I. What every physician needs to know.
Peptic ulcer disease is a common world-wide problem. It manifests as a break in the gastrointestinal mucosa that extend through the muscularis propria. It mainly occurs in the stomach and proximal duodenum. Certain other sites like esophagus, distal duodenum, jejunum and ileum may be affected in hypersecretory states (like Zollinger-Ellison syndrome), ectopic gastric mucosa (Meckel’s diverticulum), hiatal hernia etc. Most ulcers are caused by Helicobacter pylori infection or use of Non-steroidal anti-inflammatory drugs (NSAID’s). Despite common misconception in the general public there is no evidence of any link to spicy foods or stressful lifestyles.
II. Diagnostic Confirmation: Are you sure your patient has Peptic Ulcer Disease?
Patients with PUD present with a variety of symptoms. A significant proportion is asymptomatic and presents with complications like bleeding or perforation. The gold standard for diagnosis of peptic ulcers is upper gastrointestinal endoscopy (EGD). A barium swallow and upper GI series can be used in patients who are not a candidate or refuse EGD. Other imaging modalities like Abdominal computed tomography (CT) scan (with PO contrast) can sometimes identify stomach ulcers. Often the diagnosis is confirmed intra-operatively especially when a patient presents with perforation.
Forty four percent of NSAID use can be surreptitious and is detected by measuring platelet cyclooxygenase activity. Other medications, such as glucocorticoids, cytotoxic agents, alendronate, and cocaine, may also contribute to PUD or affect ulcer healing. See Figure 1.
A. History Part I: Pattern Recognition:
The most common symptom is epigastric pain which typically occurs in between meals but can occur at any time of the day. Sometimes the pain can be localized to left upper quadrant (proximal stomach ulcers) or right upper quadrant (duodenal ulcers). The pain is described as “burning” or “gnawing” though some patients present with a vague, diffuse abdominal pain. Relief with food or antacids is another characteristic feature. The classic duodenal ulcer–associated pain occurs 2 to 5 hours after a meal when acid is secreted in the absence of a food buffer and at night between 11 PM and 2 AM when circadian stimulation of acid secretion is maximal.
Other common symptoms are nausea, vomiting, heartburn and decreased appetite. Bleeding ulcers can present with hematemesis, melena, fatigue, dizziness or syncope. A perforated ulcer can present with an acute abdomen.
“Alarm features” or “red flags” can suggest malignant ulcers and need early endoscopy. These are:
Age older than 55 years with new-onset dyspepsia
Family history of GI malignancy
Unintended weight loss
Unexplained iron-deficiency anemia
Palpable mass or lymphadenopathy
B. History Part 2: Prevalence:
The most important risk factors for PUD are use of NSAID’s, H. pylori infection and smoking. Together these three account for 89%-95% of serious adverse events associated with PUD. Genetic factors play a role as well. First-degree relatives of patients with Duodenal or Gastric Ulcer have a threefold increase in the prevalence of similar ulcer. Rarely a hypersecretory tumor like gastrinoma is the cause (Zollinger-Ellison syndrome). A fasting serum gastrin level should be checked for diagnosis. Hypercalcemia may also cause ulcers. They may occur with primary hyperparathyroidism alone or in conjunction with gastrinoma in the MEN syndrome. Patients with PUD should have a calcium level for screening. Idiopathic acid hypersecretion also needs to be considered, which is defined as a condition with high basal acid output of 10 mEq/hr, with a normal basal serum gastrin or a negative secretin test.
The so called “stress ulcers” prevalent in ICU patients have two main risk factors – mechanical ventilation >48 hours and coagulopathy. There is no evidence of increased risk with stress, alcohol, caffeine, aspirin substitutes, spicy foods or salt. Glucocorticoids alone have not been shown to be ulcerogenic but increase the chances of having an ulcer when other risk factors are present (e.g., NSAID’s). The highest risk for PUD among NSAIDs is for ketorolac (RR 14.4, 95% CI 5.2–39.9)
C. History Part 3: Competing diagnoses that can mimic Peptic Ulcer Disease.
Functional (non-ulcer) dyspepsia: Difficult to distinguish based on clinical features alone. Needs EGD to document absence of ulcers.
Malignancy: mainly gastric, esophageal, pancreatic, or hepatic. Other abdominal malignancies like colon cancer and lymphoma can rarely present with similar symptoms.
Pancreatitis: epigastric pain radiating to the back; elevated pancreatic enzymes.
