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1|P age MENNONITE COLLEGE OF NURSING AT ILLINOIS STATE UNIVERSITY Family Nurse Practitioner III 475 Common Gastrointestinal Problems Acute Abdominal Pain What is it? ...A common problem that may pose diagnostic challenges for the FNP! Is it a “quick” visit? …Not usually! Need a longer appointment, if possible. An understanding of the physiology of pain and basic anatomy is essential in the evaluation of abdominal pain, but determination of an etiology can be difficult owing to overlapping symptoms in pathologic processes and to the variable response of individuals to pain. The most powerful diagnostic tools are the history and physical examination. Chronicity is a key determinant of the pace of assessment. Prompt evaluation and appropriate treatment of acute abdominal pain are crucial. Chronic abdominal pain usually may be evaluated in a more unhurried manner. Differential Diagnosis Intra-abdominal disorders Inflammatory (e.g., appendicitis, pyelonephritis, abscesses, salpingitis, PID) Mechanical (e.g., visceral obstructions, aneurysm, trauma, ectopic pregnancy, ruptured ovarian cyst) Extra-abdominal (e.g., pneumonia, myocardial infarction, shingles, sickle cell anemia, diabetic ketoacidosis, depression, anxiety) History 1. Onset (chronic or acute) 2. Progression (improving, worsening, or stable) Progression of pain from a dull, poorly localized pain to a sharp, well-defined pain signals evolution of the disease process and the need for surgical consultation 3. Migration (has it moved?) Note: The more severe the visceral pain, the more likely it is to be referred to the back. 4. Localization (generalized, periumbilical, pelvic, or quadrantal) 2|P age Some Causes of Perceived Pain in Anatomic Regions Right Upper Quadrant Cholecystitis Hepatitis Hepatomegaly Fitz-Hugh-Curtis Colitis Diverticulitis Pneumonia Pulmonary embolus Nephrolithiasis Pyelonephritis Right Lower Quadrant Appendicitis* Colitis Diverticulitis Inflammatory bowel disease IBS Ectopic pregnancy Fibroids Ovarian mass/torsion PID Nephrolithiasis Pyelonephritis Strangulated hernia Epigastric Cholecystitis Myocardial infarction Pericarditis Esophagitis Gastritis Peptic ulcer Pancreatitis Aortic dissection Mesenteric ischemia Periumbilical Intestinal obstruction Acute pancreatitis Early appendicitis* Gastritis Peptic ulcer Mesenteric thrombosis Abdominal aortic aneurysm Aortic dissection Mesenteric ischemia Suprapubic Appendicitis* Colitis Diverticulitis Inflammatory bowel disease IBS Ectopic pregnancy Fibroids Ovarian mass/torsion PID Cystitis Nephrolithiasis Pyelonephritis Left Upper Quadrant Angina Myocardial infarction Pericarditis Aortic aneurysm Aortic dissection Pneumonia Esophagitis Gastritis Gastric ulcer Pancreatitis Ruptured spleen Mesenteric ischemia Perforated colon Nephrolithiasis Pyelonephritis Left Lower Quadrant Colitis Diverticulitis Inflammatory bowel disease IBS Ectopic pregnancy Fibroids Ovarian mass/torsion PID Nephrolithiasis Pyelonephritis Strangulated hernia Any location Abdominal wall: herpes zoster, muscle strain, hernia Other: bowel obstruction, mesenteric ischemia, peritonitis, narcotic withdrawal, sickle cell crisis, porphyria, inflammatory bowel disease, heavy metal poisoning * Depending on location of appendix, may have LLQ discomfort at first. Source: Cartwrigtht, SL & Knudson, MP (April 1, 2008). Evaluation of acute abdominal pain in adults. American Family Physician, 77(7), 971-978. 3|P age 5. Character (e.g., colicky or continuous, cramping, or stabbing) Quality and Onset of Abdominal Pain Characteristic Burning Cramping Colic Aching Knife-like Gradual onset Sudden onset 6. Possible related condition Peptic ulcer Biliary colic, gastroenteritis Appendicitis with impacted feces Appendiceal irritation Pancreatitis Infection Duodenal ulcer, acute pancreatitis, obstruction, perforation Associated symptoms (e.g., nausea, vomiting, anorexia, change in bowel habits) Also: “the order”.......If pain, then vomiting, think surgical If vomiting, then pain, think medical 7. Medical history and review of systems Note: A history of abdominal surgery, chronic disease, or prior pelvic inflammatory disease should raise the index of suspicion for associated sequelae (e.g., small bowel obstruction due to postoperative intra-abdominal adhesions). Example: PID and development of Fitz-Hugh-Curtis Study published in 2004 describes symptom pattern suggestive of ovarian cancer: pelvic pain, abdominal pain, difficulty eating, bloating, increased abdominal size, and urinary urgency. These symptoms were more frequent (almost daily) compared to women without ovarian cancer, such as those with symptoms associated with menses. ************** Case Study #1 ************** Clinical Findings 1. Vital signs and general appearance (e.g., fever, shock, body position, jaundice) Note: Clients with peritoneal pain lie still with legs drawn up to chest and resist movement. Clients with colicky pain such as pain with renal stones are restless, frequently shifting positions, and lacking peritoneal signs. 2. Inspection (e.g., contour, scars, pulsations, skin or vascular lesions, visible masses, or peristalsis) 4|P age 3. Auscultation (e.g., murmurs or bruits, peristaltic sounds, succussion splash) (“succussion” is the shaking of a person to detect the presence of fluid in the body cavity by listening for a splashing sound, especially in the thorax) 4. Palpation and percussion (e.g., light and deep, guarding and tenderness, organomegaly, masses, hernias, ascites) Murphy’s sign: inspiratory arrest in response to RUQ palpation seen in acute cholecystitis CVA tenderness Obturator sign: positive if abdominal pain occurs/increases in response to passive internal rotation of the right hip from the 90-degree hip/knee flexion position; suggests appendicitis. Psoas sign: positive if increased RLQ pain when patient lifts right thigh against resistance; indicates irritation of the psoas by an inflamed appendix Rovsing’s sign: positive if RLQ pain increases with palpation in the LLQ (early sign of peritoneal irritation, possible appendicitis) 5. Rectal and/or pelvic examination (e.g., urethral or cervical discharge or bleeding, prostate or adnexal tenderness or masses, stool impaction, rectal bleeding) Note: The elderly person with an acute intraabdominal process may at first show few signs of serious illness. Peritoneal signs may be absent or minimal. The only early clues may be unexplained mild fever, tachycardia, and vague abdominal discomfort. A high index of suspicion is needed. Note: Examining for nerve and muscle wall injury is often overlooked in the urgency of searching for more worrisome pathology. Two important signs of nerve involvement are pain in a dermatomal distribution and hyperesthesia. Both occur with nerve injury due to herpes zoster or nerve root impingement; however, hyperesthesia is also seen with focal peritoneal irritation. Testing is performed by gentle stroking of the skin overlying the area of pain. Tests to Consider 1. CBC with differential 2. Urinalysis 3. Serum electrolytes, BUN, creatinine, glucose if vomiting or other symptoms are present 4. Serum lipase and amylase if pancreatic process is suspected 5. Serum bilirubin (conjugated and unconjugated), transaminase levels (AST, ALT), and albumin if hepatic process is suspected. If jaundice is present, PT and PTT may also be indicated. 6. Urine pregnancy test Rule out ectopic pregnancy in all women of childbearing age who present with acute abdominal pain 5|P age 7. Diagnostic imaging (e.g., flat and upright abdominal films, CXR, abdominal/pelvic U/S or abdominal/pelvic CT, upper and lower bowel contrast studies) Recommended Imaging Studies Based on Location of Abdominal Pain Location of Pain Imaging Right upper quadrant Ultrasonography Left upper quadrant CT Right lower quadrant CT with IV contrast media Left lower quadrant CT with oral and IV contrast media Suprapubic Ultrasonography Source: Cartwrigtht, SL & Knudson, MP (April 1, 2008). Evaluation of acute abdominal pain in adults. American Family Physician, 77(7), 971-978. 