Gastrointestinal disorders are frequently encountered by neurologists practicing in a hospital setting. Common problems include abdominal pain, upper or lower gastrointestinal bleeding, constipation with or without ileus, and diarrhea. These symptoms could be present in any hospitalized patients regardless of their primary diagnosis. However, some of these conditions may be more common in neurologically ill patients. These include dysphagia in stroke patients, altered bowel habits in patients with degenerative diseases such as Parkinson disease, or fecal incontinence in spinal cord disorders. In this chapter, we will focus on pathologies frequently seen by hospital neurologists. We will start with swallowing disorders including a discussion of their pathophysiology and the management plan. We will then discuss abdominal pain, gastrointestinal bleeding, diarrhea, and ileus, all problems that may need to be initially assessed and treated by practicing neurologists who take primary responsibility of hospitalized patients. We will finally elaborate on hepatic encephalopathy, a major complication of liver failure and a frequent cause of neurological consultation for evaluation and treatment.
CASE 45-1
A 75-year-old man with history of hypertension, type 2 diabetes, hypercholesterolemia, and prior myocardial infarction (MI) presented with acute onset of left face, arm, and leg weakness. Further diagnostic workup revealed acute ischemia in the right internal capsule. He choked badly when given a sip of water. Fluoroscopic video swallowing study showed prolonged stasis of food in the pharynx with occasional regurgitation to the nasopharynx and frequent passage into the laryngeal inlet.
The mechanism of swallowing is best described by breaking it into three important phases: oral preparatory, pharyngeal, and esophageal. The oral preparatory phase consists of chewing and making a bolus of appropriate size and consistency so that it can be propelled down the pharynx and esophagus. This phase involves CN V, VII, and XII. During the pharyngeal phase, food is propelled from the hypopharynx to the esophagus. This requires closure of the nasopharynx by approximation of the soft palate to the posterior pharynx, and closure of the laryngeal inlet by the epiglottis so that food is propelled to the esophagus and not the trachea. These actions involve CN VII, IX, X, and XII. The esophageal phase is mediated by peristalsis of the esophagus to propel food to the stomach. As food arrives to the lower end of the esophagus, the gastro-esophageal sphincter relaxes, letting the food enter the stomach.
Swallowing difficulty, or dysphagia, is a symptom of numerous medical conditions. The cause of dysphagia most commonly encountered by a neurologist is primarily neurological, although other causes should not be ignored. Common neurological problems leading to swallowing difficulty are stroke, myasthenia gravis (MG), amyotrophic lateral sclerosis (ALS), Parkinson disease (PD), multiple sclerosis (MS), and muscular disease.
Non-neurological causes of dysphagia include poor dentition, head and neck tumors, radiation injury, achalasia, Sjögren’s syndrome, scleroderma, esophageal cancer, esophagitis (infectious, eosinophilic or lymphocytic), and esophageal strictures or webs, among others.
Careful history and physical examination are the most important resources to arrive at the correct diagnosis. Common symptoms of oral dysfunction are drooling, food spillage, sialorrhea, piecemeal swallows, and dysarthria. Pharyngeal dysfunction manifests as coughing or choking during swallowing. Patients with esophageal dysphagia have difficulty swallowing several seconds after initiating a swallow and feel a choking sensation in the chest. The type of food causing the most difficulty can also help narrow the differential diagnosis. Dysphagia that occurs with both solids and liquids from the onset of the disease suggests esophageal dysmotility. On the other hand, dysphagia that starts with solid food and later progresses to occur also with liquids is more suggestive of mechanical obstruction.
Associated symptoms may also help further differentiate the cause (Table 45-1). Drooling, choking, nasal regurgitation of food, and dysarthria are often due to neurological disease. Dry eyes and mouth suggest decreased salivary production, which could be due to medication effect (anticholinergics, antihistamines) or Sjögren’s syndrome. Oral pain or referred pain (eg, otalgia) suggests tumor of the base of tongue, pharynx, or larynx. Food regurgitation, halitosis, a sensation of fullness in the neck, or a history of pneumonia accompanying dysphagia may be the result of a Zenker’s diverticulum, which may be associated with a noncompliant or excessively tight upper esophageal sphincter.1 Heart burn, emesis, chest pain, and weight loss should raise suspicion for esophageal cancer, particularly in elderly patients.
