Lecture 1: Disorders and Cancer of Salivary Glands, Parotid Glands, and Oral Cavity 1 -

1. Salivary Glands
a. Produce a quart (2 pints) of saliva each day.
b. Functions:
i. Lubricates your mouth and facilitates swallowing.
ii. Begins digestive process.
iii. Protects teeth from bacteria.
c. Salivary Gland Ductal System
i. Stenson’s Duct – Parotid – behind 2nd upper molar duct
ii. Wharton’s Duct - Submandibular and Sublingual – floor of the mouth
2. Disorders of the Salivary Glands
a. Sialoiths
i. These are small salivary stones that are the most common cause of swollen salivary glands.
ii. These tiny, calcium-rich stones block the ductal system, causing an obstruction.
iii. The etiology is dehydration in the nursing home or any condition that thickens or decreases the amount of saliva.
iv. Symptoms
1. Primary symptom is swelling and pain in the face, occurs particularly during meals, saliva is produced but can’t drain.
2. The diagnosis is made by:
a. Physical exam
b. Sometimes a CT Scan of the face
v. Treatment of Sialolithiasis
1. When conservative tx fails, which includes antibiotics and anti-inflammatories, surgical removal is indicated.
3. Salivary Gland Infections
a. Sialadenitis
i. Bacterial infection primarily of the parotid gland may result when Stenson’s Duct is blocked.
ii. Symptoms may include fever, chills, and painful swelling of parotid gland.
iii. Treatment of Acute Sialadenitis
1. Reverse condition that may have caused the problem – i.e., remove the stone (milk it out)
2. Warm compresses and antibiotics.
3. Salivary gland massage, and of all things, lemon drops (helps produce more saliva → tries to push it out) - STONEWALL
4. If conservative therapy fails, then surgical drainage may be indicated.
b. Mumps - Classic Chipmunk Look
i. This is a viral infection of children that can cause swelling of the salivary glands.
ii. It is HIGHLY contagious.
iii. In developed countries, there is now a vaccine.
iv. Treatment is supportive therapy (conservative)
4. Benign Salivary Gland Tumors
a. In the parotid gland, 85% of tumors are benign.
b. Pleomorphic Adenoma is by far the most common benign tumor of the parotid gland.
c. Second most common tumor is Warthin’s Tumor, which occurs mainly in middle-aged men.
d. Diagnosis, work-up and treatment are similar.
e. Pleomorphic Adenoma
i. Presents as a slow growing, ★mobile painless solitary mass under the skin (hard and moveable mass = pleomorphic adenoma)
ii. Diagnosis:
1. Fine needle aspiration biopsy.
2. CT scan to determine extent of disease.
iii. Surgical Treatment of Pleomorphic Adenoma
1. Why is this surgery so difficult? Proximity to facial nerve
5. Malignant Tumors of the Oral Cavity
a. Staging, Prognosis and Treatment is based upon the TNM Classification – don’t need to know – just size, nodal mets, and distant mets
6. Malignant Tumors of the Parotid Gland
a. Mucoepidermoid Carcinoma
i. Most common malignant
ii. Presents as a rapidly enlarging painless, parotid mass.
iii. Facial nerve weakness is present in 20% of the cases and usually indicates nodal metastasis and a poor survival rate.
iv. Physical Exam
1. The tumor feels rock-hard and often fixed (non-moveable) to underlying tissues.
 2. Facial nerve dysfxn as stated earlier indicates advanced disease as well as presence of palpated regional lymph nodes.
v. Diagnosis
1. Fine needle aspiration biopsy usually provides a definitive diagnosis.
2. CT scan or MRI will determine extent of disease.
vi. Treatment of MEC
1. Surgical resection is the mainstay of treatment for this dz. (completely cut out regardless of CN VII involvement)
a. Depending on CT scan, nodal dissection may be necessary.
2. Radiation therapy may be indicated for advanced disease.
3. Chemotherapy has been shown to be ineffective.
vii. Prognosis
1. If detected early enough, the five year survival rate is 88%.
2. If the tumor is greater than 4 cm with metastasis, most patients die within one to three years.
b. Adenoid Cystic Carcinoma
i. Most common malignant tumor of the submandibular and minor salivary glands.
ii. Presents as a painless mass of the submandibular gland.
iii. The tumor has an unusual propensity to spread to peripheral nerves so patients may present with pain or facial paralysis.
iv. Another unusual characteristic is that this tumor RARELY spreads to regional lymph nodes.
v. Lung is the most common site of metastasis.
vi. Recurrence is common and prognosis is poor.
vii. Diagnosis
1. Fine needle aspirate biopsy.
2. CT scan to determine extent of disease.
viii. Treatment
1. Aggressive surgical resection followed by postop radiation.
2. Some encouraging trials have been seen with external neutron beam treatment.
3. Chemotherapy – worthless.
7. Common Benign Oral Tumors
a. Leukoplakia
i. This is a white, scaly lesion seen primarily in smokers.
ii. This is considered a premalignant lesion and 20% may turn into a squamous cell carcinoma.
iii. It is often found on the tongue, but can occur anywhere within the mucosal oral cavity.
iv. The treatment is:
1. Stop smoking
2. Surgically “shave” off the lesion
b. Mucous Cyst
i. Occur when a minor salivary gland becomes blocked – often seen in “lip biters”.
ii. Treatment
1. Some may spontaneously heal
2. Or for persistent lesions, simple excision in the office
c. Ranula
i. A mucocele primarily of the sublingual salivary gland
ii. They present as translucent blue dome shaped fluctuant swelling of the floor of the mouth
1. note: same area as adenoid cystic carcinoma, but this is soft and not hard like ACC
iii. Etiology is blockage of the salivary duct
d. Black hairy tongue
i. Tongue papilla grow longer, don’t shed, and catch debris and bacteria.
ii. Multiple causes: e.g., poor oral hygiene, but seen especially in smokers.
iii. Treatment:
1. Good oral hygiene
2. Brush your tongue (literally)
3. If this doesn’t stop you from smoking, NOTHING will.
8. Malignant Tumors of the Oral Cavity
a. Squamous Cell Carcinoma
i. Accounts for the vast majority of oral cavity carcinomas.
ii. Risk factors are old friends: smoking, alcohol, and now for something new – chewing tobacco.
iii. Symptoms:
1. Most common is a persistent lip or mouth sore that bleeds.
 2. Pain or numbness of the tongue may indicate perineural invasion (metastasis)
3. A lump in the neck may indicate lymph node involvement.
b. Lip Carcinoma
i. Most common type of oral cavity cancer
ii. Causes include cigarettes as well as pipe smoking and exposure to ultraviolet radiation.
iii. Rule of 90’s.
1. 90% squamous cell carcinoma
2. 90% lower lip involvement (b/c the nose protects the upper lip from UV-B(ad) radiation that causes skin CA)
3. 90% five-year survival if less than 2 cm in diameter
iv. Diagnosis is by incisional or excisional biopsy
v. Treatment
1. Surgery is the mainstay of treatment – frozen section analysis may be helpful.
2. If lymph nodes are palpable, which is rare, a node biopsy may be indicated.
3. Reconstruction of defect depends on how much of the lower lip is removed.
a. The lower lip is a very forgiving and mobile structure. Because most of these tumors occur in elderly
patients, lower lip defects of less than 50% often can be closed primarily.
b. Larger defects will need flap closure. There have been countless different flaps described.
4. Near Total Lower Lip Reconstruction with A Karapandzic Flap
c. Cancer of the Tongue
i. Most frequent intraoral cancer
ii. 90% of these tumors are almost all squamous cell carcinoma
iii. Risk factors
1. Smoking and chewing tobacco products
2. Alcohol consumption
3. Also associated with human papilloma virus (HPV)
4. Leukoplakia
iv. Cancer of the tongue is often a debilitating disease affecting speech and swallowing.
v. Treatment
1. Surgery is mainstay of treatment
2. Neck lymph nodes may be removed depending on the extent of the disease
3. Postop radiation and chemotherapy may reduce the risk of recurrence
4. There has been some promise with the use if monoclonal antibodies
5. Partial Glossectomy, Hemiglossectomy, Total Glossectomy (no tongue)

Lecture 2: Esophageal and Gastric Cancer

1. Objectives
a. Identify general risk factors and epidemiology
b. Identify the pathogenesis and risk related to Barrett’s esophagus (esophageal adenocarcinoma precursor)
c. Recall the pathogenesis of H. pylori as it relates to gastric carcinomas and treatment
d. Discuss overall survival, prognosis and screening
e. Discuss diagnosis and treatment modalities
2. Esophageal Ca: Epidemiology
a. 5th most common GI malignancy in US
b. 10th most common malignancy worldwide
c. High incidence regions : Iran, Russia and Northern China (mainly squamous cell)
d. Hot tea, ETOH and Tobacco
3. Esophageal Ca: Pathology
a. Adenocarcinoma - glandular
i. ~50% of all cases (majority)
ii. Associated with Barrett’s esophagus
iii. Associated w/ the distal 1/3rd of esophagus
iv. Overlaps with GEJ adenocarcinoma
b. Squamous cell carcinoma – keratin pearls
i. More common in smokers and drinkers
ii. Associated with more proximal tumors
iii. Associated with HPV
4. Esophageal Ca: Pathology
5. Esophageal Ca: Epidemiology

a. Changing trends are felt to be due to obesity

6. Esophageal Cancer - Presentation
a. Dysphagia
b. Cachexia – often late stage
c. Weight loss – PEG or tube feeding during treatment
d. Melena – slow upper GI bleed
e. Hematemesis
f. Anemia – chronic blood loss, microcytic, low MCV
7. Case 1
a. 68 yo male with GERD has EGD due to dysphagia and odynophagia
b. He takes occasional H2 blockers and antacids
c. He denies weight loss or fatigue
d. CBC is normal
e. Endoscopy shows the following
f. Preferred initial diagnostic modality
8. Case 1
a. Z Line – Squamocolumnar junction
9. Barrett’s esophagus
a. 30-40x increase in adenocarcinoma of the esophagus
b. 10-15% of GERD patients undergoing endoscopy have it
c. Barrett’s is more common in Caucasians, obese, males, older adults
d. Treatment and surveillance of Barrett’s depends on severity
i. Length of esophagus involved
ii. Evidence of “dysplasia” or pre-cancer
e. Risk is 0.5-1.0% per year - Proton pump inhibitors Rx for patients to improve symptoms only not the risk of adenocarcinoma
10. Case 1 Cont…
a. 5 years later he has recurrent symptoms
b. He has not been taking his PPI and has been lost to follow up
c. He has lost 30 lbs.
d. He has occasional melena
e. He has a microcytic anemia

f. EUS – endoscopic US – good for staging – (size and depth of invasion)

g. TNM classification for size or depth of invasion
h. Also to look at paresophageal nodes – inferior phrenic, celiac, paracardiac
i. Node on the left is malignant, more irregular hyperechoic whereas the right is darker and more regular
11. Case 1

a. CT and PET – helps rule out or in cancer

12. Esophageal Ca: Staging
a. T – degree of invasion
b. N – nodal status, number involved
c. M – metastasis – yes or no
d. Biopsy gives grading, based on differentiation
13. Case 1
a. The patient has T2N1 disease (Stage II)
i. Stage 1/2/3 were going for a curative intent
ii. Stage 1 – can sometimes just do surgery
iii. Stage 2/3 – do trimodality – chemo RT and surgery
b. He undergoes chemotherapy + radiation (ChemoRT)
i. Chemo before surgery = neoadjuvant, chemo is given concurrently with the radiation
c. Carboplatin/Taxol or 5-FU/Cisplatin
i. With platinums have to watch out for neuropathies or renal insufficiency
ii. Have to give lower doses so not to make the cancer more friable
iii. Platinum increases response when given concurrently with radiation
d. Repeat endoscopy shows complete response
e. Surgery is planned within 3-4 weeks
f. NOTES
i. Despite surgery, many patients die from distant metastases or local relapse months to years later.
ii. Typical sites for metastasis include the lungs, GI nodes, liver, peritoneum.
iii. Chemotherapy is important to control the growth of distant metastases.
iv. Radiation is given to improve control of the disease returning in the resection cavity and the nodal drainage.
v. Preoperative radiation must be given at lower doses as high dose or “definitive” radiation makes the tissue too difficult to
operate upon. Radiation fibrosis and impaired wound healing are among the issues.
vi. Very rarely and generally not in the United States chemotherapy is given before and after surgery and radiation is omitted.
vii. Chemotherapy is almost never given after surgery in the United States.
14. Ivor-Lewis Esophagectomy
a. More for distal esophageal cancer
b. TEF, bleeding, perforations
15. Esophageal Ca: Treatment
a. Preoperative ChemoRT
i. 5 year survival after surgery alone ~10-15%
ii. 5 year survival after ChemoRT ~25%
iii. Trimodality (ChemoRT & Surgery) ~40% alive at 5 years
iv. Chemotherapy used are combinations of 5FU, platins and taxanes
v. Radiation is given at lower dose
16. Esophageal Ca Treatment: Prognosis
a. Stage I : 70%
b. Stage II: 40%
 c. Stage III: 30%
d. Stage IV: 5%
17. Case 1 Questions
A 58 yo immigrant from Iran develops dysphagia and weight loss. What should be your initial work up?
a. CT scan
b. PET scan
c. EUS
d. EGD
This gentleman has a squamous cell carcinoma found in the thoracic esophagus. EUS and PET scan show enlarged local nodes, but no distant
spread. What would be the best treatment supposing he is in perfect health?
e. Surgery
f. Chemotherapy
g. Radiation
h. ChemoRT followed by surgery
18. Case 2
a. 55 yo male presents with epigastric pain, fatigue and 30 lb. weight loss
b. CBC notes Hb of 7 with microcytosis
c. Stool is heme positive
d. No mass is palpable on exam
e. EGD shows a large gastric mass in the proximal portion of the stomach
19. Gastric Ca: Epidemiology
a. Tends to be more common in SA and Russia
20. Gastric Ca: Causation
a. Nitrites in smoked and salted foods
b. ETOH
c. H. pylori gastritis
d. Atrophic gastritis
e. Genetics
i. Lynch syndrome – DNA mismatch repair gene mutations
ii. Hereditary Diffuse Gastric Cancer
21. Gastric Ca: Pathology
a. Diffuse
i. Younger, poor prognosis
ii. Signet Ring Cells & Linitis Plastica
iii. Hereditary Diffuse
iv. Gastric Syndrome (CDH1) – Mutated, E-cadherin, cells are more motile, don’t hold together
b. Intestinal
i. Older, decreasing incidence
ii. Better prognosis
22. Gastric Ca: Presentation

23. Gastric Ca: Anatomy

a. Cardia = GEJ
b. Fundus
c. Antrum
 d. Corpus
e. Arterial Supply – celiac trunk, gastric arteries
f. Omentum – worry for omental seeding – essentially metastatic disease
g. NOTES
i. It is more common to see it appear in spontaneous cases in the cardia and in association with distal Barrett’s esophagus.
ii. This is typically referred to as “intestinal type” gastric adenocarcinoma.
iii. “Linitis plastica” stomach is associated with diffuse gastric carcinoma and involves non-cardia regions primarily.
24. Case 2: Pathology
a. Adenocarcinoma on the left and Silver stain for H. pylori on the right
25. Helicobacter pylori
a. H. Pylori
i. Gram negative, urease positivity - Allows bacteria to live in the stomach by making an alkaline pH
ii. 50% of world population, higher incidence in western society
iii. Attaches, disrupts mucosal layer & attaches to epithelium stimulating immune mediated inflamm. response
iv. Metaplasia into carcinoma or into MALT lymphoma
b. Staining on biopsy
c. Urea breath test or stool antigen – don’t do serum tests needed
i. Stop PPI at least 2 weeks prior
d. Treatment
i. “Triple therapy”: PPI, amoxicillin and clarithromycin for 14 days
ii. Clarithromycin resistance - 4 drug regimen
1. PPI, Bismuth, Metronidazole and Tetracycline
2. Confirm eradication 4 weeks after tx
26. Case 2
a. CT scan shows no distant spread (not sensitive enough, need to do direct visualization, an ex-lap for accurate tumor classification TNM)
b. Laparoscopic staging shows no peritoneal spread
c. He undergoes total gastrectomy
d. Multiple gastric nodes are positive
e. After recovery give adjuvant chemotherapy, typically a single agent, either 5Fluoruracil + Radiation concurrently
27. Case 2
a. Similar survival rates to esophageal – not great
28. Case 3
a. 49 yo woman has routine pelvic exam
b. She has had weight loss and some dyspepsia
c. Ovarian mass is palpated
d. Periumbilical mass is palpated
e. She has enlarged supraclavicular and axillary lymph nodes on left
f. SIDEBAR
i. The story of medicine is told by men and women whose names are attached to a particular disease. Gastric cancer was a real
scourge in the early days of modern medicine and the rush to assign one’s name to its presentation is somewhat obvious.
ii. Left supraclavicular adenopathy  Virchow’s node
iii. Left axillary adenopathy  Irish’s node
iv. Periumbilical adenopathy – Sister Mary Joseph nodes
v. Metastasis to the ovary  Krukenberg tumor
vi. Migrating thrombophlebitis  Trousseau’s syndrome
29. Case 3
a. Lymph node biopsy reveals adenocarcinoma
b. Working diagnosis is “Adenocarcinoma of Unknown Primary”
c. Differential dx on path shows likely gastric origin
d. EGD confirms gastric adenocarcinoma
30. Case 3
a. Her-2 stain is positive on path specimen – Her-2 (EGFR)
b. Trastuzumab (Herceptin) is the first targeted therapy for gastric cancer in addition to Chemo – adds 4 months or so
c. Anti-VEGF antibodies such as Ramucirumab are used as well
31. Case 3
a. Palliative 5FU/Cisplatin and Herceptin was started
b. Partial response was obtained for several months then changed to Taxol and Ramucirumab
 c. Developed “migratory phlebitis” periodically - Trousseau
d. Eventually progressed and died 2 years after diagnosis
32. Case 3 Questions
A 76 yo woman has weight loss and abdominal pain for several months. EGD shows Barrett’s esophagus and a mass in the cardia of the
stomach. What bacteria is likely to be found on biopsy?
a. Chlamydia gastroensis
b. Mycobacterium intesticum
c. Helicobacter pylori
She is found to have disease in the peritoneal cavity during exploratory laparotomy and thus is “closed up” without resecting the tumor. Why
and what can be done next?
d. Surgeons are lazy and TPN can be ordered
e. Surgery will not cure her, she should have Her2 staining done on the tumor
33. Upper GI Malignancy: Caveats
a. Older age and co-morbid disease preclude aggressive therapy
b. Surgery needs to be done by an experienced surgical oncologist or thoracic surgeon
c. Long term issues include GERD, strictures, weight loss and chronic pain
34. ECOG
a. 0 – Fully Active
b. 1
c. 2
d. 3
e. 4
f. Subjective assessment of performance
i. Once you get to 2/3 have to weigh the pros and cons
35. Upper GI Malignancy: Prevention
a. Smoking cessation
b. ETOH moderation
c. Helicobacter eradication if ulcer or gastritis present (not serology)
d. Screening in endemic areas (Lynch or
e. Prophylactic surgery for at risk family members (gastric ca)
36. Screening
a. EGD screen for Barret’s if multiple risk factors
i. 50, male, white, GERD, hiatal hernia, obese
b. Don’t screen general population

