Esophagus
#Esophageal reflux
Chronic. Currently well-controlled with PPI therapy. No acute concerns at this time.
-Continue with home medication.
#Barrett esophagus
Men with gastroesophageal reflux disease symptoms for 5 years and additional risk factors (nocturnal reflux symptoms, hiatal hernia, elevated BMI, intra-abdominal distribution of body fat, tobacco use) should be screened for Barrett esophagus
Barrett esophagus progresses as follows: intestinal metaplasia, indefinite for dysplasia, low-grade dysplasia, high-grade dysplasia, intramucosal carcinoma, and, finally, invasive adenocarcinoma
Patients with high-grade dysplasia and confirmed low-grade dysplasia should undergo treatment to eradicate all neoplastic and at-risk epithelium. Patients with Barrett esophagus without dysplasia should undergo surveillance endoscopy every 3 to 5 years to monitor for dysplasia or precancerous changes.
#Eosinophilic esophagitis
Eosinophilic esophagitis is a condition commonly associated with dysphagia and food bolus obstruction, usually found in younger men with atopic conditions.
Diagnostic criteria for eosinophilic esophagitis are dysphagia, esophageal biopsy specimens with eosinophil counts of at least 15/hpf, and exclusion of other causes of eosinophilia
#Caustic Ingestion
Figure 3, Tosca et al, AJG 2022
Bleeding
GI Bleed check list
NSAID/aspirin use, abdominal pain, alcohol, liver disease, surgery? -> gastric bypass, colectomy, AAA repair, hx of GIB, prior scope, anticoag meds
Last meal
Echo, IVC, ascites, distended stomach
CBC, CMP, coag, fibrinogen, TEG, type and cross
IV access, 2 18G; consider A line and Cordis
PCC, VitK, cryo, platelets PRN; PRN reverse anticoagulant meds
Discontinue anticoag and antihypertensives
Pantoprazole 80mg IV x1, followed by 40mg IV pantoprazole q12
If cirrhotic: octreotide 50mcg bolus, 50mcg/hr; CTX 1g IV
If upper GIB: erythromycin 250mg prior to intubation/endoscopy; over 5-30 minutes, 20-90 minutes prior to endoscopy (avoid in qtc >450 or if gastric u/s reveals empty stomach
If uremic/antiplatelets: consider DDAVP 0.3mcg/kg
Transfuse PRN
#Upper GI Bleed
Symptoms of xxx
Most recent hemoglobin: ; baseline hemoglobin x
Blatchford score of xxx
-2 large bore IVs, type and cross 2 units, pantoprazole 80mg IV once, then pantoprazole 40mg IV BID thereafter
-GI consult for endoscopy
-Give erythromycin 3mg/kg IV over 20-30 minutes, 30-90 minutes prior to endoscopy to decrease need for 2nd look endoscopy
-avoid NSAIDS and anticoagulation
-hold antihypertensives
-Coags x 1
-Lactate x 1
-CBC Q6 until Hgb is stable
#Bleeding gastric varices
In patients with gastric varices, contrast-enhanced cross-sectional imaging should be performed to determine the best treatment
Typically, octreotide is administered to reduce portal pressures, and antibiotics are provided to reduce risk for infectious complications of gastrointestinal bleeding. These complications include bacteremia, which can increase morbidity and mortality from variceal bleeding. Treatment options for gastric varices along the greater curvature of the stomach depend on the anatomy of the abdominal vasculature
#unstable GI bleed 2/2 AVM
For active lower gastrointestinal bleeding with associated hemodynamic instability, CT angiography is the study of choice.
For active lower gastrointestinal bleeding, catheter angiography and possible embolization should be performed as soon as possible after positive results on CT angiography
#acute upper GI bleed
Upper endoscopy within 24 hours
Nonbleeding visible vessel within the ulcer base, high risk for rebleeding (Forrest classification … )
-PPI IV BID for 72 hours, PO BID for 2 weeks, and PO once daily for 6 weeks
-in cirrhotic, regardless of ascites, broad spectrum abx for 7 days is recommended
#hemorrhoids
Grade 1/2/3/4; anasol/prepH; surgery needed?
#upper GI bleed
NSAIDs should be discontinued in patients with NSAID-induced bleeding peptic ulcer disease; if treatment must be continued, a selective cyclooxygenase-2 inhibitor plus a once-daily proton pump inhibitor should be used.
