Gastrointestinal Diseases and Disorders

Karen E. Hall, M.D., Ph.D.

GRECC, Ann Arbor VA Health SystemUniversity of Michigan Health System

Contributors to GI chapter:George Triadafilopoulos, MDAnnette Medina-Walpole, MDWilliam J. Hall, MD

1. Selective review of common problems

2. Address controversies in treatment

3. Convince you that you need the 5th Ed. GRS!

Purpose

Handouts on my website:

http://sitemaker.umich.edu/khallinfo

This talk

GRS questions

Handouts

Which finding is more likely due to DISEASE rather than normal AGING?

1. Colonic diverticulosis

2. Dysphagia

3. Decreased small bowel motility

4. Decreased splanchnic blood flow

5. Decreased lower esophageal pressure

Question 1: Effect of aging on GI function

Answer: 3

Which finding is more likely due to DISEASE rather than normal AGING?

1. Colonic diverticulosis

2. Dysphagia

3. Decreased small bowel motility

4. Decreased splanchnic blood flow

5. Decreased lower esophageal pressure

Small bowel “resistant” to aging

In healthy older people there is minimal change in small bowel:

Motility

Secretion

Absorbtion

Proximal and distal GI tract at greatest risk for dysfunction with aging

Proximal GI tract: Aspiration risk increases with age Swallowing studies: 40% of asymptomatic 80+ yr have significant abnormalities

Age and Swallowing111. No teeth:

Impaired mastication

2. Impaired oropharyngeal co-ordination: Slow transit of food bolus, pooling at larynx 3. Delayed relaxation of upper esophageal sphincter (UES): Food goes where it shouldn’t!

Reflux risk increases with age

LES pressure decreases with age:

Gastroesophageal reflux disease (GERD)

Achalasia

Subset of patients have pathologic increase in LES pressure:

Female: Male 4:1Age 75-85 years

Progressive dysphagia to liquids and solids

Achalasia

LES: “Bird’s beak”

LES normally closed at rest

Relaxation impaired:inhibitory NO and VIP neurons absent or dysfunctional

Achalasia Treatment

Forcible balloon distensionRupture, mediastinitis, sepsis

Botulinum toxin injectionRelief x weeks-months?Frail - high risk for balloon

Laparoscopic LES myotomy?similar risk/benefit as balloon

Splanchnic blood flow decreases with age

Upper GI tract and proximal small bowel protected due to rich anastomotic supply

Decreased blood flow to liver:Impaired metabolism: drugs, bilirubin

“Watershed” areas at risk for ischemia (colon)

Diverticular disease: ?Western Aging

Circular muscle: fewer fibers; larger spaces between fibers

Colonic collagen increases in thickness with aging:

Prolongation of muscle contraction

Intraluminal pressure increases

Mucosa/submucosa protrudes through wall = diverticulum

Aging sets the stage for clinical impairment

Physiologic effects of aging

+

Superimposed disease

Effects of medications

=

Clinical impairment in areas already at risk due to normal aging

74yo man has 1 yr trouble swallowing, nausea, weight loss 8 lbs, chronic cough. No alcohol, stopped smoking. Meds: ACE inhibitor, Fe, diuretic, K+, MVI.

Physical “normal”. Hematocrit 32.

Which would you do next?

1. Upper endoscopy (EGD) 2. Esophageal Manometry 3. pH monitoring 4. Discontinue K+ 5. Trial of H2 antagonist

Question 2: Dysphagia

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Answer: 1

Older patients may have “atypical” symptoms

Cough Pneumonia Asthma Laryngitis Hoarseness Nausea Hiccups Dental erosion

Chest pain often absent: Age-associated decrease in sensation: visceral

Gastroesophageal reflux disease (GERD)

Endoscopy indicated:

Older patients: higher risk of complicated GERD

Ulceration

Stricture

Anemia

Barrett’s esophagus Increased incidence of esophageal cancer

GERD in older patients

Barrett’s Esophagus

Mucosa: Squamous to intestinal

Pre-malignant:Dysplastic foci require biopsy for detection

High grade dysplasia (HGD) has significant risk of progression to adenocarcinoma

Barrett’s Esophagus

Earlier studies: 7-10% risk of adenocarcinoma per year?

Up to 1998-99:1. Screening EGD for patients with GERD history2. +Barrett’s: biopsy HGD: surgical referral3. Low-Moderate Grade Dysplasia: high dose PPI4. Follow-up EGD every ? 6 months – 1 year?

Should we treat Barrett’s Esophagus?

Recent RCTs of proton pump inhibitor treatment:

No significant effect on: Rate of progression of low-moderate dysplasia to HGD

Rate of esophageal adenocarcinoma

Screening EDG: esophageal cancer in 3%

Should we treat Barrett’s Esophagus?

Why didn’t PPI treatment work?

? Not long enough (6 mo – 2 years)? Genetic mutation already present? Acid exposure not the only cause? Biopsy error

Should we treat Barrett’s Esophagus?

