reduce inflammation, and improve sustained agonist-induced contraction compared with saline treatment.

Stress ulcer prophylaxis (SUP) with acid-suppressive drug therapy is widely utilized in critically ill patients following neurologic injury for the prevention of clinically important stress-related gastrointestinal bleeding (CIB). Data supporting SUP, however, largely originates from studies conducted during an era where practices were vastly different than what is considered routine by today's standard. This is particularly true in neurocritical care patients. In fact, the routine provision of SUP has been challenged due to an increasing prevalence of adverse drug events with acid-suppressive therapy and the perception that CIB rates are sparse. This narrative review will discuss current controversies with SUP as they apply to neurocritical care patients. Specifically, the pathophysiology, prevalence, and risk factors for CIB along with the comparative efficacy, safety, and cost-effectiveness of acid-suppressive therapy will be described.

The gastrointestinal tract of vertebrates is a heterogeneous organ system innervated to varying degrees by a local enteric neural network as well as extrinsic parasympathetic and sympathetic neural circuits located along the brainstem and spinal axis. This diverse organ system serves to regulate the secretory and propulsive reflexes integral to the digestion and absorption of nutrients. The quasi-segmental distribution of the neural circuits innervating the gastrointestinal (GI) tract produces varying degrees of dysfunction depending upon the level of spinal cord injury (SCI). At all levels of SCI, GI dysfunction frequently presents life-long challenges to individuals coping with injury. Growing attention to the profound changes that occur across the entire physiology of individuals with SCI reveals profound knowledge gaps in our understanding of the temporal dimensions and magnitude of organ-specific co-morbidities following SCI. It is essential to understand and identify these broad pathophysiological changes in order to develop appropriate evidence-based strategies for management by clinicians, caregivers and individuals living with SCI. This review summarizes the neurophysiology of the GI tract in the uninjured state and the pathophysiology associated with the systemic effects of SCI.

Small-scale studies indicate that spinal cord injury (SCI) may lead to significant gastrointestinal and bladder dysfunction. However, how the prevalence of chronic disease related to these dysfunctions compares with non-SCI individuals and whether there are robust relationships to level and severity of injury are still unclear. Here, our goal was to provide high-level evidence on the association between bladder and gastrointestinal dysfunction and SCI using population-level data from the Canadian Community Health Survey (CCHS) and the SCI Community Survey. Data from more than 60,000 individuals in the 2010 CCHS and 1500 individuals with SCI from the SCI Community Survey were analyzed. We used bi-variable and multi-variable logistic regression to examine relationships between explanatory and outcome variables. We found that SCI was associated with increased odds of urinary incontinence (adjusted odds ratio [aOR] = 5.0, 95% confidence interval [CI]: 3.4-7.1), bowel disorders (aOR = 2.3, CI: 1.5-3.4), as well as gastric ulcers (aOR: 3.3, CI: 2.1-4.8), even after adjusting for key confounding variables. Additionally, we found that complete SCI was associated with increased odds of urinary tract infections (aOR = 2.0, CI: 1.6-2.5) and bowel incontinence (aOR = 2.1, CI: 1.7-2.6). Individuals with SCI are at increased odds for having bladder and gastrointestinal dysfunction, certain aspects of which are dependent on the level and severity of injury. Targeted intervention and prevention strategies to manage bladder and bowel problems after SCI should be a priority for both caregivers and policy makers.

Prospective cohort study OBJECTIVES: We hypothesized that anti-muscarinic agents alter rectal compliance in SCI patients and that altered rectal compliance relates to bowel symptomatology. Our primary aim was to compare rectal compliance before and after the institution of anti-muscarinics (solifenacin and tolterodine) and an adrenoceptor agonist (mirabegron) in these patients. Additionally, we wanted to evaluate if anorectal manometry differed before and after use of anti-muscarinic agents.

Tertiary neurogastroenterology clinic, London METHODS: Thirty-five patients with supraconal spinal cord injury (SCI) underwent anal manometry, assessment of rectoanal inhibitory reflex (RAIR) and rectal compliance before and after anti-muscarinic treatment (for overactive bladder) was started (mean follow-up 12 weeks). Patients were assessed identically, pre-and post-treatment (solifenacin n = 17, tolterodine n = 10, mirabegron n = 8). Doses used were as for non-SCI patients.

Resting, squeeze and cough pressures were unchanged after anti-muscarinic treatment. Rectal compliance was significantly raised after anti-muscarinic treatment (p = 0.001). The percent amplitude of maximal sphincter relaxation of the RAIR was decreased (p < 0.001) and excitation latency was increased (p = 0.006). There was no significant change in the duration of recovery of the RAIR. There was a significant increase of the Wexner Constipation Score (p = 0.001) but no change in the Wexner Incontinence Score. There was a significant correlation between change in rectal compliance and change in Wexner Constipation Score (p = 0.001). Thus, increasing compliance of the rectum is associated with worsening of constipation after anti-muscarinic therapy. However, there were no changes in anorectal manometry or rectal compliance in those who received mirabegron.

