GI Dysmotility Clinical Correlates Mary Mc Donald MD

GI Dysmotility: Clinical Correlates Mary Mc. Donald, MD Department of Family Medicine Division of Geriatrics Landon Center on Aging

Learning Objectives After the completion of the lectures and reading assignments, the student should be able to: n n n Describe the innervation of the GI tract and prominent neurotransmitters Compare and contrast esophageal dysmotility abnormalities, including oropharyngeal dysphagia, achalasia, scleroderma of the esophagus, Schatzki’s rings and obstructive dysphagia in terms of location of defect and associated innervation and/or neuroendocrine control. Describe diagnostic approaches to the evaluation of dysphagia.

Learning Objectives (cont) n n n Define gatroparesis List risk factors for the development of gastroparesis Describe pharmacologic and nonpharmacologic treatment options for gastroparesis Distinguish acute from chronic diarrhea and list causes of each Summarize therapeutic approach to the treatment of diarrhea

Learning Objectives (cont) n n List common causes of constipation Recommend appropriate therapy for constipation dependent on its cause. Define Ileus Outline treatment modalities for ileus

Learning Objectives (cont) n n n Define and list causes of constipation Outline treatment options for constipation Define Ilius and list associated treatment options

Clinical Presentation of GI dysmotility n n n Dysphagia-mouth or esophagus Achalasia- lower esophagus Gastroparesis-stomach Diarrhea- small or large bowel Constipation- large bowel Ileus- small and large bowel

Case #1: Mr. Smith n Mr. Smith is a 74 year old male with advanced Parkinson’s disease. He has been noted by his caretakers to cough and choke during feeds, especially with liquids. He develops a right middle lobe pneumonia and requires hospitalization for IV antibiotics.

Dysphagia n n Definition-Inability or difficulty swallowing Typesn n n Oropharyngeal dysphagia Esophageal dysphagia Obstructive dysphagia

Oropharyngeal Dysphagia n n Difficulty moving food or fluid bolus from the front of the mouth to the posterior oropharynx into the esophagus. Most commonly caused by stroke Often seen in neuromuscular diseases like Parkinson’s disease, multiple sclerosis and myasthenia gravis. Also common in end-stage dementia

Mouth and oropharynx n Starts with contractions of the tongue and striated muscles of mastication. Through coordinated action, the food bolus is mixed with saliva and moved from the anterior cavity to the oropharynx where the involuntary swallowing reflex is triggered. n The cerebellum controls output for the motor nuclei of cranial nerves V, VII and XII. n In the posterior oropharrynx, a complex and precisely coordinated succession of muscular contractions and relaxations occurs M. R. SPIEKER. Evaluating Dysphagia. American Family Physician. Vol 61, No 12. June 2000

Esophageal Dysphagia n n n Caused by disordered peristaltic motility of the esophagus Most commonly caused by achalasia or scleroderma Patients describe food getting stuck in their esophagus

Esophagus Motility n As food enters the esophagus, involuntary contractions of the skeletal muscles of the upper esophagus force the bolus through the mid and distal esophagus. n The medulla controls this involuntary swallowing reflex n Cerebral cortex may voluntarily initiate a swallow. n Lower esophageal sphincter relaxes at initiation of swallow and persists until the bolus enters the stomach. M. R. SPIEKER. Evaluating Dysphagia. American Family Physician. Vol 61, No 12. June 2000

Swallowing - Esophageal Phase • • • Food from esophagus to stomach (8 -10 sec, may be 5 -8 sec) Primary peristalsis - continued peristaltic wave from that begun in pharynx Secondary peristalsis - if residual food in esophagus, initiated by intrinsic nervous system and vago-vagal responses Insert picture. 13

Achalasia n n n Disorder of the lower esophageal sphincter to relax with swallow Loss of peristalsis movement through the esophagus Presents as progressive difficulty swallowing solids and liquids, chest pain and regurgitation associated with meals.

Scleroderma n n Chronic disorder characterized by diffuse fibrosis of the skin and internal organs When fibrosis involves the esophagus, dysmotility results. Four times more common in women than men Usually occurs in 3 rd to 6 th decade of life http: //www. accessmedicine. com. proxy. kumc. edu: 2048/content. aspx? a. ID=2197876&search. Str=scleroderma

Obstructive Dysphagia n n Physical obstruction of movement of food or fluid bolus through the esophagus. Most commonly caused by strictures, Schatzki’s rings, or external compression on the esophagus by tumor or vasculature.