1. Case 1
a. 68 yo male with GERD has EGD due to dysphagia and odynophagia. He takes occasional H2 blockers and antacids. He denies weight loss
or fatigue. CBC is normal (not bleeding and no lymphopenia/HIV). Endoscopy shows the following
2. Squamocolumnar junction with an erythematous patch visible to naked eye
3. Herniation can be caused by meds, foods, increased intraabdominal pressure and requires fundoplication
4. Barrett’s esophagus
a. 30-40x increase in ★adenocarcinoma ★of the esophagus (adenocarcinoma = distal 1/3)
b. 10-15% of GERD patients undergoing endoscopy have it
c. Barrett’s is more common in Caucasians, obese, males, older adults (stoop more, gut goes out = bad mechanics for LES)
i. Note: Weakening of LES → painful esophagitis → squamous metaplasia → Barrett's Esophagus
1. ★“heartburn went away a few years ago” = worrisome for Barrett’ (Barrett’s is NOT painful)
d. Treatment and surveillance of Barrett’s depends on severity
5. Length of esophagus involved or Evidence of “dysplasia” or pre-cancer
a. Risk is 0.5-1.0% per year
b. Proton pump inhibitors Rx for patients to improve symptoms only
6. Case 1 continued…
a. 5 years later he has recurrent symptoms. He has not been taking his PPI and has
been lost to f/u. He has lost 30 lbs. He has occasional melena (dark tarry). He has a
microcytic anemia (losing blood faster than making it)
b. PPT Notes:
7. A fiberoptic scope is inserted into the mouth and down to the stomach showing in clear
detail a malignancy. Multiple biopsies may be obtained through the endoscope as well as cautery or Argon laser coagulation of bleeding
 areas. Endoscopic surgery is reserved for the smallest tumors and in those who cannot tolerate standard of care (surgery or chemoradiation).
Stents can be deployed endoscopically in the esophagus to relieve an obstruction from tumor.
1. Note: can deploy a stent to open esophagus and tamponade the bleeding or cauterize it
ii. Endoscopic ultrasound or (EUS) uses an ultrasonic transducer on the end of the endoscope to obtain more detail about the
depth of invasion as well as whether regional nodes are enlarged. EUS can accurately assess the depth of penetration in up to
90% of tumors and determine involvement of mediastinal lymph nodes in nearly all patients. It can guide a biopsy of a
suspicious node through the esophagus or stomach.
8. Staging - TNM Staging System
a. Well Differentiated - organized
b. Poorly - architecture distorted, pleomorphic nuclei, abnormal mitoses, etc
c. Wants to know where it is and where it has spread to determine if their toolkit can treat the cancer
d. Staging Imaging: Positron Emission Tomography (Initial imaging of choice = EGD)
9. Esophageal Ca: Anatomy
a. Surgeons divide the esophagus into 3 sections.
i. Note: Most common cancers are in the distal 1/3 and most of them are adenocarcinomas related to Barrett’s
b. Squamous cell carcinoma tends to be the predominant histology proximally and adenocarcinoma distally
i. Proximal disease tends to be related to tobacco and ETOH abuse.
ii. Distal esophageal adenocarcinoma has become more prevalent in North America and tracks with Barrett’s disease.
10. Case 1 Continued…
a. The patient has T2N1 disease. He undergoes chemotherapy + radiation (ChemoRT). Repeat endoscopy shows complete response. Surgery
is planned within 3-4 weeks
i. T2N1 = in at least 3-6 lymph nodes and we do not see distant spread → stage 2B (TNM Staging System)
1. Not generally resectable and prefer preoperative tx (chemotx+radiation or chemotx alone)
b. PPT Notes:
i. Carboplatin and Taxol are the preferred agents when combined with Radiation.
ii. Cisplatin and 5FU are also used as well with concurrent therapy.
11. Ivor-Lewis Esophagectomy
a. PPT Notes: Complications from this approach can be tracheo-esophageal fistula. Long term, patients will
have issues with reflux of bile and dumping syndrome (see gastric ca).
12. The Patient is stuck eating small meals until it stretches out and will most likely suffer from bile reflux and
esophagitis
13. Some patients become hyper→hypoglycemic and pass out so they need to eliminate high carb diet and eat
small meals to avoid Dumping Syndrome
14. Esophageal Cancer Treatment
a. Preoperative ChemoRT
i. 5 year survival after surgery alone ~10-15%
ii. 5 year survival after chemoRT ~25%
iii. ★Trimodality (chemoRTsurgery) ~40% alive at 5 years
iv. Chemotherapy used are combinations of 5FU, platins and taxanes
v. Radiation is given at lower dose (too much won’t allow tissues to heal and complicates surgery)
b. PPT Notes:
i. Chemotherapy is important to control the growth of distant metastases.
ii. Radiation is given to improve control of the disease returning in the resection cavity and the nodal drainage.
iii. Preop radiation must be given at low doses (high dose or “definitive” radiation makes tissue too difficult to operate)
iv. Radiation fibrosis and impaired wound healing are among the issues.
c. Note: in the old days when we just did surgery alone they ended up having recurrent or metastatic cancer. Chemoradiation therapy
increased survival, but Trimodality (ChemoRT+surgery) has increased survival the greatest
15. Esophageal Cancer Epidemiology
a. 5th most common GI malignancy in US
b. 10th most common malignancy worldwide
c. High incidence regions : Iran, Russia and Northern China (mainly squamous cell) → Hot tea, ETOH and Tobacco
16. Esophageal Cancer Pathology
a. Adenocarcinoma
i. ~50% of all cases
ii. Associated with Barrett’s esophagus
iii. Associated w/ the distal 1/3rd of esophagus
iv. Overlaps with GE junction adenocarcinoma
 v. More common in Caucasians
b. Squamous cell carcinoma
i. More common in smokers and drinkers
ii. Associated with more proximal tumors (upper-middle 2/3)
iii. Associated with HPV
iv. More common in African Americans
17. Esophageal Cancer Presentation
a. Dysphagia, Cachexia, Weight loss (30-50 lbs), Melena, Hematemesis, Anemia
b. PPT Notes:
i. Dysphagia is due to mechanical obstruction or infiltration of the myenteric plexus. Patients often complain of difficulty with
meat and bread products first (eg “food getting stuck”). This can progressively worsen which leads to pain (odynophagia) and
weight loss. Melena or “black tarry stool” is a result of bleeding as heme in the blood is broken down leading to a dark
pigmentation of the stool. Vomiting blood or “hematemesis” is common for people with bleeding esophago-gastric ulcers,
Mallory-Weiss tears of the esophagus or other benign conditions as well.
ii. Weight loss and cachexia are real concerns for patients about to undergo treatment for esophageal cancer. Nutritional support
is often necessary through a feeding tube placed in the stomach or upper intestine surgically or percutaneously.
18. Case 1 Question: A 58 yo immigrant from Iran develops dysphagia and weight loss. What should be your initial work up?
a. CT scan
b. PET scan
c. EUS
d. EGD (look at it directly - inspection)
19. Case 1 Question: This gentleman has a squamous cell carcinoma found in the thoracic esophagus. EUS and PET scan show enlarged local
nodes, but no distant spread. What would be the best treatment supposing he is in perfect health?
a. Surgery
b. Chemotherapy
c. Radiation
d. ChemoRT followed by surgery (40% 5 year survival)
20. Case 2:
a. 55 yo male presents with epigastric pain, fatigue and 30 lb. weight loss. HCT is 28 (normal: 44-48) with a
microcytosis (blood loss/iron deficiency….also men shouldn’t get this since they don’t have menses).
Stool is Heme positive. No mass is palpable on exam
21. Note: on endoscopy they see a gastric mass in the Cardia.
22. Gastric Cancer Anatomy
a. PPT Notes:
23. The epidemiology of gastric cancer has changed in recent years to more proximal. It is more common to see
it appear in spontaneous cases in the cardia and in association with distal Barrett’s esophagus. This is typically referred to as “intestinal type”
gastric adenocarcinoma. “Linitis plastica” or “leather bottle” stomach is associated with diffuse gastric carcinoma and involves non-cardia
regions primarily.
24. Case 2: Pathology
a. On the left is an H&E stain of adenocarcinoma of the stomach. On the right is a silver stain of the
Helicobacter pylori in a gastric crypt. As stated in the previous slide gastric cancer dichotomizes
into “diffuse” and “intestinal.” Intestinal is associated with H pylori and gastritis. Diffuse is more
prevalent in Asia, often hereditary and associated with “signet ring cells.”
25. Case 2 continued...
a. CT scan shows no distant spread. Laparoscopic staging shows no peritoneal spread. He undergoes
total gastrectomy. Multiple gastric nodes are positive. After recovery → 5Fluoruracil+Radiation concurrently (adjuvant therapy = given
after surgery to treat micrometastatic dz and local recurrent CA)
b. PPT Notes:
i. Unfortunately, almost 50% of patients in North America present in advanced stages of disease that is inoperable. Of those who
are operable, many have nodal or subclinical peritoneal or hepatic metastases. Treatment with adjuvant therapy has
incorporated chemotherapy and radiation in North America, while in Japan they eschew radiation feeling their surgery is
sufficient. The Europeans also use less radiation than North Americans. There is data to support all approaches but no real
world wide consensus on how best to treat patients with gastric cancer.
ii. For gastric cancer survivors, the one main issue post operatively and lifelong is a syndrome known as “dumping” syndrome.
These patient’s GI tract has been altered and the normal neurohormonal balance has been upset leading to high insulin levels
after meals. Results in hypoglycemia → anxiety, sweating, palpitations and faintness
26. Gastric Cancer Presentation:
 a. Weight loss, abdominal pain, nausea, dysphagia, melena, early satiety, ulcer-type pain
27. Gastric Cancer Epidemiology
a. Note: north america has lowered prevalence bc of eating less salty/smoked meats and increased use of refrigeration
b. PPT Notes:
i. East Asia especially Japan and Eastern Europe/Russia as well as parts of South America are hotspots for gastric cancer. It is
relatively rare in North America. Explanations for this may be dietary. Smoked and salted foods are associated with higher risk
of gastric cancer and are consumed at higher rates in these areas. Gastric cancer incidence has declined largely since
refrigeration became common place in the 1930s and 1940s.
28. Gastric Cancer Causation
a. Nitrites in smoked and salted foods
b. ETOH
c. Helicobacter pylori gastritis
d. Atrophic gastritis
e. Genetics
i. Lynch syndrome (assoc w/colorectal CA, uterine CA, and gastric CA)
ii. Hereditary Diffuse Gastric Cancer (young patients without risk factors - look at family hx)
f. PPT Notes:
i. Nitrites in cured foods when broken down in the stomach are genotoxic. Gastritis or chronic inflammation will contribute to
intestinal metaplasia very similar to Barrett’s esophagus. Over time, under the wrong kinds of environmental stressors, this
mucosa can then become dysplastic and malignant. DNA mismatch repair genetic defects predispose patients to colon, uterine
and other GI malignancies. HDGC results from mutations in the E-cadherin gene and is predominantly responsible for the more
clinically aggressive form of gastric cancer, linitis plastica. Patients with a strong family history of gastric cancer are screened
often with EGD and may have gastrectomy performed prophylactically at a young age.
29. Case 3:
a. 49 yo woman has routine pelvic exam. She has had weight loss and some dyspepsia. Ovarian mass is palpated. Periumbilical mass is
palpated. She has enlarged supraclavicular and axillary lymph nodes on left.
i. PPT Notes:
1. Left supraclavicular adenopathy → Virchow’s node
2. Left axillary adenopathy → Irish’s node
3. Periumbilical adenopathy → Sister Mary Joseph nodes
4. Metastasis to the ovary → Krukenberg tumor
5. Migrating thrombophlebitis → Trousseau’s syndrome
b. Lymph node biopsy reveals adenocarcinoma. Working diagnosis is “Adenocarcinoma of Unknown Primary”. Differential dx on path
shows likely gastric origin. EGD confirms gastric adenocarcinoma
i. PPT Notes:
1. Tumor metastases can be stained with a cocktail of antibodies called “cytokeratins” as well as markers for lymphoid
tissue and sarcoma to attempt to identify the origin of the cancer. Often an exhaustive work up is needed to find the
origin. Computed tomograms (CT) and Positron Emission Tomography (PET) are imaging modalities that aid in
isolating a dominant mass. Endoscopy can identify masses in the GI tract to a point. The small intestine is difficult to
visualize endoscopically beyond the duodenum. Fortunately, small bowel adenocarcinoma is exceedingly rare.
2. “Carcinoma of unknown primary” or specifically “adenocarcinoma of unknown primary” is a diagnosis of exclusion.
Exhaustive search for the primary disease is paramount in establishing not only diagnosis, but proper therapy. ~5% of
cancers will have an unknown primary and there are treatment protocols for this situation, but it is less than ideal.
There are newer, diagnostic tests that look at tumor genomics, rather than immunohistochemical staining pattern,
that can hone in on the diagnosis.
30. Case 3 continued…
a. ★Her2 stain (oncogene for breast and gastric CA) is positive on path specimen. Herceptin is the first targeted therapy for gastric cancer.
Anti-VEGF antibodies such as Ramucirumab are used as well
i. Palliative 5FU/Cisplatin and Herceptin was begun
ii. Partial response was obtained for several months then changed to Taxol and Ramucirumab
iii. Developed “phlebitis” periodically → Trousseau’s syndrome
iv. Eventually progressed and died 2 years after diagnosis
31. Question Case 2: A 76 yo woman has weight loss and abdominal pain for several months. EGD shows Barrett’s esophagus and a mass in the
cardia of the stomach. What bacteria is likely to be found on biopsy?
a. Chlamydia gastroensis
b. Mycobacterium intesticum
c. Helicobacter pylori
32. Question Case 2: She is found to have disease in the peritoneal cavity during exploratory laparotomy and thus is “closed up” without resecting
the tumor. Why and what can be done next?
a. Surgeons are lazy and TPN can be ordered
b. Surgery will not cure her, she should have Her2 staining done on the tumor
33. Upper GI Malignancy Caveats
a. Older age and co-morbid disease preclude aggressive therapy
b. Surgery needs to be done by an experienced surgical oncologist or thoracic surgeon
c. Long term issues include GERD, strictures, weight loss and chronic pain
d. Prevention
i. Smoking cessation
ii. ETOH moderation
iii. Helicobacter eradication if ulcer or gastritis present (not serology)
iv. Screening in endemic areas
v. Prophylaxis for family members

