Gastrointestinal system Flashcards
The acute abdomen DR DEAC PIMP
D: The ‘acute abdomen’ is defined as a sudden onset of severe abdominal pain of less than 24 hours duration. It has a large number of possible causes and so a structured approach is required.
The initial assessment should attempt to determine if the patient has an acute surgical problem that requires immediate and prompt surgical intervention, or urgent medical therapy.
R:
D:
E:
A:
C:
Acute abdomen assessment and management.
The first decision when you first see any patient is “Are they critically unwell?”. A 10-second assessment of their clinical state can be made by a general look (the “end-of-bed-o-gram”), their observations, and whether they can talk to you.
If they are critically unwell, give oxygen, start suitable initial steps, and call for help early before going into detail on the history and examination.
Presentations Requiring Urgent Surgery”
1. Bleeding
The most serious cause of intra-abdominal bleeding is a ruptured abdominal aortic aneurysm, which requires swift referral to the vascular team and immediate surgical intervention.
Other common causes usually involve a slower rate of bleeding, but with urgent surgery still required, include ruptured ectopic pregnancy, bleeding gastric ulcer, and trauma.
These patients will typically go into hypovolemic shock. Clinical features include tachycardia and hypotension, pale and clammy on inspection, and cool to touch with a thread pulse.
- Perforated Viscus
Peritonitis is the inflammation of the peritoneum, and a generalised peritonitis is most commonly caused by perforation of an abdominal viscus.
The causes of perforation are broad but include peptic ulceration, small or large bowel obstruction, diverticular disease, and inflammatory bowel disease.
Patients with a generalised peritonitis present with some characteristic features:
Patients often lay completely still, not to move their abdomen, and look unwell
This is especially important when compared to a renal colic, whereby patients are constantly moving and cannot get comfortable.
Tachycardia and potential hypotension
A completely rigid abdomen with percussion tenderness
Involuntary guarding – the patient involuntarily tenses their abdominal muscles when you palpate the abdomen
Reduced or absent bowel sounds, suggesting the presence of a paralytic ileus
3. Ischaemic Bowel
Any patient who has severe pain out of proportion to the clinical signs has ischaemic bowel until proven otherwise. They are often acidaemic with a raised lactate and physiologically compromised.
Patients will often complain of a diffuse and constant pain, however the examination can often otherwise be unremarkable. Definitive diagnosis is via a CT scan with IV contrast, with early surgical involvement. Ischaemic bowel is discussed in more detail here.
Presentations That Are Less Acute
Colic
Colic is an abdominal pain that crescendos to become very severe and then goes away completely. This is most typically seen in either ureteric obstruction or bowel obstruction.
Biliary ‘colic’ is not a true colic as the pain does not go away completely, instead getting periodically better and worse (colloquially termed ‘waxes and wanes’).
Peritonism
Peritonism (not peritonitis) refers to the localised inflammation of the peritoneum, usually due to inflammation of a viscus that then irritates the visceral (and subsequently, parietal) peritoneum.
This leads to patients stating that their abdominal pain starts in one place (irritation of the visceral peritoneum) before localising to another area* (irritation of the parietal peritoneum) or becoming generalised.
*The classic example of this is acute appendicitis, with the pain migrating from the umbilical region to the right iliac fossa.
The location of abdominal pain is perhaps the most useful initial feature to help narrow your differential. These can be classified based upon quadrant or region affected, as shown in Fig 2.
It must be remembered to always consider extra-abdominal organs as the cause for abdominal pain, including cardiac, respiratory and gynaecological or testicular conditions.)
On next fc is abdominal pain and locations.
Acute abdomen assessment and management.
The first decision when you first see any patient is “Are they critically unwell?”. A 10-second assessment of their clinical state can be made by a general look (the “end-of-bed-o-gram”), their observations, and whether they can talk to you.
If they are critically unwell, give oxygen, start suitable initial steps, and call for help early before going into detail on the history and examination.
Presentations Requiring Urgent Surgery”
1. Bleeding
The most serious cause of intra-abdominal bleeding is a ruptured abdominal aortic aneurysm, which requires swift referral to the vascular team and immediate surgical intervention.
Other common causes usually involve a slower rate of bleeding, but with urgent surgery still required, include ruptured ectopic pregnancy, bleeding gastric ulcer, and trauma.
These patients will typically go into hypovolemic shock. Clinical features include tachycardia and hypotension, pale and clammy on inspection, and cool to touch with a thread pulse.
- Perforated Viscus
Peritonitis is the inflammation of the peritoneum, and a generalised peritonitis is most commonly caused by perforation of an abdominal viscus.
The causes of perforation are broad but include peptic ulceration, small or large bowel obstruction, diverticular disease, and inflammatory bowel disease.
Patients with a generalised peritonitis present with some characteristic features:
Patients often lay completely still, not to move their abdomen, and look unwell
This is especially important when compared to a renal colic, whereby patients are constantly moving and cannot get comfortable.
Tachycardia and potential hypotension
A completely rigid abdomen with percussion tenderness
Involuntary guarding – the patient involuntarily tenses their abdominal muscles when you palpate the abdomen
Reduced or absent bowel sounds, suggesting the presence of a paralytic ileus
3. Ischaemic Bowel
Any patient who has severe pain out of proportion to the clinical signs has ischaemic bowel until proven otherwise. They are often acidaemic with a raised lactate and physiologically compromised.
Patients will often complain of a diffuse and constant pain, however the examination can often otherwise be unremarkable. Definitive diagnosis is via a CT scan with IV contrast, with early surgical involvement. Ischaemic bowel is discussed in more detail here.
Presentations That Are Less Acute
1. Colic
Colic is an abdominal pain that crescendos to become very severe and then goes away completely. This is most typically seen in either ureteric obstruction or bowel obstruction.
Biliary ‘colic’ is not a true colic as the pain does not go away completely, instead getting periodically better and worse (colloquially termed ‘waxes and wanes’).
- Peritonism
Peritonism (not peritonitis) refers to the localised inflammation of the peritoneum, usually due to inflammation of a viscus that then irritates the visceral (and subsequently, parietal) peritoneum.
This leads to patients stating that their abdominal pain starts in one place (irritation of the visceral peritoneum) before localising to another area* (irritation of the parietal peritoneum) or becoming generalised.
*The classic example of this is acute appendicitis, with the pain migrating from the umbilical region to the right iliac fossa.
The location of abdominal pain is useful feature to help narrow your differential. These can be classified based upon quadrant or region affected,
It must be remembered to always consider extra-abdominal organs as the cause for abdominal pain, including cardiac, respiratory and gynaecological or testicular conditions.)
On next fc is abdominal pain and locations.
Importantly, there are non-general surgical causes of abdominal pain that must not be missed, including testicular torsion, ruptured ectopic pregnancy, diabetic ketoacidosis, and myocardial infarction.