Patients with peptic ulcer disease and low risk for rebleeding (clean-based ulcer, ulcers with pigmented spots) can start oral feeding within 24 hours of endoscopy, receive once-daily oral proton pump inhibitor therapy, and be discharged from the hospital.
Per the ACG-ACA Clinical Practice Guideline on Anticoagulants and Antiplatelets (AJG 2022), will continue aspirin in the setting of secondary prevention
#lower GI bleed
The duration of the anticoagulant effect of the direct oral anticoagulants (DOACs) is limited because of their short half-life; in most cases of gastrointestinal bleeding, simply holding the DOAC is sufficient
In hemodynamically stable patients without evidence of rapid lower gastrointestinal bleeding, colonoscopy is the first test of choice.
Although nuclear studies may be able to detect lower gastrointestinal bleeding, precise anatomic location is inferior to that provided by first-line diagnostic tests, such as colonoscopy, CT angiography, and conventional angiography
Per the ACG-ACA Clinical Practice Guideline on Anticoagulants and Antiplatelets (AJG 2022), will continue aspirin in the setting of secondary prevention
Management of warfarin in GI bleed:
In a patient with gastrointestinal bleeding, resuming anticoagulation within the first week after discontinuation minimizes risk for 90-day thrombosis, without increasing risk for 90-day recurrent gastrointestinal bleeding.
High bleed risk procedures (>2% in 30 days): polypectomy (>1cm), PEG/PEJ placement, ERCP with sphincterectomy, EMR/ESD, EUS-FNA, endoscopic hemostasis (excluding APC), radiofrequency ablation, POEM, treatment of varices, therapeutic balloon assisted enteroscopy, tumor ablation, cystogastrostomy, ampullary resection, pneumatic or bougie dilation, laser ablation and coagulation
Low/moderate risk bleeding procedures (<2% in 30days): EGD w/w/o bx, colonoscopy with/without biopsy, flex sig with/without bx, ercp with stent, eus w/o fna, push enteroscopy and diagnostic balloon assisted enteroscopy, enteral stent deployment, APC, balloon dilation of liminal stenoses, polypectomy <1cm, ercp without sphincterectomy, marking, video capsule endoscopy
Liver
#cirrhosis ascites
Discontinue ace/arb
Consider avoiding beta blocker/NSAIDs
#compensated cirrhosis
SAVE score: ___ (Liu et al, AJG 2022)
Last known HVPG: ____
#Decompensated cirrhosis
Patient with hx of cirrhosis secondary to ****. Decompensated due to complication (variceal hemorrhage, ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatocellular carcinoma, hepatorenal syndrome, or hepatopulmonary syndrome). MELD Score of ***.
-GI consulted; appreciate recommendations
-Abdominal ultrasound and possible paracentesis
-Cefotaxime 2g q8h, Ceftriaxone 2gm IV q24hfor empiric SBP coverage (given patient has temp >100.0, abd pain/tenderness, change in mental status, PMN>250)
-Furosemide/Bumex PO daily
-Lactulose 30ml PO daily (titrate to 3-4BM's)
- Rifaxamin 550mg PO BID
-Phenergan 25mg PO Q6HR PRN for nausea
-Pain control
-Counseled on importance of routine cardiovascular exercise as tolerated (Jamali et al, AJG 2022)
#Elevated liver-associated enzymes
Elevated to ****, indicating hepatocellular/cholestatic injury. Patient with symptoms of ****. No evidence of jaundice, hypotension or mental status change to suggest intraabdominal/biliary infection. History does not support acute toxin ingestion, APAP/salicylate overdose. DDx includes viral hepatitis, DILI, shock liver, biliary obstruction; less likely autoimmune or hereditary etiology.
- Obtain RUQUS with Doppler to r/o obstructing lesions
- Obtain Iron panel, ANA panel, CT Immuno panel, Acute and Chronic Viral hepatitis panels, alpha-1 antitrypsin, Immunoglobulins, Celiac panel on admit
-LAEs qAM
- Acute Viral Hepatitis Panel, HBV DNA, HCV RNA
- CMV IgG and PCR, EBV Total IgG/IgM and PCR, HSV 1/2 IgG and DNA, HIV
- Repeat RUQUS with Dopplers
- Acetaminophen level
- Toxicology panel (UDS), pEth
- IgG, anti-smooth muscle antibodies, anti-mitochondrial antibodies
- Trend CBC, BMP, LAE and INR daily
-Monitor closely for changes in mental status/lethargy, somnolence
History of alcohol or NAFLD?