Schatzki’s rings n n n A thin submucosal circumferential ring in the lower esophagus at the squamocolumnar junction Can become increasingly stenotic when associated with gastroesophageal reflux disease Responsive to physical dilation and Reflux medications

Diagnostic Tools n n Oropharyngeal= video swallow under fluoroscopy Esophageal= Barium Swallow, esophageal manometry, endoscopy

ACHALASIA Insert picture Esophagogram showed a bird's beak appearance of the gastroesophageal junction and total aperistalsis of the esophageal body consistent with the diagnosis of achalasia.

Scleroderma of the Esophagus Insert picture This picture was taken one-half hour after patient swallowed barium. Note that barium is still present in the esophagus. There is also retained barium in the stomach. The duodenum is enlarged and the small intestine is dilated.

Barium Swallow of Schatski’s Ring Insert picture

Barium Swallow: External Esophageal Compression Insert picture

Videofluoroscopy Swallow Insert picture

Endoscopy Normal Lower Esophageal Sphincter

Case #2: Mrs. Green n Mrs. Green is a 47 year old, diabetic female with complaint of intermittent nausea and vomiting. She vomits several times a day, often several hours after eating a meal. She also reports feeling uncomfortably bloated much of the time. She has noted worsening of her blood sugar control since these symptoms began 2 months ago.

Gastroparesis n n A chronic condition of intermittent nausea and vomiting, early satiety, bloating and upper abdominal discomfort Gastric emptying studies reveal retention of 60% after 2 hours or more than 10% after 4 hours (abnormal gastric emptying time) Absence of a mechanical lesion to explain symptoms Postprandial vomiting (1 -3 hours after meals)

Who Gets Gastroparesis? n n Endocrine disorders (diabetes, hypothyroidism) Postoperative (vagotomy, gastric resection) Neurologic (Parkinsons, MS, MD) Infectious (postviral)

Stomach Motility Insert picture The stomach can be divided into two functional regions for considerations of motility

Stomach Motility n Extrinsic Neuronal Controln n Parasympathetic- primarily stimulatory, cholinergic efferents via vagal nerve. Also some inhibitory efferents releasing vasoactive intestinal polypeptide (VIP) and nitric oxide as their major neurotransmitters. Sympathetic- inhibitory control via noradrenaline

Stomach Motility n Intrinsic Neuronal Controln n pacemaker cells of the intestine, known as interstitial cells of Cajal, located within the circular muscle layers of the stomach and proximal gut. This communication establishes the rate at which contractions of the tissue maximally can occur

Factors in the Rate of Gastric Emptying n Decreased Emptying n Increased Emptying n Foods (fat>protein>CHO) n Foods (volume, liquids, low n High osmolarity p. H) n Drugs-anticholinergics n Drugs - cholinergics n GI Hormones-secretin, CCK, n GI hormones - gastrin, motilin glucagon n Diseases/surgery - irritable n Diseases/surgery-pseudocolon, pyloroplasty, partial obstruction, diabetic neuropathy, gastrectomy autonomic neuropathy n Gastric distension n Stress, fear, depression n larger food particles (~> 7 mm) n Smaller food particles (2 -3 mm) 31

Pathophysiology of Gastroparesis n n Autonomic neuropathy- a complication of longstanding diabetes as part of a more generalized neuropathy Vagotomy interrupts parasympathetic stimulation of gastric motor function

Treatment of Gastroparesis n Pharmacotherapyn n n 5 -HT 4 agonism vagal, dopamine, central 5 -HT 3 antagonism Gastric pacing with a neurostimulator Avoid opiates, anticholinergics Small, frequent meals, avoiding gas-producing foods Achieve ideal blood sugar levels in diabetics

Gastric Pacing n Implantable artificial pacemaker devices developed to deliver pulsatile electrical impulses to the pyloris of the stomach to control gastric motility.

Stomach Motility Insert picture

Case #3: Ms. Brown n Ms. Brown is a 24 year old woman who reports several month history diarrhea. She has intermittent, diffuse, crampy lower abdominal pain and feels bloated and distended. She has tried multiply over the counter remedies for diarrhea but is unable to regulate her bowels. Her symptoms are often alleviated by having a BM. She denies and fevers or chills or visible blood in her stools.