Gastroparesis: history of diabetes or other autonomic neuropathy, abdominal bloating after meals +/- vomiting of undigested food particles.
Biliary colic: abnormal LFT’s, abnormal RUQ imaging.
Inflammatory bowel disease: most often Crohn’s disease.
Ischemic bowel disease: pain is usually ill-defined and diffuse, risk factors for atherosclerosis.
Toxins/metabolic disorders: lead poisoning, acute intermittent porphyria.
D. Physical Examination Findings.
Patients with uncomplicated PUD do not have many physical findings. Epigastric tenderness on palpation is often elicited but is unreliable. One should look for signs of weight loss (temporal wasting, loose clothes), anemia (conjunctival pallor), bleeding (melena, tachycardia, orthostatic changes in blood pressure or pulse rate), gastric outlet obstruction (succussion splash) and perforation (involuntary guarding, rebound tenderness, absent bowel sounds).
E. What diagnostic tests should be performed?
Endoscopy is the study of choice for diagnosis of peptic ulcers. Upper gastrointestinal barium studies are still used in primary care. There is convincing evidence that endoscopy provides much better diagnostic accuracy in detecting ulcers. Another advantage of endoscopy is that biopsy of the ulcer could be obtained to exclude malignancy. It also permits biopsies to be taken to detect H. pylori status (rapid urease testing). Endoscopy also helps in determining ulcer size as some studies suggest that large and small gastric ulcers heal at same rate of 3 mm per week.
There is some evidence that endoscopy may improve patient satisfaction scores and reduce health care utilization in cases of previously uninvestigated dyspepsia (if endoscopy is negative).
Certain tests can help in differentiating other causes of upper abdominal pain from PUD. For example, lipase (pancreatitis), LFT’s (cholangitis). Serial hemoglobin levels may be useful if bleeding from the ulcer is suspected.
Imaging modalities like RUQ ultrasound and CT scan of abdomen may be useful to rule out cholelithiasis and abdominal malignancy.
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Once the diagnosis of ulcer is established, the H. pylori status should be evaluated. There are various endoscopic and non-endoscopic tests available for detection of H. pylori infection.
For practical purposes there are two tests available on endoscopic biopsy specimen for H. pylori: histology and rapid urease testing (RUT). Histology is considered a “gold standard” but its accuracy depends upon a number of issues including the site, number, and size of gastric biopsies, method of staining, and the level of experience of the examining pathologist. The RUT has good sensitivity and specificity. The results are available within 24 hours in most cases. Its sensitivity is reduced in post-treatment specimens. Both histology and RUT are affected by use of PPI’s, antibiotics and bismuth containing compounds. Patients should be off PPI for 1-2 weeks and off antibiotics or bismuth containing compounds for 4 weeks prior to these tests. If this is not possible then a second test should be used to improve sensitivity (e.g., antibody testing or urease breath test).
The non-endoscopic tests are Antibody testing in serum, urea breath test (UBT) and fecal antigen test (FAT). Antibody testing is inexpensive and widely available but its PPV (positive predictive value) is decreased in low prevalence populations (like North America). It is also unreliable for documenting eradication. It should only be used as an adjunct to endoscopic testing in patients who have not been able to stop PPI or antibiotics for the required time before the biopsy. UBT has excellent PPV and NPV (negative predictive value) irrespective of prevalence and is the best test for documenting eradication after treatment for H. pylori. The FAT has similar PPV and NPV as UBT and is a reliable predictor of eradication.
UBT should be performed as early during hospitalization as possible, as the sensitivity decreases with the increasing duration of antisecretory therapy. In patients treated for H. pylori, eradication should be confirmed 4 or more weeks after completion of eradication therapy to reduce the risk of recurrence of complications.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Barium follow-through is sometimes used in primary care (especially rural areas with poor access to EGD). The AGA guidelines on investigation of dyspepsia specifically advice against using radiographic studies to diagnose PUD.
For PUD-related complications, such as perforation leading to air leak, phlegmon, abscess, wall pathology, and adjoining inflammation, spiral CT with 64 slice scanner, which allows entire abdomen to be scanned in a single breath hold is more superior to ultrasound.
F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.
Many people use the serum antibody test for H. pylori to prove eradication. It has poor reliability for documenting eradication and can be positive for up to a year after therapy. Instead the UBT or FAT should be used to document eradication.
