# Clinical Cases: GI Motility

## Case 1: Achalasia

### Patient Presentation
**Demographics:** 42-year-old female

**Chief Complaint:** Progressive difficulty swallowing for 2 years

**History of Present Illness:** The patient reports gradually worsening dysphagia to both solids and liquids over the past 2 years. She describes food "getting stuck" in her chest and frequently regurgitates undigested food, sometimes hours after eating. She has lost 15 pounds unintentionally. She notes that cold liquids seem to worsen symptoms. She denies heartburn but reports intermittent chest pain.

**Past Medical History:** None significant

**Social History:** Non-smoker, no alcohol use

### Physical Examination
- **Vital Signs:** BP 118/72 mmHg, HR 74 bpm, BMI 22 (previously 25)
- **General:** Thin female, appears well-nourished despite weight loss
- **Neck:** No lymphadenopathy
- **Chest:** Clear to auscultation
- **Abdomen:** Soft, non-tender, no masses

### Workup and Results
- **Barium Swallow:** Dilated esophagus with smooth tapering at the gastroesophageal junction ("bird's beak" appearance); minimal contrast passage into stomach
- **Upper Endoscopy:** Dilated esophagus with retained food debris; tight but traversable gastroesophageal junction; no mucosal lesions or masses
- **High-Resolution Esophageal Manometry:** Elevated integrated relaxation pressure (25 mmHg, normal <15); absent peristalsis in the esophageal body; Type II achalasia pattern

![Achalasia Barium Swallow](case_01_image.jpg)
*Barium swallow demonstrating the classic "bird's beak" appearance of achalasia, with a dilated esophagus tapering smoothly to a narrowed gastroesophageal junction due to failure of LES relaxation.*

**Image Source:** Case courtesy of Radiopaedia.org

### Diagnosis
**Type II Achalasia**

### Clinical Correlation to Motility Physiology
Achalasia results from selective destruction of inhibitory neurons in the myenteric plexus that normally release nitric oxide (NO) and vasoactive intestinal peptide (VIP) to relax the lower esophageal sphincter. Without these inhibitory signals, the LES remains tonically contracted and cannot undergo swallow-induced relaxation. Additionally, the loss of coordinated peristalsis in the esophageal body means the esophagus cannot effectively propel food toward the stomach. The dysphagia to both solids and liquids from onset distinguishes achalasia from mechanical obstruction.

### Treatment
- Peroral endoscopic myotomy (POEM) - recommended given Type II pattern and good response rates
- Alternatives: pneumatic dilation or laparoscopic Heller myotomy with fundoplication
- PPI therapy post-procedure for reflux prevention

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## Case 2: Gastroparesis

### Patient Presentation
**Demographics:** 55-year-old male

**Chief Complaint:** Nausea, vomiting, and early satiety for 6 months

**History of Present Illness:** The patient reports persistent nausea, bloating, and feeling full after only a few bites of food. He vomits 2-3 times weekly, often recognizing food eaten many hours earlier. He has lost 20 pounds over 6 months due to reduced oral intake. Symptoms worsen with fatty or fibrous foods.

**Past Medical History:** Type 2 diabetes mellitus for 18 years (HbA1c 9.2%), peripheral neuropathy, hypertension, hyperlipidemia

**Medications:** Metformin, glipizide, lisinopril, atorvastatin

### Physical Examination
- **Vital Signs:** BP 132/84 mmHg, HR 88 bpm, BMI 26
- **General:** Cachectic-appearing male
- **Abdomen:** Mildly distended, succession splash present, mild epigastric tenderness, no peritoneal signs
- **Neurologic:** Decreased sensation in stocking distribution bilaterally

### Workup and Results
- **Upper Endoscopy:** Retained food in stomach despite 12-hour fast; no gastric outlet obstruction, no ulcers or masses
- **Gastric Emptying Scintigraphy:** 78% retention at 2 hours (normal <60%), 45% retention at 4 hours (normal <10%)
- **HbA1c:** 9.2%

![Gastroparesis Scintigraphy](case_02_image.jpg)
*Gastric emptying scintigraphy at 4 hours showing significant retained radiotracer in the stomach (45% retention), indicating markedly delayed gastric emptying consistent with gastroparesis.*