Per ACG guideline on elevation of abnormal liver chemistries 2017:
Confirm liver chemistry is abnormal with repeat test
Testing for HCV: anti-HCV antibody, confirm with HCV RNA by NAAT
Testing for HBV: HBsAg; IgM anti-HBc
Testing for HAV: IgM HAV
Testing for HEV: IgM HEV if acute hepatitis and returning from endemic area and Hepatitis A, B, C are negative
Testing for hereditary hemochromatosis: in absence of acute hepatitis, iron level, transferrin saturation, serum ferritin; if transferrin saturation >45% and/or elevated ferritin, HFE genetic analysis
Testing for AH: ANA, ASMA, globulin level
Testing for Wilson's Disease: ceruloplasmin; if low, confirmatory testing with 24h urinary copper and slit-lamp exam
Testing for a1AT deficiency: a1AT phenotype
Prescription and OTC medications as possible culprits:
Elevated alk phos without hepatocellular enzymes
Check GGT
PBC testing: anti-mitochondrial antibody
PSC testing: MRCP or ERCP, IgG4
If ALT/AST <5x ULN: assess for HBV/HCV, alcoholic and NAFLD, hemochromatosis, Wilson's disease, a1AT, autoimmune hepatitis, and consider drug/supplement related injury
If ALT/AST 5-15x ULN: assess for acute HAV, HBV, HCV in addition to all etiologies above
If ALT/AST >15x ULN: assess for acetaminophen toxicity and ischemic hepatopathy in addition to all etiologies above
#Drug Induced Liver Injury
RECAM score ___
#elevated alkaline phosphatase
Rule out pregnancy, postprandial increase
GGT
RUQUS
Dilated = MRCP/ERCP
Non dilated = AMA
#Hepatocellular carcinoma
Patients with hepatocellular carcinoma who have well-compensated cirrhosis, no symptoms referable to liver disease, no evidence of portal hypertension, and normal liver function markers should be referred for surgical resection.
Liver transplantation for hepatocellular cancer is the best therapy for patients who also have portal hypertension or features of liver dysfunction
#hereditary hemochromatosis
Hereditary hemochromatosis is suggested by the presence of an elevated serum ferritin level and transferrin saturation.
The diagnosis of hereditary hemochromatosis is confirmed by testing for mutations in theHFEgene
In these patients, the diagnosis is suspected by finding elevated transferrin saturation greater than 45% (guidelines vary) and an elevated serum ferritin level; diagnosis is confirmed through genetic testing
#autoimmune hepatitis
The mainstay of treatment of autoimmune hepatitis is immunosuppression with prednisone or a combination of prednisone and azathioprine.
Because autoimmune hepatitis has a high rate of relapse, therapy is recommended for at least 2 to 3 years before discontinuation of the medications.
#hepatic sarcoidosis
The most appropriate diagnostic test to perform next is upper endoscopy (Option D). Granulomatous inflammation of the liver can result in portal hypertension, even in the absence of hepatic fibrosis. Hepatic sarcoidosis is an idiopathic condition that results in non-necrotizing granulomas. The organ most commonly affected by sarcoidosis is the lung, although the liver is also often affected. Most patients with hepatic sarcoidosis are asymptomatic; if symptoms do exist, they are typically mild and may consist of pruritus or abdominal pain due to hepatic capsule stretch. It is unclear whether immunosuppressive therapy affects the clinical course of hepatic sarcoidosis, and treatment is usually not initiated unless symptoms are severe or markers of liver inflammation are significantly abnormal. Conditions such as tuberculosis, fungal infections, brucellosis, Q fever, Hodgkin lymphoma, and drug toxicity can also cause granulomatous lesions in the liver, and steps should be undertaken to exclude these conditions before a diagnosis of sarcoidosis is accepted. The presence of skin or chest imaging findings typical of sarcoidosis also supports the diagnosis of hepatic sarcoidosis. Hepatic sarcoidosis rarely results in liver failure, but portal hypertension is common. Therefore, upper endoscopy to evaluate for esophageal varices is warranted, particularly in this patient with splenomegaly and thrombocytopenia
#drug induced liver injury
Drug-induced liver disease can result from exposure to prescription and nonprescription drugs as well as herbal and dietary supplements, even if the exposure occurred 6 months before symptom onset.