Anti-muscarinic therapy for overactive bladder increases compliance of the neurogenic rectum and alters anorectal reflex activity, with worsening of constipation.

Supraconal spinal cord injury (SCI) and lower motor neurone spinal cord injury (LMN-SCI) cause bowel dysfunction; colorectal compliance may further define its pathophysiology. The aim of this study was to investigate rectal (RC) and sigmoid (SC) compliance and anorectal physiology parameters, in these subjects.

Twenty-four SCI subjects with gut symptoms (14 RC, 10 SC) and 13 LMN-SCI subjects (9 RC, 4 SC) were compared with 20 spinal intact controls (10 RC, 10 SC). Staircase distensions were performed using a barostat. Anorectal manometry, including rectoanal inhibitory reflex (RAIR) measurement, was performed in all. Data presented as mean±standard error (SCI/LMN-SCI vs. controls).

SCI subjects had a higher RC (17.0±1.9 vs. 10.7±0.5 ml/mm Hg, P<0.05) and SC (8.5±0.6 vs. 5.2±0.5 ml/mm Hg, P=0.002). LMN-SCI subjects had a lower RC (7.3±0.7 ml/mm Hg, P=0.0021) while SC was unchanged (8.3±2.2 ml/mm Hg, P>0.05). Anal resting pressure was decreased in SCI (55±5 vs. 79±7 cmH2O, P=0.0102). Anal squeeze pressure was decreased in LMN-SCI (76±13 vs. 154±21 cmH2O, P=0.0158). In SCI and LMN-SCI, the amplitude reduction of the RAIR was greater (62±4% and 70±6% vs. 44±3%, P=0.0007).

Colorectal compliance abnormalities may explain gut symptoms: increased RC and SC contributing to constipation in SCI, reduced rectal compliance contributing to fecal incontinence (FI) in LMN-SCI. Reduced resting anal pressure in SCI and reduced anal squeeze pressure in LMN-SCI along with a greater RAIR amplitude reduction may be factors in FI. These co-existing abnormalities may explain symptom overlap, and represent future therapeutic targets to ameliorate neurogenic bowel dysfunction.

Spinal cord injury (SCI) results not only in motor and sensory deficits but also in autonomic dysfunctions. The disruption of connections between higher brain centers and the spinal cord, or the impaired autonomic nervous system itself, manifests a broad range of autonomic abnormalities. This includes compromised cardiovascular, respiratory, urinary, gastrointestinal, thermoregulatory, and sexual activities. These disabilities evoke potentially life-threatening symptoms that severely interfere with the daily living of those with SCI. In particular, high thoracic or cervical SCI often causes disordered hemodynamics due to deregulated sympathetic outflow. Episodic hypertension associated with autonomic dysreflexia develops as a result of massive sympathetic discharge often triggered by unpleasant visceral or sensory stimuli below the injury level. In the pelvic floor, bladder and urethral dysfunctions are classified according to upper motor neuron versus lower motor neuron injuries; this is dependent on the level of lesion. Most impairments of the lower urinary tract manifest in two interrelated complications: bladder storage and emptying. Inadequate or excessive detrusor and sphincter functions as well as detrusor-sphincter dyssynergia are examples of micturition abnormalities stemming from SCI. Gastrointestinal motility disorders in spinal cord injured-individuals are comprised of gastric dilation, delayed gastric emptying, and diminished propulsive transit along the entire gastrointestinal tract. As a critical consequence of SCI, neurogenic bowel dysfunction exhibits constipation and/or incontinence. Thus, it is essential to recognize neural mechanisms and pathophysiology underlying various complications of autonomic dysfunctions after SCI. This overview provides both vital information for better understanding these disorders and guides to pursue novel therapeutic approaches to alleviate secondary complications.

Obstruction of the third part of the duodenum (D3) is a very rare cause of gastric outflow obstruction. Rapid weight loss is the biggest risk factor. Patients seen in acute rehabilitation settings, not uncommonly, have a period of rapid weight loss. We report two cases of superior mesenteric artery (SMA) syndrome and review the literature.

The patients presented differently, one with repeated, refractory autonomic dysreflexia and severe spasticity and one with nausea, abdominal discomfort, and vomiting. CT abdomen with contrast identified dynamic duodenal (D3) obstruction against the posterior structures by narrow angled SMA, gastric distension and, in one case, dilation of the left renal vein. Both patients responded well to optimizing nutrition in different ways. Surgery was successfully avoided.

SMA syndrome is an atypical cause of high intestinal obstruction, frequently occurring in patients who have had rapid weight loss during spinal cord injury (SCI) rehabilitation. It may co-exist with left renal vein dilation "nutcracker phenomena". The associated neurogenic bowel dysfunction due to the nature of SCI could possibly contribute to delay in diagnosis.