Lecture 3: CCC Gastritis and Peptic Ulcer Disease

1. Case 1
a. 35 year old patient of your practice calls your office . Patient notes onset of mild fever chills the preceding morning. This was associated
mild abdominal pain. Patient noted vomiting this am with a moderate amount of blood.
b. PMH no illnesses no meds no surgeries
c. Allergies none.
d. Further questions about history or present illness? - NSAIDS or Exercising
e. Physical exam Oriented white male. Slightly pale appearing HR 95 . Blood pressure 90/60. → hypovolemic b/c bleeding – send to ED
f. Abdomen mildly tender no rebound mild guarding bowel sounds hyperactive.
g. Diagnosis ?
2. Gastritis Differential Diagnoses
a. Acute Coronary Syndrome i. Esophageal Perforation, Rupture, Tears
b. Aneurysm, Abdominal j. Gastroenteritis
c. Cholangitis k. Hepatitis
d. Cholecystitis and Biliary Colic l. Inflammatory Bowel Disease
e. Cholelithiasis m. Mesenteric Ischemia – losing weight pain after food
f. Diverticular Disease n. Myocardial Infarction
g. Pulmonary Embolism o. Esophagitis
h. Renal Calculi p. Pancreatitis
3. Other Problems to be Considered
a. Gastric cancer e. Non-ulcer dyspepsia
b. Esophageal varices f. Functional gastrointestinal disorder
c. Mallory-Weiss tears g. Atypical appendicitis in the pregnant patient
d. Atrophic gastritis
4. Gastritis
a. Inflammation or irritation of the lining of the stomach, is not a single dz. Rather, gastritis is a condition that has many causes.
b. Common to all people with gastritis is pain or discomfort in the upper part of the belly (abdomen), sometimes called dyspepsia.
c. Gastritis can be a
i. brief and sudden illness (acute gastritis),
ii. a longer-lasting condition (chronic gastritis)
iii. or a special condition, perhaps as part of another medical illness.
d. An example of acute gastritis is stomach upset that may follow the use of alcohol or aspirin.
e. Helicobacter pylori is a type of bacteria that infects the stomach. Infection with this bacteria may lead to chronic gastritis.
f. Pernicious anemia (inflammatory autoimmune disease)
g. Bile reflux (bile goes back into stomach d/t weak pyloric sphincter and causes gastritis → PPI’s can cause bile reflux)
i. if you give PPI’s and it gets WORSE think about Bile Reflux Gastritis ★
h. Infections caused by bacteria and viruses
i. Gastritis is common. Up to 10% of people who come to a hospital emergency department with abdominal pain have gastritis.
j. Gastritis can be caused by irritation due to
i. excessive alcohol use, chronic vomiting, Stress, use of certain medications such as aspirin or other anti-inflamm drugs
k. Medications
 i. Aspirin (more than 300 drug products contain some form of aspirin)
ii. Nonsteroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen or naproxen)
iii. Steroids (prednisone is one example)
iv. Potassium supplements
v. Iron tablets
vi. Cancer chemotherapy medications
l. Medical and surgical conditions
i. Physical stress in people who are critically ill or injured
ii. After medical procedures (such as endoscopy, in which a specialist looks into the stomach with a small lighted tube)
iii. After an operation to remove part of the stomach
iv. After radiation treatment for cancer
v. Autoimmune diseases
vi. Pernicious anemia
vii. Chronic vomiting
m. Infections
i. Bacterial infections: H pylori infection is the most common. Many other bacteria-even those that usually cause pneumonia or
bladder infections-can cause gastritis.
ii. Viral infections
iii. Fungal (yeast) infections
iv. Parasites and worms
v. Tuberculosis
vi. Syphilis
5. Symptoms
a. Symptoms vary among individuals, and in many people there are no symptoms. However, the most common symptoms include:
i. Nausea or recurrent upset stomach
ii. Abdominal bloating
iii. Abdominal pain
iv. Vomiting
v. Indigestion
vi. Burning or gnawing feeling in the stomach between meals or at night
vii. Hiccups
viii. Loss of appetite
ix. Vomiting blood or coffee ground-like material
x. Black, tarry stools
6. Diagnosis
a. The physician may suspect gastritis by listening to the medical history. However, the only certain way to make the diagnosis is by
endoscopy and biopsy of the stomach lining.
b. Endoscopy is an exam where, under mild sedation, a lighted flexible scope is passed into the stomach.
c. Pictures can be taken but, more importantly, biopsies can be obtained for analysis under the microscope.
d. An upper GI x-ray exam and certain blood studies may be helpful.
7. Treatment
a. The treatment of gastritis will depend on its cause.
b. For most types of gastritis, reduction of stomach acid by medication is often helpful. PPI
c. Beyond that, a specific diagnosis needs to be made.
d. Antibiotics are used for infection.
e. Elimination of aspirin, NSAIDs or alcohol is indicated when one of these is the problem.
f. For the more unusual types of gastritis, other treatments may be needed.
8. Case 2
a. A 27 year old male is seen by you while covering at an Urgent care facility. Patient states that he hurt his ankle while playing basketball.
He noted landing on someone's foot on the inside of his foot and feeling his ankle roll in, he now complains of lateral ankle pain and
swelling.
b. Physical exam reveals a swollen L ankle with mild tenderness over the lateral calcaneo-fibular ligament.
c. PMH no allergies or history of hypertension or stomach problems.
d. Your diagnosis is a grade 2 ankle strain. You prescribe rest, ice, compression and elevation, Helichrysum, wild woodvine along with
naproxen 500 mg bid.(Didn’t know about Plai oil)
e. The patient calls the emergent care complaining of moderate to severe abdominal pain and blood in his stool.
f. Diagnosis? Peptic Ulcer Disease
 g. Studies? Endoscopy
h. Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa.
i. H pylori infection and NSAID use are the most common etiologic factors. ★ 2 hits
j. Other less common causes are hypersecretory states, such as
i. Zollinger-Ellison syndrome
ii. G-cell hyperplasia
iii. Mastocytosis
iv. basophilic leukemias.
9. Peptic Ulcer Disease
a. The most important risk factors for the development of peptic ulcers are infection with H. pylori and use of NSAIDs.
b. If neither of these factors is present, an alternative cause must be sought,
i. including hypersecretory states (e.g., Zollinger-Ellison syndrome [ZES])
ii. or one of the other less common causes of ulcer disease such as Crohn disease
1. vascular insufficiency
2. viral infection
3. radiation therapy, and cancer chemotherapy.
iii. Although a significant number of environmental factors, including
1. stress, personality type, occupation, alcohol, and diet, have been linked to the development of ulcers
2. there is no convincing evidence suggesting that any of these factors by itself can cause PUD.
10. PUD Pathophysiology
a. Under normal conditions, a physiologic balance exists between peptic acid secretion and gastroduodenal mucosal defense.
b. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is
disrupted.
c. Aggressive factors, such as: NSAIDs, H pylori, Alcohol, bile salts, Acid, and pepsin
d. can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury.
11. Clinical Case 3
a. Mr. Q is a 55 year old male complaining of a discomfort in his lower chest after swallowing food.
b. This discomfort is described as a squeezing sensation.
c. The symptoms occur moments after swallowing solids, but not after ingesting liquids.
d. These symptoms came on gradually, and have been slowly worsening.
e. His Past Medical History includes Hypertension, and Hyperlipidemia. He has had no surgeries
f. He takes one pill a day which is a combination anti-hypertensive and Lipid lowering agent.
g. Diagnosis? Gastric Ulcer (PUD) BUT NEED TO THINK ABOUT MESENTERIC ISCHEMIA
12. Peptic Ulcer Disease
a. Prandial Pain can also be caused by Ulcer disease
i. A spectrum of conditions involving the stomach and duodenum
ii. Starts as non-specific inflammation and progresses to ulceration.
iii. Morbidity ranges from dyspepsia to bleeding.
b. Common Causes
i. Infection – H. pylori
ii. Drugs - NSAID’s (e.g. ASA, Ibuprofen, Naproxen)
iii. Gastric Ulcers tend to hurt more with eating ★
iv. Duodenal Ulcers hurt less with eating ★
c. The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers:
d. Gastric ulcer has epigastric pain during the meal, as gastric acid production is increased as food enters the stomach.
e. Duodenal ulcers are initially relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, acid isn’t in duod.
f. Duodenal ulcer pain manifests mostly 2–3 hours after the meal, when stomach begins to release digested food & acid into duodenum.
13. Differential Diagnosis
a. Chronic gastritis h. Acute Pancreatitis
b. Myocardial ischemia
c. Acute gastritis
d. GERD
e. Pancreatic Cancer
f. Chronic Pancreatitis
g. Mesenteric Artery Ischemia★ HTN, HLD, DM, pain
14. Other Problems To Consider
a. Crohn’s disease with gastric or duodenal involvement
b. Drug-induced dyspepsia
c. Duodenitis
d. Functional (nonulcerous) dyspepsia
e. Gastric infections
f. Infiltrative diseases of the stomac
15. Treatment
a. Treatment of peptic ulcers varies depending on the etiology and clinical presentation.
b. Initial management of a stable patient with dyspepsia differs from the management of an unstable patient with upper GI hemorrhage.
c. In the latter scenario, failure of medical management not uncommonly leads to surgical intervention.
d. Treatment options include
i. Empiric antisecretory therapy
ii. Empiric triple therapy for H pylori infection
iii. Endoscopy followed by appropriate therapy based on findings of CLO test
iv. H pylori serology followed by triple therapy for patients who are infected
1. Breath testing for active H pylori infection may be used.
e. Endoscopy is required to document healing of gastric ulcers and to rule out gastric cancer.
i. This usually is performed 6-8 weeks after the initial diagnosis of PUD.
f. Documentation of H pylori cure with a noninvasive test, (urea breath test or fecal antigen) is appropriate with uncomplicated ulcers.
g. Most PUD is treated successfully with cure of H pylori infection, avoidance of NSAIDs, and appropriate use of antisecretory therapy.
i. Multiple antibiotics are required because resistance to treatment is a problem
h. Perform endoscopy early in patients
i. Older than 45-50 years
ii. Patients with associated so-called alarm symptoms
1. Dysphagia, recurrent vomiting, weight loss, or bleeding.
i. Age is an independent risk factor for the incidence and mortality from bleeding peptic ulcer, with the
i. risk increasing in persons older than 65 years
ii. increasing further in those older than age 75 years.
j. In one study, at least 2 risk factors (previous duodenal ulcer, H pylori infection, use of ASA/NSAID, and smoking) were present in two
thirds of persons with acute gastroduodenal bleeding.
16. Procedures
a. Upper GI endoscopy
i. Preferred diagnostic test in the evaluation of patients with suspected PUD
ii. Highly sensitive for the diagnosis of gastric and duodenal ulcers
iii. Allows for biopsies & cytologic brushings in the setting of a gastric ulcer to differentiate a benign ulcer from a malignant lesion
iv. Allows for detection of H pylori infection with antral biopsies for a rapid urease test and/or histopathology in patients with PUD
b. EGD
i. Indications
1. Eval for signs/symptoms suggestive of upper GI disease (dyspepsia, dysphagia, noncardiac CP, recurrent emesis)
2. Surveillance for upper GI cancer in high-risk settings (eg, Barrett esophagus, polyposis syndromes)
3. Biopsy for known or suggested upper GI disease (eg, malabsorption syndromes, neoplasms, infections)
4. Therapeutic intervention (e.g., retrieval of foreign bodies, control of hemorrhage, dilatation or stenting of stricture,
ablation of neoplasms, gastrostomy placement)
ii. Contraindications and Relative Contraindications
1. Contraindications include
a. possible perforation
b. medically unstable patients
c. unwilling patients.
2. Relative contraindications include: Anticoagulation, pharyngeal diverticulum, head and neck surgery.
iii. Complications
1. The major complications of EGD are: Bleeding, Infection, Perforation, Cardiopulmonary problems (MI)
2. Approximately 1 complication occurs for every 1000 procedures.
3. The mortality rate is estimated to be 0.5-3 deaths for every 10,000 procedures.
4. Cardiopulmonary events comprise 50% of all major complications, most of these events result from conscious sed.
c. Indications for Urgent Surgery
i. Failure to achieve hemostasis endoscopically
 ii. Recurrent bleeding despite endoscopic attempts at achieving hemostasis perforation.
iii. Maybe just simple oversewing of ulcer with treatment of the underlying H pylori infection or stopping NSAIDs for bleeding PUD.
iv. Additional surgical options for refractory or complicated PUD include:
1. Vagotomy
2. Pyloroplasty
3. Vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I)
4. Gastrojejunal reconstruction (Billroth II)
5. Highly selective vagotomy.
d. Other Tests
i. Detection of H pylori infection is essential in all patients with peptic ulcers.
ii. Endoscopic or invasive tests include a rapid urease test, histopathology, and culture.
1. Rapid urease tests are considered the endoscopic diagnostic test of choice. The presence of H pylori in gastric
mucosal biopsy specimens is detected by testing for the bacterial product urease. Three kits (ie, CLOtest, Hp-fast,
Pyloritek) are commercially available, each containing a combination of a urea substrate and a pH sensitive indicator.
a. Not good for cheap uninsured
2. Fecal antigen testing identifies active H pylori infection by detecting the presence of H pylori antigens in stools. This
test is more accurate than antibody testing and is less expensive than urea breath tests.
a. Great for cheap uninsured
3. Antibodies? (immunoglobulin G [IgG]) to H pylori can be measured in serum, plasma, or whole blood. Results with
whole blood tests obtained from finger sticks are less reliable.
4. Urea breath tests detect active H pylori infection by testing for the enzymatic activity of bacterial urease. In the
presence of urease produced by H pylori, labeled carbon dioxide (heavy isotope, carbon-13, or radioactive isotope,
carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.
5. Obtain histopath, often considered the criterion standard to establish a diagnosis of H pylori infection , if the rapid
urease test result is negative and a high suspicion for H pylori persists (presence of a duodenal ulcer).
6. Culture primarily is used in research studies and is not available routinely for clinical use.
17. Associated Complications
a. About 25 percent of patients with peptic ulcer disease have a serious complication such as
i. Hemorrhage
ii. Perforation
iii. gastric outlet obstruction
iv. Silent ulcers and complications are more common in older patients and in patients taking NSAIDs
1. The incidence of serious upper gastrointestinal complications among persons in the general population who do not
take NSAIDs is extremely low (less than one per 1,000 person-years)
18. Bleeding
a. Upper gastrointestinal bleeding occurs in 15 to 20 percent of patients with peptic ulcer disease.
b. It is the most common cause of death and the most common indication for surgery in the disease.
c. In older persons, 20 percent of bleeding episodes result from asymptomatic ulcers.17
d. Pts may present with hematemesis (bright red or “coffee ground”), melena, fatigue caused by anemia, orthostasis, or syncope.
19. Risk Stratification
a. There are several risk-stratification schemes that can help physicians determine the need for urgent intervention and predict continued
or recurrent bleeding after endoscopic therapy.
b. Rockall risk scoring system is used in stratifying patients at higher risk of rebleeding & death