III. Default Management.
Identify and treat any complications like bleeding/perforation/penetration/obstruction.
All gastric ulcers should be promptly biopsied to exclude malignancy. Duodenal ulcers are usually biopsied if they fail to heal with anti-secretory and H. pylori eradication therapy.
Stop any potential offending medications, such as NSAID’s, glucocorticoids, chemotherapy.
Test for H. pylori status. If a biopsy has been obtained then a RUT or histology should be performed. Add a non-endoscopic test if the patient has used antibiotics or bismuth compounds in past 4 weeks or a PPI in past 1–2 weeks.
If positive for H. pylori then institute eradication therapy.
– First line therapy consists of standard dose PPI twice daily + clarithromycin 500mg B.I.D., + amoxicillin 1000 mg B.I.D. for 14 days. For penicillin allergic patients substitute metronidazole for amoxicillin.
– Second line therapy for treatment failure consists of Bismuth subsalicylate 525 mg p.o. q.i.d. + metronidazole 250 mg p.o. q.i.d. + tetracycline 500 mg p.o. q.i.d. + standard dose PPI (q.d. or b.i.d.) for 14 days.
For truly H. pylori negative ulcers anti-secretory therapy should be given for 4–6 weeks (H2B or PPI).
Though no consensus exists there is widespread practice of repeat endoscopy in 6–8 weeks following therapy for gastric ulcers. Duodenal ulcers are usually benign and do not need repeat endoscopy if symptoms have resolved.
A. Immediate management.
Most of the patients who need hospitalization need so for one of the complications arising from PUD (e.g., bleeding, obstruction etc) and should be managed accordingly. There also validated prognostic scales available for risk stratification such as the Rockall score, Blatchford score or AIMS65 score.
A careful history and examination can help exclude other causes of upper abdominal pain like pancreatitis, biliary colic, gastroparesis etc.
For uncomplicated PUD – Patient should be kept NPO pending decision for EGD which is recommended within 24 hours of presentation. IV fluid boluses should be used to correct hypovolemia due to vomiting/decreased PO intake. Anti-secretory agents (PPI) should be started. IV formulations can be used while the patient is NPO. There is debate about continuous versus intermittent dosing of PPI IV as a 2014 meta-analysis found intermittent administration to be non-inferior to high dose continuous infusion which could decrease resource utilization and cost. Patients who fail endoscopic therapy should be offered transarterial angiographic embolization by interventional radiology rather than surgery as next step.
A meta-analysis of 10 studies found that predictors of recurrent bleeding included active bleeding at endoscopy, large ulcer (>2 cm), posterior duodenal ulcer, and gastric ulcers at the lesser curvature.
For treating pain NSAID’s should be avoided and opiates should be preferred. In patients with uncomplicated duodenal ulcers, the PPI given for 14 days along with eradication therapy for H. pylori is usually adequate in healing. Given low risk of malignancy in patients with duodenal ulcers, a repeat upper endoscopy is not routinely recommended after initial treatment unless symptoms do not resolve or recur.
In patients with complicated duodenal ulcers and in patients with gastric ulcers, PPI up to 8 weeks and 12 weeks respectively should be considered. In patients with gastric ulcers, PPI therapy should only be discontinued after repeat upper endoscopy at 12 weeks.
NSAID induced ulcers should be treated with PPI for minimum of eight weeks. PPIs heal NSAID induced ulcers more effectively as compared to H2RAs, so should be used preferentially.
In patients with Non-H. pylori and Non-NSAID ulcers up to 8 weeks of PPI therapy is suggested and even long term acid suppression is considered as the risk of recurrence is higher.
B. Physical Examination Tips to Guide Management.
Monitoring vital signs and serial abdominal exams are necessary to rule out occult upper GI bleed, perforation or obstruction. Orthostatic changes in BP/HR can be a useful sign to assess intravascular volume depletion. Rectal exam should be done to rule out melena and get a sample for fecal occult blood.
C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.
The response has to be monitored clinically. There is no specific laboratory test to assess response to treatment in uncomplicated PUD.
D. Long-term management.
Eradication of H. pylori and avoidance of NSAIDs are the mainstay of long term management. Smoking cessation and limiting alcohol intake should be stressed.
Long term maintenance therapy with PPIs should be considered for following high risk patients: giant ulcer (>2cm), age >50 or multiple comorbidities, Non-H. pylori and Non-NSAID ulcer, failure to eradicate H. pylori, greater than 2 recurrences of PUD in a year, continued NSAID use.