Clinicians should consider the risk of SMA syndrome in patients with SCI with rapid weight loss. Early diagnosis is possible by doing a CT abdomen with contrast and angiography if there is a high index of suspicion. SMA syndrome can be successfully treated by aggressive nutritional management. This may include total parenteral nutrition or feeding by a nasojejunal tube. Duodenojejunostomy could be required in refractory cases.

Fecal impaction (FI) is a common and potentially serious medical condition that occurs in all age groups. Children, incapacitated patients, and the institutionalized elderly are considered the highest at-risk populations. FI usually occurs in the setting of chronic or severe constipation, anatomic anorectal abnormalities, and neurogenic or functional gastrointestinal disorders. Generally, FI is a preventable disorder, and early recognition is important, as it is associated with increased morbidity, mortality, and high health care costs. Evaluation with a careful history and physical examination, in conjunction with radiologic imaging, such as an acute abdominal series or computed tomography (CT), is imperative. Prompt identification and treatment minimize the risk of complications attributable to FI, which may include bowel obstruction leading to stercoral ulcer, perforation, peritonitis, or cardiopulmonary collapse with hemodynamic instability. Treatment options include manual fragmentation and extraction of the fecal mass, distal colonic cleansing using enemas and rectal lavage with the aid of a sigmoidoscope, and/or using water-soluble contrast media such as Gastrografin to both identify the extent of the impaction and aid in cleansing and removal. Surgical resection of the involved colon or rectum is reserved for peritonitis resulting from bowel perforation. Since recurrence is common, implementing preventive measures such as increasing daily water and fiber intake, limiting medications that decrease colonic motility, using secretagogues or prokinetic agents, and treating underlying anatomic defects are highly important.

The vagus nerve is composed primarily of nonmyelinated sensory neurons whose cell bodies are located in the nodose ganglion (NG). The vagus has widespread projections that supply most visceral organs, including the bladder. Because of its nonspinal route, the vagus nerve itself is not directly damaged from spinal cord injury (SCI). Because most viscera, including bladder, are dually innervated by spinal and vagal sensory neurons, an impact of SCI on the sensory component of vagal circuitry may contribute to post-SCI visceral pathologies. To determine whether SCI, in male Wistar rats, might impact neurochemical characteristics of NG neurons, immunohistochemical assessments were performed for P2X3 receptor expression, isolectin B4 (IB4) binding, and substance P expression, three known injury-responsive markers in sensory neuronal subpopulations. In addition to examining the overall population of NG neurons, those innervating the urinary bladder also were assessed separately. All three of the molecular markers were represented in the NG from noninjured animals, with the majority of the neurons binding IB4. In the chronically injured rats, there was a significant increase in the number of NG neurons expressing P2X3 and a significant decrease in the number binding IB4 compared with noninjured animals, a finding that held true also for the bladder-innervating population. Overall, these results indicate that vagal afferents, including those innervating the bladder, display neurochemical plasticity post-SCI that may have implications for visceral homeostatic mechanisms and nociceptive signaling.

Spinal cord injuries has increased together with urban violence and show a high rates of incidence. Besides the onus to patient and society, it can also cause other serious complications to victims. Acute pancreatitis has an important impact on this disease and has been underdiagnosed in several patients.

The aim of this study was investigate the association of acute pancreatitis in acute spinal cord injuries. The secondary aim was to propose an investigation protocol to early diagnose and prevent it.

A prospective observational study was conducted in 78 patients who presented acute spinal cord injury (SCI) at our emergency department, confirmed by clinical and imaging examination, in according to the American Spinal Injury Association (ASIA) Classification. Exclusion criteria were chronic or associate diseases in spinal cord, pancreatic direct trauma, alcoholism and chronic pancreatic disease.

The association of acute pancreatitis in patients with SCI was 11.53%. The occurrence of pancreatitis or high levels of serum pancreatic enzymes in patients with ASIA A was 41.7% and only 4.17% in patients with ASIA E. In all, 55.2% of patients who presented pancreatitis or high levels of serum pancreatic enzymes had cervical level of SCI and 34.5% had thoracic level. Adynamic ileus was observed in 68.96% of this group.

We concluded that, in acute spinal cord injuries, the occurrence of acute pancreatitis or high serum levels of pancreatic enzymes are more frequent in patients with ASIA A Classification, cervical/thoracic level of spinal injury and adynamic ileus.

Retrospective review of medical notes.

To describe clinical, laboratory and examination findings of acute abdominal emergencies (AAE) in Turkish patients with spinal cord injury (SCI) and to examine diagnosis and management of AAE in early stages.

Inpatient rehabilitation unit of tertiary research hospital.

The medical records of 237 SCI patients were reviewed. The SCI patients who were recruited in the study had been diagnosed with AAE and treated medically or surgically while they were inpatients at the rehabilitation clinic.