Investigations:
Laboratory Tests
The investigations in all cases of the acute abdomen share the same generic outline:
Urine dipstick – for signs of infection or haematuria Include a pregnancy test for all women of reproductive age.
ABG – useful in bleeding or septic patients, especially for the pH, pO2, pCO2, and lactate for signs of tissue hypoperfusion, as well as a rapid haemoglobin.
Routine bloods – FBC, U&Es, Liver Function, CRP, amylase.
Consider measuring serum calcium in suspected pancreatitis.
Do not forget a group & save if the patient is likely to need surgery soon.
Blood cultures – if considering infection as a potential diagnosis
Note: Any amylase 3x greater than the upper limit is diagnostic of pancreatitis. Any raised value lower than this may also be due to another pathology, such as perforated bowel, ectopic pregnancy, or diabetic ketoacidosis (DKA)
Imaging
In the emergency setting, every patient with abdominal pain should have an ECG to exclude myocardial infarction.
Other imaging modalities that may be initially requested include:
Ultrasound:
Kidneys, ureters and bladder (‘KUB’) – for suspected renal tract pathology
Biliary tree and liver – for suspected gallstone disease
Ovaries, fallopian tubes and uterus – for suspected tubo-ovarian pathology
Radiological:
An erect chest X-ray (eCXR) – for evidence of bowel perforation (Fig. 3)
CT imaging, often best discussed with a senior depending on the suspected underlying diagnosis.
Management
The definitive management of acute abdomen depends largely on the cause. However, a good initial management plan includes the same key points – regardless of the underlying aetiology.
These include admission, IV access, NBM, analgesia +/- antiemetics, imaging (as discussed above), VTE prophylaxis, urine dip, bloods (as discussed above). Consider a urinary catheter and/or nasogastric tube if necessary. Start IV fluids and monitor fluid balance.
Central abdominal pain
Early appendicitis SBO Acute gastritis Acute pancreatitis Ruptured AAA Mesenteric thrombosis
Epigastric pain
DU / GU Oesophagitis Acute pancreatitis AAA Gastritis
RUQ pain
Gallbladder disease DU Acute pancreatitis Pneumonia Subphrenic abscess
LUQ pain
GU Pneumonia Acute pancreatitis Spontaneous splenic rupture Subphrenic abscess
Suprapubic pain
Acute urinary retention UTIs Cystitis PID Ectopic pregnancy Diverticulitis
RIF pain
Acute appendicitis Mesenteric adenitis (young) Perf DU Diverticulitis PID Salpingitis Ureteric colic Meckel’s diverticulum Ectopic pregnancy Crohn’s disease Biliary colic (low-lying gall bladder)
Loin pain
Muscle strain UTIs Renal stones Pyelonephritis AAA
LIF pain
Diverticulitis Constipation IBS PID Rectal Ca UC Ectopic pregnancy
Abdominal pain prevalence
Community prevalence 15-20%
Incidence increases in the elderly
25% consult their GP
6-10% of A/E visits
Guarding
When you pa;pate patients abdome, they tense their anterior abdominal wall. Guaarding can be voluntary or involuntary. If involuntary, patient has peritonitis, automatically they have an acute abdomen and they are potentially very seriously ill. Voluntary guarding is more subtle.
Abdominal pain management
A/B: airway/breathing, may have low oxygen sats.
-Supplemental oxygen will help them calm down.
C: Circulation
-IV access
-fluid administration
-Urinary catherisation
Disability: antiematics, abakgesics, antibiotics, radiology, re-evaluation with results (BM, blood tests, ABG, ECG, radiology).
Complications with pancreatitis
Inflamed pancreas, that inflammation can have a knock on effect on the splenic artery as it wiggles its way behind the spleen. So you can develop pseudoaneurysm of splenic artery which can rupture.
Gastrointestinal bleeding
D: Gastrointestinal (GI) bleeding is a symptom of conditions that damage the wall GI tract. GI bleeding is categorized into upper GI bleeding (UGIB) and lower GI bleeding (LGIB) depending on the source of the bleeding relative to the ligament of Treitz. In the majority of cases, bleeding is localized in the esophagus, stomach, or duodenum (UGIB). LGIB may occur in the rectum, colon, jejunum, and, in rare cases, the ileum. Gastric and duodenal ulcers are the most common causes; angiodysplasia, inflammatory diseases, and carcinomas can also cause GI bleeding. Depending on the source of the bleeding and how long the blood remains in the digestive tract, clinical symptoms may include vomiting blood (hematemesis), tarry black stool (melena), and fresh blood in the stool (hematochezia). Diagnosis includes evaluation of blood loss (e.g., hematocrit) and localization of the source of bleeding (e.g., endoscopy). Hospitalization is essential to monitor for signs of hemodynamic instability and shock caused by anemia and severe blood loss. The source of bleeding can often be located and treated simultaneously during endoscopy with injection therapy (e.g., epinephrine) or ligation.
R:
D: peptic ulcer disease, oesophagitis, cameron lesion, varices, angioma, tumours: oesophageal cancer, gastric cancer, traumatic or iatrogenic, coagulopathies, hemobilia. Erosive or inflammatory, hemorrhoids, tumours, colorectal cancer, trauma, or iatrogenic.
E:
A: Upper gastrointestinal bleeding (UGIB)
∼ 70–80% of GI hemorrhages [1][2]
The source of the bleeding is proximal to the ligament of Treitz.
Lower gastrointestinal bleeding (LGIB)
∼ 20–30% of all GI hemorrhages [3][2]
The source of the bleeding is distal to the ligament of Treitz (usually in the colon).
Other most common etiologies in document. Include:
UGIB: peptic ulcer disease, esophagitis, erosive gastritis and or duodenitis. Esophageal varices, angiodysplasia.
LGIB: diverticulosis, hemorrhoids.
C: Anemia due to chronic blood loss
Acute hemorrhage: signs of circulatory insufficiency or hypovolemic shock
Tachycardia, hypotension (dizziness, collapse, shock)
Altered mental status.
-Hematemesis: vomiting blood, which may be red or coffee-ground in appearance.
-Melenma: black, tarry stool with a strong offensive odor.
Hematochezia: The passage of bring red blood through the anus with or without stool (colonic bleeding: maroon, kelly like traces of blood in stools.
Rectal bleeding, streaks of fresh blood on stools.
P:
I: Fecal occult blood test, endoscopy, colonoscopy, nasogastric tube lavage.
M: Initial management [12]
Consider elective intubation in patients with altered mental or respiratory state and severe ongoing hematemesis.
Hemodynamic resuscitation
In case of hemodynamic instability and/or suspected ongoing bleeding
IV fluid to normalize blood pressure and heart rate (see “Fluid resuscitation”)
Transfusion of packed red blood cells in case of massive bleeding (e.g., hemoglobin < 7 g/dL)
Management of anticoagulants
INR 1.5–2.5: Endoscopic hemostasis is possible.
