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A1-G Surg Note Small Bowel > Motility Disorders of the Stomach and Small Bowel > Flashcards

Motility Disorders of the Stomach and Small Bowel Flashcards

1
Q

What controls the contractile activities of the stomach and small intestine?

A

The enteric (autonomic) neuromuscular system within the wall of the gut.

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2
Q

What role do the parasympathetic/vagal nerves and sympathetic/paravertebral nerves play in gut motility?

A

They do not control or initiate motility but can influence motor patterns

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3
Q

What are the two basic patterns of contractile activity in the stomach and small intestine?

A

One during fasting (interdigestive period) and another after feeding (postprandial period)

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4
Q

What generates the contractile activity in the gut?

A

Spontaneously active neuromotor cells within the gut wall.

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5
Q

What occurs during the interdigestive period in the stomach and small intestine?

A

Intense contractions cycle peristaltically, beginning in the stomach and moving slowly down the small intestine over 90 minutes to clear undigested food and debris.

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6
Q

How do contractile patterns change during the postprandial period?

A

The stomach mixes and breaks down food particles for digestion, while the small intestine slows transit to maximize absorption

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7
Q

What prevents larger food particles from leaving the stomach during the postprandial period

A

The antropyloric pump controls the size of the pylorus, only allowing particles smaller than 1 cm to pass.

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8
Q

What role does the proximal stomach play in gastric emptying?

A

It controls the emptying of liquids through slow, continuous tonic activity and vagally mediated “receptive relaxation.”

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9
Q

What type of contractions occur in the distal stomach?

A

Phasic contractions (2–4 per minute) arise from a pacemaker region in the mid-stomach and propagate distally to aid in the mechanical breakdown of food

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10
Q

How do injuries to the vagus nerves affect gastric motility?

A

They can impair the relaxation of the proximal stomach (emptying of liquids) and disrupt the coordination of contractions of the distal stomach (emptying of solids)

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11
Q

Where is the pacemaker region located in the small intestine, and what does it control?

A

It is in the proximal duodenum and controls the rate and direction of small intestinal contractions

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12
Q

What is the length of a true peristaltic contraction in the small intestine after a meal?

A

It typically migrates only 5 to 10 cm.

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13
Q

What is the purpose of the segmenting contraction pattern in the small intestine?

A

It increases contact of the luminal content with the mucosa, slows transit, and enhances absorption.

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14
Q

What role does the sympathetic system play in small intestinal contractions?

A

It has modulatory (primarily inhibitory) effects, as seen in conditions like postoperative ileus (POI) or adynamic ileus caused by retroperitoneal trauma or infection

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15
Q

What are common causes of gastric dysmotility seen by surgeons?

A

Operations that cut or injure the vagus nerves, such as gastrectomy, esophagectomy, and hiatal herniorrhaphy

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16
Q

How can chronic illness contribute to gastric dysmotility?

A

Neuropathy from chronic conditions like poorly controlled diabetes can damage the vagus nerves

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17
Q

What was a consequence of truncal vagotomy in past duodenal ulcer surgeries?

A

Rapid emptying of liquids leading to dumping syndrome and disrupted emptying of solids due to loss of vagally mediated relaxation

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18
Q

What syndrome can occur after the creation of a Roux-en-Y limb?

A

Roux stasis syndrome, characterized by delayed gastric emptying due to erratic, noncoordinated contractions.

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19
Q

What disrupts myoelectric continuity in a Roux-en-Y limb?

A

Transection of the jejunum, which affects the coordination of contractions with the duodenal pacemaker

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20
Q

What is “gastroparesis-like syndrome” and who typically experiences it?

A

A poorly understood condition with symptoms similar to gastroparesis, usually occurring in young females, often without objective delay in gastric emptying.

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21
Q

What are the two main types of true gastric motility disorders?

A

Delayed emptying (gastroparesis) and too rapid emptying (dumping syndrome)

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22
Q

What role does the proximal stomach play in digestion?

A

It provides vagally mediated receptive relaxation for temporary storage and starts the enzymatic and mechanical breakdown of ingested content.

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23
Q

How does the presence of amino acids in the duodenum affect the proximal stomach?