Causes of Dysphagia and Associated Symptoms
| Cause | Associated Signs and Symptoms |
|---|---|
| Stroke | Hemiparesis, facial weakness, dysarthria |
| MG | Muscle fatigability, eyelid ptosis, ocular, facial and masticatory muscle weakness |
| PD | Dementia, rigidity, bradykinesia, resting tremor |
| ALS | Fasciculations, combination of upper and lower motor neuron type of weakness |
| MS | Multiple motor and sensory deficits, unilateral visual loss, recurrent-remitting or progressive course |
| Guillain-Barré syndrome (GBS) | Acute onset of symmetric ascending muscle weakness and mild sensory changes |
| Dermatomyositis/polymyositis | Proximal muscle weakness |
| Zenker’s diverticulum | Halitosis, neck mass |
| Globus hystericus | Anxiety |
Thorough physical examination should be performed in all patients presenting with dysphagia. It must include examination of the oral cavity, head, and neck to look for lymphadenopathy or a mass. Cranial nerves should be examined with particular attention to CN V, VII, IX, X, and XII. Motor examination may show weakness suggesting stroke, MS, or MG. Proximal motor weakness can be seen in dermatomyositis or polymyositis. Masked facies along with cogwheel rigidity may suggest PD.
Diagnostic methods should be selected depending on the findings on history and physical examination. Laboratory or imaging studies (apart from video swallowing evaluation when deemed necessary) are usually not required unless the clinician is suspicious of a certain disease. Laboratory testing may involve testing for MG, MS, or muscle diseases. Most patients with dysphagia related to stroke do not need any additional laboratory test.
Swallowing assessment is recommended in all patients with stroke. In patients with mild stroke symptoms without much involvement of the lower CNs, bedside swallow assessment by nursing staff is sufficient. In other patients, formal swallowing evaluation by occupational or speech therapist may be necessary. It is first conducted at bedside by testing the swallowing of foods with different consistencies. However, a radiographic swallow assessment is often necessary to further characterize the problem and define a safe feeding plan. A barium swallow study consists of ingestion of thick barium while obtaining x-ray films at different times to see its progress. This test has been mostly replaced by the modified barium swallow under video fluoroscopy. This study is ideal for viewing the elevation of the hyoid and larynx, relaxation of the upper esophageal sphincter, and contraction of the pharynx.2 Video fluoroscopy can be used to analyze the movement of pertinent anatomic structures, evaluate pharyngeal muscle activity, and determine exact oral and pharyngeal transit times. It can also identify abnormal movement of a bolus, and identify aspiration and pooling in pharyngeal recesses. As with bedside evaluation, different food consistencies should be tested to determine the individual risk of aspiration and provide recommendations for a safe diet. If a structural abnormality of the nasopharynx is suspected, then nasopharyngeal laryngoscopy should be performed. Exclusion of esophageal pathology may require additional endoscopic or contrast radiologic studies.
Treatment depends on the cause of the dysphagia. Any tumor causing swallowing difficulty demands surgical resection, if possible. When palliation is the goal, radiotherapy could be offered to relieve obstruction caused by esophageal cancer or a compressing mediastinal tumor.
Pharmacologic treatment should also be tailored to the specific etiology. H2 blockers such as ranitidine or proton pump inhibitors such as omeprazole could be tried in patients with gastroesophageal reflux disease. If infection is the cause of dysphagia, specific antimicrobials should be prescribed (eg, dysphagia from candidiasis can be treated with fluconazole). Prokinetic drugs such as metoclopramide, erythromycin, and cisapride may be tried to increase esophageal motility in disorders such as scleroderma. Cisapride can cause ventricular tachyarrhythmia and is available via limited access protocol only in the United States. Artificial saliva is helpful in patients with xerostomia.
Compensatory swallowing strategies could be tried to reduce the risk of aspiration. They generally rely on altering the head and neck position to direct the flow of food. Modifying the texture of solid foods and consistency of liquids is widely used in the management of patients at risk for aspiration or malnutrition from dysphagia.3 Reduced bite size and frequent feeding can be useful. If the patient cannot be safely fed orally, a feeding tube should be placed after having a discussion with the patient and family.
CASE 45-2
A 58-year-old-man with history of MG complained of worsening weakness and shortness of breath. He was started on corticosteroids without much benefit. He was then admitted to hospital. His forced vital capacity and inspiratory force were inadequate. He needed mechanical ventilator support. He was on ibuprofen at home for osteoarthritis and this was continued during his hospital stay. He was not prescribed any prophylaxis for gastrointestinal stress ulcer. On day 4 of admission, he developed fever, hypotension, decreased hematocrit, and leukocytosis. Examination showed diminished bowel sounds and rebound tenderness. Upright abdominal film showed free air under the diaphragm.