INR > 2.5: Reversal agents should be considered before endoscopy.
If there is any suspicion of GI bleeding, two large-caliber peripheral venous catheters should be inserted and preparations should be made for a possible blood transfusion.
Interventions to stop bleeding [14][15]
Endoscopy
Used to locate the site of the (suspected) bleeding and to initiate therapy
Injection therapy (e.g., epinephrine): actively bleeding ulcers or blood vessels
Hemostatic surgical procedures: sclerotherapy, band ligation, cauterization, or clip placement
Polypectomy in case of bleeding polyp (e.g., in the colon)
Angiography: vasoconstriction of a bleeding vessel via e.g., intraarterial vasopressin infusion or embolization
Surgery (laparotomy): if bleeding cannot be contained through endoscopic intervention (rarely the case)
Treatment of underlying disease
See “Treatment” sections in “Crohn disease“, “Ulcerative colitis“, “Peptic ulcer disease“, “Hemorrhoids“, “Intestinal ischemia“, “Gastric cancer“, “Colorectal cancer“, and “Portal hypertension.“
Peptic ulcer – you should act immediately to reduce the amount of acid in the stomach. This will inhibit the action of pepsin, and may encourage the initial bleed to heal by itself if the first 24 hours.
The rest is then exactly the same as you would treat a normal peptic ulcer!
Oesophageal Varices– you should treat the chronic liver disease with non-selective β-blockers to lower the general venous pressure and reduce the risk of variceal bleeding.
If the varices present before they have bled, then you can treat them with ‘banding’ whereby youjust stick a little band around the bulging varices and the weakest part of the vein will be cut off from the rest, and will eventually just drop off. This treatment can be done by endoscopy.
In acute severe variceal bleeding, where the patient is in immediate danger, you may wish to use a Minnesota tube. This is a tube that is inserted down the oesophagus, into the stomach, and a small bag of air inflated at the bottom with about 300ml of air. This first bag prevents the tube being pulled out of place. There is a second bag that can also be filled with air that sits in the oesophagus. This bag is inflated to around 40mmHg pressure – just above normal venous pressure – and thus this keeps blood in the veins, rather than letting it spurt out into the oesophagus. You must be very careful when inflating the second bag as you can perforate the oesophagus!
This is only a temporary solution. It is often very uncomfortable for the patient
There are some additional steps if oesophageal varices are suspected, for example in patients with a history of chronic liver disease:
Terlipressin
Prophylactic broad spectrum antibiotics
The definitive treatment is oesophagogastroduodenoscopy (OGD) to provide interventions that stop the bleeding, for example banding of varices or cauterisation of the bleeding vessel.
NICE recommend against using a proton pump inhibitor prior to endoscopy, however you may find senior doctors that do this.
P: Hypovolemic shock
Hepatic encephalopathy (in patients with liver cirrhosis)
Aspiration pneumonia [16][17]
We list the most important complications. The selection is not exhaustive.
Gastroesophageal reflux tomach cancer
D: Gastroesophageal reflux: regurgitation of stomach contents into the esophagus (can also occur in healthy individuals, e.g., after consuming greasy foods or wine)
Gastroesophageal reflux disease (GERD): A condition in which reflux causes troublesome symptoms (typically including heartburn or regurgitation) and/or esophageal injury/complications. The most common endoscopic finding associated with esophageal mucosal injury is reflux esophagitis. [1]
NERD (non-erosive reflux disease): characteristic symptoms of gastroesophageal reflux disease in the absence of esophageal injury, such as reflux esophagitis, on endoscopy (50–70% of GERD patients) [2]
ERD (erosive reflux disease): gastroesophageal reflux with evidence of esophageal injury, such as reflux esophagitis, on endoscopy (30–50% of GERD patients).
R: Risk factors include smoking, alcohol consumption, stress, obesity, and anatomical abnormalities of the esophagogastric junction (e.g., hiatal hernia).
Risk factors/associations
Lifestyle habits such as smoking, caffeine and alcohol consumption [5][6]
Stress [2]
Obesity [7]
Pregnancy [5][3]
Diaphragm dysfunction [3]
Angle of His enlargement (> 60°) [8][9]
Iatrogenic (e.g., after gastrectomy)
Inadequate esophageal protective factors (i.e., saliva, peristalsis) [5]
Gastrointestinal malformations and tumors: gastric outlet obstruction, gastric cardiac carcinoma
Scleroderma [5]
Sliding hiatal hernia: ≥ 90% of patients with severe GERD ,
D: Other forms of esophagitis
Infectious esophagitis: generally in immunocompromised patients
Esophageal candidiasis: Endoscopy shows white or yellowish adherent plaques.
Herpes esophagitis: Endoscopy shows superficial ulcers in the upper or mid esophagus in the absence of plaques.
CMV esophagitis: Endoscopy shows distal mucosal erosions and ulcers; viral inclusion bodies in cell nuclei on biopsy.
Drug-induced esophagitis: Some medications may cause esophageal mucosal irritation, leading to erosions and ulcers.[17]
Causes:
Antibiotics (e.g., tetracycline, doxycycline, and clindamycin)
Anti-inflammatory drugs (e.g., Aspirin)
Bisphosphonates (e.g., Alendronate)
Others (e.g., potassium chloride, quinidine, and iron compounds)
Endoscopic findings: punched-out ulcers with mild inflammatory changes of the surrounding mucosa
Eosinophilic esophagitis
Associated with allergic disease (allergic asthma, allergic rhinitis) in 50% of cases
Endoscopic findings
Circumferential mucosal lesions (rings/corrugations)
Mucosal fragility
Histological finding: increased number of eosinophils.
Cardiac: See differential diagnosis of chest pain (especially angina pectoris).
Gastrointestinal
Diffuse esophageal spasm
Achalasia
Osteochondrosis
Da Costa’s syndrome (or neurocirculatory asthenia).
E: Prevalence: ∼ 15–30% in the US (increases with age) [3]
Sex: ♀ = ♂
A: Main mechanism: transient lower esophageal sphincter relaxations (tLESRs) [5]
The dysfunctional LES loosens independent of swallowing and has a decreased ability to constrict, which allows stomach contents to uncontrollably flow back into the esophagus (otherwise known as sphincter insufficiency).
Causes ∼⅔ of reflux episodes
C: The chief complaint is retrosternal burning pain (heartburn), but a variety of other symptoms, such as dysphagia and a feeling of increased pressure, are also common. Suspected GERD should already receive empirical treatment, but further diagnostic steps, such as an upper endoscopy and/or 24-hour pH test, may be indicated to confirm the diagnosis.
Chief complaint: retrosternal burning pain (heartburn) that worsens while lying down (e.g., at night) and after eating
Pressure sensation in the chest
Belching, regurgitation
Dysphagia
Chronic non-productive cough and nocturnal cough
Nausea and vomiting
Halitosis
Triggers:
Bending down, supine position
Habits: smoking and/or alcohol consumption
Psychological factors: especially stress.