A

It triggers hormonal signaling that leads to a slow tonic contraction, increasing intraluminal pressure and emptying chyme into the duodenum.

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24
Q

How do fats in the duodenum impact gastric emptying?

A

They slow gastric emptying by prolonging the relaxation of the proximal stomach

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25
Q

What factors can disrupt gastric emptying mediated by the enteric nervous system?

A

Surgical procedures, diabetes, hypothyroidism, chronic narcotic use, and cancer.

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26
Q

How does aging affect gastric emptying?

A

The rate of gastric emptying decreases with age, making older patients more susceptible to gastric motility disorders

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27
Q

What types of operations can lead to delayed gastric emptying?

A

Operations on the distal esophagus or stomach, including known or inadvertent vagotomy, Roux-en-Y gastrojejunostomy, and antireflux procedures.

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28
Q

How does the risk of delayed gastric emptying change after a gastrectomy with a truncal vagotomy?

A

The risk increases twofold

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29
Q

What is the rate of delayed gastric emptying after a classic pancreatoduodenectomy with Roux-en-Y reconstruction?

A

Up to 30%

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30
Q

What are key contributors to delayed gastric emptying after certain surgeries?

A

Vagus nerve dysfunction and disruption of the continuity between the proximal jejunum and the duodenal pacemaker

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31
Q

How can truncal vagotomy affect gastric motility?

A

It can disrupt afferent vagal signaling to the brain, leading to gastric stasis or atony.

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32
Q

What is a potential outcome of vagus nerve dysfunction after gastric surgery?

A

Incomplete gastric emptying or gastric stasis

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33
Q

What symptoms are commonly associated with true gastroparesis?

A

Epigastric fullness, early satiety, nausea, and vomiting, usually of solids more than liquids, with delayed vomiting of undigested food

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34
Q

What symptom is virtually pathognomonic of gastroparesis if there is no mechanical obstruction?

A

Delayed vomiting of undigested food hours or a day after ingestion.

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35
Q

What are the typical effects of gastroparesis on liquid and solid intake?

A

Liquids are better tolerated than solids, but early satiety and anorexia can still limit calorie intake, potentially leading to dehydration, weight loss, or malnutrition.

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36
Q

What risk factors should be evaluated in a patient with suspected gastroparesis?

A

Prior upper abdominal surgery and metabolic disturbances like diabetes or hypothyroidism

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37
Q

What physical exam finding may suggest delayed gastric emptying from mechanical obstruction?

A

A succussion splash

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38
Q

What mechanical obstructions should be excluded in the diagnostic phase of suspected gastroparesis?

A

Efferent limb syndrome, anastomotic stricture, or post-gastroenterostomy intussusception

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39
Q

What nutritional marker may be helpful in evaluating the nutritional state in gastroparesis?

A

Prealbumin, due to its shorter half-life compared to albumin

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40
Q

Why is it important to rule out NSAID or aspirin use in patients with an anastomotic stricture?

A

Because NSAIDs and aspirin can cause ulceration and anastomotic inflammation, which can contribute to stricture formation

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41
Q

What imaging technique can help rule out mechanical obstruction in suspected gastroparesis?

A

Abdominal x-rays with contrast.

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42
Q

Why is gastric distension uncommon in gastroparesis associated with vagal dysfunction?

A

Because it involves loss of proximal gastric relaxation rather than obstruction.

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43
Q

What is the gold standard test for diagnosing gastroparesis?

A

The 4-hour scintigraphic gastric emptying test for solids.

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44
Q

How is gastroparesis severity graded in the 4-hour scintigraphic gastric emptying test?

A

Based on percent retention at 4 hours: mild (<15%), moderate (16%-35%), and severe (>35%).

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45
Q

What alternative test to scintigraphy avoids radiation but is primarily used experimentally?

A

Wireless motility capsule (WMC).

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46
Q

What other test used in Japan is experimental for measuring gastric emptying in the United States?

A

Carbon breath testing.

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47
Q

Why is a barium swallow not recommended for assessing gastric emptying?

A

It is not a good measure of gastric emptying.

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48
Q

What is the initial step in treating gastroparesis?

A

Management of contributing factors, such as better glucose control or treatment of hypothyroidism.