8. 9. 10. Abdominal paracentesis Direct visualization by endoscopy, laparoscopy, or surgery With acute upper abdominal pain, CXR and EKG NOTE: Look at the total picture, not just one test…don’t forget to look at the patient!!! Beware of common misconceptions: “The white blood cell count is normal; the patient can’t have a surgical abdomen.” Studies of patients with appendicitis demonstrate sensitivities ranging from 42-90% “The white blood cell count is elevated; the patient must have a surgical abdomen.” Almost 11% of normal individuals have elevated WBC counts and 13% have left shifts. These left shifts are felt to be due to the stress response. “The patient has right lower quadrant pain, but the urinalysis shows evidence of a UTI.” Up to 30% of appendicitis cases have white blood cells in the urine secondary to periureteral inflammation. “Abdominal radiographs are often helpful in the work-up of nonspecific abdominal pain.” Abdominal radiographs are rarely helpful unless bowel obstruction, perforation, or foreign body is suspected. In healthy young individuals, these diagnoses can usually be made clinically, thus prompting the ordering of plain radiographs for confirmation. Note: They may, however, be helpful with the elderly patient. Management Although the management of abdominal pain is specific to the causative pathology, the following general measures may be useful in the management of acute abdominal pain. 6|P age Any evidence suggestive of peritoneal irritation, obstruction, or acute vascular compromise is an indication for immediate hospitalization and surgical consultation. In general, patients with unexplained abdominal pain in conjunction with recurrent nausea and vomiting, jaundice, fever, weight loss of > 10% of body weight, or the presence of blood in the stool will require more invasive testing. In patients who are older or frail: If low risk (stable vital signs, limited comorbidities), consider UTI or diverticulitis and conduct general work-up for abdominal pain If high risk (unstable vital signs, significant comorbidities), consider sepsis, perforated viscus, or ischemic bowel. Perform CT and consider hospitalization. Occult urinary tract infection, perforated viscus, and ischemic bowel disease are potentially fatal conditions commonly missed or diagnosed late in older patients. Medication Note: There is the idea that due to the fear of masking abdominal symptoms, analgesics should not be given until a probable diagnosis is made and a course of treatment is determined. Recent information suggests that some analgesics (especially parenteral NSAIDS) may not significantly interfere with the evaluation of acute abdominal pain. Meds to consider: Narcotic and non-narcotic parenteral analgesics Antiemetics and other symptomatic medications Specific pharmacotherapy as indicated (e.g., PPI in ulcer disease) Diet Nothing by mouth until a diagnosis is made; thereafter, the diet is determined by the disease. Activity Usually bedrest (especially if there is risk of medication-related falls or aortic aneurysm) Patient Education The patient should promptly report changes in symptoms. Medication information Follow-up In acute abdominal pain, even if the cause is known, follow-up may be as frequent as every few minutes. 7|P age In chronic abdominal pain, re-evaluation may be as infrequent as every several months depending on the patient, the suspected or confirmed cause, and the FNP’s degree of comfort. “Practice Pearls” Determine whether pain is acute or chronic. If acute, work-up should proceed rapidly. History and physical examination should guide focused selection of diagnostic studies. Keep patients with acute abdominal pain NPO initially. For chronic pain, recording of symptoms on a calendar along with menses, diet, and other features may be helpful. Three different categories of acute abdominal pain: Surgically Emergent Medically Emergent Self-Limiting Surgically Emergent ************** Case Study #2 ************** Appendicitis Etiology/Demographics Obstruction of the appendiceal lumen, usually by a fecalith, but occasionally by foreign bodies Most common atraumatic surgical abdominal emergency in the 10-30 year old age group. Common in this age group due to having more lymph tissue that is more likely to become hyperplastic and cause obstruction. Not as likely to see in the very young and the very old. More common in those from European and North American countries – probably related to the relative lack of fiber in the diet. Our rate of appendicitis in this country has actually decreased over the last 10-15 years as our intake of fiber has increased. Men more likely than women to be affected (1.5:1) 2/3 of cases reported between October and May. Why? May be due to influenza during those months that stimulates follicular hyperplasia, which can obstruct the appendiceal lumen. Persons with a family history of appendicitis are also at increased risk. 25% perforate by 24 hours, 75% by 48 hours. 8|P age Subjective In classic appendicitis, the pain begins as vague and poorly localized, usually felt in periumbilical area. As progresses, pain localizes to the right lower quadrant. However, need to keep in mind that appendix can have different anatomic variations (i.e. size, position) in different people…can present differently! A retrocecal appendix (15%) can cause back or flank pain A long appendix can cause pain in the LL or RUQ A retroileal appendix can lead to testicular pain A pelvic appendix may cause suprapubic pain Clinical pearl – usually pain proceeds vomiting Characteristics of pain can be highly variable – crampy to sharp to dull. Can easily confuse with PID May have obstipation Objective Physical exam reveals abdominal tenderness, RLQ tenderness, abnormal bowel sounds, +/- rebound Patient usually wants to hold still, not to move around Psoas sign/Obturator sign/Rovsing’s sign Pelvic, rectal exams as needed The 3 findings with the greatest predictive value are: Pain in the right lower quadrant Migration of that pain from the periumbilical region Abdominal rigidity on examination Source: Rubin, RN (April 1, 2003). Young man with acute right lower quadrant pain. Consultant, 538-540. ************** Case Study #3 ************** Assessment/Not to be missed Keep in mind the presentation of appendicitis is not always straightforward, especially in the very young and very old. Diagnosis is missed ½ of the time in patients over the age of 60, and most of the time in patients younger than four years old, and almost always in patients less than two years old. Don’t miss PID, ectopic pregnancy, ovarian cyst Plan Obtain labs – CBC (be sure to pay attention to manual differential – may not see rise in WBC’s, but may see increase in neutrophils), chemistries (if presentation unclear, consider including amylase), C-reactive protein, urinalysis, urine HCG if child bearing age and indicated No imaging necessary in typical appendicitis (but in non-straight-forward cases, a different diagnosis is found in 15% of cases) Source: Holden, DM, & Einstein, DM (January 2007). Imaging in practice: Which imaging test for right lower quadrant pain? Cleveland Clinic Journal of Medicine, 74(1), 37-40. Imaging may be useful in differentiating appendicitis from other conditions such as Crohn’s disease, right-sided diverticulitis, right colonic neoplasm, bowel 9|P age ischemia, acute pyelonephritis, ureteral calculus, PID, and hemorrhagic ovarian cyst. Plain-film radiography of the abdomen rarely provides useful information in the above cases (One study showed it have 