Author(s): Fareea Khaliq, MD, Andrew Tsitsilianos, MD, Sunil Sabharwal, MD
Originally published: September 20, 2014 Last updated: June 8, 2023
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Disease/ Disorder

Definition

Upper gastrointestinal (GI) complications after injuries or disorders of the central nervous system (CNS) include dental problems, gastro-esophageal reflux disease (GERD), impaired esophageal and gastric motility, erosive gastritis, cholelithiasis, cholecystitis, pancreatitis, and the superior mesenteric artery (SMA) syndrome.1-20

Dysphagia is discussed as a separate topic and will not be addressed here.

Etiology

Several disorders or injuries of the CNS, including traumatic brain injury (TBI), spinal cord injury (SCI), or severe stroke can be associated with development of erosive gastritis (stress ulcers) in the acute stage.2,3,6 Acute pancreatitis may also develop in the first few days following TBI or SCI,15-17 as may acalculous cholecystitis.10 SCI can lead to GERD,1,12,13 impaired esophageal and gastric motility,1,4,18 gallbladder disease,11 and SMA syndrome.7-9 Potential mechanisms are discussed further in the pathophysiology section.

Epidemiology including risk factors and primary prevention

Erosive gastritis and gastro-intestinal hemorrhage occur primarily during the acute stage of CNS injuries, especially in those who are critically ill or require an intensive care unit (ICU) or mechanical ventilation.3,6 An increased incidence of esophageal motility disorders after SCI has been demonstrated in some studies.4,18 Increased gastric emptying time has been shown to relate to higher level of spinal cord injury.1 GERD can develop in cervical SCI due to reduced esophageal pressure, chronic elevation of the diaphragm, increased duration in the supine position, or Valsalva maneuver performed for constipation,18 and a recent survey showed an increased prevalence of gastric ulcers in the SCI population. 23 SMA syndrome is rare and occurs primarily in those with tetraplegia.7,8 Pancreatitis occurs predominantly in the acute stage of injury, often within the first few days.15 While there is consensus that gallstones are increased after SCI, the true prevalence is unclear as many patients are asymptomatic. However, some studies have reported a higher association of acute cholecystitis in people with SCI compared to the able-bodied population.19,20 The association with the degree of neurological impairment or level of injury is inconsistent in different studies.11,18

Patho-anatomy/physiology

Individuals with neurological impairment of the upper extremity have difficulty performing dental hygiene, which contributes to an increased prevalence of dental and gum disease.14 Furthermore, there is reduced access to dental care for people with tetraplegia, as many offices cannot easily accommodate power wheelchairs. Use of a mouthpiece or mouth stick can also cause dental injury. Reduced salivary secretion may be a side effect of anticholinergic and antispasmodic medications commonly prescribed to individuals with SCI or other CNS disorders and can contribute to dental disease.

While reduced gastro-esophageal sphincter tone may contribute to GERD in some patients with SCI, studies have shown preserved lower esophageal sphincter (LES) tone even in those with complete tetraplegia.20 Increased acid secretion, medications, supine or recumbent positioning, and immobilization may contribute to a higher incidence of GERD in people with CNS injury.4, 12,13 The etiology of erosive gastritis in the setting of acute injury to the CNS is multifactorial. Intact gastric vagal innervation with loss of sympathetic innervation after SCI may contribute to increased gastric acid secretion, as well as to impaired gastric motility. CNS activity has been shown to impact gastric physiology, so these effects would be anticipated in brain injury and stroke. Gastrin release, gastric acid secretion, contractions, and emptying all are under the influence of varied CNS activities and CNS-derived neuropeptides.1

SMA syndrome occurs when the third portion of the duodenum is intermittently compressed by the overlying SMA. Predisposing factors for the SMA syndrome after SCI include rapid weight loss (with loss of mesenteric fat that separates the duodenum from the SMA), constricting spinal orthosis or body jacket, and prolonged supine positioning.7,8

Possible mechanisms for acute pancreatitis after CNS injury include parasympathetic predominance and sphincter of Oddi dysfunction. Medications, including steroids, if given after acute injury, may contribute to the risk.

Bile stasis may contribute to gallbladder disease after CNS injury. It may be caused by impaired sympathetic innervation, impaired entero-hepatic circulation, and altered biliary lipid excretion.