Small Intestine and Colon Motility n Intrinsic Neuronal Control n n Myenteric (regulates smooth muscle function), submucosal (regulates secretion and absorption), and mucosal neuronal layers Neurotransmitters- acetylcholine, opioids, norepinephrine, serotonin, ATP, and nitric oxide

Small Intestine and Colon Motility n Extrinsic neuronal control n n Parasympathetic- visceral sensory and excitatory motor innervation (via acetylcholine and substance P) Sympathetic- excitatory to sphincters and inhibitory to nonsphincteric muscle

Diarrhea n n n Defined as stool weight of more than 200 -300 g/24 hours May also be defined as stools more frequent than 3/day or liquidity of feces More than 10 Lof fluid enters the duodenum daily. All but 1. 5 L absorbed by the small intestine. Less than 200 ml reach the rectum.

Types of Diarrhea (1 of 3) n Acute Diarrhea- less than 2 weeks duration n Bacterial infection viral infection Parasitic infection

Types of Diarrhea (2 of 3) n Chronic Diarrhea- > 2 weeks duration n Osmotic Diarrhea n n n Secretory Diarrhea n n Disaccharide malabsorption Chronic laxative use Endocrine tumors Bile salt malabsorption Chronic laxative use Inflammatory Diarrhea- Inflammatory Bowel Disease

Types of Diarrhea (3 of 3) n Malabsorption Syndromes n n n Intestinal resections Intestinal bacterial overgrowth Motility Disorders n n n Irritable Bowel Syndrome Post-surgical- vagotomy, partial gastric resection Systemic diseases- diabetes, hyperthyroidism, scleroderma

Pharmacologic Treatment of Diarrhea n n n Bile Acid Sequestrants- Bile salts usually absorbed in the distal ileum. Excessive concentrations of bile salts reaching the colon results in water and electrolyte secretion. Sequestrants bind the excess bile salts, avoiding effect on Bismuth subsalicylate- converted to salisylate in the stomach and has antisecretory, antiinflammatory effects on GI tract. Loperamide- Opiate receptor activity. Does not cross the CNS

Irritable Bowel Syndrome n n n Disorder of bowel motility abnormal myoelectrical and motor abnormalities have been identified in the colon and small intestine. May have constipation-predominant or diarrheapredominant symptoms 2/3 are women No clear diagnostic study Symptoms not explained by any structural or biochemical abnormality

Treatment Modalities for IBS n n Avoid dietary triggers Pharmacologic approaches n n Antispasmodic medications- anticholinergic mechanism Antidiarrheal agents Anticonstipation agents IBS specific drugs- serotonin receptor agonists (increase motility) and antagonists (decrease motility)

Case #4: Mr. Smith n Mr. Smith is a 75 year old gentleman who reports longstanding constipation. He has bowel movements about twice a week with much straining and feeling of incomplete evacuation. He has developed hemorrhoids over the last two years and often has pain and bleeding associated with bowel movements. He reports feeling bloated and having decreased appetite. He has lost ten pounds in the last year.

Constipation n n persistent, difficult, infrequent, or seemingly incomplete defecation. Wide variability of normal bowel habits makes it difficulty to define. Often described as fewer than 3 bowel movements weekly. Hard, pellet stools indicates slowed motility.

Constipation Insert image Note dilated, stoolfilled ascending, transverse, descending colon and rectum.

Narcotic Bowel n n n Opiate–receptor activation inhibits the presynaptic release and postsynaptic response to excitatory neurotransmitters (eg, acetylcholine, substance P) from nociceptive neurons Opioids slow gastric emptying time by reducing peristalsis Tolerance develops with most side effects of chronic opiate use, except constipation

Treatment of Constipation n n n Fiber-rich (20 to 30 g daily) diet Adequate fluid intake Appropriate bowel habits and training Avoidance of constipating drugs Increase physical activity Medsn n Bulk-forming agents Laxatives Nonspecific stimulants or irritants Stool softeners (surfactants, emollients)

Laxatives n Generally act in one of the following ways: 1. 2. 3. enhancing retention of intraluminal fluid by hydrophilic or osmotic mechanisms; decreasing net absorption of fluid by effects on small- and large-bowel fluid and electrolyte transport; or altering motility by either inhibiting segmenting (nonpropulsive) contractions or stimulating propulsive contractions. Goodman and Gilman’s Pharmacology. VI. Drugs Affecting Gastrointestinal Function. Chapter 37.

Ileus n n Signs and symptoms of intestinal obstruction without mechanical cause. Also called “pseudo-obstruction” Most commonly caused by surgery, infection, inflammation or medications Postoperative ileus common in abdominal surgeries, likely due to stress-induced sympathetic reflexes, pain medications, inflammation.

Ileus Insert image Note marked dilation of small and large intestine

Treatment of Ileus n n n Tincture of time IV fluid/electrolyte/nutritional replacement Gastric decompression if nausea/vomiting Promotility agents not routinely recommended May required surgical intervention