c. Age – higher risk

d. Shock – pressure and tachy
e. Comorbid disease – liver or renal failure
f. Diagnosis – Mallory Weiss, other bleeding, upper GI cancer
g. Stigmata of recent bleeding – none or bleeding seen
20. Treatment
a. Triple therapy is considered to be the standard treatment for children
i. PPI + 2 ABXs has been shown to be very effective in clearing H pylori from the stomach.
ii. Current adult recommendation is treatment with Amoxicillin, Clarithromycin, and a PPI for 2 weeks.
iii. Current pediatric recommendation is Metronidazole + either Clarithromycin or Amoxicillin and a PPI
b. In adults, triple therapy based on amoxicillin, clarithromycin, and a proton pump inhibitor was shown to be more effective when given
for 14 days rather than for 7 days.
c. Efficacy of the 10-day treatment with proton pump inhibitor–based therapy has not been very widely studied in children and was not
recommended in
d. Quadruple therapy is used as a second-line treatment.
i. Metronidazole, clarithromycin, amoxicillin and omeprazole was effective, with an eradication rate of 94%.
e. One trial in children used bismuth-based quadruple therapy and showed an eradication rate of 84%.
f. One trial has tested the efficacy of sequential therapy in children (omeprazole plus amoxicillin for 5 d, followed by omeprazole,
clarithromycin, and tinidazole for another 5 d); eradication of H pylori infection in more than 90% of the children was reported.
21. Peptic Ulcer Disease - Surgery
a. Surgery is rare, but it is needed sometimes to treat:
b. Ulcers that don't heal (intractable peptic ulcers).
c. Life-threatening complications of an ulcer (severe bleeding, Perforation, Obstruction)
d. Surgery choices
i. When surgery is done, it usually involves one or more of the following:
ii. Cutting one or more of the nerves to the stomach (vagotomy).
iii. Widening the opening of the bottom of the stomach (pyloroplasty).
iv. Removing part of the stomach (partial gastrectomy).
22. Zollinger-Ellison Syndrome (ZES)
a. (ZES)is caused by a non–beta islet cell, gastrin-secreting tumor of the pancreas that stimulates the acid-secreting cells of the stomach
to maximal activity, with consequent gastrointestinal mucosal ulceration.
b. ZES may occur
i. sporadically or as part of an autosomal dominant familial syndrome - multiple endocrine neoplasia type 1 (MEN 1).
c. The primary tumor is usually located in the
i. Duodenum
ii. Pancreas
iii. abdominal lymph nodes
iv. ectopic locations have also been described (eg, heart, ovary, gall bladder, liver, kidney).
d. Pathophysiology
i. The symptoms of Zollinger-Ellison syndrome (ZES) are secondary to hypergastrinemia, which
1. causes hypertrophy of the gastric mucosa
2. Resulting in increased numbers of parietal cells and increased maximal acid output.
3. Gastrin by itself also stimulates acid secretion, resulting in increased basal acid secretion.
ii. The large quantity of acid produced leads to gastrointestinal mucosal ulceration. It also leads to diarrhea and malabsorption.
iii. Malabsorption in ZES usually is multifactorial, being caused by
1. direct mucosal damage by acid,
2. inactivation of pancreatic enzymes, and precipitation of bile salts.
iv. ZES is sporadic in 75% of patients, whereas in
v. The other 25% it is associated with MEN 1, an autosomal dominant condition characterized by
1. Hyperparathyroidism - hypercalcemia
2. pancreatic endocrine tumors
3. pituitary tumors.
e. Diagnosis
i. A high index of clinical awareness is needed to make a diagnosis of ZES.
ii. Abdominal pain is the most common symptom, present in 75% of patients.
iii. 73% have diarrhea, and this is the most common symptom in patients who have MEN 1/ZES and in female patients.
iv. The combination of diarrhea and abdominal pain is present in more than half the patients.
v. Heartburn is the third most common symptom
vi. Other symptoms include nausea, vomiting, gastrointestinal bleeding, and weight loss.
vii. Gastrointestinal bleeding frequently is due to ulceration in the duodenum and is the presenting symptom in 25% of patients.
viii. In patients in whom MEN 1/ZES is suspected, a history indicative of
1. Nephrolithiasis,
 2. Hypercalcemia
3. Pituitary disorders should be sought – HA, visual field cuts
f. Lab Studies
i. Fasting serum gastrin is the best single screening test.
ii. Preferably, patients should not be taking gastric antisecretory medications at the time of the test, but this is not essential for
the initial screen.
iii. Because fasting gastrin levels can fluctuate serial measurements on different days should be performed.
iv. Normal levels of serum gastrin in untreated ZES are extremely rare (< 1%).
1. Note: if gastrin is normal or low, they do not have ZES
v. Gastric acid secretory tests
1. Basal acid output (BAO) greater than 15 mEq/h or greater than 5 mEq/h in patients with a prior vagotomy and partial
gastrectomy is suggestive of ZES.
2. Basal gastric secretory volume greater than 140 mL in patients with no prior gastric acid–reducing surgery has a high
sensitivity and specificity.
3. Gastric pH less than 2.0 in the presence of a large gastric volume (>140 mL over 1 h in patients without prior gastric
acid–reducing surgery) is highly suggestive of ZES.
4. Currently, maxl acid output measurement rarely is performed if patient is a surgical candidate for tumor resection.
g. Provocative Tests
i. Elevated serum calcium levels should prompt a search for MEN 1 syndrome.
ii. A suggested algorithm for the evaluation of a patient with suspected gastrinoma is as follows:
1. Step 1: Check gastrin level. Measure at least 3 fasting levels of gastrin on different days.
2. Step 2: Perform gastric acid secretory studies.
a. A BAO value of greater than 15 mEq/h
b. gastric volume of greater than 140 mL and pH of less than 2.0 are highly suggestive of gastrinoma.
3. Step 3: Perform a provocative test. The secretin stimulation test is the preferred test.
4. Step 4: Perform somatostatin receptor scintigraphy (SRS).
5. Step 5: Perform imaging studies to stage and localize the gastrinoma.
6. Step 6: Determine if patient is a surgical candidate for tumor resection.
iii. The secretin stimulation test is the provocative test of choice because of its higher sensitivity. In this test, a 2-U/kg bolus of
secretin is administered intravenously after an overnight fast, and serum levels of gastrin are determined at 0, 2, 5, 10, and 15
minutes. An increase in serum gastrin of greater than 200 pg/mL is diagnostic.
h. Imaging Studies
i. SRS (somatostatin receptor scintigraphy) is the most sensitive imaging modality for detection of primary or metastatic lesions
in ZES and, thus, is the imaging modality of choice in ZES.
ii. CT scan can be performed to localize the tumor and is useful for evaluation for metastatic disease. However, its sensitivity for
primary tumor localization is only 50%, and frequently, tumors smaller than 1 cm are missed.
i. Medical Care
i. The goals of treatment are medical control of gastric acid hypersecretion and surgical resection of the tumor.
1. If the patient is acutely ill, immediate control of gastric acid hypersecretion can be achieved with intravenous proton
pump inhibitors.
ii. Patients who are candidates for surgical resection should be referred for resection of the tumor.
iii. For patients with metastatic disease
1. Chemotherapy, Interferon, octreotide may be helpful.
iv. The response to these agents in most studies has been low.
v. Liver transplantation for hepatic metastasis also has been reported.
vi. For patients with a single confined liver metastatic lesion, surgical resection may be attempted.
vii. Note: treatment of choice is surgery
Lecture 4: Esophageal Disorders
1. Normal Swallowing - 3 Phases:
a. Oral
i. Under voluntary control (chewing and mixed with saliva)
b. Transfer (pharyngeal)
i. Under involuntary control (getting the bolus past the UES)
ii. Bolus pushed to pharynx by tongue → automatic swallow once bolus reaches hypopharynx → UES relaxes → soft palate
elevates to block nasal cavity → epiglottis blocks larynx → tongue blocks oral cavity and propels bolus past UES
c. Esophageal
i. From the UES to the LES
ii. UES contracts → epiglottis re-opens → peristalsis carries bolus to LES → LES relaxes to allow passage to stomach → LES returns
to resting tone to prevent reflux
2. Definitions
a. Dysphagia
i. Subjective sensation of abnormal passage of food from the mouth to the stomach
ii. Inability to initiate swallow
iii. Regurgitation or coughing after the swallow
iv. Sensation that food is “stuck”
b. Ondynophagia
i. Pain with swallowing
c. Globus Sensation (Globus hystericus)
i. Non-painful sensation of lump or foreign body in the throat “feels like something is stuck in there” but no trouble swallowing
ii. Absence of Dysphagia/Odynophagia
3. History
a. Single most important part of evaluation
b. Pay special attention to timing and progression of symptoms, along with what types of food is giving them problems
c. Age, Past Medical Hx, and Medications can provide important clues
d. Dysphagia is an ALARM symptom and should never be attributed to normal aging ★ get further workup!
i. Don’t just observe
4. Getting a Good History
a. When does the trouble occur?
b. What types of food cause trouble? solids/liquids/both
c. Are the symptoms intermittent or progressive? Rapidly progressive is worrisome for malignancy
5. Other Important History
a. Associated Symptoms: Wt loss, GERD, hematemesis, odynophagia
b. Additional Medical Problems: HIV/AIDS, MS, DM, etc.
c. Current Medication: Esp. bisphosphonates, Iron, KCl, ASA, NSAIDs
6. Modified Barium Swallow
a. Videofluroscopy or Video Swallow Study
b. Patient given increasing consistencies and swallowing is recorded – thin, nectar, thick, solids
c. Transfer of bolus from mouth to esophagus (look for evidence aspiration)
d. Speech Pathology & Radiology
e. Looking for penetration of food bolus in the airway (i.e. aspiration) - is food getting past the UES correctly
7. Barium Swallow
a. Examines for Structural Abnormalities
b. Gastrografin (Diatrizoic Acid) is an alternative agent :
i. Allergy to Barium
ii. Suspected Perforation – water based so wont be bad if perforation exists
8. Esophageal Motility Testing
a. If you suspect a motility disorder, perform this test
b. Probe is inserted into nostril → pharynx → placed just proximal to the lower esophageal sphincter
i. Similar to how the EKG shows heart function electrically (X axis = time, Y axis = amplitude) – slopes down and left to right
9. EGD
a. Performed under sedation
b. Direct Visualization
c. Diagnostic (can biopsy) and Therapeutic
10. Endoscopic Dilation
a. Bougie Dilation +/- guidewire (long cylinder that stretches the length of the esophagus - stretches rings and strictures)
b. Pneumatic Dilation (balloon is inflated to maximum diameter to stretch fixed structures that area of the esophagus that needs help)
11. Oropharyngeal Dysphagia
a. “Transfer dysphagia”
b. Caused by disorders affecting the oropharynx, larynx and UES (problems with getting the bolus from the tongue past the UES)
c. Often caused by neurogenic/myogenic disorders
d. Historical Clues
i. Immediate symptoms:
1. Trouble initiating swallows
2. Coughing
3. Choking
4. Aspiration
5. Nasal Regurgitation
ii. Past Medical Hx - neurogenic/myogenic disorders (CVA, Myasthenia Gravis, Multiple Sclerosis)
e. Etiologies
i. Myopathic
1. Myasthenia gravis
2. Sarcoidosis
3. Polymyositis
ii. Neurologic
1. Brainstem tumors
2. Head trauma
3. CVA
4. MS
5. Huntington’s disease
6. Parkinson’s
iii. Structural
1. Zenker’s diverticulum
2. Cervical Webs
3. Oropharyngeal tumors
iv. Iatrogenic
1. Medication SE
2. Radiation
3. Corrosive
f. Workup and Treatment
i. Work up: Modified Barium Swallow
ii. Treatment:
1. Speech Therapy
2. Neuromuscular Electrical stimulation
3. PEG tube for refractory cases
4. PEG tube for refractory cases
12. Esophageal Dysphagia
a. Arises in the body of the esophagus, LES, and cardia (everything from the UES and downward) – now GI gets involved
b. Commonly due to mechanical obstruction or motility disorders
c. Sensation that food is getting “stuck” or is “slow to pass” seconds to minutes after the swallow
d. Solids Only: think Structural Disorder ★– Barium Swallow???
e. Solids & Liquids: think Motility Disorder ★– Esophageal Motility Testing???
f. DDx for Esophageal Dysphagia
i. Structural
1. Peptic Stricture
2. Eosinophilic esophagitis
3. Esophageal ring
4. Carcinoma
5. Vascular abnormalities
6. Radiation injury
ii. Motility
 1. Achalasia
2. DES
3. Nutcracker esophagus
4. Scleroderma
5. Sjogren’s syndrome
13. Structural Disorders
a. Peptic Stricture
i. GERD (approximately 10%)
ii. Also seen in:
1. Scleroderma – muscle cant clear acid
2. Zollinger-Ellison - hyperacidemia
3. s/p Heller myotomy – have no sphincter tone, prone to lots of ulcers
iii. Associated w/:
1. Long duration GERD
2. Male
3. Increased Age
iv. Insidious onset of symptoms – just kinda happening, solids > liquids
v. Progressive
vi. Begins w/ dysphagia to solids
vii. Progresses to both solids and liquids
viii. Treatment:
1. Acid Suppression – H2 or PPI
2. Dilation
b. Schatzki Ring (Note: this is a mucosal ring that acts as a shelf and food gets stuck)
i. Intermittent dysphagia to solids
ii. Symptoms often short-lived and associated w/ CP
iii. Relieved by regurgitation, liquids, or change in position
iv. Treatment: Dilation
c. Cervical Web
i. Incomplete mucosal fold protruding into the lumen
ii. Most common in the proximal esophagus
d. Plummer-Vinson Syndrome
i. Triad of: Dysphagia (due to esophageal web), Glossitis, Iron deficiency anemia
ii. Typically, white women, 40-70s
iii. S/Sx: dysphagia to solids
iv. Dx: Barium swallow & lab studies
v. Increased risk for Squamous Cell Esophageal Cancer
vi. Dysphagia usually improves w/ treatment of Fe deficiency
1. May need esophageal dilation
e. Eosinophilic Esophagitis
i. Adolescents/young adults w/environmental allergies
ii. Hx of food impaction
iii. Symptoms sometimes seasonal
iv. Narrowing, multiple rings
v. High Risk: Esophageal Perforation
vi. Diagnosis:
1. >15 eosinophils / HPF
2. Lack of Response to BID PPI x 2 months
vii. Treatment:
1. Swallowed aerosolized corticosteroid: Fluticasone
2. Budesonide suspension
3. Dilation
4. Elimination Diet
f. Esophageal Diverticula
i. Out pouching in esophagus
ii. Rare cause of dysphagia (< 5%)
iii. 3 locations:
 1. Above UES = Zenker’s (most important)
2. Mid-esophagus
3. Just proximal to LES (often accompany motility disorders)
g. Zenker’s Diverticulum
i. Symptoms: ★what are usually asked on the test – older people
1. Regurgitation of undigested food (ate days before)
2. Halitosis (bad breath)
3. Aspiration
4. Globus
ii. Diagnosis:
1. Barium Swallow (also seen on MBS)
2. EGD (rule out other dx)
iii. Treatment:
1. Symptoms: Surgical (by ENT surgeon)
2. Asymptomatic: Observation
h. Esophageal Carcinoma
i. Dysphagia to solids progressing to liquids
ii. Rapidly progressive symptoms
iii. Associated w/: >60 yo, Symptoms <1 yr, Anorexia, Wt. Loss (>10 kg)
i. Barrett’s Esophagus
i. Associated precursor to Adenocarcinoma
14. Esophageal Motility Disorders
a. Achalasia
i. Note: Birds Beak - proximal esophageal dilation with distal stricture
ii. Incomplete LES relaxation and Absent Peristalsis
iii. Exact etiology unknown
iv. Dysphagia to both solids and liquids
v. Male and Female equally affected
vi. Typical age of diagnosis 25-60 yo
vii. Increased Risk of ★Squamous Cell Carcinoma of Esophagus
viii. Low Surgical Risk:
1. Pneumatic Dilation or Heller Myotomy
ix. High Surgical Risk:
1. Botulinum Toxin (Botox), Nitrates, Ca-channel blockers
b. Pseudo- and Secondary Achalasia
i. Psuedoachalasia - caused by mechanical obstruction. Usually malignancy.
1. Most common - Gastric carcinoma
2. EGD in all newly diagnosed patients
ii. 2nd achalasia – to Chagas disease
1. protozoan parasite Trypanosoma cruzi
2. transmitted by triatomine bugs
c. Diffuse Esophageal Spasm (DES)
i. Note: corkscrew esophagus - alternating constrictions along the esophagus on radiology
ii. Likely caused by combination muscular and neural defects
iii. Sx provoked by stimuli:
1. Acid reflux, Stress, Hot/cold food, Carbonated beverages
iv. Intermittent dysphagia to solids and/or liquids – also complain of chest pain
v. Diagnosis:
1. Simultaneous Contractions on manometry
2. High Amplitude (>30mmHg)
3. Non-Peristaltic
vi. Treatment:
1. No good therapies, PPI a good idea for most
2. Ca-channel blockers (Diltiazem 180-240 mg/day)
3. TCA (Imipramine 25-50mg Qhs)
4. Isosorbide PRN
d. Nutcracker Esophagus
 i. Consider w/ Dysphagia and Chest Pain
ii. Peristaltic Motility Disorder
iii. Average distal esophageal amplitudes >220 mmHg
iv. Overlap with DES
v. Treatment also the same
e. Systemic Disorders Affecting the Esophagus
i. Scleroderma
1. Review: Excessive fibrosis and collagen deposition throughout body.
a. “Taut skin”, Anti-Scl-70 Ab, Can be part of CREST syndrome
2. Up to 90% of pts have GI involvement
a. Aperistalsis of distal 2/3 of esophagus
b. Severe GERD → esophageal strictures
c. Delayed gastric emptying – Reglan
3. Tx: PPI, smaller more frequent meals
ii. Amyloidosis
1. Review: extracellular tissue deposition of fibrils composed of low molecular weight subunits (5 to 25 kD) of a variety
of normal serum proteins which are misfolded
a. Stain Congo red (leading to green birefringence under polarized light)
2. Amyloid infiltrates esophageal wall and causes esophageal rigidity and loss of compliance
3. Presents similar to scleroderma. Dysphagia, severe reflux
iii. Dermatomyositis
1. Review: idiopathic inflammatory myopathies, characterized by proximal skeletal muscle weakness and muscle
inflammation
a. Gottron’s papules, shawl sign, heliotrope rash
b. Interstitial pulmonary disease
c. polyarthritis
d. Dysphagia
2. Weakness of the striated muscle of the upper one-third of the esophagus (and/or the oropharyngeal muscles)
contributes to dysphagia, nasal regurgitation, and/or aspiration
3. Tx: steroids for underlying disease
15. Odynophagia
a. General
i. Painful swallowing → think infection
ii. Most Common causes are infectious (Candida, HSV, CMV)
iii. Caustic ingestions consideration in the right clinical setting
b. Infectious
i. Candida Esophagitis
1. Common in HIV pts
a. AIDS-defining illness - primarily occurs CD4<200
2. Hematologic malignancies
3. Long Term Antibiotic Use
4. Common cause of odynophagia
5. Tx:
a. Moderate/Severe: oral fluconazole
b. Severe: IV fluconazole or amphotericin B
ii. CMV Esophagitis
1. Immune suppressed – looks more like ulcers
2. Coinfections of the esophagus are common in patients with CMV. Concomitant Infection w/:
a. Candidiasis (73%) and HSV infection (12%) have been reported among these patients.
3. Tx: IV ganciclovir or foscarnet
iii. HSV Esophagitis
1. Organism: usually HSV-1
2. Clinically similar to CMV
3. S/sx: Severe odynophagia, fever, retrosternal chest pain, usually immunocompromised pts (esp. organ transplant pts)
4. Dx:
a. EGD – multiple ulcers, friable mucosa, usually distal esophagus
b. Biopsy – intranuclear inclusion bodies
 c. Tx: Acyclovir (IV or po)
c. Pill Induced Esophagitis
i. Pathophys: prolonged contact of the caustic contents of the medication with the esophageal mucosa.
1. Often occurs at sites of anatomic narrowing: aortic arch, GE junction
2. Esophageal retention – laying flat after taking pill, no water, poor peristaltic action
3. Caustic potential of the medication: osmolar, acidic, alkaline, direct injury
ii. Meds implicated: Tetracyclines (esp. doxycycline), KCl, quinidine, ascorbic acid, ferrous sulfate, NSAIDs, Bisphosphonates
iii. S/sx: acute onset of odynophagia and retrosternal pain
iv. Dx: EGD shows isolated ulcer with normal mucosa surrounding, erosions or ulcerations and exudative inflammation
v. Tx: heal without intervention within a few days and avoid re injury
d. Caustic Esophageal Injury
i. Pathophys: severe injury (liquefactive necrosis) from highly alkaline or acidic products
1. E.g. suicide attempt from drinking lye, bleach, etc.
2. Bleach, industrial strength cleaners, button batteries, toilet bowl cleaners
ii. Dx & Tx:
1. Emergent endoscopy (unless evidence of perforation , respiratory failure)
2. DO NOT use emetic, neutralizing agents or NG suction to remove substance
3. Surgery if perforation, peritonitis or mediastinitis develops
iii. Complications: perforation (possible death), lifelong/ recurrent strictures, increased risk squamous cell esophageal cancer
e. Boerhaave’s Syndrome
i. Note: free air in the diaphragm on radiology → esophageal perforation
ii. “Effort” Rupture
iii. Associated with Eosinophilic Esophagitis
iv. Symptoms:
1. Violent Vomiting, Retching or Coughing
2. Retrosternal chest pain
3. Odynophagia
4. Tachypnea/Dyspnea
5. Fever, Shock, Cyanosis
v. Evaluation:
1. Gastrograffin Esophagram (if negative Barium swallow)
2. CT chest
vi. Treatment:
1. Contained: NPO, NG suction, IV antibiotics, TPN (feeding through the vein)
2. Free Perforation: Surgery (w/o comorbity) or Endoscopic stent
f. Esophageal Perforation
i. Typically Iatrogenic – usually during dilation
ii. Work up is identical to Boerhaave’s
iii. Therapy:
1. Surgical closure of perforation
2. Esophagectomy
3. Observation in contained perforation
g. Summary:
i. Dysphagia and odynophagia ALWAYS require further workup
ii. Be familiar with the testing modalities and the types of presentations each would be used in

Lecture 5: Upper GI Bleed

1. Definitions
a. Upper GI Tract: Esophagus, Stomach, Duodenum
b. Hematemesis: Vomiting of bright red blood or coffee ground emesis
c. Melena: Black tarry stool
d. Hematochezia: Bright red blood per rectum (BRBPR)
e. Overt Bleed: Presence of blood is obvious
f. Occult Bleed: Blood detected only with test such as stool guaiac or FIT
2. Etiologies (* =most common)
a. PUD*
 b. Esophageal/Gastric Varices*
c. Mallory-Weiss Tear
d. Vascular Lesions
e. Tumors
3. Peptic Ulcer Disease
a. Responsible for 21% of All Upper GI Bleeds
i. Gastric (55% of PUD)
ii. Duodenal
b. Primary Risk Factors:
i. H. pylori
ii. NSAIDs
iii. Physiologic Stress- burns, ICU, etc
c. H.pylori and NSAIDs account for 90% of Ulcers
4. H. pylori
a. Gram negative, 4-6 Flagella
b. Urease Producer
i. Generates Ammonia → Neutralizes Acid
c. Protease that thins protective mucus layer
d. Only colonizes Gastric Epithelium (when found elsewhere, gastric metaplasia is present) – Inlet patch of the esophagus
e. Prevalence inversely related to socioeconomic status
f. Acquired in Childhood
g. Likely Oral-Oral or Fecal-Oral Transmission
h. Complications:
i. PUD (80% Duodenal, 50% Gastric) - more likely to cause ulceration in the small bowel even though colonizes stomach
ii. Carcinoma (MALT, Adenocarcinoma)
i. Who do we Test?
i. Active PUD
ii. Hx of PUD who have not been previously treated
iii. Low Grade MALT
iv. Endoscopic Resection of early Gastric Cancer
v. Uninvestigated Dyspepsia (<55y w/o Alarm symptoms)
j. Non-Invasive HP Testing