0% sensitivity for appendicitis, pyelonephritis, pancreatitis, and diverticulitis) Role of abdominal or transvaginal ultrasound: diagnostic accuracy of > 85%, useful in the exclusion of adnexal disease in younger women Graded-compression ultrasonography is helpful in evaluating thin young children and obstetric patients Overlying bowel gas can technically limit the ability of ultrasonography to identify a normal or perforated appendix. If this occurs, CT can be used for further evaluation. CT is the imaging test of choice for suspected appendicitis in adults who are not pregnant. (NOTE: Will need to order abdominal/pelvic CT to provide visualization of entire abdomen/pelvic area….abdominal CT alone will not include total colon.) CT without contrast: lower sensitivity in thinner patients with little intraabdominal fat and in patients with early or mild appendicitis; limited ability to show inflammatory or neoplastic processes CT with IV contrast: facilities recognition of appendicitis, especially in subtle cases and in thin patient with little intra-abdominal fat; also better at showing complications of perforation such as abscess formation as well as other pathological entities that may cause abdominal pain. Complications: severe allergic reaction, renal failure. CT with enteric (oral) contrast: oral contrast is given 1.5 to 2 hours before the exam to opacify and distend the distal small bowel and cecum; this visualization of anatomic landmarks helps in identifying the appendix (differentiating it from surrounding structures). (contrast can also be given rectally) Imaging (CT of abdomen/pelvis) may be useful in patients in whom the diagnosis is uncertain Refer to surgeon for evaluation ************** Case Study #4 ************** Obstruction Etiology/Demographics Pain is caused by distention and increased wall tension of affected area Common causes – previous abdominal surgery with adhesions, tumor, constipation (obstipation) Subjective If acute onset of obstruction, the pain is intense, severe and colicky or wavelike, patient is restless. 10 | P a g e If slow onset of obstruction, pain is more vague, patient may complain of dyspepsia, bloating, etc. Signs of upper obstruction – vomiting Signs of lower obstruction – no flatus, or if partially obstructed, may see diarrhea Objective Abdominal distention Borborygmi or no bowel sounds Assessment/Not to be missed Tumor or malignancy (colon cancer to be discussed later) Plan Labs (CBC, chemistries, etc.) If concerned regarding perforation, get upright chest x-ray (check for pneumoperitonitis) Flat plate of abdomen can be helpful to visualize air in small intestine, impaction, etc. CT of abdomen/pelvis (will often show dilated loops of bowel) Refer for further evaluation. If simple obstruction, may manage medically with decompression by tube insertion. If strangulation – surgically emergent ************** Case Study #5 ************** Acute Gall Bladder (Cholecystitis, Cholelithiasis) Etiology/Demographics Cholecystitis, or inflammation of the gallbladder, may be acute or chronic Types of acute cholecystitis Acute calculus cholecystitis Inflammation of the gallbladder that develops in the presence of gallstones (cholelithiasis) 95% of cases of acute cholecystitis Acute acalculus cholecystitis Inflammation of the gallbladder in the absence of gallstones 5% of cases 11 | P a g e Age Body habitus Childbearing Drugs Ethnicity Family Gender Hyperalimentation Ileal and other metabolic diseases Risk Factors for Gallstone Formation Increasing age Obesity, rapid weight loss Pregnancy Fibric acid derivatives, contraceptives, postmenopausal estrogens, progesterone, octreotide (Sandostatin), ceftriaxone (Rocephin) Pima Indians, Scandinavians Maternal family history of gallstones Females Total parenteral nutrition, fasting Ileal disease (Crohn’s disease), resection or bypass, high triglycerides, diabetes mellitus, chronic hemolysis, alcoholic cirrhosis biliary infection, primary biliary cirrhosis, duodenal diverticula, truncal vagotomy, hyperparathyroidism, low level of HDL cholesterol Source: Ahmed, A, Cheung, RC, & Keeffe, EB (March 15, 2000). Management of gallstones and their complications, American Family Physician, 61(6), 1673-1680. Subjective Typically presents with RUQ pain, may radiate to mid-epigastric area, scapula. Pain is usually constant/steady, lasting over an hour Often accompanied by nausea, vomiting, and fever without jaundice Objective (+) Murphy’s sign If can feel gallbladder, really be concerned regarding malignancy Assessment/Not to be Missed Acalculous cholecystitis Perforation Be especially cautious in those with underlying health problems such as diabetes Pancreatitis Plan Obtain CBC (once again pay close attention to manual differential), chemistries (may or may not see increase in liver enzymes), amylase (stone obstruction of cystic duct can lead to pancreatitis) Gallbladder ultrasound If ultrasound is negative for stones, may consider ordering HIDA scan (administration of cholecystokinin [CCK] causes the gallbladder to contract; allows estimation of the ejection fraction of the gallbladder (normal ejection fraction is 35-75%) Refer to surgeon Cholecystectomy (laparoscopic vs. open) 12 | P a g e For high surgical risk or patients refusing surgery, nonsurgical therapy includes oral bile acid dissolution (ursodeoxycholic acid) or lithotripsy Some patients experience post-cholecystectomy diarrhea. Treatment: Lomotil 1 tab after each loose stool X 1-2 months. If no relief, cholestyramine daily (binds with bile) Skill Check: Try out the scenario at http://meded.ucsd.edu/isp/1999/surgery/index.html Ovarian Cyst Usually see rebound, unilateral adnexal pain with bimanual exam Usually have signs of peritoneal irritation Consider usual acute abdominal condition labs Consider pelvic ultrasound Refer to surgeon Ectopic Pregnancy Usually with rebound, signs of peritoneal irritation Suspect in women of childbearing age Urine HCG or serum HCG in addition to usual labs Pelvic ultrasound Refer to surgeon Can be life-threatening Abdominal Aortic Aneurysm (AAA) Sources: Almahameed, A, Latif, AA, & Graham, LM (October 2005). Managing abdominal aortic aneurysms: Treat the aneurysm and the risk factors. Cleveland Clinic Journal of Medicine, 72(10), 877-888. Lederle, FA (May 5, 2009). In the clinic: Abdominal aortic aneurysm. Annals of Internal Medicine, ITC5, 1-16. Risk factors: older age, smoking, male gender, white race, family history of AAA, occlusive atherosclerotic disease U.S. Preventive Services Task Force recommendations One-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men aged 65 to 75 who have ever smoked. Recommends against screening in women No recommendation regarding men 65-76 years old who never smoked Aneurysm may be asymptomatic: If small, risk of having surgery vs. risk of bleeding if does not have surgery must be weighed Are AAAs palpable? 