P: The histopathological findings vary depending on the severity of mucosal damage: [4]
Superficial coagulative necrosis in the non-keratinized squamous epithelium
Thickening of the basal cell layer
Elongation of the papillae in the lamina propria and dilation of the vascular channels at the tip of the papillae (→ hyperemia)
Inflammatory cells (granulocytes, lymphocytes, macrophages)
Transformation of squamous into columnar epithelium → Barrett’s metaplasia.
I: Empirical therapy: If GERD is clinically suspected and there are no indications for endoscopy, empiric therapy – ranging from lifestyle modifications to a short trial with PPIs – should be initiated. A GERD diagnosis is assumed in patients who respond to this therapeutic regimen. [7]
Upper endoscopy (esophagogastroduodenoscopy (EGD))
Used to classify reflux esophagitis and conduct biopsies [4]
Indications for endoscopy
Signs of complicated disease (e.g., dysphagia, painful swallowing, weight loss, iron deficiency anemia, and aspiration pneumonia) [12]
Extended course of symptoms [12][7]
Noncardiac chest pain [7]
No response to PPI treatment [13]
Esophageal pH monitoring
Measured over 24 hours via nasogastric tube with a pH probe [4]
Sudden drops to a pH ≤ 4 are consistent with episodes of acid reflux into the esophagus [4]
Indications
To confirm suspected NERD [4]
Before endoscopic or surgical treatment options are initiated in patients with NERD [7]
GERD is diagnosed when drops in esophageal pH correlate with symptoms of acid reflux and precipitating activities noted in the patient’s event diary.
Esophageal manometry
A pressure-sensitive nasogastric tube measures the muscle contractions in several sections of the esophagus while the patient swallows
Indications:
Ensure correct placement of pH probes
Evaluate peristaltic function prior to anti-reflux surgery
Exclude motor disorders that may mimic the symptoms of GERD
M: Management involves lifestyle modifications, medications, and possibly surgery. Proton pump inhibitors (PPIs) are the treatment of choice, although other agents – such as histamine H2-receptor antagonists (H2RAs) – may also be helpful. In addition to relieving symptoms, treating esophagitis is especially important, as chronic mucosal damage can lead to a premalignant condition known as Barrett’s esophagus, further progressing to adenocarcinoma of the esophagus.
Dietary
Small portions; avoid eating (< 3 hours) before bedtime [3][7]
Avoid foods with high fat content [13]
Physical
Normalize body weight [7]
Elevate the head of the bed for patients with nighttime symptoms [7]
Avoid toxins: nicotine, alcohol, coffee [13][7] , and certain drugs (e.g., calcium channel blockers, diazepam).
Medical therapy
Treatment of choice: Standard-dose of PPI for at least 8 weeks (once-daily therapy)
No response: further diagnostic evaluation
Partial response: increase the dose (to twice daily therapy) or switch to a different PPI
Good response: discontinue PPI after 8 weeks
Maintenance therapy: if symptoms recur after discontinuation of PPIs and in the case of complications (see “Complications” below)
After 8 weeks of initial treatment, reduce PPI to lowest effective dose or switch to H2RAs (only in patients without complications!).
Surgical therapy
Indications
Equally effective alternative to medical therapy in certain patients with chronic GERD [7]
Complications (e.g., Barrett esophagus, strictures, recurrent aspiration) [18][19]
Fundoplication
Symptoms resolve in 85% of cases, but recurrence is possible [19][20]
Technique: The gastric fundus is wrapped around the lower esophagus and secured with stitches to form a cuff, leading to a narrowing of the distal esophagus and the gastroesophageal junction (GEJ)and prevents reflux. [21]
Nissen fundoplication (= complete fundoplication) [18][19]
Complications [20]
Intraoperative damage to the stomach and/or surrounding organs, especially the esophagus, spleen, lungs/pleura (→ pneumothorax)
Gas bloat syndrome: inability to belch, leading to bloating and an increase in flatulence
Dysphagia (especially to solids)
Telescope phenomenon (“slipped Nissen”): the esophagus slides out of the wrapped stomach portion
Gastric denervation: Vagal nerve injury leads to bloating and cardiac complaints, resembling Roemheld syndrome
If hiatal hernia is present [19]
Hiatoplasty: margins of the widened hiatus are sutured together
Fundopexy or gastropexy: the protruding part of the stomach is tethered to the diaphragm → keeps it in place and relieves the tension placed on the cuff
P: Reflux esophagitis: most common complication of GERD [23]
Iron deficiency anemia: mucosal erosions and ulcerations → chronic bleeding → anemia
Esophageal stricture: most common sequela of reflux esophagitis [23]
Clinical features: cause solid food dysphagia
Diagnostics
Barium esophagram (best initial test): narrowing of the esophagus at the gastroesophageal junction
Endoscopy with biopsies: to rule out malignancy and eosinophilic esophagitis
Treatment
First-line treatment: dilation with bougie dilator/balloon dilator + proton pump inhibitors in patients with reflux
In refractory cases (multiple recurrences): steroid injection prior to dilation, endoscopic electrosurgical incision
Recurrence occurs in the majority of patients; often multiple treatment attempts necessary
Esophageal ring: [24]
Schatzki rings at the squamocolumnar junction are the most common type
Clinical features and management similar to that of an esopahgeal stricture
Aspiration of gastric contents leads to:
Aspiration pneumonia
Chronic bronchitis
Asthma (exacerbation)
Laryngitis and hoarseness
Barrett esophagus
Pathophysiology
Reflux esophagitis → stomach acid damages squamous epithelium → squamous epithelium becomes replaced by columnar epithelium and goblet cells (intestinal metaplasia, Barrett’s metaplasia) [3]
The physiological transformation zone (“Z-line”) between squamous and columnar epithelium is shifted upwards
Pathology
Short-segment Barrett’s esophagus (< 3 cm of columnar epithelium between Z-line and GEJ)
Long-segment Barrett’s esophagus (> 3 cm of columnar epithelium between Z-line and GEJ) → higher cancer risk!
Complications: precancerous condition for adenocarcinoma (see esophageal cancer)
Management and surveillance [25]
Medical treatment with PPIs
Endoscopy with four-quadrant biopsies at every 2 cm of the suspicious area (salmon colored mucosa)
If no dysplasia: repeat endoscopy every 3–5 years
If indefinite for dysplasia: repeat endoscopy with biopsies after 3–6 months of optimized PPI therapy
If low-grade dysplasia
Endoscopic therapy of mucosal irregularities
Alternatively: surveillance every 12 months with biopsies every 1 cm
If high-grade dysplasia: endoscopic therapy of mucosal irregularities
Barretts oesophagus
Constant reflux of acid results in the lower oesophageal epithelium changing in a process known as metaplasia from a squamous to a columnar epithelium. This change to columnar epithelium is called Barretts oesophagus. When this change happens patients typically get an improvement in reflux symptoms.