The most common cause of cholestatic hepatitis is drug-induced liver injury.
#concern for hepatorenal syndrome
The initial management of acute kidney injury in patients with cirrhosis is to stop diuretic therapy.
In patients with hepatorenal syndrome, β-blocker therapy should be discontinued
Consider terlipressin per CONFIRM trial; NNT HRS of ~6, NNH at 90 day mortality ~20
#sbp
Spontaneous bacterial peritonitis is diagnosed by an ascitic fluid neutrophil count of 250/μL (0.25 × 109/L) or higher.
Treatment of spontaneous bacterial peritonitis includes a third-generation cephalosporin; albumin is infused in the presence of hepatic (bilirubin level >4 mg/dL [68.4 μmol/L]) or kidney dysfunction
#Budd Chiari
Budd-Chiari syndrome is suggested by right-upper-quadrant abdominal discomfort, hepatomegaly, and ascites.
Budd-Chiari syndrome can be diagnosed with Doppler ultrasonography of the abdomen; it demonstrates absence of flow in the hepatic veins as well as hepatic congestion
Long-term anticoagulation is required in patients with Budd-Chiari syndrome, although bleeding risks are significant in patients with acute or chronic liver disease, portal hypertension, and esophageal varices. Angioplasty of the hepatic veins and/or placement of a transjugular intrahepatic portosystemic shunt (TIPS) can be used to reestablish adequate hepatic venous drainage. If liver failure develops, liver transplantation may be considered.
#Alcoholic hepatitis
fever, jaundice, tender hepatomegaly, and leukocytosis
Maddrey score:
Prednisolone is the treatment for severe alcoholic hepatitis, defined as a Maddrey discriminant function score of 32 or greater or the presence of hepatic encephalopathy.
Patients with alcoholic hepatitis treated with prednisolone who do not respond after 7 days should have the prednisolone discontinued; otherwise, prednisolone should be continued for 28 days.
The 2018 American College of Gastroenterology guideline on alcoholic liver disease makes a conditional recommendation against the use of pentoxifylline
#pyogenic liver abscess
In patients with pyogenic liver abscess, empiric broad-spectrum parenteral antibiotics that cover streptococci, enteric gram-negative bacilli, and anaerobes should be initiated.
Hepatic abscesses 3 cm or greater in diameter typically do not resolve with antibiotic therapy alone, and aspiration of the abscess by percutaneous needle approach is warranted.
CTX + flagyl
Serology for entameba histolytica
#HCC screening and cirrhosis
Patients with cirrhosis who have undergone virologic cure for hepatitis C virus infection should undergo surveillance for hepatocellular carcinoma every 6 months with ultrasonography.
No information indicates that the addition of α-fetoprotein (AFP) to ultrasonography screening for hepatocellular carcinoma leads to improved survival; therefore, surveillance using ultrasonography may be performed with or without AFP measurement every 6 months
Pancreas
#Pancreatitis
Revised Atlanta Classification 2012, 2 of 3: epigastric pain radiating to the back, lipase 3x ULN, CT findings
Etiology possibilities: EtOH, gallstone, hypercalcemia, HyperTG, ERCP, steroid induced, medication induced, trauma
-Per WATERFALL trial, 10ml/kg bolus if hypovolemic, then 1.5ml/kg/hr mIVF (NNH of aggressive fluid resuscitation is ~7 when compared to moderate as above)
-treatment of nausea/vomiting/pain with:
-zofran 4mg IV q6 PRN
-dilaudid 2mg IV q4 PRN
-Recheck labs (CBC, CMP) every 12 hours
-Transabdominal ultrasound to evaluate for fluid collections, evaluate the CBD (understanding mild dilation is to be expected with a post CCY patient)
-If concerning findings on US then consider abdominal CT or MRI pancreas
-resume oral feedings when pain improves and any nausea or vomiting subsides
-if oral feeding not tolerated, enteral feeding should be considered within 72 hours
#autoimmune pancreatitis
High dose prednisone 2-3 months
IgG4
#Walled off pancreatic necrosis
Per POINTER trial (NEJM 2021), early catheter drainage is not superior to delayed drainage
#Pancreatic serous cystadenoma
Mucin-producing cysts, including intraductal papillary mucinous neoplasms and mucinous cystic neoplasms, are thought to have malignant potential.