E. Common Pitfalls and Side-Effects of Management
Failure to recognize complications like bleeding, perforation etc.
Failure to check for H. pylori and provide eradication therapy.
IV. Management with Co-Morbidities
During pregnancy, treat with older PPIs, such as omeprazole and pantoprazole, but typically H. pylori eradication is deferred until after delivery.
A. Renal Insufficiency.
Some H2B (e.g., famotidine) need dose reduction or increase in dosing interval in renal failure (CrCL <50 ml/min).
B. Liver Insufficiency.
Certain PPI’s (e.g., esomeprazole) need dose reduction in severe liver failure (Child-Pugh Class C).
C. Systolic and Diastolic Heart Failure
Careful attention should be paid to volume status during fluid resuscitation/maintenance therapy to avoid pulmonary edema.
D. Coronary Artery Disease or Peripheral Vascular Disease
Patients with known PUD (current or prior) who are on prophylactic aspirin (including low dose) or clopidogrel are classified as high risk for GI toxicity of NSAID’s. In these patients alternatives to NSAID’s should be used.
For patients who need to continue aspirin or clopidogrel a PPI can be used to decrease incidence of GI bleeding. There is some concern about lowered efficacy of antiplatelet agents due to PPI but the benefit of reduced GI complications far outweighs the risk of increased cardiovascular events.
E. Diabetes or other Endocrine issues
No change in standard management.
No change in standard management.
G. Immunosuppression (HIV, chronic steroids, etc.).
Patients using chronic steroids in addition to NSAID’s are at increased risk of developing peptic ulcers. These patients should be tested for H. pylori and treated if positive.
In such patients if there is a history of previous complicated ulcer then a COX-2 inhibitor (like celecoxib) should be used in conjunction with a PPI or misoprostol (400–600 mcg daily in divided doses).
If the patients have a history of uncomplicated ulcer then unselective NSAID’s could be used in conjunction with PPI or misoprostol.
H. Primary Lung Disease (COPD, Asthma, ILD)
No change in standard management.
I. Gastrointestinal or Nutrition Issues
Avoid smoking and excessive alcohol.
J. Hematologic or Coagulation Issues
Anticoagulants pose a significant risk for GI bleeding. The risk is increased even more with concomitant use of NSAIDs. As such their use together should be avoided as much as possible. In the event both have to be used together an H. pylori test and treat regimen should be followed. For long term NSAID use in these patients, addition of a PPI or misoprostol would lead to reduction in GI toxicity.
For patients with recent resolved upper gastrointestinal bleed who have been tested and treated for H. pylori the risk of recurrent bleed is not increased with warfarin. As such in these patients warfarin can be resumed if indicated.
K. Dementia or Psychiatric Illness/Treatment
No change in standard management.
V. Transitions of Care
A. Sign-out considerations While Hospitalized.
B. Anticipated Length of Stay.
The length of stay depends on presence or absence of complications. For most admissions for uncomplicated PUD a LOS of 1–2 days is sufficient.
C. When is the Patient Ready for Discharge.
For uncomplicated PUD as soon as the presenting symptoms are resolved (e.g., abdominal pain, vomiting etc) patient can be discharged.
D. Arranging for Clinic Follow-up.
1. When should clinic follow up be arranged and with whom.
Patients should follow up with either a gastroenterologist or a primary care physician within 2 weeks to discuss results of biopsy (if taken), H. pylori testing (if not known at time of discharge) and need for repeat EGD (for gastric ulcers).
2. What tests should be conducted prior to discharge to enable best clinic first visit.
H. pylori testing should be performed in all patients diagnosed with PUD.
3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.
E. Placement Considerations.
F. Prognosis and Patient Counseling.
The prognosis is usually good in patients with uncomplicated peptic ulcers. For the vast majority of patients 8 to 12 weeks of anti-secretory therapy is sufficient to heal the ulcers.
Ulcers which do not heal even with 8-12 weeks of potent anti-secretory therapy (full dose PPI) are considered as “refractory ulcers”. The most common causes for refractory ulcers are persistent H. pylori infection, continued use of NSAID’s, giant ulcers (>2–3 cm in size), malignancy and hypersecretory states (ZE syndrome).
Given the many benefits of smoking cessation, patients should be advised to stop smoking and limit alcohol use to one alcoholic beverage per day.
