Other upper gastro-intestinal problems in disorders of the CNS (excluding dysphagia)

Author(s): Robert S. Winston, DO, Sunil Sabharwal

Originally published:09/20/2014

Last updated:09/20/2014

1. DISEASE/DISORDER:

Definition

Upper gastrointestinal (GI) problems after injuries or disorders of the central nervous system (CNS) include: gastro-esophageal reflux disease (GERD), impaired gastric motility, erosive gastritis, gallbladder disease including gallstones and cholecystitis, pancreatitis, and the superior mesenteric artery (SMA) syndrome. Dental problems are also common.

Dysphagia, which occurs with several CNS disorders, is discussed as a separate topic.

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.1,2Acute pancreatitis may also develop in the first few days following TBI or SCI,3 as may acalculous cholecystitis.4 SCI can lead to GERD,5,6 impaired gastric motility, gallbladder disease,7 and SMA syndrome.8,9 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 after acute CNS injuries, especially in those who are critically ill or require intensive care unit (ICU) stay or mechanical ventilation. Increased gastric emptying time has been shown to relate to higher level of SCI. SMA syndrome is rare and occurs primarily in those with tetraplegia. Pancreatitis occurs predominantly in the acute stage of injury, often within the first few days. While there is general consensus that gallstones are increased after SCI, the true prevalence is unclear because many patients are asymptomatic; association with the degree of neurological impairment or level of injury is inconsistent in different studies.

Patho-anatomy/physiology

Individuals with neurological impairment of upper extremity function have difficulty performing dental hygiene, contributing to an increased prevalence of dental and gum disease.10 An additional contributing factor to potential dental problems after tetraplegia is reduced access to dental care, since only some dental offices are able to accommodate power wheelchairs. Use of a mouthpiece or mouth stick can also cause dental injury.

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. Increased acid secretion, medications, recumbancy, and immobilization may contribute to a higher incidence of GERD in people with CNS injury. 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.

SMA syndrome can occur if 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.

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

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 diagnosis is missed and management is delayed. Dental disease may result in caries and/or occlusion problems. Esophageal stricture or aspiration are potential complications of GERD.

2. 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 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 and epigastric bloating.

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.

Abdominal emergencies may present with autonomic dysreflexia in people with SCI above the T6 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

Lab 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.11 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.

Imaging

Imaging studies such as plain abdominal films, abdominal ultrasound, and/or computerized tomography (CT) are often needed to evaluate upper GI problems, including gallbladder or pancreatic disease. Plain films may 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 is also used in evaluation of SMA syndrome. 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.

Supplemental assessment tools

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

3. 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.12 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 temporarily withholding oral feeding, decompressing the gut through nasogastric suctioning, providing parenteral nutritional support, and correcting fluid and electrolyte balance as needed. 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 modification 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. Surgical options such as fundoplication may be considered for those resistant to medical therapy. Surgery can often be performed laproscopically, with reduced post-operative recovery time.

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.

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. 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 T6. A low threshold for lab testing and imaging is warranted for non-specific findings that are not readily explained.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Certain vasoactive metabolites of angiotensin are being evaluated as gastro-protective agents for stress ulceration, with promising results in preliminary animal studies.13

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

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 of 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.

REFERENCES

1. 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.

2. 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.

3. Nobel D, Baumberger M, Eser P, Michel D, Knecht H, Stocker R. Nontraumatic pancreatitis in spinal cord injury.Spine. 2002; 27(9):E228-232.

4. Branch CL Jr, Albertson DA, Kelly DL. Post-traumatic acalculous cholecystitis on a neurosurgical service.Neurosurgery. 1983;12(1):98-101.

5. Singh G, Triadafilopoulos G. Gastroesophageal reflux disease in patients with spinal cord injury.J Spinal Cord Med. 2000;23(1):23-27.

6. 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.

7. Tola VB, Chamberlain S, Kostyk SK, Soybel DI. Symptomatic gallstones in patients with spinal cord injury.J Gastrointest Surg. 2000;4(6):642-647.

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. 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.

11. 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.

12. 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.

13. Magierowski M, Jasnos K, Pawlik M, Krzysiek-Maczka G, Ptak-Belowska A, Olszanecki R, Kwiecien S, Korbut R, Brzozowski T. Role of angiotensin-(1-7) in gastroprotection against stress-induced ulcerogenesis. The involvement of masreceptor, nitric oxide, prostaglandins, and sensory neuropeptides.J Pharmacol Exp Ther.2013 Dec;347(3):717-26

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 clinicalperspective.J Gastrointestin Liver Dis. 2012;21(1):75-82.

Author Disclosures
ROBERT S. WINSTON, DO
Author indicated he/she has no relevant financial relationships to disclose.
SUNIL SABHARWAL
Author indicated he/she has no relevant financial relationships to disclose.

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