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49
Q

What dietary modifications are recommended for patients with gastroparesis?

A

Ingesting more liquids than solids
eating smaller and more frequent meals (ideally six or more per day)
and following a low-residue, softer food diet

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50
Q

What types of liquid formulations are suggested for patients with nutritional challenges in gastroparesis?

A

High-calorie, high-protein, low-fat small particle liquid formulations, unless associated with problematic dumping syndrome > give high Protein Formula for Dumping

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51
Q

What prokinetic drugs may be tried if dietary changes do not alleviate gastroparesis symptoms?

A

Metoclopramide, domperidone (for patients with an antrum), and low-dose erythromycin (125 mg).

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52
Q

What is a key side effect of metoclopramide that physicians need to warn patients about?

A

Extrapyramidal side effects, such as spasmodic dystonias and tardive dyskinesia, especially in the elderly.

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53
Q

What are the concerns associated with domperidone, which is used outside the US?

A

Cardiovascular proarrhythmic risks, such as QT prolongation and tachyphylaxis

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54
Q

Why might erythromycin be used short-term for gastroparesis?

A

It can improve gastric emptying but may develop tachyphylaxis, requiring “drug holidays.”

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55
Q

What role do tricyclic antidepressants play in treating gastroparesis?

A

They may be considered for refractory nausea and vomiting, but they can potentially worsen symptoms due to their anticholinergic effects

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56
Q

When might total parenteral nutrition (TPN) or enteral nutrition be necessary for gastroparesis patients?

A

In severe and life-threatening cases of malnutrition; enteral nutrition should be tried before TPN.

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57
Q

What is a limitation of the newer 5HT3 antagonists and 5HT4 receptor agonists in gastroparesis treatment?

A

They may help with nausea and vomiting but do not increase effective gastric emptying.

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58
Q

When should operative intervention for gastroparesis be considered?

A

For patients with severe, medically refractory symptoms affecting quality of life and nutritional health.

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59
Q

What is essential before placing a jejunal feeding tube in gastroparesis patients?

A

A trial of nasoenteric feeding to evaluate tolerance

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60
Q

What indicates a poor prognosis for successful enteric feedings in gastroparesis patients?

A

Inability to tolerate feedings due to severe bloating or exacerbation of abdominal pain

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61
Q

What might be the only viable option for severe refractory gastroparesis when enteric feedings fail?

A

Total parenteral nutrition (TPN).

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62
Q

What is the purpose of a venting gastrostomy tube in gastroparesis?

A

To relieve gastric fullness or persistent vomiting.

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63
Q

Why should the volume loss from a gastrostomy tube be monitored?

A

To ensure volume replacement and prevent loss of bile salts, which may require reinfusion

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64
Q

What surgical approach might be considered for patients with postsurgical gastroparesis after a total vagotomy?

A

Near total or completion gastrectomy, but only in selected patients who tolerate enteric feedings

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65
Q

What recent interest has emerged in surgical treatments for gastroparesis?

A

Pyloroplasty and endoscopic procedures like G-POEM or per-oral pyloromyotomy (POP)

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66
Q

What preoperative measure should be considered before a pyloroplasty in gastroparesis patients?

A

Injection of botulinum toxin into the pylorus as a trial.

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67
Q

What is the potential role of sleeve gastrectomy in gastroparesis treatment?

A

It may increase gastric emptying, especially in patients with obesity or diabetes, but data are limited.

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68
Q

What is gastric electrical stimulation (GES), and who might it benefit?

A

A treatment involving an electrical stimulator implanted in the stomach wall, suggested for severe gastroparesis patients, particularly with diabetes or predominant nausea/vomiting

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69
Q

Does gastric electrical stimulation (GES) reliably increase gastric emptying?

A

No, GES may help with nausea and vomiting but does not reliably increase effective gastric emptying

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70
Q

Why is the use of gastric electrical stimulation (GES) considered controversial?

A

Success rates vary significantly among different groups, and it does not function like a cardiac pacemaker to “pace” the stomach.

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71
Q

What are symptoms of gastroparesis-like syndromes, and who is most affected?