1. Antibody – serum, low cost, good negative predictive value – can’t determine eradication (always positive)
a. Good for young person, undiagnosed
2. Urea Breath Test – good test, shows active infection
3. Stool Antigen Test – common for adults, good for active infection, prevalence doesn’t matter
ii. Note: serum antibody is easiest but cannot document active infection, only identifies exposure
1. Patient needs to be off of PPI’s 2 weeks before doing these tests
k. Endoscopic HP Testing
 1. Histology – expensive due to the pathology costs
2. Rapid Urease Testing – inexpensive, very sensitive and specific – changes color, not as sensitive with treatment
3. Culture – not done often, expensive not available
4. PCR – test for antibiotic specificity
l. Standard First Line Treatment
i. Tx for H.pylori is PPI + Antibiotics - don’t need to memorize slide
ii. BID PPI + two antibiotics
iii. Quadruple therapy is becoming more positive
m. Documenting Eradication
i. Some suggest documenting eradication in all treated patients
1. Breath Test, Stool Antigen, or Endoscopic
ii. Definitely Document Eradication In:
1. Complicated PUD (Bleeding or Perforation)
2. Family or Personal History of Gastric Cancer
3. Need for Future NSAID therapy
5. NSAID Gastropathy/PUD
a. Multifactorial Injury
i. Topical Injury
ii. Inhibition of Prostaglandin Synthesis
b. Enteric Coated or IV Administration does NOT affect decrease GI toxicity ★
c. PPI Prophylaxis in High Risk Pts.
i. >60,
ii. History of PUD
iii. Concurrent use of Anticoagulants or Steroids
iv. Comorbidities
6. Stress Gastritis
a. ICU setting: Burns, Major Surgery
b. Risk Factors:
i. Mechanical Ventilation (over 48 hrs)
ii. Coagulopathy
iii. Hypotension
c. Diagnosis: Shallow ulcers on EGD
d. Prophylaxis: ALL pts on Prolonged Ventilation and Coagulopathy
i. Treatment: IV PPI or H2-RA (while risk factor is present → while on mechanical ventilation)
7. Portal System: Quick Review
a. Responsible for directing blood from all parts of the GI tract to the Liver
b. Supplies majority of the Liver’s blood supply
i. Portal Vein 80%
ii. Hepatic Artery 20%
iii. These 2 systems converge to form the Hepatic Sinusoids
8. Portal Hypertension
a. Elevated Gradient between Portal and Hepatic Veins
b. Ohm’s Law
i. Pressure = Resistance x Flow
c. Resistance: Difficult to Fix
i. Fibrosis and nodularity of Cirrhotic liver
ii. Distortion of Vascular Architecture – irreversible
d. Vascular Flow: Potentially Reversible, Therapy Target
 i. Intrahepatic Vasoconstriction
ii. Splanchnic Vasodilation
iii. Systemic Vasodilation
9. Portal Hypertension Consequences
a. Portal HTN leads to formation of collaterals
i. Low pressure veins incapable of handling increased pressure
b. Insufficient to normalize portal pressure
i. Esophageal Varices – lumpy bumps in the esophagus
ii. Gastric Varices – lumpy bumps in the stomach
iii. Portal Hypertensive Gastropathy – “snakeskin appearance”
10. Vascular Disorders
a. Mallory Weiss Tear
i. Longitudinal mucosal lacerations (intramural dissections) in the distal esophagus and proximal stomach
ii. Associated with forceful Retching
iii. Prevalence among upper GI bleeds = 5%
iv. Prolonged symptoms can be associated with perforation (Boerhaave’s Syndrome)
b. Arteriovenous Malformations (AVM)
i. AKA – Angioectasias, Vascular ectasia
ii. Telangiectasias (implies congenital or systemic disease, anatomically similar)
iii. Most common vascular anomaly of the GI Tract
iv. Patient age >60
v. Increased in: ESRD, von Willebrand’s disease and possibly Aortic Stenosis
vi. Usually multiple
vii. Can present as either overt or occult bleeding
c. Hereditary Hemorrhagic Telangiectasia
i. Osler-Weber-Rendu
ii. Autosomal Dominant, 1:5,000-8,000
iii. Mucocutaneous Telangiectasias
iv. AVM GI tract, Liver, Pulmonary and Cerebral Vasculature
v. Most Common Findings: Epistaxis, GI Bleed → Iron Deficiency Anemia
vi. Increased Risk of Colon Cancer ★ (showed pic and asked what type of Cancer is the patient most at risk for)
d. Dieulafoy Lesion
i. Aberrant submucosal vessel that erodes into overlying epithelium without overlying ulcer
ii. Exact Etiology Unknown
iii. Triggers for Bleeding Unknown:
1. Males
2. CVD, CKD, DM or ETOH abuse
3. NSAIDs
iv. Bleeding is self-limited but at times profuse – squirts blood
v. Diagnosis: Endoscopic
e. GAVE (Gastric Antral Vascular Ectasia)
i. Watermelon Stomach
ii. Etiology: Uncertain
iii. Oozes blood
iv. Associated with: Cirrhosis and Systemic Sclerosis
v. Clinical Scenario: >70 yo, Female, Iron deficiency anemia, Occult GI Bleeding
11. Cancer
a. Gastric Adenocarcinoma
i. 90% of all Gastric Tumors
ii. Diffuse and Intestinal Types
iii. Intestinal Type Progression:
1. Superficial Gastritis
2. Chronic Atrophic Gastritis
3. Intestinal Metalplasia
4. Dysplasia
5. Carcinoma
 iv. H.pylori related to both types (Eradication reduces Gastric Cancer Risk)
v. Risk Factors:
1. Pickled/Smoked Foods
2. Smoking
3. Obesity
4. Developing Countries (Eastern Asia and Central America)
vi. Symptoms:
1. Wt. Loss
2. Vague Abdominal Pain
3. Dysphagia (Proximal tumors) - pseudoachalasia
4. Occult GI Blood loss (<20% have overt hematemesis/melena)
vii. At Diagnosis:
1. 50% will have disease extending beyond locoregional confines
2. Only 50% of those will have locoregional Involvement that can undergo resection
b. MALT Lymphoma (Mucosa Associated Lymphoid Tissue)
i. Strong Association with H. pylori
ii. Peak Incidence 50-60 yo, Slight Male predominance
iii. Occult GI Bleed seen in on 19%
iv. Most Common Symptoms: Epigastric pain (78-93%), Anorexia (47%), Wt. Loss (25%)
c. GIST (Gastrointestinal Stromal Tumor)
i. Mesenchymal Tumors (connective tissue, not epithelial)
ii. Most common in the stomach (70%) and proximal small bowel
iii. 5,000 new cases each year in the US
iv. 50-70yo, Equal M-F
v. 40% Develop Overt GI bleed from
vi. Tumors enlarge enough to outstrip blood supply, creating a characteristic central tumor cavity filled w/hemorrhage & necrosis
12. Evaluation of an Upper GI Bleed
a. Initially
i. Use History, Physical and Basic Lab work up to :
1. Determine Severity of the Bleed
2. Identify Possible Causes of the Bleeding
3. Determine if there are Conditions Present that may affect future Management
ii. This will guide:
1. Patient Triage – where does the patient go
2. Resuscitation – what to do
3. Empiric Medical therapy
4. Further Diagnostic Testing
b. Historical Clues
i. Bleeding Manifestations: Hematemesis? or Melena?…Hematochezia?
ii. Associated Symptoms:
1. Retching → Mallory-Weiss
2. Dizziness/Lightheadedness → bleeding a lot
3. Abdominal Pain → perforation? Do we need surgery on board
iii. PHx:
1. Recent NSAID or Steroid use, Anticoagulation, Antiplatelet Agents (Coumadin, Xarelto, Plavix)
2. Hx of PUD or GI bleed
3. Known Coagulopathy
4. Liver Disease or risk factors (ie prolonged ETOH abuse or Hx of IVDA)
c. Examination – Clinical Assessment of Hemodynamic Status – MOST IMPORTANT FIRST STEP
i. Resting Tachycardia
1. Mild to moderate volume loss
ii. Orthostatic Hypotension ★ good bedside evaluation of volume status
1. Systolic BP decrease of ≥20mmHg and/or HR increase of ≥20 bpm moving from recumbent to standing
2. Indicates volume loss of at least 15%
iii. Supine Hypotension
1. Indicates volume loss of at least 40%
d. Examination
i. Is this a possible perforation?
1. Significant Tenderness to palpation
2. Involuntary Guarding
3. Peritoneal Signs
a. Note: if patient is stiff as a board it’s because they’re having peritoneal signs & don’t want to move around
ii. Looks for hints to possible undiagnosed disease, particularly liver disease and might be a varices rather than just an ulcer ★
1. Ascites
2. Jaundice/Scleral Icterus
3. Spider Angiomas
iii. Start with:
1. CBC
2. CMP Chemistries and Liver Function
3. Coagulation studies (PT/INR, PTT)
4. EKG and Troponins in at risk groups
iv. Expect Hgb to decrease initially with hydration
v. Look for 20:1 (or higher) BUN:Cr Ratio
1. Higher the ratio = higher likelihood of upper GI bleed
2. Blood is absorbed as it passes through the Small Bowel, causing decreased renal perfusion
e. Triage and Support
i. ICU Admission:
1. Hemodynamically Unstable
2. Active Overt Bleeding
ii. Support:
1. Supplemental O2 via Nasal Cannula
2. 2 Large bore IV’s or Central Line
3. Elective Intubation for airway protection in selected pts (ongoing hematemesis, altered respiratory or mental status)
iii. ★ Fluids are Priority One:
1. Start with a liter bolus of normal saline and adjust based on individual needs
iv. Transfusions: (comes a little later in the process…)
1. Hgb <7 g/dL for most
2. Hgb <9 g/dL for those with symptomatic CAD
3. Avoid over transfusion, especially in Portal HTN
v. Correct Coagulopathy and Low Platelets:
1. FFP for INR ≥1.5 and active bleeding
2. Platelets for Plt <50,000
f. Medications
i. ★ IV PPI (Proton Pump Inhibitors) High Dose, continuous Infusion
1. Lowers rate of Ulcer Re-bleed
2. Decrease Length of Hospital Stay
3. Decrease Need for Transfusions
4. Reduces Need for Intervention at Endoscopy
5. Promotes stabilization of blood clots by neutralizing gastric acid
ii. Erythromycin
1. Used in selected patients to improve visualization at endoscopy
2. Motilin Receptor agonist
a. Promotes gastric emptying
b. Given 20 min to 2 hours prior to EGD
c. Reduces need for second look endoscopy
iii. Metoclopramide (Reglan) is also used, but not preferred (d/t extrapyramidal side effects)
g. Medications for Patients with Cirrhosis
i. Octreotide (Somatostatin Analog)
1. Suspected Variceal Bleeding (not routine)
2. IV bolus of 50 mcg, then 50 mcg/hr infusion
3. Mechanism of Action:
 a. Increases Splanchnic Resistance by Inhibitor hormones that cause vasodilation (glucagon, VIP)
ii. Prophylactic Antibiotics
1. Gram negative coverage (Ceftriaxone, Zosyn, Levaquin)
2. Decrease in All Cause Mortality
3. Reduce Infectious complications, SBP
4. Reduce Re-bleed risk
h. Nasogastric Lavage
i. NG Tube? Generally not necessary
ii. May be useful:
1. Determining if bleeding is ongoing
2. Remove particulate matter, clots or fresh blood prior to EGD
i. Role of EGD
i. Diagnostic Modality of Choice in Acute UGIB:
1. Diagnosis/Source of bleed
2. Prognostic Information
3. Therapeutic Intervention
ii. In General should be performed within 24 hrs of presentation (High risk within 12 hrs)
j. EGD and PUD
i. Stigmata of Recent Hemorrhage (SRH) predict need for therapeutic intervention & re-bleed
ii. Stigmata: (Descending Risk of Re-bleed)
1. Active Spurting - most worrisome, bleeding now
2. Active Oozing – bright red
3. Non-bleeding visible vessel
4. Adherent clot – harbinger of recent bleed, need to look under – often re bleeds
5. Flat pigmented spot
6. Clean base - least worrisome
13. Endoscopic Therapy
a. Epinephrine Injection
i. Vasoconstrictor
ii. Diluted w/ Normal saline 1:10,000
iii. Must be used with Additional Modality
b. Heater Probe:
i. Initial hemostasis (alone or with Epi) = 78-100%
ii. Re-Bleed rate = 0-18%
iii. Direct Contact Method → applies heat
c. Endo clips
i. Used alone or combination
ii. Useful For: PUD, Mallory Weiss Tear, Dieulafoy Lesions, AVM
d. Argon Plasma Coagulation
i. Non-contact
ii. Uses Argon gas along with a high voltage spark delivered to the tip of the probe
iii. Used most commonly in UGI tract with: AVM, GAVE, Dieulafoy’s lesion (useful for vascular lesions, not ulcers)
e. Endoscopic Variceal Band Ligation (EVL)
i. Treatment of Esophageal Varices (Not Gastric Varices)
ii. Can be used for Hemostasis as well as secondary prophylaxis of variceal bleed
14. What about Gastric Varices?
a. Cyanoacrylate Glue
i. Limited by Availability and Local Expertise
ii. Injected directly into varix
b. TIPS (Transjugular Intrahepatic Portosystemic Shunt)
i. Uses: Esophageal Varices (re-bleed following EVL), Gastric Varices, Refractory Ascites
15. Endoscopic Treatment Failures (Non-Variceal)
a. Bleed is localized: Endoscopy, TRBC Scan, CT
b. Arteriography with Embolization
i. Bleed rate must be ≥0.5 mL/minute – pretty brisk
ii. Selective cannulation of the bleeding vessel is achieved then Embolization is performed w/ various agents
iii. Efficacy up to 95%, but “fairly low re-bleed rate” (last year he said fairly common)
16. Angiography Fails, Now What? → Surgery
a. Medical, Endoscopy and/or Radiographic Failures undergo resection
b. Billroth II
17. Conclusion
a. Good History/Physical to generate differential diagnosis
b. Determine Hemodynamic Stability (if not stable…get them that way!)
c. Correct Coagulopathy and Replace blood products
d. Start Appropriate Medication prior to Endoscopy
e. Perform appropriately timed EGD w/ therapeutic modalities as needed

Lecture 6: GERD and Barrett’s Esophagus

1. Anatomy of the Esophagus
a. Hollow, muscular tube with mucosa, submucosa, and muscularis layers
b. Histo: stratified squamous that transitions to columnar epithelium at the GE junction
i. Characterized by tight intercellular junctions, cell membrane ion transporters
c. 2 sphincters: UES and LES
d. Goal: transfer food bolus to the stomach and prevent its regurgitation
e. The external longitudinal layer of muscle:
i. superior 1/3 is striated muscle (voluntary control)
ii. middle 1/3 is a mixture of smooth and striated muscle
iii. Inferior 1/3 is smooth muscle (peristalsis) - (note: pts w/scleroderma develop dysphagia d/t smooth muscle atrophy)
f. Muscle layers close esophageal lumen & shorten the esophagus to transfer to the bolus. In the distal portion, peristalsis transfers bolus.
g. LES maintains tonic high-pressure passage of food, relaxing for transfer of food. This sphincter tonicity prevents regurgitation.
h. Esophagus protected by refluxed gastric contents by:
 i. Anatomic/Physical anti-reflux barrier
1. LES – elevated resting pressure
2. Crural diaphragm
3. Phrenoesophageal ligament
4. Angle of His – positioning of the stomach
i. Esophagus protected by refluxed gastric contents by continued...
i. Esophageal clearance mechanisms of peristalsis
ii. Neutralization by alkaline saline
iii. Epithelial defensive factors (tight junctions)
2. GERD
a. Definition: Reflux of stomach contents causes symptoms or complications that are troublesome for the pt
i. Also acid can lead to tissue injury
b. Some reflux is physiologic and normal (“happy spitters”)
c. Heartburn and regurgitation are NOT the only indicators of disease
d. Epi: ~7% of Adult Americans have daily symptoms – $10-$21 Billion dollars per year
e. Pathophysiology
i. 3 Major Mechanisms of reflux:
1. Transient lower esophageal sphincter relaxations (tLESRs)
a. Longer than swallow-induced LES relaxation, w/o pharyngeal contraction & esophageal peristalsis
2. Hypotensive lower esophageal sphincter
a. Gastric distention, cholecystokinin, foods (fat, chocolate, caffeine, alcohol), smoking, and drugs
3. Anatomic disruption of the gastroesophageal junction, often associated w/ hiatal hernia
a. Thus, decreased pressure from the diaphragm keeping the LES closed
ii. Prolonged esophageal acid clearance
1. E.g. peristaltic dysfunction, decreased salivation
iii. Esophageal hypersensitivity
1. E.g. visceral hyperalgesia
iv. Obesity & pregnancy increase intrabdominal pressure and disrupts GE junction.
v. Pregnancy hormones also adversely affect LES tone.
vi. Note: there are physical, physiologic reasons etc that can play into GERD
3. Definitions
a. Heartburn – burning substernal pain; postprandial. Also called pyrosis.
b. Regurgitation – perception of gastric content into mouth or hypopharynx (“tastes like a penny”)
c. Dyspepsia - burning epigastric pain, abdominal discomfort
d. Water brash – hypersalivation in response to reflux (rare)
e. Dysphagia – difficulty swallowing
f. Odynophagia – painful swallowing
g. Globus sensation - perception of a lump or fullness in the throat that is felt irrespective of swallowing
4. GERD Signs and Symptoms
a. Esophageal symptoms (typical)
i. Heartburn (pyrosis)
ii. Regurgitation
iii. Dysphagia
iv. Atypical esophageal symptoms - chest pain, water brash, globus sensation, odynophagia, and nausea
b. Extraesophageal symptoms (atypical)
i. Bronchospasm, laryngitis, dental erosions, asthma, chronic cough
ii. Possibly may also cause sinusitis, recurrent otitis media and pulmonary fibrosis
iii. Up to 1/3 of pts evaluated for heartburn have extraesophageal symptoms
iv. Note: cough is the #4 most common symptom of GERD, even though it’s an extra-esophageal/atypical sx
5. Chest Pain due to GERD
a. Most common cause of non-cardiac chest pain
b. Must rule out cardiac cause in at-risk patients (since that would be life-threatening)
c. Symptoms overlap due to similar neural visceral neural pathways
d. May be relieved by nitrates – doesn’t differentiate
e. Chest pain that wakes a patient from sleep, however, is uncommon in true cardiac disease and may suggest an esophageal disorder, as
does pain that is relieved with antacids or pain that lasts for several hours without associated symptoms.
f. 8-10 week PPI trial may be indicated if cardiac CP ruled out.
6. GERD Risk Factors
a. Obesity (also in pregnancy)
b. Increased intraabdominal pressure
c. Hiatal hernia
d. GERD Worsened by
i. Xerostomia (decreases saliva production)
ii. Sjogren’s syndrome (decreased saliva production)
iii. Scleroderm (reduced LES pressures)
iv. Gastroparesis (delayed clearance of stomach contents) - side effect of DM
v. Nicotine (induces LES relaxation and decreases saliva production)
7. Hiatal Hernia
a. Co-morbid condition which often worsens GERD
b. Define: Herniation of viscera, most commonly the stomach, into mediastinum through the esophageal hiatus of the diaphragm
c. Sliding hiatal hernia is most common (Type I)
i. A sliding hiatal hernia is one in which the GE junction and gastric cardia slide upward as a result of weakening of the
phrenoesophageal ligament attaching the gastroesophageal junction to the diaphragm at the hiatus
ii. Result from increased intraabdominal pressure: pregnancy, obesity
iii. More at risk to have GERD
8. Red Alarm Symptoms -These symptoms require further diagnostic evaluation. Usually with an EGD.
a. Dysphagia
b. Involuntary weight loss
c. Anemia
d. Vomiting
e. GI bleeding
9. History
a. Symptom location, duration
b. Remitting/exacerbating factors – many patients will have tried OTC meds before presenting to you
c. ROS – ask about red alarm symptoms
d. PMHx
e. Complete list of meds, including OTC meds
f. Social Hx: tobacco history
10. Physical Exam
a. Usually benign
b. Look for connective tissue diseases which can exacerbate
c. Severe disease may see dental erosions (severe disease or bulimia)
d. Signs of chronic sinusitis
e. Abnormal supraclavicular lymph nodes – suggest esophageal or gastric cancer
11. Differential Diagnosis
a. Achalasia
b. Infectious esophagitis
c. Pill esophagitis
d. Eosinophilic esophagitis
e. Esophageal motor disorders
f. Peptic ulcer disease
g. Non-ulcer dyspepsia
h. Biliary tract disease
i. Coronary artery disease
j. Esophageal cancer
12. Diagnosis of GERD
a. Clinical diagnosis
i. unless unsure of diagnosis or red alarm symptoms present → then perform additional testing
b. Generally just do empiric trial with PPIs,
i. If favorable response this supports dx
ii. If empiric therapy not effective perform EGD
c. If refractory ds, consider further testing
i. EGD, ambulatory pH
d. Barium swallow not indicated for GERD. Used for dysphagia and can show a peptic stricture.
13. What is an EGD?
a. Esophagogastroduodenoscopy
b. Patients usually minimally sedated and maintaining their own airway.
c. Use a camera with ports for tools to visually inspect the oropharynx, esophagus, stomach, and proximal duodenum
14. Indications for EGD

i.
15. GERD on EGD
a. 2/3 of pts w/ symptomatic disease won’t have visible evidence of disease on endoscopy
b. Absence of endoscopic features of GERD does not exclude the diagnosis
c. May be normal or have varying degrees of esophagitis
i. Histologically – cell proliferation, thickening of the basal cell, and elongation of the papillae
ii. Macroscopically – see erosions on EGD
16. Ambulatory pH testing for GERD
a. Used to confirm diagnosis in pts w/ persistent symptoms (whether typical or atypical) who do not have evidence for mucosal damage on
endoscopy or to monitor the adequacy of tx in those with continued symptoms.
b. Withhold reflux meds prior to testing
c. Thin probe inserted through the nose to the esophagus (placement confirmed by x-ray) and then measures pH for 24 hours – push button
d. Documents number, severity and duration of reflux events and correlate to patient’s symptom diary
17. Management of GERD

i. Symptoms of esophageal without ALARM – PPI – better good, refractory send to GI

