This document was supplied by the Gastroparesis and Dysmotilities Association (GDPA). Their web site can be found at www.gdpa.net.
These motility problems present as a spectrum from mild through severe. Although, each affected region has its own diagnostic term; but all share a weakened to flaccid, discordant function of motility. As many as a third of those suffering for years from troublesome, non-specific digestive motility symptoms may slowly progress to a more severe state. Generally speaking, young to middle-aged females make up the largest group to move on to a more severe state, for which no known cause can be identified. This unknown cause is labeled “idiopathic”. These idiopathic forms show a variable course over the years, with symptom flair-ups followed by periods of quiescence. As well, many individuals affected with an enteric infection (whether bacterial, parasitic or viral) can then develop a post-infection dysmotility (or abnormal motility), which may slowly resolve (over a period of from two to five years) but, in the interim, can significantly impact quality of life to a disabling degree. [Dysmotilies can also develop after surgery - more details about this on www.gdpa.net]
The four major motility diseases:
Gastroparesis (GP) refers to the motility disturbance occurring primarily in the stomach.
The term “gastro” refers to the stomach while “paresis” means weakness or paralysis. Also called “delayed gastric emptying” to describe the observed phenomenon found in gastric emptying studies, it is the most common of all the digestive motility diseases.
In its severe, classical form, gastroparesis is easily recognizable by most gastroenterologists. In its less severe form, it may take years to gain a proper diagnosis. Often, diagnosis rests upon the experience of the clinician since there is not a great deal of research nor is there a consensus to guide the definition or diagnosis of this disease.
The most troubling signs and symptoms of severe gastroparesis are unrelenting nausea and vomiting. These symptoms frequently occur along with abdominal pain due to the distended, poorly functioning stomach, and also with pain from chronic acid reflux into the esophagus and mouth as a consequence of gastric stasis. These symptoms currently have very few effective treatments, while some patients do not respond to any remedy.
Nutritional compromise is the hallmark of these unrelenting symptoms. Patients suffering from gastroparesis show a slow, insidious progression of malnourishment, and many will require jejunostomy tubes or total parenteral nutrition in order to stabilize their weight loss. The placement of tubes to re-hydrate and provide nutrition does not alleviate symptoms. Patients still “pool” secretions in their stomachs and vomit these up. Venting by gastrectomy tubes allows for the drainage of stomach secretions and gastric decompression, but this process further jeopardizes hydration and electrolyte balance, and again, does not alleviate the confounding and enormously difficult-to-manage symptom of nausea. Patients may require two or three prescription, anti-nauseant medications in their attempt to control this very debilitating symptom.
Chronic Intestinal Pseudo-obstruction (CIP) is the diagnostic name applied to the regional, paralytic motility disease affecting the small intestine. It often leads to a general failure of the entire digestive tract. Also called CIP, this motility disease has the greatest degree of morbidity and mortality. CIP usually has an insidious onset and may take from three to ten years for an accurate diagnosis to be obtained. The diagnosis of CIP is usually preceded by several years with nonspecific abdominal symptoms. During this time, many patients may undergo unnecessary, multiple, surgical interventions in the attempt to find a mechanical bowel obstruction. Delayed gastric emptying (gastroparesis), as well as puzzling autonomic nervous system (ANS) dysfunction, is also frequently found with CIP. The ANS dysfunction creates baffling symptoms resulting in urinary retention, sweating abnormalities, changes in heart rate, and blood pressure fluctuations.
The dyspeptic symptoms described above also occur with CIP, but this group of patients suffers to a far greater degree from intense abdominal pain. This intense pain often requires narcotic use. The narcotics then have the effect of further slowing down the weak digestive tract. Intractable constipation is also a predominating symptom with CIP, creating problems of severe fecal impaction. Secondary problems, such as “small bowel bacterial overgrowth”, commonly occur and greatly impair the already compromised digestion. As well, co-morbidities of chronic pancreatitis, gall bladder failure, and/or liver impairment are not uncommon, and reflect a motility derangement of even the pancreatic and biliary ducts, causing pooling and stasis within these organs.