A

Early satiety, nausea, and vomiting, often seen in young females in their 20s or 30s

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72
Q

How do symptoms of gastroparesis-like syndromes relate to objective gastric emptying results?

A

There is often poor correlation, with many patients having normal gastric emptying despite significant symptoms.

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73
Q

What alternative mechanisms might contribute to gastroparesis-like syndromes?

A

Impaired gastric accommodation and sensitization of vagal afferent pathways.

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74
Q

What is the initial step in diagnosing gastroparesis-like syndromes?

A

Excluding true gastroparesis with a formal radionuclide gastric emptying study.

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75
Q

What is the primary treatment focus for patients with gastroparesis-like syndromes?

A

Symptomatic treatment for nausea and vomiting, starting with antiemetics and antinausea medications.

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76
Q

Which antiemetic medications are typically used first for treating nausea in these patients?

A

Metoclopramide and 5HT3 receptor antagonists like ondansetron or granisetron.

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77
Q

What neuromodulator has been used for gastroparesis-like syndrome, and what were its results in studies

A

Tricyclic antidepressants, like nortriptyline, showed no improvement in nausea in a randomized controlled study.

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78
Q

Which agent has shown promise for treating nausea and improving appetite in gastroparesis-like syndromes?

A

Mirtazapine, due to its 5HT3 receptor antagonism.

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79
Q

What role does buspirone play in treating gastroparesis-like symptoms?

A

It may improve gastric accommodation, useful for patients with early satiety.

anxiolytic that is an agonist of the 5HT1A receptor

80
Q

What is Gastric Electrical Stimulation (GES), and for whom is it FDA-approved?

A

A technique using serosal electrodes on the gastric antrum for “drug refractory disease.

81
Q

What is the presumed mechanism of action for GES?

A

Modulation of vagal signaling, not improved gastric emptying.

82
Q

What is diabetic gastroparesis primarily related to?

A

Poor glucose control and its effects on vagal nerve function.

83
Q

How does the symptomatology of diabetic gastroparesis typically present?

A

It waxes and wanes in severity, making irreversible interventions usually inadvisable.

84
Q

What initial steps are recommended for managing diabetic gastroparesis?

A

Better control of glucose intolerance and dietary modifications, along with pharmacologic agents used for other forms of gastroparesis.

85
Q

How might insulin pumps benefit patients with diabetic gastroparesis?

A

They can lead to fewer hyperglycemic events, a decrease in HbA1c, and symptom improvement.

86
Q

What is the role of a venting gastrostomy in diabetic gastroparesis?

A

It can relieve bloating symptoms, but continuous drainage should be avoided to prevent dehydration and bile salt loss

87
Q

How should gastric resection be considered for diabetic gastroparesis?

A

It should be avoided in most patients, except in highly unusual and severe cases.

88
Q

What role might Gastric Electrical Stimulation (GES) play in treating diabetic gastroparesis?

A

It may help with symptoms of vomiting and nausea, although it may not necessarily improve gastric emptying.

89
Q

What is dumping syndrome, and how does it occur?

A

It is the overly rapid emptying of gastric contents into the duodenum or jejunum, commonly occurring after gastric operations involving a vagotomy.

90
Q

What types of meals exacerbate symptoms of dumping?

A

Carbohydrate-rich or hyperosmolar liquid meals.

91
Q

What was disproven as the primary cause of dumping symptoms?

A

The old theory that a rapid fluid shift into the gut causes relative hypovolemia.

92
Q

What symptoms are commonly associated with early dumping syndrome?

A

Abdominal bloating, nausea, and the need to lie down after eating; diarrhea may occur but is not universal.

93
Q

Which type of gastric surgery most frequently results in dumping syndrome?

A

Subtotal gastrectomy with vagotomy.

94
Q

When do early dumping symptoms typically occur?

A

Within 30 minutes of eating.

95
Q

How does late dumping differ from early dumping?

A

Late dumping occurs 90 minutes to 3 hours after eating and often involves symptoms of hypoglycemia and potentially diarrhea.

96
Q

What causes hypoglycemia in late dumping syndrome?

A

High-calorie meals overwhelming insulin regulation, leading to a delayed insulin release and rapid reactive hypoglycemia

97
Q

What are severe symptoms that can result from hypoglycemia in late dumping?