Barretts oesophagus is considered a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus (3-5% lifetime risk with Barretts). Patients identified as having Barretts oesophagus are monitored for adenocarcinoma by regular endoscopy. In some patients there is a progression from Barretts oesophagus (columnar epithelium) with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.
Treatment of Barretts oesophagus is with proton pump inhibitors (e.g. omeprazole). There is new evidence that treatment with regular aspirin can reduce the rate of adenocarcinoma developing however the is not yet in guidelines.
Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the epithelium so that it is replaced with normal cells. This is not recommended in patients with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.
Barrett’s oesophagus
D: lso known as Columnar Lined oesophagus (CLO)
This is a complication of long term oesophageal reflux.
It looks a bit like white pasty finger like projections coming up from the bottom of the oesophagus.
Strictly speaking it is defined as >3cm columnar epithelium present at the bottom of the oesophagus.
The mechanism by which it occurs is not fully understood. Some argue that it is a migration of the epithelium of the bottom 2cm of the oesophagus further up the lumen – i.e. a migration of essentially the gastric epithelium. Others would say that as both squamous and columnar epithelium are derived from the same stem cells, it is just perhaps a change in the intra-luminal conditions that determine what those stem cells develop into; more acidic conditions will cause a columnar epithelium to form. The second idea is more popular.
It is found in 10% of patients who have an endoscopy for reflux symptoms.
It is seen endoscopically as a pinker/redder epithelium as opposed to the whiter epithelium that lines the rest of the oesophagus. At first it may just extend up as thin bands of epithelium, but later it may encircle the entire lower oesophagus.
On microscopic examination, the cells resemble those of the stomach, however they secrete intestinal-like mucins, and as a result, Barrett’s oesophagus is actually a form of intestinal metaplasia.
Metaplasia – This usually occurs as a result of an environmental factor. It is when an existing epithelium is replaced by a different one; one that now has an ‘advantage’ due to the change in environmental conditions.
It is a major risk factor in oesophageal adenocarcinoma – there is a lifetime risk of 5-10%. Only about 5% of Barrett’s patients will actually ever get dysplasia. The risk for a Barrett’s patient to get ANY CANCER in their lifetime is:
No dysplasia – 2% (this is almost exactly the same as the general population)
Low-grade dysplasia – 30%
High-grade dysplasia – 50%
As such is defined as a ‘premalignant condition’, and patients who have it are at 100x times greater risk of cancer than the general population.(i.e. risk of oesophageal adenocarcinoma goes from 4 in 100 000 to 400 in 100 000. This however, is still a relatively small risk overall (0.4%), and as such the patients overall risk of getting any cancer is still about 2-3%.
95% of Barrett’s patients will die of another cause other than oesophageal cancer.
Most cases of CLO are not detected until cancer develops.
R:
D:
E: Associated with men >50, particularly Caucasians.
Increased risk due to smoking (but not alcohol)
A:
C:
P:
I: When you first find Barrett’s/if you suspect oesophageal carcinoma then you would biopsy the oesophagus. This has very strict guidelines, and you have to biopsy every quadrant (i.e. imagine the oesophagus as having a square lumen, and biopsy all four sides) for every 2cm of Barrett’s present. So if the patient has 6cm of Barrett’s, you have to do 12 biopsies. The idea behind this is so that you don’t miss any possible areas of high grade dysplasia, because macroscopically (ie as you look at the oesophagus down the endoscope) you cannot see a difference between areas of low grade and high grade dysplasia.
The evidence for surveillance is not conclusive. The current BSG (British society of Gastroenterologists) guidelines state that you can do surveillance if you want to, but you don’t have to. As a result, some trusts offer it and some don’t.
If you do offer surveillance, then you must be sure that if anything is found, that the patient is fit enough to undergo surgery. E.g. do you really want to offer surveillance to a 90 year old man?
Where it is offered, surveillance is currently recommended for those with low grade dysplasia about every 6-12 months, and for those without dysplasia every 2-3 years. Dysplasia takes about 2-5 years to develop.
Even with surveillance, it is not that likely you will find a carcinoma any sooner (hence the option not to survey). For example, you might have missed an area of high dysplasia last time round, and by the time you survey again it has developed beyond a treatable stage.
M: There is no evidence that treatment with PPI’s or anti-reflux medicine leads to recession of Barrett’s.
However, treatment is basically that of GORD.
P:
Oesophageal carcinoma
Osophageal cancer typically assumes the form of adenocarcinoma or squamous cell carcinoma, although there are some rarer tumors. Adenocarcinomas are considered the fastest-growing neoplasia in Western countries, while squamous cell carcinoma is still most common in the developing world. Adenocarcinoma, which usually affects the lower third of the esophagus, may be preceded by Barrett’s esophagus, a complication of gastroesophageal reflux disease (GERD). In addition to GERD, other risk factors include obesity and smoking. Squamous cell carcinomas mostly occur in the upper two-thirds of the esophagus. Known risk factors for squamous cell carcinoma include carcinogen exposure from alcohol and tobacco consumption, and dietary factors (e.g., diet low in fruits and vegetables). Esophageal cancers are often asymptomatic in early stages of the disease. Locally advanced disease is common at presentation, progressive dysphagia being the primary symptom. Hoarseness, weight loss, and hematemesis may also be present. Endoscopy is the primary diagnostic test, enabling direct visualization and biopsy of the lesion for histopathological confirmation. Curative surgical resection may be considered for locally invasive cancers. Esophageal cancer is unresectable at presentation in about 60% of patients. Chemotherapy, radiation, and palliative stenting play a role in the management of unresectable disease.
oesophageal cancer
D:
R: Adenocarcinoma
Risk factors
Gastroesophageal reflux: Barrett’s esophagus
Obesity
Smoking
Achalasia
Localization: mostly in the lower third of the esophagus
Squamous cell carcinoma (SCC)
Risk factors [4]
Alcohol consumption
Smoking
Diet low in fruits and vegetables
Drinking hot beverages
Achalasia
Nitrosamines exposure (e.g., cured meat, fish, bacon) [5]
Plummer-Vinson syndrome
Caustic strictures
Diverticula (e.g., Zenker’s diverticulum)
Radiotherapy
Esophageal candidiasis
Betel or areca nut chewing
Localization: mostly in the upper two-thirds of the esophagus
The primary risk factors for squamous cell esophageal cancer are alcohol consumption, smoking, and dietary factors (e.g., diet low in fruits and vegetables)!
D:
E: Sex: ♂ > ♀ (3:1)
Peak incidence: 60–70 years of age
Adenocarcinoma: most common type of esophageal cancer in the US [1]
Squamous cell carcinoma (SCC): most common type of esophageal cancer worldwide [2]
Adenocarcinoma is more common in the US of America.