Intractable nausea, vomiting, and the vomiting of bile are seen with CIP. Nutritional support for this group of patients, having intestinal failure, is more dependent upon total parenteral nutrition (TPN). This method is required since insufficient nutrient absorption can occur with the poorly functioning intestines.
For clarification, enteral and total parenteral nutrition (TPN) are forms of nutritional support in which a liquid formula is infused through a catheter via an infusion pump. For enteral support, a catheter is run through the abdomen into the small intestine (jejunostomy). For TPN, a catheter is threaded through the chest wall into a large vein (central venous catheter) or a PICC line (peripherally inserted central catheter). Infusion rates with enteral feeding can be very slow due to intestinal spasms, and with TPN, due to vascular spasms. A meal can take many hours or as long as all day to infuse. This intervention usually does not halt nausea, vomiting, or abdominal pain. Finally, many who rely on parenteral nutrition, suffer, on average, approximately two life threatening blood infections each year as a complication of this form of feeding. TPN also carries a risk of liver failure and small bowel bacterial overgrowth.
If liver failure ensues from TPN, the only treatment option left for these patients is an intestinal transplant. Before the advent of total parenteral nutrition in the 1970s, many more patients died of CIP.
Even if good nutrition is restored with TPN, symptom bouts persist with flare-ups of pseudo-obstruction, creating a medical emergency. These unpredictable flare-ups lead to vomiting, excruciating abdominal pain, and abdominal distention from the air-filled small bowel. Life with CIP means repeated and prolonged hospital stays, a future inescapably intertwined with a local hospital. This patient group is often medially mismanaged since few patients are seen by any one medical centre. Patients become fearful as they are at the mercy of poor management. There are no centres of excellence to which these patients can turn for support, and no treatment consensus guidelines for physicians in order to help guide them in their medical management.
Colonic Inertia (CI) is the regional motility disease that primarily affects the colon. Also called slow transit constipation, it too is characterized by weak to flaccid tone with uncoordinated contractile activity within the colon. Its onset is insidious. Severe constipation with fecal impaction may result in problems of overflow diarrhea and fecal incontinence with bleeding anal fissures. This motility disease causes severe abdominal distention, unrelenting pain, and great risk of severe fecal impaction leading to complete blockage, dilation of the colon, and risk of intestinal rupture. A rupture results in spillage of fecal matter into the abdominal cavity causing a life-threatening infection known as “peritonitis”. Surgical remedies are not always a quick fix since the motility disturbances can progress farther up the digestive tract, thus representing a more generalized disease of impaired motility.
The motility disease affecting the esophagus is known as “achalasia,” meaning “failure to relax”. Characterized by dysphasia (difficulty in swallowing) of solids and liquids, substances entering the esophagus become trapped due to the persistent contraction of the lower esophageal sphincter (LES), a ring-like muscle surrounding the esophagus and acting as a valve at the gastroesophageal junction. Achalasia is further characterized by weak to absent peristaltic waves of motility within the esophagus. If unable to pass naturally into the stomach, these trapped contents must be expelled through voluntary regurgitation. Patients present with a number of symptoms, depending upon the stage at which the disease is diagnosed. In addition to the aforementioned difficulty in swallowing and regurgitation, symptoms can include severe chest pain due to esophageal muscle spasms (a sub-condition known as “vigorous achalasia”), heartburn/GERD, coughing, wheezing, and pneumonia. Progressive intolerance for food substances and consistencies, along with unanticipated obstructive instances, adversely affects a patient’s general quality of life. Indeed, the unpredictable nature of the aperistalsis and LES malfunction makes achalasia an oppressive condition, with frequent choking, dramatic weight loss and malnutrition commonly experienced.
Many patients suffering from the more severe digestive motility diseases will often present with a blending of all the above-identified diseases.
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