A

Disturbed thinking, seizures, and coma

98
Q

What modern bariatric syndrome is similar to late dumping?

A

Noninsulinoma postprandial pancreatogenous hypoglycemia syndrome (NIPPS)

99
Q

After which surgery is dumping syndrome most commonly seen today?

A

Roux-en-Y gastric bypass surgery.

100
Q

Is dumping syndrome usually permanent after gastric bypass?

A

No, most patients do not have prominent or persistent symptoms after the first 3 months.

101
Q

What percentage of patients with dumping syndrome present with early symptoms?

A

About 75%.

102
Q

What should be included in the differential diagnosis for dumping syndrome?

A

Afferent loop syndrome
pancreatic insufficiency
and bowel obstruction after prior gastric surgery.

103
Q

What symptoms are associated with early dumping syndrome?

A

Early satiety, abdominal pain, nausea, and autonomic dysfunction (e.g., racing heartbeat, sweating, dizziness, and tremors)

104
Q

Is diarrhea common with early dumping syndrome?

A

No, diarrhea is not commonly associated with early dumping

105
Q

How long do symptoms of early dumping typically last?

A

About an hour.

106
Q

What triggers the release of vasoactive substances in early dumping syndrome?

A

The high osmolarity of the gastric contents.

107
Q

What are the characteristic symptoms of late dumping syndrome?

A

Similar to early dumping but also include fatigue, mental changes, and fainting due to reactive hypoglycemia.

108
Q

When does late dumping syndrome typically occur after a meal?

A

Approximately 90 minutes to 3 hours after eating

109
Q

What test can be used to help confirm late dumping syndrome?

A

Provocative testing with 50 g of orally administered glucose followed by measurements of glucose, plasma insulin, heart rate, and symptoms.

110
Q

What is the sensitivity and specificity of the heart rate increase and hydrogen breath excretion test for late dumping syndrome?

A

Sensitivity of 94% and specificity of 92%.

111
Q

Is an upper GI series typically necessary for diagnosing dumping syndrome?

A

No, it may help define anatomy but is often not necessary, as the diagnosis is usually evident from patient symptoms and clinical context.

112
Q

What is the primary treatment for dumping syndrome?

A

Dietary modification.

113
Q

Which types of foods should patients with dumping syndrome avoid?

A

Simple sugars, alcohol, and most dessert-type food items

114
Q

What simple dietary measure can help minimize dumping syndrome symptoms?

A

Avoiding drinking fluids 30 minutes before, during, and after meals

115
Q

How can fiber supplements and complex carbohydrates benefit patients with dumping syndrome?

A

They help slow transit and alleviate symptoms.

116
Q

What postural advice should be given to patients with dumping syndrome?

A

Patients should avoid an upright posture while eating and recline after meals

117
Q

What medication may be used for patients with refractory dumping syndrome symptoms?

A

Octreotide

118
Q

How should subcutaneous octreotide be administered for optimal effect?

A

30 minutes before a meal.

119
Q

What side effect may occur with long-acting octreotide, and how can it be managed?

A

Steatorrhea, which can be managed with pancreatic enzyme replacement.

120
Q

What outdated surgical procedure for severe diarrhea due to rapid gastric emptying is no longer recommended?

A

The use of a 10-cm reversed jejunal limb

121
Q

What endoscopic procedure may benefit patients with late dumping syndrome and hypoglycemia after Roux-en-Y gastric bypass?

A

Endoscopic transoral outlet reduction (TORe)

122
Q

What are potential surgical options for severe cases of late dumping syndrome?

A

Reversing the gastric bypass or redirecting the Roux limb into the duodenum

123
Q

Why is subtotal pancreatectomy not recommended for hypoglycemia associated with late dumping?

A

It has proven to be ineffective in long-term outcomes

124
Q

What is a true small intestinal “ileus,” and how common is it after intraabdominal operations?

A

It is very unusual and not commonly seen after intraabdominal operations.

125
Q

What is a “physiologic ileus,” and when does it typically occur?

A

It is a transient form of ileus, occurring in the first 1 to 4 days postoperatively, often referred to as “postoperative ileus.”

126
Q

What causes the transient postoperative ileus?