Non–mucin-producing cysts, such as a serous cystadenoma, have no malignant potential
#h pylori
For patients with dyspepsia, a “test and treat” strategy forHelicobacter pyloriinfection is recommended.
In a person from an area with a low prevalence ofHelicobacter pylori,a positive serologic result is likely a false positive and should be followed by a stool antigen test or a13C urea breath test.
#pancreatic pseudo cyst
Pancreatic pseudocysts are peripancreatic fluid collections that occur with acute pancreatitis and do not contain solid material or debris.
Pancreatic pseudocysts do not require drainage unless the patient is symptomatic or the pseudocysts become infected
Autoimmune
#Celiac disease
Iron deficient anemia, diarrhea, malabsorption, weight loss, failure to thrive, dermatitis herpetiformis
-GI symptoms began:
-Oral ulcers, rashes, neuropathy?
-family history of Celiac or other autoimmune disease?
-IgA TTG + total IgA level ordered; positive **/**/****
-if second test necessary: deaminated gliadin peptide antibodies
- patient instructed to continue gluten challenge for minimum 2 weeks prior to testing
-small bowel biopsy performed **/**/****
-HLA-DQ2 and HLA-DQ8 to rule out disease in borderline cases (100% sensitivity)
-CBC, ferritin, vitamin D/A, vitamin B12, LFTs, folate; zinc/copper, TSH, morning cortisol
-recommended family screening of 1st degree relatives
-DEXA:
-referred to dietician for gluten free diet; patient instructed to specify "celiac disease" instead of gluten free at restaurants
-follow up in 4-6 months for clinical improvement, recheck serology and vitamin deficiencies
-follow up serology in 12 months, and q1yr
-repeat biopsy in 24 months, repeat DEXA if abnormal
-patient counseled on importance of dietary compliance for symptom control and prevention of T cell lymphoma
-avoid ARBs, checkpoint inhibitors, mycophenolate mofetil, MTX
-consider autoimmune enteropathy, CVID, tropical sprue, Whipple disease
-symptoms not improving?
-correct diagnosis?
-inadvertent gluten? Review meds with pharmacist
-microscopic colitis? SIBO? Carb malabsorption? IBS/IBD?
#celiac disease, refractory
10% of patients with celiac disease and recurrent symptoms have a concurrent diagnosis. Conditions to consider include HIV infection, irritable bowel syndrome, small intestinal bacterial overgrowth, microscopic colitis, and pancreatic insufficiency
#ulcerative proctitis
Patients with ulcerative proctitis should receive topical therapy with 5-aminosalicylate suppositories; once remission is achieved, 5-aminosalicylates are effective in maintaining it.
Combined 5-ASA therapy (oral and topical) is superior for inducing remission in patients with left-sided or extensive ulcerative colitis compared with oral or topical therapies alone.
#PSC
Primary sclerosing cholangitis (PSC) is associated with inflammatory bowel disease (IBD) in approximately 85% of cases; therefore, all patients with PSC without known IBD should have colonoscopy with biopsies at the time of PSC diagnosis.
Patients with PSC have a 15% lifetime risk for cholangiocarcinoma; annual or biannual magnetic resonance cholangiopancreatography and carbohydrate antigen 19-9 measurement is recommended for cholangiocarcinoma surveillance
There is also an increased risk for gallbladder cancer in PSC, and regular annual screening with ultrasonography is recommended
Liver transplantation (Option D) should be considered for patients with PSC and decompensated cirrhosis, recurrent bacterial cholangitis, and hilar cholangiocarcinoma
Transplant outcomes for patients with PSC are excellent, with 1-year survival rates of at least 90% and recurrence rates of approximately 20% at 5 years after liver transplantation
#crohn disease
An anti–tumor necrosis factor agent is most likely to induce and maintain remission of moderate to severe ileocolonic Crohn disease resistant to glucocorticoids or immunomodulators.