A:
C: Early stages: Often asymptomatic but may present with swallowing difficulties or retrosternal discomfort
Late stages
Common
Progressive dysphagia (from solids to liquids) with possible odynophagia
Weight loss
Retrosternal chest or back pain
Anemia
Less common
Hematemesis, melena
Hoarseness
Esophageal cancer is a “silent” disease and typically becomes symptomatic at advanced stages!
P: Adenocarcinoma
Histological characteristics: often present with adjacent Barrett mucosa (columnar epithelium with goblet cells) and high-grade dysplasia
Squamous cell carcinoma
Histological characteristics
Breakdown of uniform tissue structure
Squamous cell carcinoma clusters with circular keratinization
Lymphocytic infiltration between the carcinoma clusters
I: Esophagogastroduodenoscopy (best initial and confirmatory test) [8]
Direct visualization of the tumor
With biopsy of any suspicious lesions
Barium swallow: asymmetrical and irregular borders of the esophagus with characteristic stenosis and proximal dilatation (apple core lesion)
Sensitive, but does not allow confirmation or staging of a malignancy. Inferior to endoscopy, but indicated in the case of:
Severe stricture that inhibits endoscopic evaluation
Suspected tracheoesophageal fistula due to esophageal cancer
Staging [8]
Transesophageal endoscopic ultrasound
Chest and abdominal CT and/or PET
Bronchoscopy or laparoscopy
M: Curative
Indication
Locally invasive disease that has not invaded surrounding structures
High-grade metaplasia in Barrett syndrome
Methods
Neoadjuvant chemoradiation
For downstaging → potentially allows for later resection
As definitive treatment in patients with proven complete response (e.g., during endoscopy)
Surgical resection
Endoscopic submucosal resection for removal of superficial, epithelial lesions
Subtotal or total esophagectomy with gastric pull-through procedure or colonic interposition
Palliative
Indication: patients with advanced disease (majority of patients)
Methods:
Chemoradiation
Stent placement
Other endoscopic treatments (e.g., laser therapy
P: Esophageal stenosis Tracheoesophageal fistula: passage of food and fluid into the respiratory tract Postoperative Anastomotic leak or stricture Recurrent laryngeal nerve injury.
Generally poor prognosis due to an aggressive course (due to an absent serosa in the esophageal wall) and typically late diagnosis.
The more distal the tumor, the better the prognosis
Esophageal cancer has an aggressive course and metastasizes early because of the absence of serosa in parts of the esophagus!
Peptic ulcers
Peptic ulcer disease (PUD) refers to the presence of one or more ulcerative lesions in the stomach or lining of the duodenum. Possible etiologies include infection with the bacterium Helicobacter pylori (most common), prolonged use of nonsteroidal anti-inflammatory medicines (possibly in combination with glucocorticoids), conditions associated with an overproduction of stomach acid (hypersecretory states), and stress. Epigastric pain is a typical symptom of PUD, however, some patients may remain asymptomatic. Diagnosis occurs via direct visualization of the ulcer on esophagogastroduodenoscopy (EGD) and H. pylori detection (via biopsy or non-invasive testing). The first-line treatment for most peptic ulcers involves H. pylori eradication via triple therapy (a course of two different antibiotics in combination with a proton-pump inhibitor) and the withdrawal of offending agents. Antisecretory drugs (e.g., proton-pump inhibitors, or PPIs), which reduce stomach acid production, are continued for 4–8 weeks after eradication therapy and may be considered for maintenance therapy if symptoms recur. Surgical intervention may be necessary in rare cases, especially if complications such as perforation or massive bleeding occur. Stomach cancer is an important differential diagnosis and must be ruled out if risk factors are present.
Peptic ulcers DR DEAC PIMP
D: Gastric ulcer: an ulcerative lesion in the stomach lining; typically manifests along the lesser curvature and the gastric antrum
Duodenal ulcer: an ulcerative lesion located in the duodenum, typically in the first part (i.e., the duodenal bulb)
Erosive gastritis: acute mucosal inflammation of the stomach that does not extend beyond the muscularis mucosae
An atypical location is suspicious for carcinoma!
R: Risk factors
Chronic gastritis caused by H. pylori, a curved, flagellated gram-negative rod
Duodenal ulcers: up to 90% are due to H. pylori infection
Gastric ulcers: up to 80% are due to H. pylori infection
Chronic gastritis of other etiology
Long-term use of NSAIDs (e.g., patients with rheumatoid arthritis, SLE, etc.):
Risk for gastroduodenal ulcers increases 5-fold.
NSAID use seems to have a stronger association with gastric ulcers than with duodenal ulcers.
Long-term use of NSAIDs plus glucocorticoids: Risk increases 10 to 15-fold!
SSRIs
Smoking
Chronic alcohol consumption
Patients with blood type O have a higher risk for duodenal ulcers.
Age > 65 years
Stress (see “Subtypes and variants” below)
Rare risk factors:
Zollinger-Ellison syndrome (can result in duodenal ulcer)
Hyperparathyroidism
E:Incidence: > 6 million cases annually in the US
Duodenal ulcers are 3 times more common than gastric ulcers.
Duodenal ulcers occur on average 10–20 years earlier than gastric ulcers.
Sex: ♂ = ♀
A:
C:Findings common to both (gastric and duodenal):
Dyspepsia: postprandial heaviness, early satiety, and gnawing, aching or burning epigastric pain
Pain relief with antacids
Potential signs of internal bleeding (anemia, hematemesis, melena)
∼ 70% of patients with PUD are asymptomatic
Stool sample positive for occult blood (see gastrointestinal bleeding).
For gastric ulcers:
-pain increases shortly after eating -> weight loss.
-Nocturnal pain in 30-40% of patients.
Duodenal ulcer:
Pain increases 2-5 hours after eating. Pain on an empty stomach (hunger pain) that is relieved with food intake -> weight gain.
Nocturnal pain in 50-80% of patients.
Gastric ulcer is associated with pain after light (weight loss) Gorging. Duodenal ulcer is associated with relief after massive (weight gain) Desserts.
“
Taking NSAIDs can often mask PUD symptoms until complications such as hemorrhage and perforation occur!
P:
I: ≤ 60 years of age without alarm features: Urea breath test for H. pylori
> 60 years of age or presence of ≥ 1 alarm features: EGD with biopsies and rapid urease testing for H. pylori
Negative for H. pylori infection and NSAID intake; trial therapy unsuccessful
Measure serum gastrin level at baseline and after secretin stimulation test: high levels in gastrinoma (Zollinger-Ellison syndrome)
Measure serum calcium and parathyroid hormone: high levels in primary hyperparathyroidism
Testing for Helicobacter pylori
See “Helicobacter pylori diagnostics”
Esophagogastroduodenoscopy (EGD)
Most accurate test
Patients > 60 years of age or presence of ≥ 1 alarm features, which include:
Certain symptoms: progressive dysphagia, painful swallowing (odynophagia), and/or persistent vomiting
Signs of active GI bleeding (e.g., melena, unexplained iron-deficiency anemia)
Signs of malignancy (e.g., unintended weight loss, lymphadenopathy, palpable mass)
Family history of upper GI malignancy in a first-degree relative
Jaundice
Biopsy samples from:
Edge and base of the ulcer (essential to rule out malignancy) .