A

It is primarily a gastric and colonic response to abdominal wall trauma from a laparotomy

127
Q

Is postoperative ileus a result of small bowel dysmotility?

A

No, small intestinal contractile activity is present during and after the operation

128
Q

How can small intestinal contractile activity be demonstrated intraoperatively?

A

By “tweaking” the small bowel and observing it contract, unlike the stomach and colon

129
Q

Can intraintestinal feeding be administered postoperatively?

A

Yes, it can be administered immediately as the small intestine functions relatively normally.

130
Q

What causes the absence of “bowel sounds” in the early postoperative period?

A

The loss of gastric emptying of swallowed gas, which leads to the absence of the gas/liquid interface that produces bowel sound

131
Q

What is adynamic ileus, and how does it differ from physiologic ileus?

A

Adynamic ileus is a rare, generalized motor disorder affecting the entire gut, involving the stomach, small intestine, and colon.

132
Q

What are common causes of adynamic ileus?

A

Systemic inflammatory disorders (e.g., sepsis), retroperitoneal operations (e.g., kidney transplantation), or retroperitoneal conditions (e.g., trauma, hematoma)

133
Q

What is isolated colonic ileus (colonic pseudo-obstruction), and what does it involve?

A

It involves only the colon, not the stomach or small bowel, and can complicate procedures like total hip arthroplasty or retroperitoneal operations

134
Q

What symptoms are indicative of adynamic ileus?

A

Vomiting, bloating, abdominal distention, obstipation of stool and gas, and tinkling bowel sounds.

135
Q

What is distinctly unusual in adynamic ileus compared to a mechanical small bowel obstruction?

A

Crampy abdominal pain

136
Q

What imaging can confirm the diagnosis of adynamic ileus?

A

A simple abdominal radiograph showing dilation of the stomach, small intestine, and entire colon

137
Q

What should be included in the differential diagnosis for adynamic ileus?

A

Exclusion of an obstructing rectal lesion, which may require proctoscopy or a transrectal contrast radiograph.

138
Q

What is the primary treatment focus for adynamic ileus?

A

Treating the underlying cause, most commonly sepsis.

139
Q

Are pharmacologic or operative interventions effective for adynamic ileus?

A

No, they are neither needed nor effective

140
Q

What conservative management approach is commonly used for adynamic ileus?

A

The use of a nasogastric tube

141
Q

Are prokinetic agents effective in treating adynamic ileus?

A

No, prokinetic agents are not effective.

142
Q

What is the prognosis for adynamic ileus once the systemic cause is controlled?

A

It is transient and resolves when the underlying cause is treated.

143
Q

What is the primary difference between POI and adynamic ileus?

A

POI is a physiologic response to abdominal wall trauma, while adynamic ileus is a pathologic response to conditions like infection.

144
Q

Which parts of the gut are affected by POI?

A

POI involves the stomach and colon but not the small intestine.

145
Q

Which parts of the gut are involved in adynamic ileus?

A

Adynamic ileus affects the entire gut, including the stomach, small intestine, and colon

146
Q

How significant is POI in modern surgical practice, especially with the increase in laparoscopic operations?

A

POI is considered less relevant or problematic with the rise of laparoscopic surgeries

147
Q

What has recent work with enhanced recovery after surgery (ERAS) shown about postoperative feeding?

A

Early postoperative feeding of the stomach or small intestine is beneficial and reinforces the lesser importance of POI

148
Q

What common belief about POI has been disproven by studies?

A

The belief that POI is related to the extent of handling of the intestine has been disproven; it is more related to abdominal wall trauma and factors like opioid medications.

149
Q

Which types of surgeries are less susceptible to POI?

A

Laparoscopic surgeries, such as laparoscopic colectomy.

150
Q

What is a notable exception where gastric emptying recovery can be delayed postoperatively

A

After a distal gastrectomy when there has been mechanical obstruction of the gastric outlet and stomach dilation.

151
Q

Are prokinetic medications effective for treating POI? after distal gastrectomy for gastric obstruction

A

Most prokinetic medications, including erythromycin, domperidone, and prucalopride, have minimal or no benefit for POI

152
Q

What should be avoided when treating rare cases of delayed gastric emptying after distal gastrectomy?