Combination therapy with an anti–tumor necrosis factor and an immunomodulator is more efficacious than monotherapy with either agent alone in achieving glucocorticoid-free remission and mucosal healing in moderate to severe Crohn disease
#ulcerative colitis
Combination therapy with infliximab and azathioprine is more efficacious than monotherapy with either agent alone in achieving glucocorticoid-free remission and mucosal healing in ulcerative colitis.
Before initiation of anti–tumor necrosis factor agents, patients should undergo testing for latent tuberculosis and hepatitis B virus infection
#UC flare
Labwork ordered: CMP, CBC, Pre-albumin, ESR, CRP, Total cholesterol, TPMT Enzyme, Quantiferon, Stool culture, C. Diff PCR, CMV PCR, GI PCR, Iron saturation
- Abdominal series ordered
- GI consult in AM to schedule flexible sigmoidoscopy. Greatly appreciate recs
- Record: # stools, # with stool blood, urgency time, signs of toxicity
- IV fluids to produce clear urine, goal output >50 cc/hr x > 8 hours: goal >5L in 1st 24 hours
- patient will be made NPO
- IV steroids
- can consider rectal Messalamine if appropriate
#left sided UC
5-Aminosalicylate enemas are an appropriate and effective treatment for mild, left-sided ulcerative colitis.
5-Aminosalicylate suppositories are an appropriate and effective treatment for mild to moderate ulcerative proctitis
#elevated LFTs in UC
Cholestatic? Get an MRCP. Normal? Get a liver biopsy for small duct PSC
Biliary
#Choledocholithiasis
2019 ASGE Guidelines
Cancer
#Lynch syndrome
Consider 600mg daily aspirin per CAPP2 trial, number needed to prevent colorectal cancer at 10 years of ~25
Symptoms
#Nausea and vomiting
-Zofran 4mg IV Q4 PRN
-Compazine 10mg Q6
-EKG x 1 to evaluate QTc
#Constipation
-Senna 8.6mg PO QHS
-Miralax 17g in 8oz water PRN for constipation
#constipation
Constipation can be secondary or functional (idiopathic); medications are the most common cause of secondary constipation.
Colonoscopy is the initial evaluation of constipation in elderly patients with acute constipation and patients with unintentional weight loss, family history of colorectal cancer, unexplained anemia, and age older than 50 years with no previous colonoscopy
Medications are the most common cause of secondary constipation. Other causes of this common condition include mechanical obstruction, systemic illnesses, altered physiologic states, and psychosocial conditions. Once secondary causes have been excluded, chronic constipation is considered functional. Functional constipation is subtyped into categories of slow transit, normal transit, or dyssynergic defecation. Slow-transit constipation is defined as the delayed passage of fecal contents through the colon based on objective transit testing. Normal-transit constipation is functional constipation in which colonic transit times are adequate. Dyssynergic defecation refers to difficulty with or inability to expel stool as a result of some combination of abnormalities in contraction and/or relaxation of the muscles of the pelvic floor during defecation
Colonoscopy is the initial evaluation of constipation in elderly patients with acute constipation and patients with unintentional weight loss, family history of colorectal cancer, unexplained anemia, and age older than 50 years with no previous colonoscopy. This patient is age 52 years, and colonoscopy should be performed as the initial study to evaluate for mechanical causes of constipation.
Treatment options for chronic constipation include serotonergic prokinetic agents (prucalopride [Option B]), bulking agents (psyllium [Option C]), stimulant laxatives (senna, bisacodyl), osmotic laxatives (polyethylene glycol, lactulose, sorbitol), stool softeners (docusate), secretagogues (lubiprostone, linaclotide, plecanatide), and/or biofeedback. These therapeutic modalities are appropriate after evaluation for a cause of constipation.
Physiologic testing, including colon transit testing with a radiopaque marker study (Option D), scintigraphy, or the wireless motility capsule, is reserved for patients with constipation symptoms that do not respond to initial trials of lifestyle modification and laxative therapy.
Motility
#ileus
Etiology: surgery, inflammation, hematoma, hypokalemia, hypomagnesemia, medication (opioid, anticholinergic)
Treatment: NPO, NG tube set to continuous wall suction, IVF, aggressive electrolyte repletion (K>4), avoidance of opioids and anticholinergics
#IBS
The diagnosis of irritable bowel syndrome requires symptoms of recurrent abdominal pain at least 1 day a week for 3 months, along with at least two of the following: pain related to defecation, change in stool frequency, or change in stool consistency.