Nine out of 237 SCI patients had been diagnosed with one of the AAE. Three patients were AIS A, three patients were AIS B and three patients were AIS C. The most common AAE was acute cholecystitis; three patients were diagnosed with this. The others were single cases of intra-abdominal hemorrhage, intra-abdominal abscess, tuba-ovarian abscess, subileus, Crohn's disease and cholangitis. Three of the patients were treated with surgery and six were treated medically. The most common symptoms in patients were fever, abdominal pain and abdominal discomfort (four of AAE). Three patients had abdominal tenderness and abdominal distension. The expected findings of AAE, rebound and defense, were positive only in two patients.

Gall bladder disease is a common cause of AAE. The classic symptoms and examination findings will usually not facilitate acute abdomen diagnosis in the SCI group, so we should be aware of patients' subjective complaints and when necessary use advanced imaging techniques immediately.

Critically ill spinal cord injury (SCI) patients are at high risk for pressure ulcers. Research is needed to identify risk factors for pressure ulcers. The aim of this study was to investigate risk factors and outcomes of pressure ulcers in critically ill SCI patients. This is a retrospective cohort study. Data were gathered from medical records of adult patients with SCI admitted to surgical intensive care units. Ninety-four SCI patients participated in this study. Clinical variables associated with pressure ulcers were as follows: fecal management systems, incontinence, acidosis, support surfaces, steroids, and additional equipment. Hypotension was the strongest predictor of pressure ulcers. Nursing interventions may address risk factors and improve patient outcomes.

Despite the widely recognized prevalence of gastric, colonic, and anorectal dysfunction after spinal cord injury (SCI), significant knowledge gaps persist regarding the mechanisms leading to post-SCI gastrointestinal (GI) impairments. Briefly, the regulation of GI function is governed by a mix of parasympathetic, sympathetic, and enteric neurocircuitry. Unlike the intestines, the stomach is dominated by parasympathetic (vagal) control whereby gastric sensory information is transmitted via the afferent vagus nerve to neurons of the nucleus tractus solitarius (NTS). The NTS integrates this sensory information with signals from throughout the central nervous system. Glutamatergic and GABAergic NTS neurons project to other nuclei, including the preganglionic parasympathetic neurons of the dorsal motor nucleus of the vagus (DMV). Finally, axons from the DMV project to gastric myenteric neurons, again, through the efferent vagus nerve. SCI interrupts descending input to the lumbosacral spinal cord neurons that modulate colonic motility and evacuation reflexes. In contrast, vagal neurocircuitry remains anatomically intact after injury. This review presents evidence that unlike the post-SCI loss of supraspinal control which leads to colonic and anorectal dysfunction, gastric dysmotility occurs as an indirect or secondary pathology following SCI. Specifically, emerging data points toward diminished sensitivity of vagal afferents to GI neuroactive peptides, neurotransmitters and, possibly, macronutrients. The neurophysiological properties of rat vagal afferent neurons are highly plastic and can be altered by injury or energy balance. A reduction of vagal afferent signaling to NTS neurons may ultimately bias NTS output toward unregulated GABAergic transmission onto gastric-projecting DMV neurons. The resulting gastroinhibitory signal may be one mechanism leading to upper GI dysmotility following SCI.

The aim of this study is to review and summarize the relevant literature regarding pharmacologic and non-pharmacologic methods of prophylaxis against gastrointestinal (GI) stress ulceration, and upper gastrointestinal bleeding in critically ill patients. Stress ulcers are a known complication of a variety of critical illnesses. The literature regarding epidemiology and management of stress ulcers and complications thereof, is vast and mostly encompasses patients in medical and surgical intensive care units. This article aims to extrapolate meaningful data for use with a population of critically ill neurologic and neurosurgical patients in the neurological intensive care unit setting. Studies were identified from the Cochrane Central Register of controlled trials and NLM PubMed for English articles dealing with an adult population. We also scanned bibliographies of relevant studies. The results show that H(2)A, sucralfate, and PPI all reduce the incidence of UGIB in neurocritically ill patients, but H(2)A blockers may cause encephalopathy and interact with anticonvulsant drugs, and have been associated with higher rates of nosocomial pneumonias, but causation remains unproven and controversial. For these reasons, we advocate against routine use of H(2)A for GI prophylaxis in neurocritical patients. There is a paucity of high-level evidence studies that apply to the neurocritical care population. From this study, it is concluded that stress ulcer prophylaxis among critically ill neurologic and neurosurgical patients is important in preventing ulcer-related GI hemorrhage that contributes to both morbidity and mortality. Further, prospective trials are needed to elucidate which methods of prophylaxis are most appropriate and efficacious for specific illnesses in this population.

Cross-sectional study.

To analyze the predictors of severe neurogenic bowel dysfunction (NBD) in persons with spinal cord injury (SCI).

The Kaohsiung Medical University Hospital, Taiwan.

Two questionnaires-the NBD score and the Beck Depression Inventory second edition-were sent to 232 persons with SCI by mail. The demographic factors and injury-related factors were recorded to evaluate any relationships with severe NBD. The associations between the severity of NBD and psychological condition were also measured.