A

Reoperation to “redo” the gastroenteric anastomosis should be avoided

153
Q

What is chronic idiopathic pseudo-obstruction?

A

A family of rare heritable disorders that mimic mechanical small bowel obstruction with progressive and disorganized motility patterns.

154
Q

What are the three most common forms of chronic idiopathic pseudo-obstruction?

A

Histopathologic myopathy of smooth muscle, histopathologic neuropathy, and neuromotor dysmotility without definitive histopathologic findings.

155
Q

What is mitochondrial neurogastrointestinal encephalopathy disease (MNGIE)?

A

An extremely rare genetic cause of GI pseudo-obstruction with peripheral and GI dysfunction and associated neurological symptoms (e.g., ptosis/ophthalmoplegia, peripheral neuropathy, leukoencephalopathy), caused by a mutation in the thymidine phosphorylase gene

156
Q

What characterizes the motility patterns in chronic idiopathic pseudo-obstruction?

A

Ineffective, uncoordinated contractile activity leading to intestinal distention and stasis.

157
Q

Which organs can be initially affected by chronic idiopathic pseudo-obstruction?

A

The esophagus (megaesophagus), duodenum (megaduodenum), colon (megacolon), or urinary system (megaureter).

158
Q

How does chronic idiopathic pseudo-obstruction progress over time?

A

It eventually affects all smooth muscle in the gut and genitourinary system to varying extents.

159
Q

What type of biopsy is needed to diagnose chronic idiopathic pseudo-obstruction?

A

A full-thickness biopsy, not just an endoscopic biopsy, requiring specialized staining and reading.

160
Q

What role does the autonomic nervous system play in chronic idiopathic pseudo-obstruction?

A

It leads to discoordinated contractile activity and ineffective transit in the gut

161
Q

Can chronic idiopathic pseudo-obstruction be associated with neoplasms?

A

Yes, it is rare but possible as a paraneoplastic phenomenon mediated by an uncharacterized humoral agent

162
Q

What is a common initial presentation of hereditary dysmotility syndromes?

A

Severe constipation, which may progress to involve the small intestine over time.

163
Q

What inappropriate treatment have some patients with hereditary dysmotility syndromes received?

A

Colectomy for a diagnosis of colonic inertia

164
Q

How can hereditary dysmotility syndromes mimic achalasia?

A

Patients may present with isolated megaesophagus, which eventually involves the distal gut over time

165
Q

What is a common presentation of pseudo-obstruction in teenagers?

A

Megaduodenum of the first and second portion of the duodenum, often confused with superior mesenteric artery syndrome

166
Q

What key aspect differentiates SMA syndrome from pseudo-obstruction?

A

SMA syndrome usually follows marked weight loss rather than preceding it.

167
Q

Why should a family history be considered in patients with hereditary dysmotility syndromes?

A

These disorders are often familial and heritable, so there should be a history of esophageal, colonic, or genitourinary issues unless it is a new mutation

168
Q

At what age do symptoms of intestinal pseudo-obstruction typically begin?

A

Symptoms often start in late childhood/early teenage years or may appear in the 20s and 30s.

169
Q

What are common early symptoms of hereditary dysmotility syndromes?

A

Vague, chronic GI complaints such as substantial constipation, dysphagia, gastroesophageal reflux, or intermittent abdominal distention/cramping

170
Q

What is a clinical clue that a patient may have a hereditary dysmotility syndrome?

A

A history of surgery for presumed mechanical small bowel obstruction without convincing evidence of such obstruction during exploration

171
Q

How do the symptoms of hereditary dysmotility syndromes often behave over time?

A

They frequently wax and wane, raising questions about whether current symptoms are due to dysmotility or adhesions from prior surgery

172
Q

How is the diagnosis of chronic idiopathic intestinal pseudo-obstruction typically made?

A

It is most often a diagnosis of exclusion, unless there is a strong family history

173
Q

What is a key radiographic finding that suggests chronic idiopathic intestinal pseudo-obstruction?

A

Small intestinal and often gastric distention extending to the cecum without a clear transition point.

174
Q

What should raise suspicion for chronic idiopathic intestinal pseudo-obstruction in younger patients?