Specific secondary or associated conditions and complications

Gingivitis and periodontal disease may be more severe in individuals who are unable to perform oral hygiene independently. Dental disease may result in caries or occlusion problems. Erosive gastritis following an acute neurological event or injury can cause gastrointestinal hemorrhage. Severe pancreatitis may rarely lead to pancreatic necrosis. Gangrene of the gallbladder is a serious complication of cholecystitis if the diagnosis is missed, and management is delayed. Esophageal stricture or aspiration are potential complications of GERD.

Essentials of Assessment

History

Depending on the degree and nature of neurological impairment, typical symptoms of upper GI disorders may not be present. Obtunded sensorium in those with intracranial injury or pathology may limit clinical evaluation. Pain may be poorly localized in those with sensory impairment or referred to distant skin areas. Heartburn may not be present with GERD in those with complete tetraplegia, although would be expected in those with neurological level of injury below T7. Sensory deficits may also mask the symptoms of pancreatitis or gallstones, although in some studies a significant proportion of patients with SCI and cholelithiasis did have right upper quadrant pain that is typical of the condition.

Impaired gastric motility may lead to early satiety, epigastric bloating and abdominal discomfort.

Symptoms of SMA syndrome include epigastric pain, postprandial fullness, nausea and vomiting, especially when supine. Some patients may report relief with a hyper-flexed “knees-to-chest” position.  Secondary features may include autonomic dysreflexia or increased spasticity in response to the noxious stimulus.7,8

Abdominal emergencies may present with autonomic dysreflexia in people with SCI above the T7 neurological level.

Physical examination

A careful abdominal examination should be performed in patients with gastrointestinal symptoms such as nausea, bloating, or vomiting and in those with sensory impairments who present with non-specific symptoms of uncertain etiology such as fatigue, increased spasticity, or autonomic dysreflexia. Tachycardia or low-grade fever may be present. Loss of motor and reflex function may mask rigidity and guarding, even in the presence of abdominal emergencies. Rigidity of the abdominal wall may also be difficult to evaluate in the presence of abdominal spasticity.

Laboratory studies

Laboratory studies may provide a clue to diagnosis of several upper GI problems, especially in the setting of atypical or vague symptoms, but can be non-specific. Leukocytosis is typical with acute pancreatitis or cholecystitis. Amylase and lipase levels are increased after pancreatitis; lipase levels may be more specific than amylase although both have been reported to be elevated in acute intracranial pathology in the absence of pancreatitis.16 Cholecystitis causes elevated serum bilirubin, alkaline phosphatase, and liver enzymes, though these could also result from other pathologies or as side effects of some medications.10

Imaging

Imaging studies such as plain abdominal films, abdominal ultrasound, and/or computerized tomography (CT) are often needed to evaluate upper GI problems. Plain films may be limited by lack of specificity and sensitivity, but can provide the diagnosis of perforated viscus, bowel ischemia, or renal stones. Ultrasound is especially useful in detecting gallbladder disease, while also being able to examine the liver, pancreas, kidneys, and bile ducts. In SMA syndrome, barium study shows a cutoff between the 3rd and 4th portions of the duodenum in the supine position. CT scan with contrast is an investigation of choice in evaluation of SMA syndrome.7 It provides 3-dimensional measurements that assist in diagnosis, e.g., showing reduced angle between the aorta and SMA (to less than 22 degrees) and reduced distance between the aorta and SMA where the duodenum passes between them.7,8

Supplemental assessment tools

Diagnosis of GERD typically requires an esophagogastroduodenoscopy (EGD); manometric studies may also be considered. Radioisotope scan may be indicated to diagnose cholecystitis if ultrasound examination is unclear.

Rehabilitation Management and Treatments

At different disease stages

Stress ulcer prophylaxis is indicated for the first 4 weeks after CNS injury, with proton pump inhibitors (PPI) or histamine H2-receptor antagonists, especially in critically ill patients or those requiring ICU stay.21,22 However, it should not be continued indiscriminately since the risk diminishes significantly after that period. Prolonged PPI use has been associated with increased Clostridium difficile infection.

General principles of management of acute pancreatitis also apply to those with CNS injuries. These include temporary withholding of oral feeding, decompressing the gut through nasogastric suctioning, providing parenteral nutritional support, and correcting fluid and electrolyte imbalances. Similar measures of nil per oral (NPO) and intravenous fluids are instituted for other causes of acute abdomen such as acute gastric dilation or cholecystitis. Cholecystectomy is indicated for symptomatic gallbladder disease. The role of prophylactic cholecystectomy in the presence of incidentally identified, uncomplicated and asymptomatic, gallstones in patients with SCI is not clear.