Fecal calprotectin testing to assess for inflammatory bowel disease and stool testing for giardiasis and celiac disease should be considered in patients with chronic diarrhea
#SIBO
Causes of fat malabsorption include pancreatic dysfunction, infections (e.g., giardiasis and Whipple disease), celiac disease, tropical sprue, and small intestinal bacterial overgrowth.
Small intestinal bacterial overgrowth can be diagnosed in the appropriate clinical context with both typical symptoms (abdominal discomfort, flatulence, bloating, and diarrhea) and a positive result on a glucose breath test
#osmotic diuresis
Chronic diarrhea can be classified as osmotic, secretory, steatorrhea, inflammatory, motility, or miscellaneous
In patients with liquid stool, a calculated osmotic gap of greater than 100 mOsm/kg suggests osmotic diarrhea.
The fecal osmotic gap is calculated as follows: 290 – (2 × [stool sodium + stool potassium]).
#achalasia
Achalasia is associated with dysphagia with both solids and liquids, along with nonacidic regurgitation of undigested food.
Achalasia treatment includes botulinum toxin injection, pneumatic balloon dilation, peroral endoscopic myotomy, or laparoscopic myotomy
#dumping syndrome
Dumping syndrome results from rapid gastric emptying after gastric surgery; symptoms can include abdominal pain, epigastric fullness, diarrhea, nausea, vomiting, borborygmi, and bloating.
First-line treatment of dumping syndrome is smaller, more frequent meals.
Classic vasomotor symptoms can include palpitations and tachycardia, faintness or syncope, diaphoresis, and flushing and pallor. Symptoms typically occur within 1 hour of eating. Treatment should be tiered, beginning with dietary modifications and patient education by a trained dietitian. Dietary interventions can include the pursuit of smaller and more frequent meals (at least six per day); delayed intake of fluids by at least 30 minutes after intake of solids; avoidance of rapidly absorbable carbohydrates and alcohol; increased intake of high-fiber, high-protein foods; and lying down after a meal for 30 minutes. The use of dietary supplements, such as guar gum or pectin, to increase food viscosity can also be helpful.
Pharmacologic interventions can be considered when the previously mentioned measures fail, although no pharmacologic treatment has been approved for dumping syndrome
Abdominal pain
#diverticulitis
Uncomplicated diverticulitis is treated with oral antibiotics (ciprofloxacin or metronidazole) and a liquid diet.
Hospitalization and intravenous antibiotics are required to treat acute diverticulitis in patients who cannot tolerate an oral diet; patients with severe comorbidities, advanced age, or immunosuppression; and patients for whom oral antibiotics have been ineffective
CTX+flagyl
Zosyn
Merrem
>2-3 years since last CSP, per guidelines, should have repeat after resolution of inflammation to evaluate for obstruction/malignancy
Peritonitis/persistent sepsis —> surgery
Diverticulitis
“Immunocompetent patients not requiring hospitalization and without evidence of significant inflammation, who are not medically frail, able to tolerate oral intake, and with adequate follow-up capabilities, can safely avoid a course of antibiotics and the potential adverse effects associated with antibiotics, including but not limited to the disruption of their microbiome
“Clinicians should treat with antibiotics when the patient has complicated diverticulitis, has comorbid unstable conditions, is immunosuppressed, or has signs of a systemic inflammatory response
Internists could also initially treat with antibiotics when symptoms have lasted longer than five days, the patient cannot tolerate oral intake, and he or she has other significant comorbidities, said Dr. Lin. “Also, patients who initially are managed with conservative care who do not improve or who have new or worsening symptoms should be started on antibiotics.”