If these causes have been excluded then prolonged maintenance therapy with a PPI should be continued till response is achieved.
Elective surgery for refractory peptic ulcers is an option but is rarely done nowadays.
VI. Patient Safety and Quality Measures.
A. Core Indicator Standards and Documentation.
B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.
H. pylori testing and treatment, avoiding use of NSAIDs.
VII. What’s the Evidence?
” in peptic ulcer disease. NIH Consensus Development Panel on Helicobacter pylori in peptic ulcer disease”. JAMA. vol. 272. 1994. pp. 65
Malfertheiner, P, Megraud, F, O’Morain, C. “Current concepts in the management of infection: the Maastricht III consensus report”. Gut. vol. 56. 2007. pp. 772
Marshall, BJ, Goodwin, CS, Warren, JR. “Prospective double-blind trial of duodenal ulcer relapse after eradication of “. Lancet. vol. 2. 1988. pp. 1437
Chiorean, MV, Locke, GR, Zinsmeister, AR. “Changing rates of testing and treatment in patients with peptic ulcer disease”. Am J Gastroenterol. vol. 97. 2002. pp. 3015
Li, LF, Chan, RL, Lu, L. “Cigarette smoking and gastrointestinal diseases: the causal relationship and underlying molecular mechanisms (review)”. Int J Mol Med. vol. 34. 2014. pp. 372
Gudmand-Høyer, E, Jensen, KB, Krag, E. “Prophylactic effect of cimetidine in duodenal ulcer disease”. Br Med J. vol. 1. 1978. pp. 1095
Gisbert, JP, Pajares, JM. “Systematic review and meta-analysis: is 1-week proton pump inhibitor-based triple therapy sufficient to heal peptic ulcer?”. Aliment Pharmacol Ther. vol. 21. 2005. pp. 795
Lam, SK, Ching, CK, Lai, KC. “Does treatment of with antibiotics alone heal duodenal ulcer? A randomised double blind placebo controlled study”. Gut. vol. 41. 1997. pp. 43
Sung, JJ, Chung, SC, Ling, TK. “Antibacterial treatment of gastric ulcers associated with “. N Engl J Med. vol. 332. 1995. pp. 139
Buckley, M, Culhane, A, Drumm, B. “Guidelines for the management of -related upper gastrointestinal diseases”. Ir J Med Sci. vol. 165. 1996. pp. 1
” eradication therapy in dyspeptic disease: A clinical guideline”. 1996.
Gisbert, JP, Khorrami, S, Carballo, F. “Meta-analysis: eradication therapy vs. antisecretory non-eradication therapy for the prevention of recurrent bleeding from peptic ulcer”. Aliment Pharmacol Ther. vol. 19. 2004. pp. 617
Gisbert, JP, Calvet, X, Feu, F. “Eradication of for the prevention of peptic ulcer rebleeding”. Helicobacter. vol. 12. 2007. pp. 279
Lai, KC, Lam, SK, Chu, KM. “Lansoprazole for the prevention of recurrences of ulcer complications from long-term low-dose aspirin use”. N Engl J Med. vol. 346. 2002. pp. 2033
McColl, KE. “How I manage -negative, NSAID/aspirin-negative peptic ulcers”. Am J Gastroenterol. vol. 104. 2009. pp. 190
Dammann, HG, Walter, TA. “Efficacy of continuous therapy for peptic ulcer in controlled clinical trials”. Aliment Pharmacol Ther. vol. 7. 1993. pp. 17
Bianchi Porro, G, Parente, F. “Long term treatment of duodenal ulcer. A review of management options”. Drugs. vol. 41. 1991. pp. 38
Lauritsen, K, Andersen, BN, Laursen, LS. “Omeprazole 20 mg three days a week and 10 mg daily in prevention of duodenal ulcer relapse. Double-blind comparative trial”. Gastroenterology. vol. 100. 1991. pp. 663
Penston, JG, Wormsley, KG. “Review article: maintenance treatment with H2-receptor antagonists for peptic ulcer disease”. Aliment Pharmacol Ther. vol. 6. 1992. pp. 3
Penston, JG. “A decade of experience with long-term continuous treatment of peptic ulcers with H2-receptor antagonists”. Aliment Pharmacol Ther. vol. 7. 1993. pp. 27
Mahadevan, U, Kane, S. “American gastroenterological association institute technical review on the use of gastrointestinal medications in pregnancy”. Gastroenterology. vol. 131. 2006. pp. 283