A

A prior history of negative laparotomy
recurrent childhood complaints of abdominal distention or constipation
and no history of potential mechanical obstruction

175
Q

Why is diagnosing chronic idiopathic intestinal pseudo-obstruction challenging?

A

Because it mimics mechanical obstruction, and delaying necessary operative treatment is a concern

176
Q

What is a key finding during laparoscopic exploration that confirms the diagnosis of chronic idiopathic intestinal pseudo-obstruction?

A

Distention of the entire small intestine down to the cecum without any convincing site of obstruction

177
Q

What might a previous operative note imply if a patient is suspected of chronic idiopathic intestinal pseudo-obstruction?

A

It may reveal the surgeon’s attempt to justify an obstruction that was not clearly identified, hinting at pseudo-obstruction

178
Q

What has proven unreliable in diagnosing chronic idiopathic intestinal pseudo-obstruction?

A

Characterizing the motor (contractile) pattern and measuring the amplitude of contractions

179
Q

What preoperative diagnostic tool is considered most reliable for chronic idiopathic intestinal pseudo-obstruction?

A

Diagnostic laparoscopic exploration for visualizing the distended bowel.
no signs of concurrent or prior obstruction, such as adhesions, hernia, or intraluminal mass.

180
Q

What type of treatment is available for intestinal pseudo-obstruction?

A

Only symptomatic and supportive treatment.

181
Q

Why should resections and internal bypasses be avoided in patients with intestinal pseudo-obstruction?

A

Because it is a progressive disorder involving the entire small intestine, making resections or bypasses ineffective

182
Q

Is a full-thickness biopsy usually helpful in diagnosing intestinal pseudo-obstruction?

A

No, it is often debatable and most centers lack the expertise for specialized neuromuscular staining

183
Q

Why should nonreversible treatments be avoided in the early course of intestinal pseudo-obstruction?

A

Because symptoms and severity tend to wax and wane, making irreversible procedures risky.

184
Q

What supportive measure can be used when the disease affects the esophagus, stomach, and/or duodenum?

A

Intrajejunal feedings, to delay the need for chronic parenteral feeding

185
Q

What becomes the mainstay of treatment in advanced stages of intestinal pseudo-obstruction?

A

Chronic parenteral nutrition

186
Q

What procedure might be considered for chronic and symptomatic abdominal distention?

A

Decompressive tube enterostomy (not a formal enterostoma due to risk of stomal prolapse)

187
Q

What alternative feeding measure can be taken if vomiting is problematic?

A

A venting tube gastrostomy, with careful fluid replacement

188
Q

What is a potential treatment option for highly selected individuals with severe intestinal pseudo-obstruction?

A

Intestinal transplantation

189
Q

When does small bowel involvement typically occur in the course of scleroderma?

A

Usually later in the disease course

190
Q

Which part of the gastrointestinal tract is more commonly involved in scleroderma?

A

The esophagus, often presenting with gastroesophageal reflux.

191
Q

What is the most prevalent finding in the small bowel wall of scleroderma patients?

A

myopathy with hypoplasia of the intestinal wall muscles.
leads to poor amplitude contractions and dyscoordination of contractile patterns, resulting in poor propulsion of luminal content.

192
Q

What treatments have been attempted for small bowel dysmotility in scleroderma?

A

Pyridostigmine
octreotide
oral antibiotics for bacterial overgrowth

193
Q

How common is postvagotomy diarrhea?

A

It is a very rare form of dysmotility with no known effective treatment.

194
Q

What is believed to be the underlying pathophysiology of postvagotomy diarrhea?

A

Dysmotility causing rapid transit through the small intestine rather than malabsorption

195
Q

What are the primary symptoms of postvagotomy diarrhea?

A

Diarrhea and cramping after eating, without symptoms between meals.

196
Q

What is a key diagnostic feature of postvagotomy diarrhea when analyzing the stool?

A

The diarrhea is watery, and the presence of undigested foodstuffs indicates rapid transit.

197
Q

How is postvagotomy diarrhea diagnosed? and Tx

A

It is a diagnosis of exclusion

Supportive treatment.

A1-G Surg Note Small Bowel (10 decks)

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