Ciprofloxacin with metronidazole is probably the most commonly used antibiotic regimen for patients with diverticulitis, and amoxicillin and clavulanic acid is a reasonable single agent,
Per DINAMO trial, supportive therapy non inferior to antibiotics at 90 days for mild acute diverticulitis
Mora-López L, Ruiz-Edo N, Estrada-Ferrer O, et al; DINAMO-study Group. Efficacy and safety of nonantibiotic outpatient treatment in mild acute diverticulitis (DINAMO-study): a multicentre, randomised, open-label, noninferiority trial. Ann Surg. 2021;274:e435-e442. [PMID: 34183510] doi:10.1097/SLA.0000000000005031
Per AJG 2017:An average red meat intake of less than 51 g/d, dietary fiber intake of about 23 g/d, roughly two hours of vigorous physical activity weekly, a normal body mass index, and never smoking were associated with lower diverticulitis incidence in men
-Liu PH, Cao Y, Keeley BR, et al. Adherence to a healthy lifestyle is associated with a lower risk of diverticulitis among men. Am J Gastroenterol. 2017;112:1868-1876. [PMID: 29112202] doi:10.1038/ajg.2017.398
#narcotic bowel syndrome
Narcotic bowel syndrome is characterized by paradoxical worsening of abdominal pain despite dose escalation; complete cessation of narcotic use is the only effective treatment
Malignancy:
#Peutz Jeugers
The diagnosis of Peutz-Jeghers syndrome (PJS) is based on the presence of two of the following three criteria: two or more PJS-type hamartomatous polyps in the gastrointestinal tract; multiple melanotic macules in the mouth, buccal mucosa, nose, eyes, genitalia, or fingers; and family history of PJS.
#Fundic gland polyps
Fundic gland polyps are the most common benign epithelial gastric polyp and require no endoscopic follow-up.
#Gastric ulcer
Routine repeat upper endoscopy for gastric ulcer is not recommended.
Repeat upper endoscopy for gastric ulcer is reasonable for ulcers that appear suspicious for malignancy, ulcers that were not biopsied originally, ulcers with an unclear cause, or continued symptoms despite adequate therapy
#Gastric metaplasia
Gastric intestinal metaplasia is a premalignant condition; patients have up to a 10-fold increased risk for gastric cancer compared with the general population
#Hepatic adenoma
Factors posing an increased risk for malignant transformation of hepatic adenomas include adenomas greater than 5 cm in diameter, adenomas with β-catenin activation, or adenomas found in men.
Oral contraceptives should be discontinued in women with hepatic adenomas with follow-up CT or MRI at 6-month intervals to confirm stability or regression in the size of the lesion
Hepatobiliary:
#Acute cholecystitis
Acute cholecystitis can be diagnosed by ultrasonography showing gallbladder wall thickening and/or edema and a positive Murphy sign elicited during ultrasonography.
Treatment of acute cholecystitis includes analgesia, intravenous antibiotics with gram-negative and anaerobic coverage, and cholecystectomy before hospital discharge.
Vascular
#Chronic mesenteric ischemia
The diagnosis of chronic mesenteric ischemia requires exclusion of alternative causes of postprandial abdominal pain and weight loss, along with compatible imaging findings.
CT or magnetic resonance angiography findings suggesting chronic mesenteric ischemia include severe stenosis (>70%) of two of the three mesenteric arteries
#Acute mesenteric ischemia
Early acute mesenteric ischemia most commonly presents with abrupt onset of severe periumbilical abdominal pain followed by the urge to defecate and an unremarkable abdominal examination.
CT angiography is the recommended imaging modality for the diagnosis of acute mesenteric ischemia
#Colonic ischemia
Colonic ischemia is the most common form of ischemic bowel disease and usually results from a nonocclusive low-flow state in microvessels.
Colonic ischemia presents with abrupt-onset lower abdominal discomfort and cramping, followed within 24 hours by hematochezia
Abdominal CT is indicated to assess the severity, phase, and distribution of colonic ischemia. CT findings are nonspecific, including segmental bowel wall thickening and pericolonic fat stranding, often in the distribution of the “watershed” areas of the colon (splenic flexure and rectosigmoid junction). Colonoscopy is the primary method to diagnose colonic ischemia, usually after CT has shown a thickened segment of colon.
#Unintentional weight loss
Consider EGD. PMID 28350752. 46% of patients with weight loss and GI symptoms had abnormalities on EGD.
Dysphagia
Solid or liquid?
Oropharyngeal or esophageal?
-coughing, gagging, point to where it gets stuck
History of eosinophilia?
Pill esophagitis?
History of GERD?
Anemia? Consider Plummer Vinson test
EOE
>15 eosinophil per hpf