Although most causes of abdominal pain are related to GI disease, extraintestinal conditions involving the genitourinary tract, abdominal wall, thorax, or spine can cause abdominal pain. Some of the main causes of abdominal pain are listed in Table 45-2.
Most Frequent Causes of Abdominal Pain
|
Appendicitis, cholecystitis and choledocholithiasis, intestinal obstruction, pancreatitis, mesenteric ischemia, bowel perforation, and diverticulitis account for two thirds of hospital admissions for acute abdominal pain and are associated with significant morbidity and mortality. A dynamic ileus and, to a lesser extent, gastroparesis and neurogenic bowel are the most frequent neurological causes of abdominal pain.
The wide differential diagnosis can be narrowed based on acuity, location, nature, and severity of pain, along with associated symptoms. Physical examination helps narrow the differential diagnosis even further, and history and physical data must be used to obtain targeted investigations to confirm the correct diagnosis.
Acute pain is seen with bowel perforation, biliary and renal colic, ruptured aortic aneurysm, and referred pain from myocardial infarction. Gradual onset of pain with rapid worsening suggests pancreatitis, strangulated bowel, or mesenteric artery thrombosis. Gradual-onset pain with progressive worsening is seen with appendicitis, diverticulitis, and retroperitoneal hematoma.
Defining the location of pain is important. Somatic pain is well localized, while visceral pain is more diffuse and poorly localizing. Pain arising from the right lower quadrant is usually caused by appendicitis. Pain in the right upper quadrant is seen with cholecystitis and biliary lithiasis. Left lower quadrant pain is often caused by diverticulitis or sigmoiditis. Epigastric pain can be a symptom of gastritis or pancreatitis. Costovertebral angle tenderness is characteristic of renal colic. Pain caused by ischemia, bowel obstruction, and inflammatory bowel disease is usually diffuse.
Inflammation of parietal peritoneum, obstruction of a hollow viscus (intestines, biliary tract, and ureters), vascular events (mesenteric ischemia, aortic dissection/rupture), abdominal wall processes (trauma, rectus sheath hematoma, myositis), and referred pain are the common mechanisms of abdominal pain. In patients with neurological disease, alterations in gastric and intestinal peristalsis can be associated with abdominal pain.
Obstruction, peritonitis, and bowel infarction can cause large amounts of intra-abdominal accumulation of fluid (third spacing) and vasodilatation from cytokine release, which, if severe, can produce distributive shock. Patients with peritonitis try to avoid any abdominal movements, while patients with biliary or renal colic move constantly.
Examination should start with inspection to identify abdominal distension or skin color changes in cases of jaundice. Abdominal palpation should precede palpation to determine the characteristic of the bowel sounds before altered by the manual examination of the abdominal wall. Abdominal silence indicates ileus, especially adynamic (bowel sounds may be decreased in some areas and increased in others when ileus is caused by obstruction). Increased bowel sounds can be heard in patients with colitis. Gentle palpation is usually sufficient to elicit signs of peritonitis. If superficial palpation does not produce overt tenderness, deep palpation should follow to examine for rebound tenderness and organomegalies. Localized rebound tenderness suggests specific diagnoses. Murphy’s sign is a useful sign in cases of acute cholecystitis. It is tested by asking the patient to take a deep breath while pressing the area of gall bladder just beneath the liver edge. This sign is present when the patient feels increased discomfort with the deep palpation and interrupts the deep inspiration. Tenderness at McBurney’s point in the right lower quadrant is a sign of appendicitis. Abdominal percussion can elicit guarding in patients with peritonitis and can be used to gauge organomegalies and evaluate for ascites. Exquisite flank tenderness to percussion is a classical sign of renal colic.
Rectal examination can identify fecal impaction (common in elderly patients with constipation), and tenderness when pressing on posterior wall of the rectum may be the only sign of retrocecal appendicitis. In women, a pelvic examination should also be performed to evaluate the possibilities of pelvic inflammatory disease, an adnexal mass or cyst, uterine pathology, or an ectopic pregnancy.