In all, 39.4% of the respondents suffered from severe NBD. Multiple logistic regression analysis showed that those with a cervical injury (odds ratios (OR)=10.5, 95% confidence interval (CI) 1.6-67.7) or a thoracic injury (OR=7.1, 95% CI 1.2-40.3) had a higher risk of severe NBD than those with a lumbar injury. Persons with American Spinal Injury Association (ASIA) A had a 12.8-fold higher risk of severe NBD than persons with ASIA D (OR=12.8, 95% CI 3.3-50.1). Longer duration of injury (> or =10 years) was another risk factor of severe NBD. Moderate-to-severe depression was associated with reduced bowel function.

This study showed that high level of cord lesion, completeness of cord injury and longer duration of injury (> or =10 years) could predict the severity of NBD in patients with SCI.

Spinal cord injury (SCI) is associated with severe autonomic dysfunction in both the acute and chronic phases. Upper gastrointestinal (GI) motor dysfunction has been previously reported in humans and rats. Gastric emptying (GE) of a solid meal--as measured by the [(13)C]-octanoic acid breath test--is delayed in the first 3 weeks after either spinal cord transection (SCT) or contusion (SCC) in rats. This is one of the main findings of a new paper by Qualls-Creekmore et al. in the current issue of this journal. Previous studies in rats only reported impairment of GE, intestinal and GI transit of liquid after SCI, but the authors observed that the delay of the GE of solid was more prominent after SCT than SCC. Recovery of the delay of GE of solid occurred at 6 weeks after SCC, but not after SCT. However, gastric motility changes persisted despite the functional normalization of the GE in rats with SCC. Bowel dysfunction is a major physical and psychological burden for SCI patients. Collaborative efforts, like the development of international standards to evaluate autonomic function after SCI will likely clarify the mechanisms of dysfunction and lead to the development of new therapeutic strategies.

Cross-sectional and nonexperimental.

To detect and compare functional abnormalities in the esophagus and esophagogastric junction in 2 groups with chronic spinal injuries, 1 with injuries at the phrenic innervation level and the other at upper thoracic levels, and to relate these to gastroesophageal reflux containment.

There are no studies on esophageal manometry with pH metering among spinal cord injury patients. Worldwide statistics reveal that the prevalence of gastroesophageal reflux disease among spinal cord injury patients is greater than among the general population, at around 22% to 27%. The "diaphragmatic crura" has been recognized as an important antireflux barrier and should functionally be considered to be a muscle separated from the costal diaphragm. However, doubts remain regarding whether this difference relates to its innervation.

This was a cross-sectional study on 29 patients with complete spinal cord injuries: 14 quadriplegics (level C4) and 15 paraplegics (levels T1-T7). Functional abnormalities of the esophagogastric junction, esophagus, and diaphragm were investigated using esophageal manometry and diaphragmatic video fluoroscopy. Presence of gastroesophageal reflux was investigated subjectively (pyrosis and regurgitation) and objectively (pH metering and endoscopy).

The incidence of gastroesophageal reflux disease was 27.6%, without difference between the groups. This became statistically significant when the mean diaphragmatic crural pressures were compared (quadriplegics: 37.5 +/- 17.8; paraplegics: 26.6 +/- 7.2; P = 0.048). It was also significant in relation to the prevalence of at least one of the objective and/or subjective reflux findings and/or esophageal peristaltism (quadriplegics: 85.7%; paraplegics: 40.0%; P = 0.011).

Spinal injury at the level of the phrenic innervation did not predispose the quadriplegics toward greater risk of developing gastroesophageal reflux disease. Paradoxically, manometry showed significantly greater crural contractility among the quadriplegics.

Cross-sectional studies suggest that colorectal dysfunction after spinal cord injuries (SCI) worsens as time goes by. However, follow-up studies are needed to prove this.

Prospective study.

To describe long-term colorectal function in SCI patients.

Members of the Danish Spinal Cord Injuries Association.

In 1996, 424 members of the Danish Paraplegic Association answered a detailed questionnaire describing their colorectal function. In 2006, those who continued as members (n=284) received an identical questionnaire. Data for patients responding both in 1996 and in 2006 (n=159) were compared.

In 1996, 25% of the respondents reported that colorectal dysfunction had some or a major impact on their quality of life. At follow-up 10 years later, it was 38% (P<0.005). In 1996 11% defecated less than every second day and 16% spent more than 30 min at each defecation; in 2006, it was 19% (P<0.01) and 25% (P<0.00001), respectively. Digital anorectal stimulation or evacuation was performed at least once every week by 48% in 1996 and by 56% in 2006 (P<0.0001). Fecal incontinence was reported at least once a month by 22% in 1996 and by 17% in 2006 (P<0.001).

While the frequency and severity of constipation-related symptoms increase with time since SCI, there is a decrease in the frequency of fecal incontinence.