3-3.9 cm = palpable 29-61% of the time > 5 cm = palpable 76-82% of the time Do yearly ultrasound to check if getting larger 3-4 cm. Check every 12 months 4-4.5 cm Check every 6 months 13 | P a g e > 4.5 cm Refer to vascular subspecialist Surgery usually recommended for aneurysms 2 inches (5.5 cm) or more in diameter for men (5 cm in women) and for aneurysms that are enlarging quickly (> 0.6-0.8 cm/yr) Surgery may be a traditional (open) repair or endovascular stent grafting (endograft) Endograft good for older patient or patients at higher operative risk Open repair for younger patients After endograft, CT at 1, 6, and 12 months, and then yearly (AAA should decrease in size). If AAA leaking: Patients may complain of tearing pain that radiates to back; pain is severe Pain may radiate to groin, testicles, legs, or buttocks May feel pulsating mass (approximately 83% of the time) Hypotension present (45% of the time) Will need open repair (outcome usually good if repaired before it ruptures; < 40% survive a ruptured AAA) Trauma ************** Case Study #6 ************** Medically Emergent Acute Pancreatitis Sources: Amerine, E. (June 2007). Get optimum outcomes for acute pancreatitis patients. The Nurse Practitioner, 32(6), 44-48. Etiology/Demographics Inflammatory breakdown of pancreatic architecture, with release of digestive enzymes into the interstitium of the gland, leading to autolysis (= “autodigestion”) Two forms of acute pancreatitis Edematous (or interstitial) is usually mild and resolves in about 7 days Severe or necrotizing is associated with a high degree of complications and mortality More than 80% of cases of acute pancreatitis can be attributed to ethanol abuse or biliary stones Other causes: hypertriglyceridemia, tumor, mumps Use of some medications such as thiazide diuretics, furosemide, nitrofurantoin [Macrobid], and GLP-1 meds used in diabetes, including Byetta, Bydureon, and Victoza 14 | P a g e Subjective Sharp, periumbilical pain History of alcoholism, gallbladder disease, mumps, use of meds noted above May complain of persistent vomiting Pain is worse with food, somewhat better with upright position Objective Acutely ill, very uncomfortable May have abdominal distention, tenderness, diminished bowel sounds, fever Assessment/Not to be Missed Perforation (check bowel sounds, CXR) Plan CBC, CMP, amylase, lipase Amylase – found primarily in pancreas and salivary glands; begins to rise 3-6 hours after onset of acute pancreatitis and peaks in approximately 24 hours; returns to normal within 2-3 days after onset Lipase – found only in pancreas; increases in blood within 24-36 hours after onset; remains elevated up to 14 days longer than amylase Imaging Ultrasound: main role is to detect gallstones as the likely cause CT: Most useful in patient with severe or atypical presentation; may be helpful in differentiating acute pancreatitis from conditions such as perforated peptic ulcer, mesenteric ischemia, acute cholecystitis, and bowel obstruction or perforation. Mild pancreatitis requires supportive therapy Discontinue offending drug if acute pancreatitis drug-induced Pain control, antiemetic medications, IV fluids Diet: NPO to avoid recurrence of pain resulting from the activation of pancreatic enzymes; begin diet after pain, tenderness and ileus have resolved (start with clear liquids, progress to full diet Re-evaluate labs until normal Recovery usually within 5-7 days Pancreatitis due to obstruction from gallstones, dysfunction of the Sphincter of Oddi, or malignancy requires endoscopic retrograde cholangiopancreatography (ERCP) with possible stone extraction and/or sphincterotomy of the ampula, or stent placement in the biliary duct Moderate to severe pancreatitis: admit to critical care unit Local complications include formation of pseudocyst or pancreatic abscess, requiring percutaneous aspiration or drainage. (may take up to 4 weeks to develop) 15 | P a g e Pyelonephritis Etiology: Infection of the upper urinary tract/kidney Subjective: Presents with complaints of flank pain, often accompanied by nausea and vomiting Usually febrile Objective: On exam – acutely ill, CVA tenderness Diagnosis/Plan: What would urinalysis results likely be? Definitely need urinalysis and culture. Start on fluoroquinolones while awaiting C & S results May need IV fluids May need hospitalization for fluids and IV antibiotics if unable to keep oral antibiotics down or if pregnant Follow closely Kidney Stones Subjective: Pain is result of obstruction/partial obstruction of urinary tract Patient complains of colicky pain – usually flank May also report diminished urinary stream Patient appears restless, can’t get comfortable Diagnosis/Plan: Blood noted in urine dipstick; can do CT "Stone protocol" (doesn't require contrast media...great for folks with renal insufficiency) May need admission for fluids, pain control If manage outpatient, follow frequently, give urine strainer to hopefully catch stone Pelvic Inflammatory Disease Pain with pelvic/bimanual, may be excruciating Fever May need hospitalization Increased risk of infertility, scarring, ectopic pregnancy May say she is monogamous, but “serially” monogamous Ischemic Bowel Disease (See Mesenteric Ischemia later in this handout) Arteries that supply oxygenated blood to the large and small intestines become narrowed or blocked. At risk: age > 50, smoking, obesity, high cholesterol, HTN, CVA, afib, DVT, MI 16 | P a g e Presentation variable May have rectal bleeding Self Limiting Gastroenteritis Viral Most common cause of gastroenteritis Patient presents with complaints of abdominal cramping, accompanied by diarrhea, often times emesis. No blood is present in stool or emesis Heavy fruit syrup may help settle stomach Many times report someone else in family or someone exposed to is ill with same thing On exam will see generalized abdominal tenderness – bowel sounds generally hyperactive, although may be hypoactive/absent if has just thrown up Examine/investigate signs of dehydration – i.e. orthostatics, mucous membranes, skin turgor, last void, etc. If dehydrated consider IV fluids (avoid fluids with dextrose for first liter – leads to more fluid loss related to relative hypertonicity) Usually lasts for 24-72 hours – if longer, at least consult, if not refer Treatment – clear liquids, bland foods (BRAT diet = bananas, rice, applesauce, toast), gradually adding regular foods (fatty and dairy products last), also avoid alcohol (gastric irritant) and smoking If nausea is severe, consider antiemetic such as phenergan or Zofran. Otherwise, antidiarrheals/antiemetics are not recommended. Wait 30 minutes after vomiting before taking something by mouth – allows reverse peristalsis to correct itself Food Poisoning Likely to have a more abrupt onset in comparison with viral gastroenteritis Self-limiting, need to evaluate for dehydration/need for IV fluids or other supportive measures If gotten from a restaurant, report to Health Department Same treatment as for viral gastroenteritis Traveler’s Diarrhea Prevention is the best strategy o If traveling in North America, advise not to drink any untreated water (i.e., mountain streams, lakes, etc.) due to risk of Giardia or similar organisms. o If traveling to underdeveloped countries, advise no water, drinks with ice cubes or made with water, fresh vegetables or fruits that may have been washed in water. Bottled water is best! In past, some have promoted antibiotic prophylaxis for travelers, however with emergence of resistant strains, there is concern about this practice. 17 | P a g e o One option is to treat with Pepto Bismol 60 ml QID. Warn patient that stool will turn dark. (can also get black tongue) If acutely ill, treat with Cipro 500 mg bid for 3 days or Bactrim DS one bid for 3 days. Consideration can be given to sending antibiotics with patient to take if becomes symptomatic while traveling. Gastritis Associated with alcohol intake, smokers Patient complains of nausea, burning, gnawing pain Treat by having patient discontinue alcohol/smoking Also use Mylanta or OTC H2 Blocker Chronic Abdominal Pain Ovarian Cancer Need high index of suspicion since symptoms are nonspecific Consider ovarian cancer in the differential diagnosis of women who present with unexplained abdominal pain, abdominal swelling, GI symptoms such as constipation, and/or pelvic pain. Abdominal bloating increased abdominal size urinary urgency One study found 40% of women with ovarian cancer visited their doctor at least once because of abdominal or pelvic symptoms between 36 and 4 months before their cancer was diagnosed. However, only 25% of these patients received pelvic imaging or CA-125 testing during that time. In contrast, 61% received abdominal imaging and about 30% received GI tests. Source: Smith, LH et al. Ovarian cancer: Can we make the clinical diagnosis sooner. Cancer. Advanced online publication. August 22, 2005. To avoid delay in diagnosis, order pelvic imaging and CA-125 Pancreatic Cancer (PC) Source: Abbruzzese, JL, Lowy, AM, Pleskow, D, & Xiong, HQ (February 2006). Update on the approaches to pancreatic disease. Patient Care. 15-24. Pancreatic carcinoma (August 24, 2011) accessed at http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001283/?report=printable 4th leading cause of cancer-related mortality Fewer than 5% of patients survive beyond 5 years Risk factors o Smoking Smoking + family history = doubles the risk of PC o Diabetes o Long-term inflammation of pancreas (chronic pancreatitis) o Age o Genetic susceptibility (BRCA2 gene, familial polyposis gene, and Lynch syndrome o Lynch syndrome= Hereditary Nonpolyposis Colorectal Cancer, an autosomal dominant problem. 