Complete blood cell counts with differential can be informative. Leukocytosis is expected in inflammatory diseases of the intestine, pancreas, gallbladder, and pelvic organs, but is also present in noninflammatory acute conditions, such as renal colic, mesenteric ischemia, or aortic perforation. Acute anemia can alert the clinician to the presence of internal bleeding. Elevated serum amylase is in the laboratory hallmark of pancreatitis but is also seen in patients with perforated gastroduodenal ulcer, intestinal obstruction with strangulation, and acute cholecystitis. Lipase is more specific than amylase for the diagnosis of pancreatitis. Liver function tests can identify hepatic disease and determine if cholestasis is present (signaled by a rise in serum levels of direct bilirubin and alkaline phosphatase). Urinalysis helps identify urinary infection or nephrolithiasis as the cause of pain. In women of childbearing age, it is essential never to forget checking a pregnancy test to rule out ectopic implantation and because the results can affect subsequent decisions on diagnostic testing (eg, use of radiation) and prescribed medications (requiring avoidance of teratogenic agents).
Plain abdominal radiographs are useful to exclude intestinal perforation and obstruction. Dilated colon or small bowel with air fluid levels suggests ileus, and the distribution of the dilated loops can help discriminate between obstructive and adynamic forms of the disease. The presence of free air indicates perforated viscus, most often bowel perforation. Although plain films are cheaper and easier to obtain, abdominal CT is the study of choice in the evaluation of undifferentiated abdominal pain.4 In addition to providing the information offered by plain films, CT scan can also detect thickened colonic or appendiceal wall and streaking of the mesocolon or mesoappendix seen in diverticulitis or appendicitis, signs of gallbladder inflammation, enlarged pancreas, ruptured spleen, adnexal mass, ascites, or retroperitoneal hematoma. Ultrasonography can detect enlarged gallbladder, gallstones, enlarged ovary, or tubal pregnancy, although CT can also be diagnostic in these conditions. Ultrasound is usually preferred as initial modality in pregnant women. Further diagnostic testing such as CT angiography or peritoneal lavage, or specialized tests such as hepatobiliary iminodiacetic acid (HIDA) scan may be needed in selected cases. In some cases, diagnostic laparoscopy is needed to come to the final diagnosis.
In daily practice, a hospital neurologist faced with a patient with abdominal pain should obtain a careful history, perform a detailed general and abdominal examination, and obtain basic laboratory work and, perhaps, initial imaging studies. It may be cost-effective to involve surgeons or gastroenterologists before proceeding to specialized tests.
Ruptured aortic aneurysm is a surgical emergency. Acute onset of pain with a pulsatile mass, with or without bruit, demands immediate surgical consultation. These patients may have orthostatic hypotension or overt shock. Obstruction and peritonitis are also common conditions that need urgent surgical evaluation. Symptoms of intestinal obstruction are anorexia, bloating, nausea and vomiting, and obstipation. Plain radiograph shows dilated bowel loops proximal to the obstruction. CT abdomen is more sensitive and helps locate the level of obstruction. It can also identify the cause of obstruction, such as hernias and mass lesions. Peritonitis is usually caused by perforation of an abdominal or pelvic viscus, including the lower esophagus (eg, Boerhaave syndrome), stomach (peptic ulcer), and intestine (duodenal ulcer, mesenteric infarction, strangulation, carcinoma). CT abdomen can be diagnostic. Supportive care with fluid resuscitation and broad-spectrum antibiotics (including anaerobic coverage) are needed in anticipation of surgical intervention.
CASE 45-3
A 65-year-old man with long-standing history of atrial fibrillation (AF) on chronic anticoagulation with warfarin had an MI 2 months before. High-grade stenosis of the left anterior descending coronary artery was treated with a stent. Consequently, he was prescribed aspirin and clopidogrel while being kept on warfarin for stroke prevention. He was now admitted after a seizure. Head CT showed a subdural hematoma. Further workup revealed a hemoglobin of 6.5 g/dL. Stool test for occult blood was positive.
Signs and symptoms of GI bleeding depend on the acuity of the problem and whether it is due to upper or lower GI bleeding. Acute upper GI bleeding manifests with hematemesis, melena or, rarely hematochezia when the bleeding is very brisk. Symptoms of lower GI bleeding are rectal bleeding and hematochezia. Chronic bleeding from either site may present with anemia, lethargy, and weight loss.
Common causes of upper GI bleeding include:
Gastric and/or duodenal ulcers
Gastroesophageal varices with or without portal hypertensive gastropathy
Esophagitis
Erosive gastritis/duodenitis
Mallory-Weiss syndrome
Angiodysplasia
Mass lesions (polyps/cancers)
Dieulafoy’s lesion
Although the etiologies are variable, the most common cause of upper GI bleeding is gastroduodenal ulcer.5
Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin, physiologic stress, and excess gastric acid are the most common causes of gastroduodenal bleeding. Physiological stress and aspirin use are perhaps the most common causes among patients admitted with neurological problems.
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