ii. Symptoms with ALARM – go to GI

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 iii. Esophageal + non-esophageal – PPI
iv. Non-esophageal without Esophageal – maybe not GERD
18. Treatment
a. Lifestyle modifications
i. Wt loss and smoking cessation – Evidence Based
ii. Avoidance of triggering foods – limited data
iii. Postural changes (elevating the head of the bed) – limited data
iv. Eat smaller, more frequent meals and >4 hrs prior to bedtime
b. Medication Treatments for GERD
i. Usually chronic therapy required
ii. Antacids
1. Mylanta (Aluminum & Magnesium hydroxide), Maalox (Calcium carbonate), Tums (Calcium carbonate) – work to
neutralize acid
2. Use for symptoms that occur < 1x/week
iii. PPI (proton pump inhibitors) - (PPI’s are more efficacious than H2 or Antacid)
1. e.g. Omeprazole (Prilosec), Esomeprazole (Nexium), Pantoprazole (Protonix)
2. MOA: decrease acid secretion & gastric volume by irreversibly binding to and inhibiting the H+-K+ ATPase pump
3. Should be taken daily and not on-demand based on MOA
4. PPI superior for healing esophagitis and controlling symptoms
5. PPI side effects – nausea, diarrhea.
6. Long term may have increased risk of C. diff, CAP, hip fx and Vitamin B12 def
7. Safety excellent – many OTC
iv. H2 blockers (Histamine 2 inhibitors) – A NICE ADD ON
1. e.g. Famotidine (Pepcid), Ranitidine (Zantac), Cimetidine (Tagamet) - Cimetidine has a lot of Drug Interactions ★
2. MOA: work to decrease acid secretion by inhibiting the histamine-2 receptor on the gastric parietal cell
3. Develop tachyphylaxis w/i 2-6 weeks of initiation - Safety excellent – all OTC
4. H2 can be used to supplement PPI at bedtime w/ persistent symptoms
c. Surgery Treatments for GERD
i. Usually for those with refractory, long duration of symptoms, or persistent s/sx in young person
ii. Nissen fundoplication (360-degree wrap)
iii. Outcomes are very similar if not more favorable for surgery over meds in some studies
d. OMT Considerations for GI/Reflux
i. Think About:
1. Viserosomatic reflexes (both Sympathetic and Para-Sympathetic)
2. Treating surrounding structures (bowel, diaphragm, ribs, etc)
3. Treating lymphatic congestion
ii. Remember:
1. All viscera have nerve endings in their walls that are activated by spasm/stretch. This pain signal is then carried by
2. visceral Afferent fibers back to the dorsal horn where they increase Efferent activity to all areas innervated by that
spinal segment → Paravertebral Vasomotor & Muscle tone changes = facilitated segments from viserosomatic reflex.
3. Facilitation is directly proportional to intensity of input
e. OMT - GI Viscerosomatic Reflexes
i. Parasympathetic association Look for changes in the high cervical (vagus) and sacrum
ii. Sympathetic association palpable tissue texture changes in thoracolumbar paravertebral soft tissues
T3 – T6 R Esophagus
T5 – T10 L Stomach
T6 - T8 R Duodenum
T5 – T9 B/L Pancreas
T5 –T10 R GB
T8 –T10 B/L Small intestine
T9 - T12 R Appendix
T11 – L1 R Cecum and ascending colon
L1 - L3 L Descending colon
iii. C2L, T3-6R, T5-10L, T6-8R - common upper GI/Reflux pattern
f. OMT - Treatment for GI/Reflux

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 i. Treat areas of Sympathetic / Para-Sympathetic facilitation with the OMT treatment of your choice. For example:
1. Treating Upper cervicals and thoracics with ME
ii. Treat surrounding structures as needed with the OMT treatment of your choice. For example:
1. Treating the Lower rib dysfunctions with ME and Rib Raising
2. Treating abdominal diaphragm with an indirect or direct abdominal diaphragm release
3. Treating the bowel with mesenteric release
4. Some DO’s will also treat the stomach itself with visceral treatments
iii. Treating Lymphatic congestion with Pedal Pump (best to open up the abdominal diaphragm first to help with lymph drainage)
iv. PPT notes:
1. RIB RAISING WILL OF COURSE AFFECT SYMPATHETICS AS WELL
2. MESENTERIC RELEASE HELPS FLOW THROUGH GI SYSTEM – AFTER ALL CONSTIPATION WILL AGGRAVATE REFLUX
v. OMT will improve somatic dysfxn but if from a viserosomatic reflex it will return until underlying visceral pathology addressed.
1. So if you have a recurrent somatic dysfunction in an area think about what viscera could be causing facilitation at that
level and use this to guide your history taking. You may discover additional symptoms or disease processes/symptoms
that the patient had not previously mentioned!
19. Complications of GERD - (+/- hiatal hernia → GERD → Barrett Esophagus → Adenocarcinoma)
a. General
i. Reflux esophagitis
ii. Bleeding
iii. Stricture
iv. Barrett esophagus
v. Adenocarcinoma
vi. Reflux-induced asthma
vii. Severity of reflux does not correlate well to severity of mucosal damage on endoscopy
b. Peptic Stricture
i. Strictures are a result of the healing process of ulcerative esophagitis
ii. Deposited collagen fibers contract and narrow the lumen of the esophagus
iii. Usually near the GE junction
iv. S/sx: solid food dysphagia, episodic esophageal obstruction
v. Dx: Barium swallow or EGD
vi. Tx: EGD balloon dilation
c. Reflux Induced Asthma
i. GE reflux can be seen in 30-90% of pts w/ asthma
ii. Esophageal acid may produce bronchoconstriction and therefore exacerbate airflow obstruction in asthmatics by:
1. Increased vagal tone → substance P → increased respiratory resistance
2. Increase bronchial reactivity
3. Microaspiration of gastric contents into the upper airway
d. Barrett’s Esophagus
i. Acquired precancerous condition resulting from severe mucosal injury
ii. Metaplastic change in the lining of the distal tubular esophagus
1. Normal squamous epithelium is replaced by intestinal columnar epithelium ★
iii. Association with ★adenocarcinoma of the esophagus
1. Overall risk of cancer in individual pt is low
iv. Epi: 1.3% prevalence, 45% of pts don’t have reflux s/sx (Primarily middle age white males)
v. Risk factors: frequent and long-standing reflux, smoking, male, older age, central male pattern obesity
vi. S/sx: development of reflux at earlier age, increased duration, increased severity, prior complication of GERD (e.g.
esophagitis, ulceration, stricture, bleeding)
vii. Difficult to clinically distinguish from GERD
viii. Dx: EGD w/ biopsy at-risk pts
1. Chronic GERD, hiatal hernia, age ≥50, male, white, elevated BMI, and intra-abdominal body fat distribution
2. See displacement of the squamocolumnar junction so that it is now proximal to the GE junction
ix. Tx: somewhat controversial
1. Treat the associated GERD w/ PPI indefinitely
a. Efficacy of cancer prevention by PPI not proven yet
b. Anti-reflux surgery not more effective at cancer prevention than medical therapy

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 2. EGD surveillance w/ biopsy at regular intervals depending on dysplasia prevalence
a. 3 mo for high-grade and 6-12 mo for low-grade
3. High-grade mucosal abnormalities should be radiofrequency ablated endoscopically or endoscopically resected
a. May progress to needing esophagectomy (esp when have invasive adenocarcinoma)
4. Prognosis: 0.5 % to 0.7% annually will go on to develop esophageal adenocarcinoma
a. 30-125 times increased risk of esophageal cancer. (relative risk)
20. Summary:
a. Pathophys of GERD:
i. Impaired LES and relaxation of the sphincter
ii. Decreased acid clearance from impaired peristalsis or abnormal saliva
iii. Delayed gastric emptying
b. Associated risk factors:
i. Delayed gastric emptying (seen in gastroparesis w/ diabetes)
ii. Hiatal hernia – Lose the physical anti-reflux barrier with the crura of the diaphragm when the stomach is herniated above the
diaphragm so impairs the LES ability to work
iii. Obesity
c. Workup for GERD
i. Clinical diagnosis.
ii. If red alarm symptoms, unclear diagnosis or refractory to empiric treatment, do EGD or alternative testing.
iii. Usually empiric trial of PPI (which is superior to H2 antagonist).
d. Barrett’s esophagus
i. Metaplastic change from squamous to columnar epithelium in the esophagus.
ii. At increased risk for adenocarcinoma.
iii. Do EGD to diagnosis and surveillance for cancer.

Lecture 7: Congenital Disorders of the Abdominal Wall and GI System

1. Malformations of the GI Tract
a. Esophagus
i. Tracheoesophageal Fistrula
ii. Esophageal Atresia
b. Small Intestine
i. Congenital Diaphragmatic Hernia
c. Abdominal Wall Defects
i. Omphalocele
ii. Gastroschisis
iii. Prune Belly Syndrome
iv. Umbilical Hernia
v. VACTERL
2. Case 1
a. You are the intern on call. You are asked to come see this baby in respiratory distress. What are some questions you might ask:
i. Gestational age (preterm [37 wks] or term) vi. Maternal fever (infection environment)
ii. Mode of delivery (vaginal vs. c-section) vii. Baby Ethnicity (caucasian M’s do worse [lungs])
iii. Prenatal complications. viii. Rupture of membranes. (no longer sterile envt)
iv. GBS status ix. Prenatal US results (organ development)
v. Vitals (Temp, Respiratory rate, Pulse, Pulse Ox) x. Serologies (Hep B, Rubella, etc)
b. You walk in the room and you see a neonate with grunting, nasal flaring and subcostal retractions = (working to breathe)
i. Vitals: P 180 (fast; normal is 130-150), R 56 (normal: 50), Sats 85% on RA (low).
c. Differential Diagnosis
i. Prematurity vi. Respiratory distress syndrome (RDS)
ii. Transient tachypnea of the newborn. vii. Sepsis
iii. Congenital cardiac abnormality. viii. Tracheoesophageal fistula (TEF)
iv. Congenital diaphragmatic hernia. ix. Tracheomalacia
v. Meconium aspiration (increases risk of PTX) x. Pneumomediastinum/ Pneumothorax
3. Development of the GI Tract

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 a. Foregut b. Midgut
i. Pharynx i. Distal duodenum
ii. Lower respiratory system ii. Jejunum and ileum
iii. Esophagus iii. Appendix
iv. Stomach iv. Ascending colon
v. Proximal duodenum v. Proximal transverse colon
vi. Liver and the biliary tree c. Hindgut
vii. Pancreas i. Distal transverse colon
ii. Descending colon, sigmoid, and rectum
iii. Proximal anal canal
4. Tracheoesophageal fistula (TEF) / Esophageal fistula (EF)
a. Esophageal atresia (EA) is the most frequent congenital anomaly of the esophagus (1:4000 neonates).
i. Caused by malformation of the esophagus.
ii. 90% of EA is associated with TEF
b. TEF is a congenital communication between the esophagus and the trachea (fistula connecting the 2→ sx after feeding)
c. 50% associated with a syndrome:
i. VATER/VACTERL - (V) Vertebral, (A) Anorectal, (C) Cardiac, (T) Tracheal, (E) Esophageal, (R) Renal, (L) Limb defects
ii. CHARGE syndrome
iii. Anopthalmia-esophageal genital syndrome
d. Symptoms
i. Frothing and bubbling at the mouth after birth
ii. Coughing with feeding ★
iii. Cyanosis
iv. Respiratory distress
v. Symptoms exacerbated with feeding.
e. Diagnosis
i. Prenatal clues:
1. Maternal polyhydramnios, absence of fluid filled stomach in baby. – baby cant swallow pee
ii. Inability to pass nasogastric tube or an orogastric tube.
iii. CXR showing coiled feeding tube.
iv. Esophagram with contrast.
f. Management/Outcome
i. Prevent aspiration.
ii. Prone position minimizes movement of gastric fluids.
iii. Avoid Endotracheal intubation (because air will go into stomach and lungs cannot expand)
iv. If surgical correction not possible, consider placement of G tube.
v. Surgical correction within few days of life.
vi. Complications of surgery usually seen in infancy:
1. Anastomotic leak and stricture, Refistulization, GERD.
vii. Most patients lead normal/healthy lives.
5. VATER/VACTERL Syndrome
a. A disorder that affects many organ systems.
i. (V) Vertebral → Defects in the bones of the spine such as fused bones, missing or extra bones (60-70%)
ii. (A) Anorectal → Anal atresia. Can also association with genitourinary abnormalities
iii. (C) Cardiac (40-80%) - need an ECHO
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 iv. (T) Tracheal → TEF
v. (E) Esophageal → EA
vi. (R) Renal
vii. (L) Limb defects → Missing thumbs, malformation of arms and forearms
b. Noted in 1 in 10,000 to 40,000 children
c. Sporadic mutations/multifactorial etiologies
d. Prenatal screening
i. Fetal Ultrasound
e. Screening:
i. Echocardiogram
ii. Comprehensive metabolic panel (looking for renal fxn - BUN/Creatinine)
iii. Abdominal Ultrasound - kidneys
iv. X-rays (confirm placement of NG tube)
f. KNOW THE DIFFERENT COMPONENTS OF VACTERL
6. Congenital Diaphragmatic hernia
a. Defined as communication between the abdominal and thoracic cavities with or without abdominal contents in the thorax.
b. Varying in location:
i. Esophageal hiatus (hiatal hernia)
ii. Paraesophageal (adjacent to the hiatus)
iii. Retrosternal (Morgagni)
iv. Posterolateral (Bochdalek) ** most common position
1. CDH usually refers to the Bochdalek form (90%).
2. Note: you will hear bowel sounds in the lung fields
c. The diaphragm is a dome shaped musculoskeletal structure.
d. The fetal diaphragm forms around 8 week gestation.
i. CHD usually when abdominal contents return to abdomen from the umbilical sac at 10 wk gestation → lung doesn’t form
e. Major limiting factor for survival is pulmonary hypoplasia.
f. Epidemiology: 1/2000 to 1/5000 live births.
g. Females 2x affected than males.
h. Presentation:
i. Respiratory distress within the first several hours after birth
ii. Level of distress is consistent with degree of pulmonary hypoplasia and persistent pulmonary hypertension
iii. Barrel-shaped chest
iv. Scaphoid abdomen (because of loss of the abdominal contents into the chest)
v. Absence of breath sounds on the ipsilateral side (might hear bowel sounds)
vi. Heartbeat (PMI) is displaced to the right because of a shift in the mediastinum
i. Diagnosis:
i. Prenatal Ultrasound (polyhydramnios, chest mass, gastric bubble)
ii. CXR after delivery.
j. Management:
i. Debate on the time for surgery. Typically done when the neonate is stable.
ii. If small: Sutured closed
iii. If large: Synthetic flap, Muscle flap
iv. Initial management in the nursery includes immediate endotracheal intubation (high Frequency oscillation ventilation),
sedation, NG tube to allow for constant decompression of the GI tract, avoid positive pressure ventilation (like bagging).
v. ECMO (Extracorporeal membrane oxygenation) - machine does work for lungs to oxygenate blood
k. Outcome:
i. Overall survival of live births is 67%. Some spontaneously abort.
ii. Pulmonary issues, neurodevelopmental delays, growth retardation, GERD, Hearing loss, growth delay.
iii. Some of the morbidities are not associated with the CDH but the treatment options used
7. Omphalocele
a. Herniation of abdominal contents into the base of the umbilical cord
b. Sac is covered with peritoneum but NOT overlying skin
i. + intestines 1/5,000
ii. + liver and intestines 1/10,000

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 c. The abdominal cavity is proportionately small/underdeveloped
d. Defect may vary from 2-10 cm
e. EMBRYO: The abdominal contents should return to the abdominal cavity by 10 weeks gestation
i. Note: the contents didn’t turn around and go back in correctly
f. Tissue must be covered with saline soaked sterile dressings to avoid the tissue from drying.
g. Care must be taken to avoid rupture of the sac.
h. If sac ruptures, Mersilene mesh or similar synthetic material can be used to cover the tissue and organs.
i. KNOW THIS ★ Elevated maternal serum alpha-fetoprotein concentration (MSAFP) is elevated in 70%
j. Diagnosed at 2nd trimester Ultrasound.
k. Associated with syndromes:
i. Beckwith Wiedemann (omphalocele, hypoglycemia, macrosomia)
ii. Trisomy 13 and 18.
l. Management in delivery room
i. Need to stabilize child before going into surgery
ii. Preserve heat and minimize insensible fluid loss
iii. Orogastric tube to decompress the stomach
iv. Stabilize the airway
m. Surgical repair - depends on size of lesion
i. Primary closure for small defects (<2 cm)
ii. Staged closure for larger defects (Dacron-reinforced silastic silo)
n. Prognosis
i. Improved if no associated anomalies
ii. Overall survival is 79 percent
iii. Note: problems are associated with the genetic syndromes, not the omphalocele or its repair itself
iv. Note: babies with omphalocele are delivered by c-section
8. Gastroschisis
a. Defect lateral to the median plane of the anterior abdominal wall
b. Extrusion of the abdominal viscera without involving the umbilical cord
i. Note: intestines come out through the defect but not through the umbilical cord or within a sac
c. Exact cause of gastroschisis is uncertain
i. involve defective formation or disruption of body wall in the embryonic period, with subsequent herniation of bowel
ii. Typically not associated with extra intestinal anomalies.
d. Incidence is 1/10,000.
e. Elevated maternal serum alpha fetoprotein (MSAFP) level during 2nd trimester in 90%
f. Prenatal ultrasound
g. Intestine is usually only herniated organ
h. Decreased association with chromosomal and other associated congenital anomalies
i. Bowels often thickened, matted and edematous → less likely to fxn later on
j. Higher incidence of intestinal atresia, stenosis, perforation, necrosis, or volvulus
k. Note: different from omphalocele bc no membrane covering...the more you leave the gut like that, higher chance of obstruction
l. Management in delivery room (same as omphalocele)
i. Preserve heat and minimize insensible fluid loss
ii. Orogastric tube to decompress the stomach
iii. Stabilize the airway
m. Surgical repair
i. Primary closure
ii. Staged closure
iii. Dacron-reinforced silastic silo
iv. “Gentle touch”
1. Slower process allowing gravity to reduce bowel before closure
n. Prognosis
i. Overall survival is 90 percent

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9. Prune Belly Syndrome
a. Also called Triad syndrome OR Eagle-Barrett Syndrome.
b. Incidence: 1/40,000 births.
c. 95% affected are males
d. Deficient of abdominal muscles, undescended testes, and urinary tract abnormalities.
e. Oligohydraminos (urine output is low bc kidney fxn is low) and pulmonary hypoplasia are common prenatal complications.
f. Kidneys show varying degrees of dysplasia.
g. Malrotation of the bowel is often present.
h. Note: child looks fine until you look at their belly muscles and they “look flappy”
i. Clinically
i. Poor musculature in the bladder making it difficult to empty the bladder. ( need cath )
ii. If no urethral obstructions → Antibiotic prophylaxis to prevent UTI.
iii. If urethral obstruction → Vesicostomy until old enough for surgery.
iv. Orchiopexy (bringing down the scrotal sac) is typically done in the first 6 months of life.
j. Prognosis:
i. Depends on the extent of pulmonary hypoplasia and renal dysplasia.
ii. 1/3rd are stillborn or die in the first few months of life.
iii. 30 % of survivors develop end stage renal disease and require renal transplant.
10. Umbilical Hernia
a. Defined as protrusion of intestines through a defect in the abdominal wall muscles.
b. Also associated with diastasis recti (abdominal muscles don’t come together properly)
c. Mostly seen in African American/Asian children and low birth weight babies.
d. Symptoms:
i. soft reducible bulge over the umbilicus which becomes more protuberant during crying, coughing or straining.
ii. Ranges in size from less than 1 cm to as large as 5 cm (rare).
e. Complications:
i. Concern if the intestines become strangulated and not reducible. This becomes a surgical emergency.
f. Treatment:
i. Most resolve without intervention by 1 year of age. (bc 6-9 mos kids start sitting up and strengthen belly muscles)
ii. If still present or worsening, it requires surgical intervention.