Golberg, D, Szilagyi, A, Graves, L. “Hyperemesis gravidarum and infection: a systematic review”. Obstet Gynecol. vol. 110. 2007. pp. 695
Mansour, GM, Nashaat, EH. “Role of in the pathogenesis of hyperemesis gravidarum”. Arch Gynecol Obstet. vol. 284. 2011. pp. 843
Nikfar, S, Abdollahi, M, Moretti, ME. “Use of proton pump inhibitors during pregnancy and rates of major malformations: a meta-analysis”. Dig Dis Sci. vol. 47. 2002. pp. 1526
Marshall, JK, Thompson, AB, Armstrong, D. “Omeprazole for refractory gastroesophageal reflux disease during pregnancy and lactation”. Can J Gastroenterol. vol. 12. 1998. pp. 225
Plante, L, Ferron, GM, Unruh, M, Mayer, PR. “Excretion of pantoprazole in human breast”. J Reprod Med. vol. 49. 2004. pp. 825
Nava-Ocampo, AA, Velázquez-Armenta, EY, Han, JY, Koren, G. “Use of proton pump inhibitors during pregnancy and breastfeeding”. Can Fam Physician. vol. 52. 2006. pp. 853
Barkun, A, Leontiadis, G. “Systematic review of the symptom burden, quality of life impairment and costs associated with peptic ulcer disease”. Am J Med. vol. 123. 2010. pp. 358
Earlam, R. “A computerized questionnaire analysis of duodenal ulcer symptoms”. Gastroenterology. vol. 71. 1976. pp. 314
Kang, JY, Yap, I, Guan, R, Tay, HH. “Acid perfusion of duodenal ulcer craters and ulcer pain: a controlled double blind study”. Gut. vol. 27. 1986. pp. 942
Gururatsakul, M, Holloway, RH, Talley, NJ, Holtmann, GJ. “Association between clinical manifestations of complicated and uncomplicated peptic ulcer and visceral sensory dysfunction”. J Gastroenterol Hepatol. vol. 25. 2010. pp. 1162
Lu, CL, Chang, SS, Wang, SS. “Silent peptic ulcer disease: frequency, factors leading to "silence," and implications regarding the pathogenesis of visceral symptoms”. Gastrointest Endosc. vol. 60. 2004. pp. 34
Matthewson, K, Pugh, S, Northfield, TC. “Which peptic ulcer patients bleed?”. Gut. vol. 29. 1988. pp. 70
Wilcox, CM, Clark, WS. “Features associated with painless peptic ulcer bleeding”. Am J Gastroenterol. vol. 92. 1997. pp. 1289
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- I. What every physician needs to know.
- II. Diagnostic Confirmation: Are you sure your patient has Peptic Ulcer Disease?
- A. History Part I: Pattern Recognition:
- B. History Part 2: Prevalence:
- C. History Part 3: Competing diagnoses that can mimic Peptic Ulcer Disease.
- D. Physical Examination Findings.
- E. What diagnostic tests should be performed?
- 1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- 2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.
- III. Default Management.
- A. Immediate management.
- B. Physical Examination Tips to Guide Management.
- C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.
- D. Long-term management.
- E. Common Pitfalls and Side-Effects of Management
- IV. Management with Co-Morbidities
- A. Renal Insufficiency.
- B. Liver Insufficiency.
- C. Systolic and Diastolic Heart Failure
- D. Coronary Artery Disease or Peripheral Vascular Disease
- E. Diabetes or other Endocrine issues
- F. Malignancy
- G. Immunosuppression (HIV, chronic steroids, etc.).
- H. Primary Lung Disease (COPD, Asthma, ILD)
- I. Gastrointestinal or Nutrition Issues
- J. Hematologic or Coagulation Issues
- K. Dementia or Psychiatric Illness/Treatment
- V. Transitions of Care
- A. Sign-out considerations While Hospitalized.
- B. Anticipated Length of Stay.
- C. When is the Patient Ready for Discharge.
- D. Arranging for Clinic Follow-up.
- 1. When should clinic follow up be arranged and with whom.
- 2. What tests should be conducted prior to discharge to enable best clinic first visit.
- 3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.
- E. Placement Considerations.
- F. Prognosis and Patient Counseling.
- VI. Patient Safety and Quality Measures.
- A. Core Indicator Standards and Documentation.
- B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.