**Image Source:** Case courtesy of Radiopaedia.org

### Diagnosis
**Diabetic Gastroparesis**

### Clinical Correlation to Motility Physiology
Diabetic autonomic neuropathy damages vagal nerve fibers that coordinate gastric motility. The proximal stomach (fundus) normally provides reservoir function through receptive relaxation mediated by vagal inhibitory neurons releasing NO and VIP. The distal stomach (antrum) generates grinding contractions at 3 cycles per minute, driven by interstitial cells of Cajal (ICC) pacemaker activity modulated by vagal cholinergic input. In diabetic gastroparesis, impaired vagal function and potential ICC loss result in poor fundic accommodation and weak antral contractions, leading to retained gastric contents, nausea, and vomiting.

### Treatment
- Glycemic optimization (reduces acute hyperglycemia-induced slowing)
- Dietary modifications: small, frequent, low-fat, low-fiber meals; liquid nutritional supplements
- Metoclopramide 10 mg before meals (with caution regarding tardive dyskinesia)
- Consider gastric electrical stimulation (Enterra) for refractory symptoms
- Pyloric interventions (G-POEM) for selected patients

---

## Case 3: Small Intestinal Bacterial Overgrowth (SIBO)

### Patient Presentation
**Demographics:** 67-year-old female

**Chief Complaint:** Bloating, diarrhea, and weight loss for 8 months

**History of Present Illness:** The patient reports progressive abdominal bloating and distension, particularly after meals. She has 4-6 loose, foul-smelling, fatty stools daily. She has lost 12 pounds despite adequate oral intake. She also notes fatigue and occasional tingling in her feet.

**Past Medical History:** Type 2 diabetes (15 years), diabetic autonomic neuropathy with orthostatic hypotension, chronic PPI use for GERD (10 years)

**Surgical History:** None

### Physical Examination
- **Vital Signs:** BP 128/76 mmHg (sitting), 108/68 mmHg (standing), HR 82 bpm
- **General:** Thin, fatigued-appearing female
- **Abdomen:** Distended, tympanitic, mild diffuse tenderness, hyperactive bowel sounds
- **Neurologic:** Decreased vibration sense at ankles bilaterally

### Workup and Results
- **CBC:** Hemoglobin 10.8 g/dL, MCV 108 fL (macrocytic)
- **Chemistry:** Albumin 3.2 g/dL
- **Vitamin Levels:** B12 low (180 pg/mL), folate elevated (>20 ng/mL)
- **Glucose Hydrogen Breath Test:** Positive (hydrogen rise >20 ppm within 90 minutes)
- **Stool Studies:** Elevated fecal fat

![SIBO Breath Test](case_03_image.jpg)
*Hydrogen breath test graph showing an early rise in breath hydrogen concentration (>20 ppm) after lactulose ingestion, consistent with small intestinal bacterial overgrowth.*

**Image Source:** Case adapted from clinical literature

### Diagnosis
**Small Intestinal Bacterial Overgrowth (SIBO)**

### Clinical Correlation to Motility and Protective Mechanisms
SIBO occurs when protective mechanisms that maintain near-sterile small bowel conditions are compromised. Normal defenses include: (1) gastric acid killing ingested bacteria - chronic PPI use eliminates this barrier; (2) the migrating motor complex (MMC) sweeping bacteria distally during fasting - diabetic autonomic neuropathy impairs this "housekeeper" function; (3) the ileocecal valve preventing colonic bacterial reflux. This patient has multiple risk factors. The characteristic finding of low B12 with elevated folate reflects bacterial consumption of dietary B12 and bacterial folate synthesis. Deconjugation of bile acids by bacteria impairs fat absorption, causing steatorrhea.

### Treatment
- Rifaximin 550 mg three times daily for 14 days
- Address underlying causes: consider reducing PPI dose, prokinetic therapy for dysmotility
- B12 supplementation
- Low-FODMAP diet may reduce symptoms
- Anticipate need for cyclic antibiotic therapy if symptoms recur