Lecture 8: Pediatric Upper Gastrointestinal Disorders Including Reflux and Pyloric Stenosis
Case 1- Approach to an infant with vomiting (cc: 4 week old infant with vomiting)
a. Questions to ask
i. Frequency
ii. Duration of illness x. Travel
iii. What is the color of emesis xi. Toxic ingestion
iv. Food/fluid intake based on developmental stage xii. Tick exposure
v. Output xiii. Foreign body ingestion
vi. Change in stool pattern/ consistency or color xiv. Change in vision
vii. Fever xv. Recent new medications
viii. Abdominal distention xvi. Food allergies
ix. Mental status of the child xvii. Trauma/ signs of ICP (hx of OCP’s?)
b. HPI: 5 week old infant has been “happy spitter” since birth, with an increase in the amount and frequency of vomiting over the last 5-6
days. He is vomiting milk immediately after every feed and at times the milk seems to shoot out of his mouth and covers his clothing.

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 Mother denies fever. No changes in stooling. Voiding at least 3-4 times a day (normal for pt is almost after every feed, 6-7 times a day)
He is breastfeeding approx 15 mins on each breast every 3-4 hours. No perceived aversion to feeding.
c. Birth History: Term AGA male infant born via vaginal delivery to a G1P1 mother without any complications. Birth weight = 7lbs 3 ounces.
Negative prenatal labs including negative maternal GBS
i. Family History: Negative for milk protein allergy, lactose intolerance, Celiac, IBS, IBD
d. Social History: Lives with parents. No smokers in the home. Sleeps in crib on his back. City water. No sick contacts. No recent travel.
e. Decreased urine output is concerning, spitting up more than expected maybe????
2. Differential Diagnosis for Vomiting in an Infant
a. Infectious: d. GI continued….
i. Infectious Acute Gastroenteritis i. Appendicitis
ii. Pertussis ii. Intussusception
b. External iii. Hirshsprungs disease
i. Overfeeding iv. GER
ii. Incorrect preparation of formula v. GERD
iii. Foreign body vi. Biliary atresia/ Biliary colic
iv. Food poisoning/ Allergy vii. Esophageal strictures
v. Medication e. Metabolic/ Electrolyte disorders
c. GI: i. Adrenal Crisis
i. Lactose intolerance ii. Hyponatremia
ii. Milk protein allergy iii. Inborn metabolic errors
iii. Pyloric stenosis f. Neuro
iv. TEF i. Hydrocephalus or other ICP (NAT)
v. Malrotation ii. Adrenal crisis
vi. Volvulus iii. Migraine

3. Red Flags with the history and physical of vomiting

a. Bilious emesis – white stools i. Abnormal NBS
b. Hematemesis j. Lack of meeting developmental milestones OR/
c. Hematochezia/ Melena developmental regression
d. Fever k. Change in mental status
e. Dehydration l. Respiratory distress
f. Hepatosplenomegaly m. Night sweats
g. Distended abdomen n. Low socio-economic status
h. Poor weight gain/ Failure to thrive
4. Growth Curves
a. Want to make sure that they are clinically stable along curves
5. Overview of Normal Exam

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6. Pyloric Stenosis
a. Hypertrophy and hyperplasia of muscular layers of pylorus causing a functional gastric outlet obstruction
b. Etiology unknown: Multifactorial
c. “The Olive” - firm moveable mass palpable on the right side of abdomen = hypertrophied pyloric muscle
d. Incidence 2.5-3/1000 of live births
e. 95% of cases diagnosed between 3-12 weeks of age
f. 30% of cases occur in firstborn
g. 5:1 Male predominance - First born males
h. Clinical Presentation
i. Projectile vomiting after feeds
ii. Non-bilious vomiting
iii. Infant is hungry and wants to feed frequently
iv. Mild to severe dehydration
v. Poor weight gain
vi. Peristaltic waves
vii. Palpable olive
i. Labs:
i. Complete metabolic profile
1. Hypochloremic, hypokalemic, metabolic alkalosis ★ KNOW THIS
2. Hyperbilirubinemia (5-14%) – icteropyloric syndrome
j. Imaging:
i. Abdominal Ultrasound - Diagnostic modality of choice
ii. Barium study (String sign)
k. Treatment
i. Correct dehydration and metabolic derangements
ii. Pyloromyotomy (shave off pylorus)
7. Case 2: Multiple episodes of spitting up in infant (CC: 4 month old with multiple episodes of vomiting/spitting everyday)
a. Note: this is the happy spitter
b. Growth chart = good for height
8. GER vs. GERD
a. Gastroesphogeal reflux (GER)
i. the retrograde movement of gastric contents across the lower esophageal sphincter (LES) - due to weak LES
ii. Frequent regurgitation
iii. Good weight gain
iv. Not irritable
v. “Happy spitter”
b. Gastroesophageal reflux Disease (GERD)
i. When the reflux has pathological consequences including esophagitis, nutritional compromise, or respiratory complications
ii. Frequent regurgitation
iii. Poor weight gain
iv. Feeding refusal
v. Irritability - Arching back and lifting chin
vi. Respiratory complications
c. Note: baby with reflux arches their back to try to close off the sphincter and are at higher risk for aspiration
9. Difference between Case 1 and 2

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10. GERD
a. Peaks at 4 months
b. Usually resolves by age 12-18 months
i. 90% by 12 months
c. Likely genetic and environmental predisposition – SMOKING
d. More common in
i. premature infant
ii. Children with neuromuscular disorders
1. Muscular dystrophy, cerebral palsy & Down syndrome
e. Symptoms in Infants
i. Postprandial regurgitation
ii. Signs of esophagitis - irritability, feeding aversion, discomfort of pain symptoms such as arching/stiffening
iii. +/- Failure to thrive
iv. Respiratory symptoms
1. Obstructive apnea
2. Stridor
3. Lower airway disease
v. Sandifer’s syndrome (<1%) ★
1. Seizure like activity with neck contortions, lifting of the chin, eye deviations or arching of the back
a. Note: looks like seizure but there is no abnormal neural activity
f. Symptoms in Preschoolers and Older Children
i. Preschool age
1. Regurgitation
2. Abdominal pain
3. Decreased food intake
4. Respiratory symptoms (wheezing, dry cough) - treat them for reflux and their cough will go away
ii. Later childhood and adolescents
1. Nausea/ Epigastric abdominal pain
2. Chest pain
3. Airway manifestations related to asthma, laryngitis, sinusitis, dry cough
4. Weird taste in mouth
g. Diagnostic Modalities of GERD
i. History and Physical exam – most info, try not to do studies
ii. Upper GI (barium, radiographic study)
1. Rule out anatomic abnormalities
a. achalasia, esophageal stricture and stenosis, hiatal hernia, gastric outlet or intestinal obstruction
iii. Esophageal pH monitoring- Probe placed in the distal esophagus, rarely used for diagnosis
1. Helpful in assessing acid suppression during treatment
2. Helpful in evaluating apneic episodes or atypical GERD presentations
iv. Endoscopy
h. Treatment - Infants
i. Most infants do not need any treatment for “asymptomatic” GER
ii. Dietary changes
1. Adjust feeding volumes and frequency (feed less more frequently)
2. Thickening of feeds with rice cereal – lots of iron can cause constipation leading to vomiting, just use a little
3. Trial of hypoallergenic diet (exclude dairy or soy proteins) in maternal diet when breastfeeding.
iii. Positioning
1. Prone positions and upright carried positions can minimize reflux
2. Burping multiple times between feeds.
iv. Pharmacology
i. Treatment - Preschoolers and Older Children
i. Conservative therapy and lifestyle changes
1. Avoid tobacco smoke exposure
2. Avoid acidic or reflux inducing foods (caffeine)
3. Weight reduction

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 ii. Pharmacology
1. Acid suppression
2. Antacids
3. H2RA (H2- receptor antagonist) - Ranitidine (Zantac)
4. PPI (Protein pump inhibitors) - Omeprazole (Prilosec)
5. Prokinetic agents
11. Summary Slide
a. Pyloric stenosis
i. is stenosis of pylorus seen in 3-12 week olds
ii. hallmark is “projectile vomiting”
iii. is diagnosed with pyloric ultrasound
b. GER
i. Happy spitter - Good weight gain with regurgitation
ii. Does not need treatment – physiologic
c. GERD
i. Regurgitation with other associated symptoms
ii. irritability, respiratory difficulty, poor weight gain
iii. Initial treatment conservative, then may consider pharmacologic treatment – stop smoking near the patient
iv. Diagnosis made clinically, but other modalities are available to rule out other cause of vomiting
12. Differential Diagnosis of Bilious Vomiting
a. Intestinal malrotation
b. Intestinal duplication
c. Annular pancreas
d. Midgut volvulus
e. Intestinal atresia
13. Summary Slide
a. Pyloric stenosis
i. is stenosis of pylorus seen in 3-12 week olds
ii. hallmark is “projectile vomiting”
iii. is diagnosed with pyloric ultrasound
b. GER
i. Happy spitter - Good weight gain with regurgitation
ii. Does not need treatment – physiologic
c. GERD
i. Regurgitation with other associated symptoms
ii. irritability, respiratory difficulty, poor weight gain
iii. Initial treatment conservative, then may consider pharmacologic treatment
iv. Diagnosis made clinically, but other modalities are available to rule out other cause of vomiting
14. Differential Diagnosis of Bilious Vomiting
a. Intestinal malrotation
b. Intestinal duplication
c. Annular pancreas
d. Midgut volvulus
e. Intestinal atresia
f. Duodenal, Jejunal and Ileal obstruction

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15. Duodenal Atresia
a. Seems to arise in the 5th week of gestation secondary to failure of recanalization of the lumen.
b. Incidence: 1/10,000 births.
c. Associated with other abnormalities such as Down’s syndrome, esophageal atresia, malrotation. ★
i. 25% of infants with Duodenal atresia have Down’s syndrome.
d. Hallmark symptom is bilious vomiting.
e. Presentation:
i. Bilious vomiting
ii. Peristaltic waves noted
iii. Hx. of polyhydramnios in the prenatal ultrasound.
iv. Jaundice
f. Diagnosis:
i. KUB showing “double bubble sign ★
1. Note: question will be → child with Down’s Syndrome with abdominal distension presenting with bilious vomiting -
has double bubble on radiologic studies
g. Treatment:
i. NG/OG decompression
ii. Duodenoduodenostomy.
iii. Echocardiogram and Spine and Chest X-ray to rule out other abnormalities.
16. Biliary Atresia
a. A rare but life threatening condition with obstruction in the biliary system
b. Bile is formed in the liver and travels to the gallbladder via the biliary ducts.
c. 1 in 18,000 infants. F > M
d. Types:
i. Fetal - Noted in the womb
ii. Perinatal - Noted within 2-4 weeks of life.
e. Symptoms:
i. Non-Bilious vomiting
ii. Dark urine
iii. Jaundice
iv. Gray or white stools
1. Due to lack of bilirubin getting to the intestines
f. Diagnosis/ Labs:
i. Serum Total and Direct bilirubin
ii. Liver enzymes
iii. Abdominal Ultrasound
iv. Liver scan /biopsies
g. Treatment:
i. Kasai Procedure – reconstruct biliary symptom
ii. Liver transplant

Lecture 29: Encopresis, Constipation, Hirschsprung’s Disease, and Megacolon in Children

1. Constipation
a. Accounts for 5% of general pediatric office visits and 25% of all referrals to pediatric gastroenterologists
b. Rarely associated with significant, serious illness or disease
c. Negatively impacts quality of life and causes parental frustration
d. Children often complain of abd pain, decreased appetite, & painful BMs – distressing not only to the child but to the parents as well
e. Causes a vicious cycle if unrecognized and untreated early leading to disruption of toilet training and difficulty with achieving and
maintaining bowel continence
2. Case 1: CC- Constipation
a. HPI: A mom brings her 4 week old male into your office complaining of “constipation”
b. What is NOT a normal characteristic of baby poop?
A) Yellow or green color
B) Multiple small pellet shaped stools
C) A thin watery applesauce consistency
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 D) Pooping after every feeding
E) Pooping 2-3 times a week
c. Normal Baby Poop
i. Greenish Black and Sticky – Meconium
ii. Yellow and Seedy – next few days after starting breast feeding
iii. Greenish Brown
iv. Tan and Thick
v. Dark Green
vi. Bright Green
d. Abnormal
i. Dry Brown and Hard – constipation
ii. Chalky White – biliary
iii. Black or Red Streaked - blood
e. Significant HPI and ROS
i. Stool frequency, size, color, and consistency?
ii. Hematochezia? Pain with defecation?
iii. When did he have his 1st stool? How many hours after birth?
1. If they don’t poop in 1st 24 hrs thats bad – could be meconium ileus
iv. Vomiting? If so, how often? What color? Hematemesis? Bilious emesis?
1. Bilious emesis – bowel obstruction distal to Sphincter of Oddi bc you can’t get bile if obstruction is above
v. Changes in voids? Hematuria?
vi. Any change in appetite, diet, or formula?
vii. Any other associated symptoms? Fever, rash, decreased activity, seizures?
f. HPI – Mom states “He did not stool in the nursery for the first 2 days. He finally pooped after the nurse took a rectal temp.” He has
stooled once since coming home. It was about 2 weeks ago and “came out like thin ribbons.” It was light brown with no mucous or
blood. The baby did seem “upset when he was pooping.” Normally he is breastfed but he has not been feeding well over the last couple
of days and has not wanted to eat at all today.
i. ROS – Gen - Afebrile, fatigue but not lethargic, no rash, no recent illness
ii. GI - “Puffy Abdomen”, decreased appetite, no vomiting
iii. GU - 6-8 wet diapers a day but only 3 so far today
iv. Allergies – NKDA
v. Birth History – Term, vaginal birth, uncomplicated
vi. Medical History – Constipation. No hospitalizations. No surgeries
vii. Family History – Diabetes II and HTN
viii. Social History – Lives with mom, dad, and an older brother. Dad smokes “outside”. No recent travel. Pet hamster named Rocky.
ix. Medications – None
x. Immunizations – UTD
3. Differential for Constipation in an Infant or Child?

4. Constipation
a. Constipation: 2 or fewer stools per week OR passage of hard, pellet-like stools for at least 2 weeks
b. Functional Constipation: Voluntary withholding of stool; infrequent passage of large diameter, often painful, stools
c. Encopresis: fecal incontinence caused by leakage of retained stool
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 d. Caused by either a defect in filling or emptying the rectum
e. Causes:
i. Nonorganic (Functional)
ii. Organic
f. It is often self-perpetuating:
i. VOLUNTARY WITHHOLDING → large hard stool → pain → more withholding → larger harder stool → pain →
g. One of the most common causes for generalized abdominal pain in children
h. PE - LLQ mass, impacted stool may be felt
i. Long term effects:
i. Patient anxiety and family stress
ii. Encopresis
iii. Enuresis
iv. Accompanying urinary tract/bladder stasis leading to UTIs
5. Encopresis
a. Fecal incontinence caused by leakage of stool around retained stool
b. Watery stool from the proximal colon leaks around hard retained stool and may pass unnoticed by the child
c. 5-10 year olds typically affected
d. Children typically present with soiling
e. Often mistaken for diarrhea
f. Note: watery stool goes around the mass trying to get around it → soiling themselves w/o realizing it
i. Need to fix the constipation/get out the hard stool to relieve the problem
6. By what age should all normal children have attained fecal continence?
A) 18 months
B) 2 years
C) 3 years
D) 4 years
E) 5 Years
7. Diagnosis of Constipation/Encopresis
a. Diagnosis is clinical★ (DON’T need to get an xray!)
b. Based primarily on history
c. PE may feel impacted stool in colon on abdominal exam and/or impacted hard stool in rectum on rectal exam
d. KUB = AP Abd Xray – you will see large amounts of stool in the colon
8. Functional Constipation/Encopresis Treatment
a. Disimpaction
i. Enemas
ii. Glycerin suppositories
iii. Oral laxatives: Polyethylene glycol (Miralax) 1.5g/kg/day
iv. Manual
b. Maintenance
i. Diet modification – water, fiber, fruit juices
ii. Behavioral Therapy – scheduled toilet times
iii. Laxatives - Polyethylene glycol 1g/kg/day, Lactulose 1-3 ml/kg/day, Glycerin suppositories
c. Long treatment course with frequent relapses
d. Note: advise miralax for first few days….then wean down to every other day for 6 months
9. Constipation: Oral Medication
a. Osmotic agents – lactulose (a synthetic disaccharide), sorbitol, and polyethylene glycol
b. Lubricants – mineral oil
c. Stimulants – promote enhanced colonic transit (Senna, Bisacodyl); avoided as long term tx and can cause discomfort
10. How much Fiber Should a Child Eat?
a. age + 5 = # of grams of fiber per day
b. However, more recently a number of nutrition experts advise the following:
i. 1 to 3 year olds - 19g of fiber a day
ii. 4 to 8 year olds - 25g of fiber a day
iii. 9- to 13-year-old girls - 26g of fiber a day
iv. 9- to 13-year-old boys - 31g of fiber a day