Treatment of identified GERD is similar to that in the general population and includes lifestyle modifications such as smoking cessation, reduced alcohol, coffee, mint, and chocolate intake, and avoiding meals just before bedtime or assuming the supine position. Pharmacological treatment includes PPI or H2-receptor antagonists. For refractory cases, fundoplication may be considered, with reduced post-operative recovery time noted with laparoscopic surgical options.

Management of SMA syndrome includes upright positioning for meals, assuming the side-lying position (vs. supine) after eating, and restoration of lost weight. Surgical options to relieve duodenal compression include duodenojejunostomy in resistant cases, though surgery is only rarely needed.7,8

Coordination of care

Adequate access to preventive dental examinations and hygiene are especially important in this patient population to reduce dental complications.

Patient & family education

Patients with sensory impairments of the abdomen and trunk due to tetraplegia or high paraplegia should be educated about the importance of seeking timely evaluation for persistent or acute onset of new non-specific symptoms to avoid delayed diagnosis and management of abdominal emergencies.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Special consideration is needed for timely recognition and management of abdominal emergencies such as a perforated viscus, acute pancreatitis, or acute cholecystitis in people with sensory impairments due to CNS injury. Pain and tenderness may be absent or atypical. A high index of suspicion is warranted to avoid missed or delayed diagnosis. The presence of nausea, vomiting, or non-specific malaise may be the only clinical symptoms. Low grade fever or tachycardia may be the only clinical findings. Bowel sounds may be increased, decreased, or absent, depending on the pathology. Increased spasticity may occur. The presentation may include autonomic dysreflexia in people with SCI above T7. A low threshold for lab testing and imaging is warranted for non-specific gastrointestinal symptoms or exam findings that are not readily explained.

Cutting Edge/ Emerging and Unique Concepts and Practice

Emerging data suggests diminished sensitivity of vagal afferents to gastrointestinal neuroactive peptides and neurotransmitters, which may be one mechanism contributing to upper GI dysmotility following SCI.1

Gaps in the Evidence-Based Knowledge

There is controversy about the indications for prophylactic cholecystectomy in patients with SCI. Some have advocated routine screening ultrasounds to detect the presence of gallbladder disease and a low threshold for surgery, based on higher risk of delayed diagnosis and problematic complications in these patients and a potentially higher complication rate after emergency surgery in the setting of acute cholecystitis. Others believe no specific interventions are indicated in asymptomatic patients.  Another area for additional study is to better define the potential associations between esophageal dysmotility, gastroesophageal reflux disease, and pulmonary function after SCI.4

In recent years, the microbiome-gut-brain axis has become a rapidly expanding interest regarding human health and disease.  The role of the microbiome in GI dysfunction following SCI is a potential area for future research.1

Epidural spinal cord stimulation is a promising technology and an area for ongoing research, not only for locomotor function and pain management but also as a plausible intervention for autonomic dysfunction following SCI, including bowel function.1