Traditional literature regarding acquired bowel dysfunction for persons with spinal cord injury (SCI) has focused on clinical assessments of bowel dysfunction and bowel management programs. These studies make reference to the effects of bowel dysfunction on quality of life (QOL), but none systematically study the relationship. This study develops 4 scales that measure impediment to community integration (ICI) due to bowel dysfunction and then examines the relationship between bowel dysfunction, ICI, and QOL.

A structured telephone survey was conducted with a convenience sample of 103 SCI consumers. Survey questions documented bowel dysfunction (ie, severity and number of accidents), bowel management (ie, how often bowels are evacuated), ICI, and satisfaction with 4 life domains.

Correlation analyses showed that subjective bowel dysfunction severity and number of days per month a respondent had to stay home because of lack of bowel control were associated with barriers to personal relationships, feelings about self, and home life. Also, the number of bowel accidents per month was associated with feelings about self. ICI scales were shown to be related to lower levels of satisfaction with free time, friendships, family life, and life in general. No statistically significant relationships were found between bowel dysfunction and satisfaction with life.

Bowel dysfunction is a barrier to community integration and is related to low levels of life satisfaction. Also, it is possible to quantify ICI related to bowel dysfunction. Educational programs can reduce the stigma associated with bowel dysfunction. Further research into the intricate relationships between bowel problems, barriers to participation in the community, and life satisfaction is needed.

Mechanical ventilation has evolved greatly over the last half century, guided primarily by improved comprehension of the relevant pathology/physiology. Neurosurgical patients are a unique subgroup of patients who heavily use this technology for both support, and less commonly, as a therapy. Such patients demand special consideration with regard to mode of ventilation, use of positive end-expiratory pressure, and monitoring. In addition, meeting the ventilatory needs of neurosurgical patients while minimizing ventilatory-induced lung damage can be a challenging aspect of care.

This is a retrospective study of 500 patients with spinal cord injury who underwent abdominal ultrasonography as a routine screening test from 2000 to 2003. We analyzed the results according to the different abdominal organ systems. Among the 500 cases, 226 (45.2%) showed abnormal findings. 98 cases of abnormal findings in the liver included 75 of fatty liver and 13 of mass. The 88 cases of abnormal findings in the bladder included 56 of bladder wall thickening, 14 of cystitis and 10 of urinary stone. The 35 cases of abnormal findings in the kidney included 19 of renal cyst and 6 of pelvic dilatation. The 35 cases with gallbladder abnormalities included 19 with gallstones and 11 with biliary sludge. Excluding the cases with bladder wall thickening, there were still 170 cases with abnormal ultrasonographic findings. Abdominal sonography seems to be a useful tool in detecting hidden intraabdominal pathologies in patients with spinal cord injury.

The impact of spinal cord injury on an individual's gastrointestinal tract function is often poorly understood by the general public and also by those involved with persons with spinal cord injury. This chapter reviews the anatomy, physiology and function of the gastrointestinal tract, with particular emphasis on neurological control mechanisms. In turn, it relates the effect that spinal cord injury has on the neurological control of the gastrointestinal tract. The symptoms that are encountered by patients in the acute phase following injury, and by individuals in the months/years after injury, with particular reference to the effect of altered autonomic nervous system control of the gastrointestinal tract, are discussed. Together with a following summary of current bowel management regimens and techniques, this chapter aims to provide an overall view of the effect that autonomic dysfunction due to spinal cord injury has on gastrointestinal function.

Defecatory complications are common after spinal cord injury (SCI) and have been attributed, in part, to an imbalance of the autonomic nervous system between parasympathetic and sympathetic effects on the colon. Because parasympathetic (i.e., cholinergic) input to the bowel may be downregulated after SCI, it was hypothesized that neostigmine, a medication that increases cholinergic tone by blocking the metabolism of acetylcholine, might promote bowel evacuation in these persons. Since neostigmine is known to cause bradycardia and bronchoconstriction, we also assessed whether these side-effects could be prevented by coadministration of neostigmine with glycopyrrolate, an anticholinergic agent that has limited activity on the muscarinic receptors of the colon. The hypothesis was tested in 13 persons with SCI in whom videofluoroscopy was carried out after instillation of a barium oatmeal paste into the rectum and descending colon. On separate days, subjects received, in a randomized, blinded design, one of three intravenous infusates (normal saline, 2 mg neostigmine, or 2 mg neostigmine + 0.4 mg glycopyrrolate). The effect of these infusates on bowel evacuation of the barium paste, heart rate, and airway resistance was determined. Both neostigmine and neostigmine + glycopyrrolate resulted in prompt bowel evacuation. The nadir heart rate was lower after neostigmine alone than with the combination. Neostigmine administration increased both total and central airway resistance, an effect that was not observed with the coadministration of glycopyrrolate. Other side-effects of neostigmine and the combination of drugs included muscle fasciculations and dry mouth, both of which were mild and short-lived. Abdominal cramping was noted in subjects with spinal cord lesions below thoracic level 10. These results indicated that neostigmine/glycopyrrolate administration is safe and well tolerated in persons with chronic SCI.