Stomach lining distant from the ulcer (Helicobacter pylori testing for detection of underlying type B gastritis)
If active bleeding, EGD can be performed for diagnosis and subsequent hemostasis treatment (electrocautery) in the same session.
Alarm features of PUD include progressive dysphagia, odynophagia, persistent vomiting, jaundice, signs of GI bleeding, signs of malignancy, and a family history of upper GI malignancy!
To rule out gastric cancer, patients with stomach ulcers should undergo follow-up EGD and histology until the ulcer has healed completely!
M: General management of dyspepsia
H. pylori positive → eradication therapy (with antibiotics and a PPI) and supportive treatment → continue PPIs for 4–8 weeks → follow-up
H. pylori negative → medical acid suppression (with a PPI) and supportive treatment for 4–8 weeks → follow-up
Medical treatment
Helicobacter pylori eradication therapy (with antibiotics)
Acid suppression: PPIs (most effective), H2 blockers, antacids (mainly used for symptom relief)
Mucosal protection: misoprostol , sucralfate (both substances are rarely used in PUD)
Supportive treatment
Discontinue NSAIDs
Restrict alcohol use/smoking/emotional stress
Avoid eating before bedtime
Surgical treatment
With the advent of potent acid suppression in the form of PPIs, surgical intervention is rarely needed.
Indications
Refractory syndromes despite appropriate medical treatment
If cancer is suspected
Complications that cannot be treated endoscopically (see “Complications” below)
Partial gastrectomy (Billroth)
Billroth I: distal gastrectomy with end-to-end or side-to-end gastroduodenostomy
Billroth II: resection of the distal ⅔ of the stomach with a blind-ending duodenal stump and end-to-side gastro-jejunostomy. The Billroth I and II methods without a Brown’s anastomosis often lead to bile reflux into the stomach. This may result in type C gastritis in the region of the anastomosis. The chronic inflammation causes atrophic changes and increases the risk of cancer (anastomosis carcinoma).
Vagotomy
P: Bleeding (see gastrointestinal bleeding)
Most common complication of PUD
Located posterior more commonly than anterior
Perforated gastric ulcers of the lesser curvature may cause hemorrhage of the left gastric artery.
Duodenal ulcers of the posterior wall are more likely to cause massive bleeding because of their proximity to the gastroduodenal artery.
Gastric/duodenal perforation (see also secondary peritonitis and gastrointestinal perforation)
Second most common complication of PUD
Located anterior more commonly than posterior
Duodenal ulcers of the anterior wall are more likely to perforate into the abdominal cavity, causing pneumoperitoneum (free air below the diaphragm) and irritation of phrenic nerve (e.g., shoulder pain).
Subhepatic abscess
Etiology: may result from a perforated duodenal or gastric ulcer
Clinical presentation: fever and vomiting (see also “Gastric/duodenal perforation” above)
Diagnosis: subhepatic gas on abdominal x-ray
Management
Treat underlying cause
IV antibiotics, percutaneous drainage
See also “Therapy” in pyogenic liver abscess.
Gastric outlet obstruction (GOO)
Definition: mechanical obstruction of the pyloric channel or duodenum
Etiology
Malignancy (most common)
PUD
Acute PUD → inflammation and edema
Chronic PUD → scarring and fibrosis
Gastric volvulus
Less common causes that cause strictures in the pyloric channel: Crohn disease, history of ingestion of a caustic substance, chronic pancreatitis
Clinical presentation
Postprandial, nonbilious vomiting
Succussion splash
Early satiety
Progressive gastric dilation
Weight loss
Diagnosis
Barium swallow
Upper endoscopy (confirmatory test): identification of the gastric pathology
Laboratory tests: hypokalemic hypochloremic metabolic alkalosis
Saline load test
Management
Symptomatic: nasogastric suction, electrolyte and fluid replacement, and parental nutrition
Definitive: surgery or endoscopic dilation
Fistula formation
Clinical presentation
Increased severity of pain, which is no longer relieved by eating; radiation of pain to the back
Weight loss, diarrhea
Malignant transformation
Gastric ulcers: high malignant potential (progression to cancer in 5–10% of cases) → malignancy should be ruled out with biopsy [20]
Duodenal ulcers: usually benign → routine biopsy is not required
Postgastrectomy syndromes
Posterior ulcers are more likely to bleed and anterior ulcers are more likely to perforate: Postal workers wear Blue collars and should not have an Antisocial Personality.
Gastric cancer Dr Deac Pimp
D: Gastric cancer refers to neoplasms in the stomach, including cancers of the esophagogastric junction. The incidence is declining in the United States and Europe, while it is rising in Japan and South Korea. Gastric cancer is associated with several risk factors (e.g., consumption of foods high in nitrates, increased nicotine intake, Helicobacter pylori infection). In its early stages, the disease is often asymptomatic or accompanied by nonspecific symptoms (e.g., epigastric discomfort, postprandial fullness, or nausea). Late-stage disease may present with gastric outlet obstruction (mechanical obstruction of the pyloric canal), leading to weight loss and vomiting. Biopsy during endoscopy confirms the diagnosis. Adenocarcinomas are the most common form of gastric cancer. Treatment includes endoscopic or surgical resection. Depending on staging, chemotherapy may be indicated before or after surgery (neoadjuvant or adjuvant chemotherapy), or as a palliative therapy.
R:
D: Gastric ulcer Gastroesophageal reflux disease (GERD) Ménétrier's disease Non-ulcer dyspepsia Other types of cancer MALT lymphoma Sarcoma Gastrointestinal stromal tumor (GIST)
E: Sex: ♂ > ♀
Peak incidence: 70 years
Geographical distribution: strong regional differences
High incidence in South Korea and Japan
Declining incidence in the United States and Europe
A: Exogenous risk factors
Diet rich in nitrates and/or salts (e.g., dried, preserved food)
Nicotine use
Low socioeconomic status
Endogenous risk factors
Diseases associated with a higher risk of gastric cancer
Atrophic gastritis
H. pylori infection: associated with a higher risk of intestinal gastric cancer but not with diffuse gastric cancer
Gastric ulcers
Partial gastrectomy
Gastroesophageal reflux disease (GERD; for cancers of the gastroesophageal junction)
Adenomatous gastric polyps
Hereditary factors (positive family history, hereditary non‑polyposis colorectal cancer)
Higher incidence in individuals with blood type A.