References

  1. Holmes GM, Blanke EN. Gastrointestinal dysfunction after spinal cord injury. Exp Neurol. 2019 Oct;320:113009. doi: 10.1016/j.expneurol.2019.113009. Epub 2019 Jul 9. Review. PubMed PMID: 31299180
  2. Ullman T, Reding M. Gastrointestinal dysfunction in stroke. Semin Neurol. 1996. Sep;16(3):269-75
  3. Larson GM, Koch S, O’Dorisio TM, Osadchey B, McGraw P, Richardson JD. Gastric response to severe head injury. Am J Surg. 1984;147(1):97-105.
  4. Radulovic M, Schilero G, Yen C, et al. Greatly increased prevalence of esophageal dysmotility observed in persons with spinal cord injury. Dis Esophagus. 2015;28(7):699–704.
  5. Fynne L, Worsøe J, Gregersen T, Schlageter V, Laurberg S, Krogh K. Gastric and small intestinal dysfunction in spinal cord injury patients. Acta Neurol Scand. 2012 Feb;125(2):123-8.
  6. Berlly MH, Wilmot CB. Acute abdominal emergencies during the first four weeks after spinal cord injury. Arch Phys Med Rehabil.1984;65(11):687-690.
  7. Desai MH, Gall A, Khoo M. Superior mesenteric artery syndrome – A rare presentation and challenge in spinal cord injury rehabilitation: A case report and literature review. J Spinal Cord Med. 2015 Jul;38(4):544-7.
  8. Welsch T, Büchler MW, Kienle P. Recalling superior mesenteric artery syndrome. Dig Surg. 2007;24(3):149-156
  9. Laffont I, Bensmail D, Rech C, Prigent G, Loubert G, Dizien O. Late superior mesenteric artery syndrome in paraplegia: case report and review. Spinal Cord. 2002;40(2):88-91
  10. Branch CL Jr, Albertson DA, Kelly DL. Post-traumatic acalculous cholecystitis on a neurosurgical service. Neurosurgery. 1983;12(1):98-101.
  11. Tola VB, Chamberlain S, Kostyk SK, Soybel DI. Symptomatic gallstones in patients with spinal cord injury. J Gastrointest Surg. 2000;4(6):642-647.
  12. Singh G, Triadafilopoulos G. Gastroesophageal reflux disease in patients with spinal cord injury. J Spinal Cord Med. 2000;23(1):23-27.
  13. Silva CB, Martinez JC, Yanagita ET, et al. The repercussions of spinal cord injury on the action of the diaphragmatic crura for gastroesophageal reflux containment. Spine. 2008;33(26):2892-2897.
  14. Stiefel DJ, Truelove EL, Persson RS, Chin MM, Mandel LS. A comparison of oral health in spinal cord injury and other disability groups. Spec Care Dentist. 1993;13(6):229-235
  15. Nobel D, Baumberger M, Eser P, Michel D, Knecht H, Stocker R. Nontraumatic pancreatitis in spinal cord injury. Spine. 2002; 27(9):E228-232
  16. Liu KJ, Atten MJ, Lichtor T, et al. Serum amylase and lipase elevation is associated with intracranial events. Am Surg. 2001;67(3):215-219.
  17. Pirolla EH, de Barros Filho TE, Godoy-Santos AL, Fregni F. Association of acute pancreatitis or high level of serum pancreatic enzymes in patients with acute spinal cord injury: a prospective study. Spinal Cord. 2014 Nov;52(11):817-20
  18. Enck, P. et al. Upper and Lower Gastrointestinal Motor and Sensory Dysfunction after Human Spinal Cord Injury. Prog Brain Res. 2006;152:373-384.
  19. Gartenberg A, Nessim A, Cho W. Acute cholecystitis. An emerging complication in spinal cord injury patients in the United States. J Neurol Surg. 2022;83:478-480.
  20. Ho P, Yeh K, Pan S. Increased risk of acute pancreatitis in persons with spinal cord injury: a population-based, propensity score-matched longitudinal follow-up study. Spinal Cord. 2021;59:1170-1176.
  21. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis in critically ill patients. Resolving discordant meta-analyses. JAMA. 1996;275(4):308-314.
  22. Lin PC, Chang CH, Hsu PI, Tseng PL, Huang YB. The efficacy and safety of proton pump inhibitors vs histamine-2 receptor antagonists for stress ulcer bleeding prophylaxis among critical care patients: a meta-analysis. Crit Care Med. 2010;38(4):1197–1205.
  23. Squair JW, Dhaliwal R, Cragg JJ, Charbonneau R, Grant C, Phillips AA. National Survey of Bladder and Gastrointestinal Dysfunction in People with Spinal Cord Injury. J Neurotrauma. 2019;36(12):2011-9.

Bibliography

Sabharwal S. Gastrointestinal consequences. In: Sabharwal S, ed. Essentials of Spinal Cord Medicine. New York, NY: Demos Publishing; 2014:313-315.

Ebert E. Gastrointestinal involvement in spinal cord injury: a clinical perspective. J Gastrointestin Liver Dis. 2012;21(1):75-82.

Original Version of the Topic

Robert S. Winston, DO, Sunil Sabharwal, MD. Upper gastro-intestinal problems in disorders of the CNS (excluding dysphagia). 9/20/2014

Previous Revision(s) of the Topic

Sameer Siddiqui, MD, Kayla Roddick, MD, Michael Ortiz, MD, Sunil Sabharwal, MD. Upper gastro-intestinal problems in disorders of the CNS (excluding dysphagia). 10/31/2019

Author Disclosure

Fareea Khaliq, MD
Nothing to Disclose

Andrew Tsitsilianos, MD
Nothing to Disclose

Sunil Sabharwal, MD
Demos Medical/ Springer Publishing, Honorarium, Book Author/Editor
American Board of PM&R, Non-remunerative Positions of Influence, Board Director