A descriptive, cross-sectional, multicentre design was used.

To analyse bowel management in patients with spinal cord injury (SCI) especially the occurrence of unplanned bowel evacuations and duration of planned bowel evacuation.

In total, 29 rehabilitation facilities for SCI patients in Austria, Germany, the Netherlands and Switzerland, with a total of 837 hospitalized SCI patients.

Data were collected by nurses within 1 week in November 2001 using a quantitative questionnaire containing 14 questions. For data analysis, a chi (2)-test was used for differences in the outcome of bowel evacuation procedures associated with different interventions. Stepwise multiple logistic regression was used to analyse the relationship between the outcome of bowel management and the interventions as well as intervening factors.

More unplanned bowel evacuations were associated with usage of oral laxatives (n=444, P<0.001) as well as bowel evacuation every day (n=270, P<0.05) or every second day (n=368, P<0.05). The outcome of less unplanned bowel evacuations was associated with manual removal of stool combined with digital stimulation (n=35, P<0.05) and spontaneous bowel evacuations (n=104, P<0.001). Short duration of bowel evacuation (<60 min) was associated with manual removal of stool (n=64, P<0.05), the sitting position at defecation (n=494, P<0.001) and low frequency of bowel evacuation (>or=3 days) (n=638, P<0.05). Duration >60 min was associated with the use of oral laxatives (n=444, P<0.001) and complete loss of sensory function (n=349, P<0.05). Stool of hard consistency was associated with the manual removal of stool (n=64, P<0.001), the manual removal of stool in combination with digital stimulation (n=53, P<0.001) and the sitting position at defecation (n=494, P<0.05). Stool of soft consistency (n=341) was associated with the complete motor lesion (n=443, P<0.05).

Manual removal of stool was combined with low risk of unplanned bowel evacuations and short duration of evacuation time. These results are useful to improve the outcomes of bowel management in SCI patients.

Constipation defined as changes in the frequency, volume, weight, consistency and ease of passage of the stool occurs in any age group. The most important factors known to promote constipation are reduced physical activity and inadequate dietary intake of fibres, carbohydrates and fluids. Fluid losses induced by diarrhoea and febrile illness alter water balance and promote constipation. When children increase their water consumption above their usual intake, no change in stool frequency and consistency was observed. The improvement of constipation by increasing water intake, therefore, may be effective in children only when voluntary fluid consumption is lower-than-normal for the child's age and activity level. In the elderly, low fluid intake, which may be indicative of hypohydration, was a cause of constipation and a significant relationship between liquid deprivation from 2500 to 500 ml per day and constipation was reported. Dehydration is also observed when saline laxatives are used for the treatment of constipation if fluid replacement is not maintained and may affect the efficacy of the treatment. While sulphate in drinking water does not appear to have a significant laxative effect, fluid intake and magnesium sulphate-rich mineral waters were shown to improve constipation in healthy infants. In conclusion, fluid loss and fluid restriction and thus de-or hypohydration increase constipation. It is thus important to maintain euhydration as a prevention of constipation.

Neurogenic bladder dysfunction after spinal cord injury (SCI) is a major medical and social problem for which there is no definitive solution. After the successful establishment in animals of a skin-central nervous system-bladder reflex pathway for micturition we performed this procedure on 15 patients with SCI who had 3 years of followup.

A total of 15 male volunteers with hyperreflexic neurogenic bladder and detrusor external sphincter dyssynergia (DESD) caused by complete suprasacral SCI underwent limited hemilaminectomy and ventral root (VR) micro anastomosis, usually between the L5 and S2/3 VRs. The L5 dorsal root was left intact as the trigger of micturition after axonal regeneration. Mean followup was 3 years. All patients underwent urodynamic evaluation before surgery and during followup.

Preoperative studies in patients with complete suprasacral SCI revealed hyperreflexic neurogenic bladders and DESD with some differences in storage function during infusion cystometrograms. Of the 15 patients 10 (67%) regained satisfactory bladder control within 12 to 18 months after VR micro anastomosis. Average residual urine decreased from 332 to 31 ml and urinary infection as well as overflow incontinence disappeared. Urodynamic studies revealed a change from detrusor hyperreflexia with DESD and high detrusor pressure to almost normal storage and synergic voiding without DESD. Impaired renal function returned to normal. Two patients (13%) who required a skin stimulator to evoke voiding following the VR anastomosis had partial recovery but more than 100 ml residual urine. One patient was lost to followup and 2 had failure.

An artificial somatic-central nervous system-autonomic reflex arc can be established surgically to provide a novel method for controlling bladder function in patients with complete suprasacral SCI who have hyperreflexic bladder and DESD. Nerve impulses delivered from the efferent neurons of a somatic reflex arc can be transferred to initiate the response of an autonomic effector.