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 v. 14- to 18-year-old girls - 26g of fiber a day
vi. 14- to 18-year-old boys - 38g of fiber a day
c. Fiber foods: lentils > black beans > peas > raspberries….etc
11. Red Flags Based on History 12. Red Flags Based on PE
a. Delayed passage of meconium (after 48 hrs of life) j. Severe abdominal distension
b. Rectal bleeding (unless attributed to an anal fissure) k. Lower spine abnormalities
c. Bloody stools l. Lumbosacral dimple, hair tuft, lipoma, gluteal cleft dev.
d. Constipation present from birth or early infancy m. Anal scars
e. Ribbon stools (very narrow in diameter - Hirschsprung) n. Anteriorly displaced anus
f. Failure to thrive or delayed growth o. Perianal fistula
g. Urinary incontinence or bladder disease p. Tight anal canal with empty rectum
h. Congenital anomalies or syndromes a/w Hirschsprung’s q. Explosive expulsion of stool after digital rectal exam
i. Down Syndrome r. Absent anal wink
i. Fever or vomiting s. Abnormal LE DTR, absence of delay in relaxation phase
i. Hypothyroidism
13. Meconium Plug
a. Part of the meconium forms a plug that creates a functional distal colonic obstruction
b. Incidence 1:500 - 1:1,000
c. Meconium is retained in the colon > 24-48 hrs after birth
d. Most cases are thought to be due to immaturity of intestinal ganglion cells but etiology not fully understood
e. Additional risk factors: maternal DM, prematurity, Cystic Fibrosis ★
f. Meconium plug syndrome is a diagnosis of exclusion
i. DDx includes Hirschsprung Disease, Meconium Ileus, Intestinal Atresia
g. PE: Abdominal distension
h. Imaging:
i. Xray – may show obstruction
ii. Contrast enema – retained meconium will show up as a filling defect in the colon
i. Treatment: Rectal stimulation, enema; Keep a high index of suspicion for underlying issues
j. Symptoms typically resolve & infants pass normal stools once plug is passed, however if symptoms persist additional work up needed
14. Meconium Ileus
a. All meconium is very thick inspissated typically in the terminal ileum leads to Ileus and/or obstruction
b. More severe than just a plug
c. No stool in > 24-48 hrs after birth
d. Causes 30% of bowel obstructions in neonates
e. 50% of patients have no underlying disorder
f. Most patients who do have an underlying disorder have CF
g. PE: Abdominal distention, bilious emesis
h. Imaging:
i. Xray - dilated loops of bowel, air fluid levels, Ground Glass/Soap Bubble appearance (Meconium mixed with air) and if
obstruction no air in rectum
ii. Contrast Enema - Micro colon & small bowel with filling defects d/t meconium. Area proximal to meconium is dilated.
i. Treatment: IV fluids and Gastrografin enema (15-50% success rate)
j. Surgical evacuation is often necessary, sometimes resection or ostomy are needed
k. Nutrition and fluid support required post operatively
15. Hirschsprung’s Disease
a. Congenital aganglionic megacolon, A motor disorder of the colon
b. Occurs in 1 of 5,000 live births, Male : female ratio 3-4:1
c. Absence of ganglion cells that starts in the internal anal sphincter and extends proximally
d. Colon wall is unable to relax and thereby creates a functional obstruction
e. 75% of patients have disease isolated to the rectum and distal sigmoid colon but it can involve proximal segments
f. Associated with other congenital defects such as Down Syndrome ★
g. Cause: Disorder of migration of neuroblasts from neural crest or in differentiation of neuroblasts into colonic ganglion cells
i. At least 8 genetic mutations have been identified but most of the time it is idiopathic
h. Presents frequently after birth with FAILURE TO PASS MECONIUM IN THE 1st 24-48 HRS OF LIFE
i. Severe disease may present like bowel obstruction (bilious vomiting) or with fever and pain from enterocolitis
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 ii. Mild disease may present as a history of chronic constipation and FTT. May not be diagnosed until later in childhood as adults.
i. PE - RECTAL EXAM - NO STOOL IN THE RECTUM
i. Children will have a large expulsion of gas and stool after rectal exam (BLAST SIGN)
ii. Abdominal distension
iii. A mass of stool can be felt in the left lower quadrant
j. Radiologic studies
i. Xray – 1st if concerned for obstruction or perforation
ii. Barium Enema – shows an abrupt narrow transition zone and is helpful in showing the extent of the dz (un-prepped)
k. Gold standard is rectal biopsy ★
i. Lack of ganglion cells seen on rectal biopsy with Hirschsprung’s
l. Anorectal manometry
i. Measures pressure of the internal anal sphincter in response to the dilated balloon
ii. Should have symmetric spikes when you dilate the balloon (normal) but you don’t (Hirschsprung’s)
iii. With normal constipation, you will have relaxation of the internal anal sphincter
iv. With Hirschsprung’s, you have failure of relaxation b/c of the lack of ganglion cells ; int anal sphincter fails to relax in response
to rectal distension
m. Note: the first test you do might be an XRAY….but if asking gold standard pick rectal biopsy!!
n. Treatment:
i. First stabilize the patient – NG tube to decompress, fluids and antibiotics if necessary.
ii. Surgical removal of the aganglionic segment and placement of a temporary colostomy for about 6-12 months and then will get
a definitive repair.
16. Back to Case 1….
a. HPI: Previously healthy 4 week old male with constipation. Last stool 2 weeks ago. Thin light brown “ribbon” like. No blood No bile. ?
Possible pain with defecation. No stool in first 24 hrs of life.
b. VS – Wt 4 kg T 98.7 RR 44 HR 132 BP 90/52 O2 100% RA
c. Gen –Resting comfortably, in no acute distress
d. HEENT – Normocephalic, No nasal congestion, TMs clear, Mucous membranes moist, OP within normal limits. Neck soft and supple, no
mass or lymphadenopathy.
e. Resp – CTA Bilaterally without wheezes or crackles. No retractions or distress.
f. CV – Regular rate and rhythm. No murmur. 2+ pulses in all extremities. Capillary refill brisk.
g. Physical Exam
i. Abd – Distended, generalized tenderness throughout, hypoactive bowel sounds. No HSM. Palpable mass in the left lower
quadrant.
ii. GU – Normal circumcised male. Testes descended bilaterally.
iii. Rectal – Good rectal tone, no stool in rectum. After rectal exam, the patient had an explosive burst of gas and stool.
iv. MS – No deformities, moving all extremities equally
v. NEURO – No obvious defects, reflexes intact, tone is normal
h. What Labs do you want?
i. CBC, CMP, liver function, thyroid function, Hemoccult stool
i. Question 3: What key PE finding helps us make our diagnosis?
A) Hypoactive bowel sounds and distended abdomen
B) Abdominal mass
C) Abdominal pain with normal rectal tone
D) Empty rectum with expulsion of stool and air after rectal exam
E) There is nothing on PE that will help us with the diagnosis…..We need tests!
j. What Test do you want to do to confirm your Dx?
i. Rectal Biopsy
k. Eli’s Treatment
i. Eli was stabilized and had a bowel resection and colostomy. His final repair was scheduled for age 12 months
17. Megacolon
a. Idiopathic or acquired megacolon
i. Chronic constipation of any etiology
ii. Intestinal pseudo-obstruction
b. Should be differentiated from toxic megacolon and lack of systemic toxicity is what distinguishes this from toxic megacolon
c. A descriptive term describing dilatation in the colon NOT caused by mechanical obstruction

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 d. 3 categories:
i. Acute – Pseudo-obstruction from altered motility
ii. Chronic – Congenital or Idiopathic
iii. Toxic
18. Toxic Megacolon
a. An acute form of colonic distension
b. Typically a complication of IBD; particularly fulminant Ulcerative Colitis
c. Symptoms: Abdominal pain and Distension, Fever, Dehydration, Shock
d. PE: Abdominal tenderness, Abdominal distension, Possible loss of bowel sounds, Tachycardia, tachypnea, delayed capillary refill
e. Labs – Nonspecific. Elevated WBC
f. ABD XR – Colonic Dilatation
i. There will be air in the rectum since this is not an obstruction.
ii. Look for free air to rule out bowel perforation
iii. Note: bowel perforation will show free air in the diaphragm
g. Treatment initially conservative
h. Bowel decompression (NG tube)
i. Fluid and electrolyte management
ii. Steroids if active IBD
iii. Antibiotics if concern for sepsis
i. If no improvement in 24 hours, a colectomy is indicated.
j. If the condition does not improve, there is a SIGNIFICANT RISK OF PERFORATION, SEPSIS, AND DEATH.
k. COLONOSCOPY IS CONTRAINDICATED as it may rupture the dilated colon.

Lecture 10: Intussusception, Midgut Volvulus, and Necrotizing Enterocolitis

1. Case 1: CC - Vomiting and Diarrhea
a. HPI : 12 month old male who was previously in good health presents to the ER with sudden onset of vomiting and diarrhea
b. Important HPI and ROS
i. How long has he been vomiting? How often?
ii. When does the vomiting occur? Around feedings?
iii. Characterize the vomiting. Color? Blood? Projectile?
iv. Does the child seem to be in pain with the vomiting?
v. Changes in stools or voids? Frequency of stool? Color of stool?
vi. Any change in appetite, diet, or formula?
vii. Any associated symptoms? Fever, rash, decreased activity?
c. Case HPI and ROS
i. HPI – Periodic vomiting x 8 hrs. Occurring about every 20 min and associated with increased fussiness, crying, and belly pain.
Emesis was initially clear but now green-yellow in color, non-bloody, not projectile, not associated with feeding. In between
vomiting, he appears almost normal and has been taking sips of Pedialyte. He had 6 episodes of diarrhea which was watery
with mucous and blood mixed in.
ii. ROS – Afebrile, fatigued but not lethargic, no rash, no URI sx. Decreased urine production today, not crying tears.
d. What does “projectile” vomiting mean?
A) Vomit dribbling out of the mouth
B) Forceful vomit shooting out a couple inches
C) Forceful vomit shooting out several feet
D) What difference does it make?
e. Case Medical Hx
i. Allergies – NKDA iv. Medical History – One ear infection
ii. Medications – Fluoride v. Hospitalizations – None
iii. Birth Hx – Term, uncomplicated SVD vi. Surgical History - None
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 vii. Family History – Heart dz, Breast CA ix. Immunizations – UTD
viii. Social History – Lives with mom, dad, and a
goldfish named Nemo. No smokers. No travel.
f. Case Physical Exam → DEHYDRATED
i. VS – Wt 10.5 kg T 98.3 RR 36 HR 168 BP 92/56 O2 98% RA
ii. Gen – Fatigued but resting comfortably. Half way through your exam draws his legs up and curls up in obvious pain and begins
vomiting.
iii. HEENT – Normocephalic/atraumatic, eyes mildly sunken, no nasal congestion, TMs clear, mucous membranes dry, OP no
erythema or lesions. Neck soft and supple, no mass or LAD.
iv. Resp – CTA bilaterally, no wheezing or crackles. No retractions.
v. CV – Tachycardic, Regular rhythm. No murmur. 2+ pulses in all extremities. Capillary refill 3 seconds.
vi. Abd – soft, non-distended, generalized pain with palpation, a long thin mass is palpated on the right side of the abdomen. No
HSM.
vii. GU – Mild diaper rash, otherwise normal circumcised male. Testes descended bilaterally.
viii. Rectal – good tone, no mass or hernia
ix. MS – No deformities, moving all extremities equally
x. Neuro – no obvious defects, reflexes intact, tone is normal
g. Dehydration Status

h. What clues in the history should we focus our differential diagnosis on?
A) Emesis and dehydration
B) Tachycardia and dehydration
C) Bilious emesis and heme positive stool
D) Abdominal pain and diarrhea
E) Nemo the fish
2. How to Approach the Differential
a. BILIOUS VOMITING = OBSTRUCTION distal to the sphincter of Oddi
b. BLOOD MIXED IN STOOL = Bowel injury (ischemia, ulceration, polyps)
3. What is the DDx for Obstruction in an infant or child
a. Intussusception
b. Volvulus
c. Congenital anatomic abnormalities (duodenal atresia or stenosis)
d. Annular pancreas
e. Incarcerated hernia
f. Adhesions
g. Abdominal mass (cancer)
h. Hirschprung’s
i. Meconium Ileus
j. Gastroesophageal reflux
k. Pyloric stenosis

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4. Intussusception
a. Invagination of part of the intestine into itself (portion is telescoped into an adjacent segment) → TELESCOPING
b. Typically near the illeocecal junction but can be anywhere
c. Most are idiopathic but occasionally a pathologic lead point is discovered (Meckel’s diverticulum, polyps, LNs)
d. Occurs in 1-4 per 1,000 live births
e. Boys > Girls (4:1)
f. Idiopathic 90 %
g. Some correlation with prior or concurrent respiratory illness such as Adenovirus ★
h. Past association with the older Rotavirus vaccine formulation
i. Clinical Presentation:
i. Presents around 3-36 months of age
ii. Inconsolable crying
iii. Vomiting – may be non-bilious initially and then become bilious
iv. Intermittent colicky pain
v. Pulling legs up
vi. Note: sometimes you see them during the pain free period….need to ask good questions to look for these sx
j. Physical Exam
i. Fatigue, sometimes lethargy
ii. Abdominal distension
iii. 25% have right sided, “sausage shaped” abdominal mass
iv. “Currant jelly” stools **(buzzword) - late finding (may not always be present in clinical picture)
v. If untreated, the invagination leads to decreased blood supply bowel → bowel wall swelling → necrosis → perforation → fever
→ septic shock death
k. Labs: Nonspecific
l. Abdominal Xray - may show obstruction or free air but TYPICALLY NORMAL
i. Bowel Obstruction = distended loops of bowel with absence of air in the colon and rectum, air fluid levels
ii. Bowel Perforation = Free air and distended loops of bowel
m. Abdominal Ultrasound ** Initial Diagnostic test of choice
i. Shows a ★ “Bulls Eye” or Coiled Spring lesion
n. Barium Enema of Intussusception
i. **Air Contrast or Barium Enema – can be both diagnostic and therapeutic ★
ii. It is therefore the 1st line choice in diagnostic imaging
iii. Shows a coiled spring shape to the bowel or a filling defect in the bowel
o. Note: if you're not sure what you’re looking for….do the Abdominal US first but what is diagnostic/therapeutic or if you know that they
have intussusception with high clinical suspicion then do the Air Contrast Enema
p. Treatment
i. 1st stabilize – IV fluid and electrolyte resuscitation, nasogastric tube
ii. Non-operative reduction with barium or air contrast enema
1. Treatment of choice for stable pts, Contraindicated in patients with peritonitis or perforation
2. 80-95% success rate. ~ 10% recurrence rate
q. Surgical Treatment
i. Indicated first line for
1. Severely ill appearing patients
2. Evidence of perforation
3. Concern for peritonitis
4. Patients with prolonged symptoms
5. Patients who non-operative reduction failed
ii. Open manual reduction is attempted but if not successful then a resection is preformed
iii. Recurrence occurs in 1% of cases after manual reduction and almost nonexistent after resection
5. Midgut Volvulus
a. Occurs when the small bowel twists around the SMA resulting in vascular compromise
b. Malrotation of the intestine usually the underlying predisposing defect

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 c. Volvulus → Bowel Ischemia → Necrosis → Perforation → Sepsis
d. A high index of suspicion, rapid recognition, and rapid treatment are essential
e. Clinical Presentation
i. Typically present within the ★first year of life (60% by 1 month of age) with bilious emesis and abdominal pain
ii. PE = symptoms of acute bowel obstruction:
1. Ill-appearing /toxic
2. Bilious emesis
3. Abdominal pain and distension
iii. May also present with signs of septic shock
iv. Labs: Nonspecific
f. What are the symptoms/signs of septic shock?
i. Tachypnea and tachycardia
ii. Fever and elevated WBC
iii. End organ failure (kidney, liver, mental status changes)
iv. Hypotension
v. All of the above
g. Abd X-Ray – Often nonspecific but may show decreased intestinal gas with gastric and duodenal bulb distention
h. Midgut Volvulus: Upper GI
i. corkscrew sign: spiral appearance of the distal duodenum and proximal jejunum
i. Treatment
i. NPO (Nothing by mouth)
ii. NG tube for gastric decompression
iii. Fluid resuscitation – correcting any electrolyte imbalances
iv. Antibiotics
v. Surgical reduction and removal of any necrotic areas of bowel (Ladd’s Procedure)
vi. Prognosis depends on amount of necrotic bowel
6. Back to Case 1….
a. HPI – Previously healthy 12 mon male with episodic belly pain bilious emesis with mucous and blood in his stool
b. PE- Tachycardic, moderately dehydrated with abd pain to palpation and a RLQ mass
c. What labs should we get? CBC, BMP, amylase, lipase, Hemoccult stool
i. CBC: WBC 7 Hb 12 Plt 274; normal diff
ii. BMP: Na 145, K 3.8, Cl 110, BUN 10, Cr 0.8, glu 100
iii. Amylase 58, lipase 32
iv. Stool heme positive
v. Helpful in stabilizing patient and for making the diagnosis
d. Has Our Differential Diagnosis For Jack Changed ?
i. Intussusception, Volvulus, Annular Pancreas, Abdominal Mass (Cancer)
e. What imaging studies do we need?
i. Ultrasound (if you don’t know what it could be) or Air Contrast/Barium Enema (if 100% sure its intussusception)
f. What initial steps do we need to take to ensure Jack is stable and/or make Jack comfortable?
i. NPO
ii. NG tube and IV placement
iii. Fluid resuscitation
iv. Air contrast enema → If no resolution with the enema, then surgery
g. What Imaging would you get?
i. Abdominal US – shows Bullseye
7. Necrotizing Enterocolitis (NEC)
a. Intestinal wall necrosis
b. The most common life threatening GI emergency in the newborn period
c. Usually seen in premature babies, most cases in infants born < 34 weeks gestation
d. Occurs in 1-7% of neonates in the NICU
e. Occurs in 10% of infants weighing <1500g (3.3lbs) at birth
f. Risk Factors:
i. 2 wks - 3 mons of chronologic age **
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 ii. Prematurity is the major risk <34wk or <1500g
iii. Rarely occurs before feeding is started → starts when you start introducing feeding
g. Etiology is multifactorial:
i. Overactive innate immune response to intestinal microbiota
ii. Decreased integrity of intestinal mucosa
iii. Depressed mucosal enzymes
iv. Suppressed GI hormones
v. Poor coordination of GI motility
vi. Difficulty with GI blood flow regulation
h. Clinical Presentation
i. Physical Exam:
1. Abdominal distension 6. Temperature instability – low/high
2. Heme positive stools 7. Lethargy
3. ★Increased residuals (undigested 8. Apnea
9. Respiratory distress
food)
10. Metabolic acidosis
4. Tachycardia/Bradycardia
11. DIC
5. Tachypnea
ii. Modified Bell Staging criteria for severity
iii. NEC → Bowel Wall Necrosis → Perforation → Sepsis
iv. High index of suspicion and rapid diagnosis and treatment are essential
i. Imaging: Diagnosis is made by clinical suspicion and Abd Xray
i. **Pneumatosis Intestinalis** = Gas within the intestinal wall
j. Treatment
i. NPO
ii. NG tube for gastric decompression
iii. IV nutrition (TPN)
iv. Broad spectrum antibiotics
v. Frequent monitoring with X-rays (to make sure they are not getting worse or perforation)
vi. If conservative treatment fails (perforation or clinical deterioration)
1. Primary Peritoneal Drainage
2. Laparotomy with removal of the necrotic bowel – traditional tx
k. PROGNOSIS
i. 70-80% survival with only half having long term sequelae
1. Short bowel syndrome, strictures, poor growth, neurodevelopmental issues
l. Prevention
i. Breastfeeding is the most important strategy associated w/lower risk of NEC
ii. Experimental methods – antenatal steroids, enteral antibiotics, prebiotics, probiotics, IgA supplementation erythropoietin,
arginine supplementation. More research is needed to determine how effective these methods are.
iii. Avoidance of histamine 2 blockers (Zantac)
iv. Avoidance of prolonged empirical antibiotic use

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