Current recommendations:

1. Screening EGD for patients with GERD history2. +Barrett’s: biopsy +for HGD: surgical referral3. M-LGD: ?PPI + Follow-up EGD ?timing

Watch for future developments

What about the other options? Manometry, pH monitoring: may confirm acid or spasm but will not diagnose dysplasia or cancer Discontinuing K+: Yes, if ulceration and/or stricture observed with EGD Discontinue Iron: may cause strictures, not indicated H2 antagonist: Acid reduction less than PPI Side effects increased in geriatric population

Back to Question 2

Question 3

66yo male NH resident with schizophrenia, GERD, tardive dyskinesia has productive cough, fever, hypoxia. CXR: bilateral LL pneumonia. After treatment of pneumonia, what you do next?

1. Cervical xray to check for cervical spurs

2. Discontinue antipsychotic medication

3. Start metoclopramide

4. Perform swallowing evaluation

5. Place feeding tube

Answer: 4. Swallowing evaluation

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Aspiration pneumonia

Major risks for aspiration pneumonia in this patient: Oropharygeal dyskinesia: medication, age GERD Anticholinergic medication Swallowing study Diagnostic (severity; complications); guide therapy

Aspiration pneumonia

What about the other options? Cervical spurs common, rarely cause dysphagia Discontinuing antipsychotic or adding metoclopramide may worsen dyskinesia Titrate antipsychotic down gradually to lower dose

Feeding Tube?

Significant complications and ethical issues Swallow study, adjust diet, medication first

Feeding tubes in Dementia

Are feeding tubes indicated in dementia? Controversial topic Demented patients live a year longer with a tube Increased calories Cost: Poor quality of life Pain; restraints; ER visits; infection; bleeding Aspiration and pneumonia unchanged or worse

Bacteria in saliva; reflux liquid diet

Question 4: “The Bottom End”

89 yo woman NH resident with abdominal distension, and emesis.

Parkinson’s disease; hypertension; CHF; hypothyroidism; immobility

No pain, weight loss, appetite change. Meds: Ca antagonist, digoxin, diuretic, levothyroxine, carbidopa/levodopa

Px: afebrile, abdomen distended, not tender, hard stool in rectum, no occult blood, CBC normal

Question 4

What should you do next? 1. Abdominal ultrasound 2. Colonoscopy 3. Discontinue Ca antagonist 4. Administer enema 5. Start prokinetic medication

Answer: 4. Enema

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Constipation

Mulifactorial:

Aging-related colonic slowing

Immobile

Parkinson’s disease

Medications (Ca antagonist, diuretic, levodopa)

Constipation

Initiate a bowel regimen

1. “Get things moving from below first”

2. Disimpaction (by your assistant!)

3. Tap water enema (phospho-soda; suppository)

4. Optimize hydration (?mobility)

5. Maintainance: cathartic/osmotic laxative (MOM; Dulcolax; senna; PEG solution)

Constipation

Avoid:

1. Initial oral cathartics: potentially dangerous if severely constipated

Use once things on the move

2. Mineral oil by mouth: lipoid pneumonia

3. Fiber alone: unlikely to work and may cause impaction

Question 5

86 yo man NH resident has fever, emesis x 36 hours. Other problems: HTN, CAD, diabetes, mild dementia, acute MI 1 mo ago.

Temp 99.5, HR 102, BP 110/66, abdo nontender, WBC 8; rest of lab tests normal; EKG: nonspecific ST changes.

Advance directives: hospital management of “reversible conditions”, no CPR.

Question 5

What would you do next? 1. Serial abdominal exams and xrays in NH 2. Serial EKGs and cardiac enzymes in NH 3. Bowel regimen for constipation 4. Fluids and antibiotics in NH 5. Urgent surgical evaluation

Answer: 5. Surgical Evaluation

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Acute Abdomen in the Older Patient

Morbidity and mortality: higher in geriatric patients

Delayed diagnosis: “high index of suspicion needed”

Symptoms vague/atypical: Rebound and guarding absent in 50-70% WBC: “normal” but may have left shift Confusion, anorexia

Acute Abdomen in the Older Patient

Acute abdomen: potentially treatable (appendicitis; diverticular abcess; ischemic colitis; cholecystitis, etc.)

Patient’s Advance Directives – indicated desire for treatment of potentially reversible conditions

Appendicitis in the Older Patient

Diagnosis at surgery: Appendicitis

Increased incidence: men aged 80+

70-90% have rupture at time of surgery delay in diagnosis a major factor 6-10% mortality vs 0.5% in young 50% of deaths from appendicitis occur in aged

Finally - Back to Question 5

What about the other options? Patient already too ill for serial abdominal exams or cardiac enzymes in nursing home

Bowel regimen contraindicated if acute abdomen suspected – may cause perforation

Fluids and antibiotics in nursing home: Unlikely to prevent deterioration if surgical disease ? Patient/family: no hospitalization; “trial of therapy” rather than comfort care

Colon cancer and gastric cancer

Anemia and bleeding

Diarrhea

Flatulence

Peptic Ulcers and H. Pylori

http://sitemaker.umich.edu/khallinfo

For Additional Information: GRS Syllabus