18 | P a g e Associated with increased risk of other cancers (ovarian, endometrial, renal, gastric, hepatobiliary, small intestine) S/S: fatigue, weight loss, anorexia, nausea and vomiting, abdominal/back pain (from local invasion), jaundice o If head of pancreas affected (exocrine function), frequently present with progressive obstructive jaundice from blockage of bile drainage into the small intestine; manifests as dark urine and pale stools o If PC in endocrine portion of pancreas (tail), new-onset diabetes or changes in glucose tolerance in patients with diabetes is also a frequent finding. o Possible Sister Mary Joseph Nodule…what is this? Imaging: Helical CT remains the test of choice for diagnosing pancreatic masses and extra-pancreatic metastases and for determining resectability of the tumor. Management o Resectable in approximately 15% of patients on initial presentation Whipple resection (pancreaticoduodenectomy) if PC in head of pancreas o Standard chemotherapy for advanced pancreatic cancer is gemcitabine (Gemzar), but research continues. ************** Case Study #7 ************** Gastroesophageal Reflux Disease (GERD) Source: Hart, AM (August 2013). Evidence-based recommendations for GERD treatment. The Nurse Practitioner, 38(8), 26-34. Demographics/Etiology Reflux of acid into the esophagus Associated risk factors include obesity, pregnancy, nicotine, caffeine, and alcohol use Other associated risks are decrease in sphincter tone of the lower esophageal sphincter (LES), decreased secondary peristalsis, defective mucosal resistance, delayed gastric emptying, gastroparesis secondary to diabetes, IBS, peptic ulcer disease, asthma, COPD, angina More prevalent with use of anticholinergics, nitrates, and oral corticosteroids Cochrane review found patients presenting with concomitant GERD and H. Pylori infections typically experience improvement in GERD symptoms with H. Pylori eradication. Prevalence rate in US 15-20% Occurs equally in men and women; more common in whites than non-whites 44% of U.S. adult population have heartburn once/month 14% have symptoms weekly; 7% have daily symptoms 50-80% of patients with asthma have GERD (remember, bronchodilators also loosen the LES) GERD is the most common cause of non-cardiac chest pain 19 | P a g e Clinical pearl: Patients with chronic cough have high likelihood of having GERD and should receive a trial of antisecretory therapy. Subjective Gnawing, burning, reflux sensation up the chest that is worse after large meals, lying down, bending over Pain at least temporarily alleviated with the use of antacids Objective Usually a normal exam May have mid-epigastric tenderness to palpation Not to be Missed MI, PUD, cholelithiasis, scleroderma, gastric cancer Plan Stool guaiac Weight loss if obese Wear loose clothing (tight clothes around the waist and abdomen put pressure on the stomach, aggravating the symptoms) Avoid late evening meals Avoid lying down or bending right after eating. Elevate head of bed with bricks or blocks (simply raising head on extra pillows does not work!) Avoid high fat and high carbohydrate foods Avoid medications that decrease lower esophageal sphincter tone, including: Beta2-agonists (bronchodilators) Alpha-adrenergic antagonist Nitrates Anticholinergics Theophylline Morphine Meperidine Barbiturates Avoid medications that irritate/promote breakdown of the esophageal mucosa such as NSAIDs, steroids D/C nicotine, caffeine, alcohol Antacids after meals and at HS If antacids not sufficient, can try OTC H2 blocker – split into BID dose works better (i.e. Zantac or Axid 150 mg bid) or OTC PPI (omeprazole) Other options would be a prescription proton pump inhibitor (such as lansoprazole [Prevacid], rabeprazole [AcipHex], esomeprazole [Nexium], or pantoprazole [Protonix]) or a promotility agent such as metaclopramide (Reglan, which increases peristalsis) 20 | P a g e Take PPIs 30 minutes before breakfast (if bid, take before breakfast and evening meal) If this is not sufficient to control symptoms, referral to gastroenterology usually made for further evaluation by EGD (esophagogastroduodenoscopy) Two strategies for treating GERD: Step-up approach Phase I: Lifestyle modification Phase II: Treatment with an H2 receptor antagonist (H2RA) or promotility agent Phase III: Increase in dose or frequency of H2RA monotherapy, or treatment with H2RA combined with a promotility agent Phase IV: Treatment with proton pump inhibitor (PPI) or surgery Step-down approach – give highest dosage of PPI for symptomatic control and step down once it is achieved To avoid “rebound reflux,” PPIs should be gradually discontinued over a few weeks (halving the dose every week, until on lowest dose, then taking lowest dose for 1 week) Concerns regarding use of PPI’s Gastric acid has a protective effect against enteric infections; therefore gastric acid suppression can permit pathogens to more readily colonize in the upper GI tract and predispose individuals to infections, such as pneumonia and Clostridium difficile associated diarrhea. Association between prolonged PPI use (> 1 year) and a moderately increased risk of hip and vertebral factures Prolonged PPI use may impact vitamin B12, iron, and magnesium absorption Interaction of clopidogrel (Plavix) with omeprazole (Prilosec) and esomeprazole (Nexium) use. Clopedogrel is a prodrug metabolized in the liver to an active form that inhibits platelet aggregation. Cytochrome CYP2C19, an enzyme involved in this activation process, is inhibited by PPIs, a phenomenon that can decrease antiplatelet response and increase risk for CV events. Complications Dental erosions Pharyngeal ulcerations Laryngeal damage Reflux esophagitis Esophageal ulcers and strictures (Schlotsky's ring) Barrett’s esophagus o Replacement of the normal squamous epithelium of the esophagus with a metaplastic columnar epithelium, a risk factor for developing esophageal adenocarcinoma o Mechanism: Barrett’s esophagus linked to repeated and prolonged exposure of the esophageal mucosa to gastric material refluxed into the esophagus 21 | P a g e o 10% of individuals with chronic GERD have Barrett’s esophagus o 0.5-1% of Barrett’s esophagus patients develop adenocarcinoma of the esophagus every year o More common in those who smoke or drink alcohol. o Mean age at diagnosis = 55, men:women 2:1 o Increased risk with longer duration of GERD symptoms o Treatment: radiofrequency ablation of abnormal tissue Esophageal adenocarcinoma Refractory GERD In the event of failed response to a PPI, it is important to both reconfirm the diagnosis of GERD (focusing on ruling out alarm symptoms) and ensure proper administration of PPIs 30 minutes prior to breakfast. Alarm symptoms of GERD suggesting complicated disease: o Black or bloody stools o Choking o Chronic cough o Dysphagia o Early satiety o Hematemesis o Hoarseness o Iron deficiency anemia o Odynophagia o Weight loss Source: Heidelbaugh, JJ, Gill, AS, Harrison, RV, & Nostrant, TT. (August 15, 2008). Atypical presentations of gastroesophageal reflux disease. American Family Physician, 78(4), 483-488. Dyspepsia Source: Talley NJ, Vakil N. (2005) Guidelines for the management of dyspepsia. Am. J. Gastroenterol, 10: 2324-2337. Vague discomfort in the upper abdomen or chest described as gas, feeling of fullness, gnawing, or burning May have GERD, peptic ulcer, functional (nonulcer) dyspepsia, or (rarely) malignancy Patients with the onset of dyspepsia at age 56 or older or those with alarm symptoms at any age should undergo immediate upper endoscopy. o Alarm symptoms: see those listed above, along with persistent vomiting, family history of GI malignancy, previous documented peptic ulcer, abdominal mass, or lymphadenopathy. Patients with reflux-predominant symptoms should be treated as if they have GERD If prevalence of H. pylori infection in the community is < 10%, a trial of a PPI is recommended. If trial fails, a test for H. Pylori infection followed by eradication if positive should be pursued When H.pylori is more common, test for H. pylori first, then trial a PPI. If this fails, may consider upper endoscopy. 22 | P a g e Peptic Ulcer Disease (PUD) Etiology/Demographics Ulceration of the duodenal or gastric mucosa Number of associated factors including the interplay of acid production, pepsin secretion, and mucosal defense mechanisms, also Helicobacter pylori infection Male:Female ratio 2:1 Smoking Alcohol use Stress NSAID use – serves as a local irritant, but most importantly is a prostaglandin inhibitor, which interferes with the normal synthesis of mucosa Long-term or high dose steroid use Family history (to a degree) Type O blood Symptoms Peptic ulcer disease is typically manifested by symptoms including burning pain or discomfort localized in the center part of the abdomen PUD pain is often worse when the stomach is empty, allowing gastric acid to come in contact with the ulcer; improved when a patient consumes food to satiety. Helicobacter pylori Source: Saad, R, & Chey, WD (February 2005). A clinician’s guide to managing Helicobacter pylori infection. Cleveland Clinic Journal of Medicine, 72(2), 109-124. H. pylori is now widely accepted as a contributing factor in peptic ulcer disease (many feel that it is the underlying etiology of PUD) Prevalence of H. pylori varies geographically o It is associated with lower socioeconomic status, poor hygiene (very prevalent in underdeveloped countries, even in children, however most are asymptomatic) In the US, H. pylori infection occurs in approximately 20% of those younger than 40 and in approximately 50% of those older than 60 There seems to be a decreasing incidence of H. pylori in the US due to improving socioeconomic conditions over the century Mode of transmission is unclear, although person-to-person fecal-oral spread is suspected because clusters occur in families. Gastric adenocarcinoma and gastric lymphoma have been epidemiologically linked to H. pylori There are a wide variety of serological tests available for screening of H. pylori for the office to the laboratory, all with varying sensitivities/specificities C-labeled urea breath test: Patient takes urea orally which is labeled with an isotope. If H. pylori is present in the stomach, labeled carbon dioxide (CO) is produced as a result of the interaction. This CO can be detected in the patient's breath within minutes of the urea ingestion. The patient breathes into a collection bag or onto a flat breath card. (NOTE: Patient must stop treatment for GERD for 2 weeks prior to the test, except can use antacids.) 23 | P a g e Number of different treatment options for H. pylori. First line regimens (14 day duration) are: o Clarithromycin-based triple-drug therapy used in patients who are not allergic to penicillin Omeprazole 20 mg twice daily, plus amoxicillin 1 g twice daily plus clarithromycin 500 mg twice daily o Bismuth-based quadruple therapy used in penicillin-allergic patients Bismuth subsalicylate (Pepto-Bismol) 525 mg four times daily, plus metronidazole 250 mg four times daily, plus tetracycline 500 mg four times daily, plus histamine H2 Not to be Missed GI cancer Plan If the patient has any “red flags” (i.e. sustained progressive weight loss, dysphagia, odynophagia [pain with swallowing], persistent vomiting, nocturnal wakening, hematemesis, melena) refer for endoscopy. If patient with no “red flags” and has no previous documented ulcer disease, treat empirically with H2 blocker or PPI for at least a full 4 weeks (if large ulcer or a gastric ulcer, may need up to 8 weeks of therapy). If patient does well, follow. If no response, refer. If patient has no “red flags”, but gives a history of a previously documented ulcer, test for H. pylori and treat with one of the above mentioned therapies if positive. If H. pylori negative, treat with H2 blocker or PPI as previously discussed. Follow up is important with all groups! Strongly encourage smoking cessation if appropriate Avoid eating before bedtime (helps prevent increased nighttime gastric acid production) Avoid medications that injure the mucosal barrier (i.e. NSAID, steroids) Alleviate emotional stress. Can try antacids Chronic Pancreatitis Mild to severe recurrent epigastric pain, usually after years of alcohol abuse, however also may be due to gallbladder obstruction Often times these individuals are very difficult to manage due to pain control issues. Refer Chronic Cholecystitis/Cholelithiasis Patient gives history of recurrent episodes of biliary colic that has resolved spontaneously. Symptoms may be worsened by fatty intake or caloric excess. Ultrasound is first line test of choice 24 | P a g e For patients that are symptomatic and have gallstones documented on ultrasound, refer to surgeon for evaluation for elective cholecystectomy For those patients who are asymptomatic and stones are found coincidentally (i.e. on CT scan done for another reason): do not treat or recommend surgery. Only 20% will develop active disease in their lifetime Do recommend that patients with chronic disease discontinue estrogens, as they promote gall bladder disease. Recommend gradual weight loss for obese patients (avoid drastic diets/severe calorie restrictions as this may actually exacerbate symptoms) The Acute Abdomen in the Older Patient Acute Abdomen in the Elderly Source: Burg, MD, & Francis, L. (August 2005). Acute abdominal pain in the elderly. Emergency Medicine. 8-13. A common and life-threatening condition Elderly often delay seeking health care Cognitive impairment? Decreased mentation? Fear of loss of independence? Neuropathy or chronic use of meds such as corticosteroids or pain relievers may blunt pain perception Presentation may be atypical…Need high index of suspicion Consider the possibility of an intra-abdominal process in all older patients seeking treatment for an acute illness Many medical conditions that cause or lead to painful abdominal disorders are more common in the elderly, such as intra-abdominal malignancies, vascular disease, cholelithiasis, and diverticulosis History “Have-To’s” Duration and location of pain Presence/absence of vomiting Whether patient is passing flatus What abdominal surgery has previously been performed Physical Signs Physical signs are conspicuous by their absence in some older patients with acute abdominal disease Peritonitis is less likely to cause rebound tenderness Pyrexia and tachycardia less likely to be present 25 | P a g e Physical Examination Careful inspection of inguinal and femoral areas for presence of incarcerated hernia Listening for bowel sounds Rectal examination to rule out fecal impaction and GI bleeding Diagnostic Tests to Consider CBC with differential o WBC’s may not be elevated o Significant left shift o Low Hct with