C: Gastric cancer is often asymptomatic. Early signs are nonspecific and often go unnoticed. At later stages the following symptoms may occur:
General signs
Weight loss
Chronic iron deficiency anemia (paleness, fatigue, headaches)
Gastrointestinal signs
Abdominal pain
Early satiety
Nausea or vomiting
Dysphagia
Acute gastric bleeding (hematemesis or melena)
Late stage gastric cancer
Palpable tumor in epigastric region
Gastric outlet obstruction
Hepatomegaly, ascites
Virchow’s node: left supraclavicular adenopathy, located where the thoracic duct joins the subclavian vein at the venous angle.
Sister Mary Joseph’s node: umbilical node indicating metastasis from a gastrointestinal or abdominopelvic malignancy
Malignant acanthosis nigricans (in particular associated with gastric adenocarcinoma).
Subtypes and variants
Metastatic Disease
Lymphangitic spread
All local lymph nodes (lesser and greater curvature)
Celiac, paraaortic, and mesenteric lymph nodes
Carcinoma of the cardia may spread to mediastinal lymph nodes.
Hematogenous spread: liver, lung, skeleton, brain
Local invasion of adjacent structures
Peritoneal carcinomatosis
Esophagus, transverse colon, pancreas, etc.
Direct seeding
To the ovaries (Krukenberg tumor): an ovarian malignancy comprised of signet ring cells that has metastasized from a primary site, most commonly the stomach
To the pouch of Douglas.
P: Adenocarcinoma (90% of cases)
Typically localized, exophytic lesion +/- ulceration
Arise from glandular cells in the stomach; usually located on the lesser curvature of the stomach
Signet ring cell carcinoma
Diffuse growth
Multiple signet ring cells = round cells filled with mucin, with a flat nucleus in the cell periphery
Less common
Adenosquamous carcinoma
Squamous cell carcinoma.
Lauren classification of gastric adenocarcinoma
Intestinal type (∼ 50% of cases): polypoid, glandular formation; expanding (not infiltrative) growth pattern; clear border
Diffuse type (∼ 40% of cases): infiltrative growth and diffuse spread in the gastric wall, no clear border
Mixed type (∼ 10% of cases)
I: Diagnostic procedures
Upper endoscopy with biopsy (best initial test) : Biopsy confirms the diagnosis
Barium upper GI series may be considered and would show loss of intestinal folds and stenosis
Laboratory test
Iron deficiency anemia
Serologic markers : TNF-α as possible future tumor marker
Staging
Abdominal ultrasound
Endosonography
Assessment of tumor depth and local lymph nodes
Abdominal and pelvic CT-scan using intravenous and oral contrast;
Thoracic CT-scan
Diagnostic laparoscopy.
M: Exact therapy, which may be either curative or palliative, depends on staging and the type of tumor.
Endoscopic resection
Surgery
Perioperative chemotherapy, sometimes radiotherapy
Trastuzumab is indicated for HER2+ gastric adenocarcinomas
Surgery
Radical gastrectomy and lymphadenectomy (operative standard)
Resection of the lesser and greater omentum and radical lymphadenectomy
Roux-en-Y gastric bypass
The surgeon separates the proximal jejunum from the duodenum and creates an end-to-end anastomosis of the jejunum with the remaining part of the stomach (gastrojejunostomy), or in the case of a total gastrectomy, with the esophagus (esophagojejunostomy).
Duodenal stump is connected distally with the jejunum using an end-to-side anastomosis.
Alternative: subtotal gastrectomy
Total gastrectomy (with Roux-en-Y anastomosis)Subtotal gastrectomy (with Roux-en-Y anastomosis)
P: Malignant acanthosis nigricans
A paraneoplastic syndrome seen in adenocarcinomas of GI origin, especially in gastric adenocarcinoma
Pathophysiology: caused by exogenous transforming growth factor TGF-α and epidermal growth factor (GF)
Clinical findings
Brown to black, intertriginous and/or nuchal hyperpigmentation that can turn into itching, papillomatous, poorly-defined efflorescence
Rapid growth and verrucous or papulous surface helps to differentiate it from benign acanthosis nigricans
Localization: axilla, groin, neck
Malignant acanthosis nigricans always requires further diagnostic measures to look for malignancy!
Postgastrectomy syndromes
Related to resorption
Maldigestion
Consequences and management
Iron deficiency → supplement iron
Pernicious anemia due to lack of intrinsic factor, usually produced by gastric parietal cells → supplement vitamin B12
Related to anastomosis
Small intestinal bacterial overgrowth (SIBO)
Definition: bacterial overgrowth within the small intestine
Causes
Anatomic abnormalities: (e.g., surgery causing blind intestinal loops – blind loop syndrome ), strictures)
Motility disorders
Pathophysiology: bacterial overgrowth → bacteria deconjugate bile acids, increase vitamin B12 turnover, and produce increased amounts of vitamin K and folic acid
Clinical features: diarrhea, steatorrhea, weight loss, malabsorption (e.g., deficiency of vitamin B12, A, E, D, zinc, and iron)
Diagnostics
Jejunal aspirate cultures collected during endoscopy
Positive lactulose breath test
Treatment: antibiotics and parenteral supplementation of vitamins and proteins, possibly surgical treatment
Related to motility
Dumping syndrome: rapid gastric emptying due to either defective gastric reservoir function or pyloric emptying mechanism, or anomalous postsurgery gastric motor function.
Early dumping
Cause: rapid emptying of undiluted chyme into the small intestine caused by a dysfunctional or bypassed pyloric sphincter
Clinical features
Appears within 15–30 minutes after ingestion of a meal
Symptoms may include nausea, vomiting, diarrhea, and cramps, as well as vasomotor symptoms such as sweating, flushing, and palpitations.
Management
Dietary modifications: Small meals that include a combination of complex carbohydrates and foods rich in protein and fat to cover protein and energy requirements are preferable.
30–60 min of rest in the supine position after meals
Often spontaneous improvement after a couple of months
Late dumping
Cause: postprandial hypoglycemia; dysfunctional pyloric sphincter → chyme containing glucose immediately reaches the small intestine → glucose is quickly resorbed → hyperglycemia → excessive release of insulin → hypoglycemia and release of catecholamines
Treatment
Dietary modifications
Octreotide and surgery are second and third-line therapies
Suspect late dumping syndrome in a patient with previous gastric surgery and hypoglycemia!
Remnant carcinoma is a complication associated with the remnant stomach. Follow-up is important!
prognosis: Since there are no early signs, gastric cancer is often diagnosed very late. At diagnosis, 60% of cancers have already reached an advanced stage that does not allow for curative treatment.
Early gastric cancer has the best prognosis .
Distant metastases or peritoneal carcinomatosis dramatically worsen the prognosis and are lethal most of the time.