We report an unusual case of aerophagia after traumatic spinal cord injury (SCI), which shows the profound effects of abdominal distension on respiratory ability in such individuals. In this case, abdominal distension resulting from aerophagia reduced the effectiveness of phrenic nerve pacing on diaphragm function necessitating greater use of positive-pressure ventilatory (PPV) support. Reduction of postprandial gastric air and abdominal distension with insertion of a percutaneous endoscopic gastrostomy tube ameliorated the condition and allowed for more effective phrenic nerve pacing and greater PPV-free breathing. We are unaware of a similar case involving an individual with an SCI.

In persons with spinal cord injury (SCI), several studies have shown that large bowel transit is decreased at the level of the left colon and rectum, and that postprandial colonic response to food is absent. To define these parameters further, the effects of food on colonic motility in persons with SCI were studied and compared to those of spinally intact (SI) individuals.

The study was conducted in eight subjects with SCI (four paraplegic and four quadriplegic) and six age-matched SI subjects. After routine bowel preparation, colonoscopy was performed with the proximal end of a solid state pressure transducer catheter (four sensors each separated by 10 cm) tethered to the splenic flexure using endoclips (Olympus). The subjects were then allowed to carry out their usual daily activities. Two phases were compared: 1 h before breakfast, designated as the "resting phase," and 1 h during breakfast, designated as the "food-ingestion phase."

Baseline colonic activity of the SCI group was significantly less than in SI subjects. During meals, the motility index, mean amplitude of the waves, percent activity, and number of waves was significantly less in the SCI group. In both the SI and SCI groups, a postprandial colonic response was observed. However, in the SCI group, the response was seen only in the descending colon and not in the rectosigmoid region.

SCI decreases colonic motility, and this alteration may relate to difficulty with evacuation. The postprandial colonic response in SCI is present but is suboptimal and confined to the descending colon.

A retrospective analysis of 10 patients with pancreatitis after traumatic spinal cord injury.

To determine the conditions leading to nontraumatic pancreatitis in spinal cord injury.

Little is known in the literature about pancreatitis after spinal cord injury. A few authors suggest a multifactorial pathogenesis.

Over a 4-year period the case reports of 338 patients with traumatically caused SCI were reviewed concerning p-amylase and/or lipase elevations. Acute pancreatitis was defined as an elevation of p-amylase and/or lipase of more than three times the upper normal limit.

Ten of 338 patients had p-amylase and/or lipase elevations three times higher than the upper normal limit. All 10 were male with a mean age of 40.4 years. The average onset time of acute pancreatitis was 16 +/- 5.5 days after trauma. The usual etiologic factors of acute pancreatitis such as obstructive, toxic, or traumatic events were excluded.

The clinical recognition of acute pancreatitis in paraplegic and quadriplegic patients is hampered by diminished or lost visceral sensitivity and therefore is based on laboratory investigations. The current authors therefore hypothesize that acute pancreatitis in the setting of high-level spinal cord injury may result from a combination of locally mediated sphincter of Oddi dysfunction and vagal dominant innervation of the pancreatic gland in autonomic failure.

Numerous secondary neurologic and systemic complications can occur in the face of a spinal cord injury. The goal of immediate treatment is early spine immobilization and realignment, stabilization of hemodynamic and pulmonary status, prompt radiographic evaluation, and prevention of medical complications. These measures should optimize the chances for neurologic recovery.

A case report of superior mesenteric artery syndrome (SMA syndrome) occurring in a paraplegic patient 3 months after injury.

To report an unusual case and review the literature of SMA syndrome in spinal cord injured patients, focusing on paraplegic subjects and on tardive presentations.

A Physical Medicine and Rehabilitation Center in Garches (France).

Current medical literature includes reports of only 14 spinal cord injured patients with SMA syndrome. This syndrome has been often described in anorexia nervosa, burns or other causes of cachexia, following correction of spinal deformities or after application of body casts.

In spinal cord injured patients SMA usually occurs in tetraplegic patients during the first weeks after injury. Only four cases of SMA syndrome in paraplegic patients have been described. Late forms are less common than acute ones: only three cases among 14. SMA syndrome consists of a vascular compression of the third part of the duodenum between the ventrally oriented SMA and the aorta. The normal aorto-mesenteric angle ranges between 38 degrees and 65 degrees and can be as low as 6 degrees in patients with SMA syndrome. The diagnosis is usually based on upper gastro-intestinal contrast X-ray study, which shows abrupt vertical compression of the third part of the duodenum. CT scan with angiography is useful in some difficult cases. Conservative management includes early correction of dehydration and electrolyte imbalance, insertion of a nasojejunal tube beyond the obstruction and renutrition. Duodenojejunostomy may be necessary in case of failure of conservative treatment.

SMA syndrome is an unusual gastro-intestinal complication that may occur in paraplegic patients, even late after injury.