perforated peptic ulcer BUN, Creatinine o Increased with dehydration, GI bleed Electrolytes o Low K from vomiting, diarrhea o Low Na with acute illness Liver function o Increased with cholelithiasis, hepatitis, cholangitis ABGs EKG o Inferior wall MI – abdominal pain, intractable vomiting Imaging o Abdominal x-ray (erect/supine) o Abdominal ultrasound o Abdominal/pelvic CT o Laparoscopy for continued diagnostic uncertainty ************** Case Study #8 ************** Cholecystitis Most common cause of acute abdominal pain in the older patient Complications o Ascending cholangitis o Empyema of the gallbladder o Perforation of the gallbladder o Pancreatitis (high amylase) o Indications of gallstone in common duct: elevated bilirubin Bowel Obstruction Responsible for 25% of acute abdomens in older patients Common causes o Incarcerated hernia o Carcinoma o Adhesions o Volvulus (a twisting of the bowel on itself) 26 | P a g e o Fecal impaction Appendicitis 14% of cases of acute abdomen in elderly Mortality rate up to 15% o Late presentation o Inaccurate diagnosis o High prevalence of perforation at time of presentation o Decreased blood flow to appendix o Narrower lumen, thinner wall Signs/symptoms o Less likely to have classic RLQ pain, fever, or elevated WBC o More likely to have Diffuse abdominal pain Abdominal guarding Abdominal mass Peptic Ulcer Disease (PUD) Incidence increases with age More likely to be taking both Rx and OTC NSAIDs Smoking, heavy alcohol intake Empirical anti-ulcer therapy without endoscopy not suggested o Greater risk of malignant ulcer ************** Case Study #9 ************** Diverticulitis Source: Wu, JS, & Baker, ME (July 2005). Recognizing and managing acute diverticulitis for the internist. Cleveland Clinic Journal of Medicine, 72(7), 620-627. Diverticulosis increases with age (5% in the 5th decade to about 50% in the 9th decade) Most commonly affects sigmoid (BUT can occur anywhere in the colon…check for recent colonoscopy results) Associated with long-term low-fiber diets 27 | P a g e 10-25% of patients with diverticulosis eventually develop inflammation in the diverticula = diverticulitis o Often found during colonoscopy with recommended treatment being highfiber diet o Historically, providers have recommended avoiding ingestion of seeds, corn, popcorn, and nuts for fear that they might become entrapped in diverticular, but no controlled studies support this dietary restriction (Source: Salzman, H, & Lillie, D. (October 1, 2005). Diverticular disease: Diagnosis and treatment. American Family Physician, 72(7), 1229-1234. Common symptoms o Classic, but may be absent in older patient: Pain in LLQ Fever Tender mass in LLQ o Alternating diarrhea and constipation, rectal bleeding Discomfort decreased after passing stool o Malaise, anorexia, N & V Clinical Pearl: Tenderness tends to be focal if the process is contained and contamination is minimal, and generalized if inflammation extends to a large area. Diagnosis: labs (CBC, ESR), imaging (CT abdomen/pelvis) CT most helpful for patients with a confusing clinical presentation, those with a palpable LLQ mass which might be a drainable abscess, and to evaluate patients whose condition is not responding to standard therapy for acute diverticulitis If has not had a colonoscopy previously, will need one...however cannot scope during acute diverticulitis due to risk of diverticular blowout Treatment o If symptoms and findings are minor: Outpatient treatment Rest the bowel: Liquid diet or low-residue diet Adequate hydration Oral antibiotic effective against colonic flora Flagyl plus fluoroquinoline X 7-10 days OR Augmentin NOTE: Patients usually respond fairly quickly (first day) to antibiotic therapy. If not, may need CT and possible admission. o If patient cannot tolerate oral intake and/or elderly: Admit IV fluids IV antibiotics Bowel decompression via NG o Surgery if abscess, peritonitis, or sepsis 28 | P a g e Mesenteric Ischemia Source: Nishijima, DK. (May 1, 2012). Mesenteric ischemia in emergency medicine. Accessed at http://emedicine.medscape.com/article/758674-overview A disease of old age due to atherosclerosis or clot o > 2/3 of cases in those age 70+ Mortality rate > 80% 3 major arteries supply blood to the stomach, small intestine, and large intestine o Significant collateral circulation provides some protection from ischemia (able to compensate for approximately a 75% acute reduction in mesenteric blood flow for up to 12 hours without substantial injury) o No symptoms until 2 of 3 of these are blocked/narrowed Causes: o Chronic: long-standing atherosclerotic disease of 2 or more of the mesenteric vessels o Acute: causes include: arterial embolism usually from a dislodged cardiac thrombus arterial thrombosis due to acute worsening of ischemia in patients who have preexisting atherosclerosis severe and prolonged intestinal vasoconstriction most commonly from severe systemic illness with systemic shock secondary to reduced cardiac output can also occur with cocaine ingestion, ergot poisoning, digoxin use, and use of alpha-adrenergic agonists Symptoms o Chronic: severe abdominal pain (periumbilical) 30-60 minutes after eating; decreased intake wt. loss, diarrhea, N&V, constipation o Acute: sudden, severe abdominal pain, vomiting, diarrhea Diagnosis is difficult; CT scan and angiography are best for diagnosing this (note: MRI no better than CT) Suggestive findings o Pain more severe than expected; pain is disproportionate to physical examination findings o History of arteriosclerosis o Postprandial abdominal pain o Diarrhea (heme +) o Leukocytosis Treatment o Chronic: no smoking, diet/exercise, cholesterol & BP control o Acute: surgery 29 | P a g e Colon Cancer Demographics Colorectal cancer (cancer of the colon or rectum) is the 2nd leading cause of cancer-related death in the United States In 2003, there were an estimated 147,500 new cases and 57,100 deaths from colorectal cancer o Of those diagnosed, 93% are aged 50 and older Who is at Risk? Risk increases with advancing age Inflammatory bowel disease Personal or family history of colorectal cancer or colorectal polyps Certain hereditary syndromes (Lynch syndrome – CRC; familial polyposis) Lack of regular physical activity contributes to risk for colon cancer, but does not affect rectal cancer risk Low fruit and vegetable intake Low-fiber and high-fat diet Obesity Alcohol consumption Tobacco use Survival If colorectal cancer is detected early, while the disease remains localized, the 5year survival rate can exceed 90% in men and women A 2012 study found about 2/3 of Americans ages 50-75 have had the recommended screenings for colorectal cancer If the tumor is not detected early, morbidity and mortality increase rapidly. o In the U.S., the current 5-year rate is only 50-55%, because, regardless of sex, 65% of patients present with advanced stage disease What is needed: more aggressive screening and prevention strategies to facilitate earlier detection and improved treatment outcomes Pathophysiology Colon cancer is believed to arise from polyps, which are protrusions that extend from the mucosal surface of the colonic wall. Colon polyps may be nonneoplastic, or neoplastic, based on their histopathology o Nonneoplastic polyps include hyperplastic, inflammatory, and lymphoid polyps o Neoplastic polyps, which are generally called adenomas, can be further subdivided into benign or malignant adenomas Malignant = polypoid carcinoma Benign adenomas have the potential to become malignant Tubular adenomas represent 75% of all neoplastic polyps and are the least likely to progress to a malignant state. 30 | P a g e Villous adenomas are the mostly likely to progress to becoming cancerous Tubulovillous adenomas have an intermediate potential for becoming cancerous Predicting the probability that an adenoma will develop into cancer o Overall, fewer than 1% of all polyps progress to cancer o However, from 5% to 40% of adenomas are estimated to progress to cancer Generally, the smaller the polyp, the lower the likelihood of cancer o The process by which normal mucosa is converted into an adenoma and then cancer is gradual, occurring over approximately 5-10 years. Clinical Presentation Most cases are diagnosed between the ages of 60 and 75 o At diagnosis, almost 25% of patients have distant disease, while another 40% have regional disease involving the surrounding lymph nodes, which increases the risk for metastases. Most common site is on the right side of the colon, frequently involving the ascending or transverse colon Without screening, early detection of colorectal cancer is difficult, because patients with localized tumors are often asymptomatic Most common symptoms include: o Appearance of blood on or around the stool o Abdominal pain (frequently crampy and intermittent) o A change in bowel habits (constipation, diarrhea, or a change in stool caliber or frequency) o Iron deficiency anemia secondary to clinically silent GI bleeding o Unexplained weight loss (in patients with more advanced disease) Screening and Early Detection With the conversion of normal mucosa to carcinoma taking up to 10 years, there is a large window of opportunity to use screening procedures to detect polyps, the precursors of this cancer, and to remove them before they become cancerous. Approximately 70-80% of all cases occur in people at “average risk,” meaning that screening of the general population (as opposed to high-risk groups only) is appropriate. US Preventive Services Task Force: o Recommends screening for colorectal cancer (CRC) using fecal occult blood testing (FOBT), sigmoidoscopy, or colonoscopy in adults, beginning at age 50 years and continuing until age 75 years. o Recommends against routine screening for CRC in adults age 76-85 years. There may be considerations that support CRC screening in an individual patient. o Recommends against screening for CRC in adults older than age 85 years. o Insufficient evidence regarding use of CT colonography and fecal DNA testing as screening modalities for CRC. 31 | P a g e Recommend regular screening for all adults aged 50 years or older, including: o FOBT every year o Flexible sigmoidoscopy every 5 years o Double-contrast barium enema every 5 years o Total colon examination by colonoscopy every 10 years NOTE: High-risk individuals (those with a genetic predisposition for colorectal cancer, a family history of the disease, or inflammatory bowel disease) typically begin screening at an earlier age and undergo more frequent surveillance, usually with colonoscopy. o With first-degree relatives with CRC, recommendation for colonoscopy every 5 years, beginning at age 40 or 10 years than the earliest family diagnosis (whichever comes first) First-degree relatives include parents, siblings, and children Postpolypectomy surveillance strategies according to risk of recurrent advanced adenoma Colonoscopic Findings Recommendation Above Average Risk Small, left-sided hyperplastic polyps in a Continue average risk screening strategy patient who does not meet criteria for hyperplastic polyposis syndrome 1-2 small (< 1 cm) tubular adenomas Colonoscopy every 5-10 years High Risk 3-10 adenomas, or any adenoma > 1 cm with Colonoscopy every 3 years villous features or high-grade dysplasia >10 adenomas Colonoscopy more often than every 3 years, consider genetic counseling for familial syndrome Hyperplastic polyposis syndrome Colonoscopy, no clear recommendation on interval, further investigation needed Source: Bianchi, LK & Burke, CA (June 2008). Understanding current guidelines for colorectal cancer screening: A case-based approach. Cleveland Clinic Journal of Medicine, 75(6), 441-448. American Cancer Society advertising in medical journals: “Keep talking to your patients about colon cancer screening, so you won’t have to talk to them about colon cancer.” Chemoprevention In population-based observational studies, people had lower rates of colorectal cancer if they were taking various agents, including NSAIDs, calcium, and folate. o Aspirin has shown a modest risk reduction, but is associated with concomitant risks. o COX-2 inhibitors are under study as an adjunct to endoscopic surveillance and surgery in patients with familial adenomatous polyposis. o Exisulind, the sulfone metabolite of sulindac (NSAID) reduces adenomas in patients with familial adenomatous polyposis. o Calcium and folate supplementation have been found to moderately reduce adenoma formation without significant risk. 32 | P a g e References regarding colorectal cancer: www.cdc.gov website (Center for Disease Control) Kamakshi, V.R., & Goodin, S. (2001). Prevention and management of colorectal cancer in women. Journal of the American Pharmaceutical Association, 4 (4), 585-595. Burke, C.A., Bauer, W.M., & Lashner, B. (April 2003). Chemoprevention of colorectal cancer: Slow, steady progress. Cleveland Clinic Journal of Medicine, 70 (4), 346-350. Hepatic Problems Cirrhosis and Chronic Liver Failure Cirrhosis is a consequence of chronic liver disease, with liver tissue being replaced by fibrosis, scar tissue, regenerative nodules, and leading to loss of liver function; final stage of chronic liver damage/disease Liver failure occurs when >75% of the liver is no longer able to function due to inflammation of the liver. Acute liver failure: loss of function occurs within days to weeks; may be reversible (acetaminophen overdose is leading cause) Chronic liver failure: damage is severe; occurring over years to decades; generally irreversible (Hepatitis C and ETOH abuse are leading causes) Most common ages 40-50 years; men>women; 10th leading cause of death in men; 12th in women Best treatment is prevention, with emphasis on: - reducing alcohol consumption - limiting occupational hepatotoxin exposure, and - preventing parenteral transmission of hepatitis B and C. The overall goal is to minimize hepatocellular injury and the risk of progressing to chronic liver failure and cirrhosis. Symptoms Most symptoms are nonspecific and may include: o easy bruising (WHY?) o fatigue o malaise o weight loss Other symptoms or diseases may occur as a result of the primary disorder that caused the cirrhosis. These symptoms and diseases may be a clue to the cause and include Addison’s disease, arthralgia, autoimmune disease, bone pain, 33 | P a g e diabetes mellitus, heart failure, hyperpigmentation, hypothyroidism, loss of libido, night blindness, pruritus, and steatorrhea. Clinical Findings Physical examination abnormalities include: - clubbing - hepatomegaly - jaundice - lacrimal and parotid gland enlargement - muscle wasting - gynecomastia and testicular atrophy in men (WHY?) - palmar erythema - spider angioma - splenomegaly Portal hypertension is suggested by abdominal collaterals (caput medusae), ascites, encephalopathy, esophageal varices, hemorrhoids, and splenomegaly. Staging and Treatment of Ascites Source: Fowler, C. (April 2013). Management of patients with complications of cirrhosis. The Nurse Practitioner, 38(4),14-22. Stage 1 2 3 Refractory Description Minimal ascites; only detectable by ultrasound Moderate ascites with abdominal distension Massive ascites with marked abdominal distention Ascites that is unresponsive or inadequately responsive to diuretics or excessive adverse reactions from diuretics Treatment Sodium restriction Sodium restriction and diuresis Sodium restriction, diuretics, therapeutic paracentesis, and TIPS (transjugular intrahepatic portosystemic shunt) Therapeutic paracentesis and TIPS Palpation of the liver reveals variable findings: o Enlarged and easily palpable liver o Regenerating macronodules along the liver border (micronodules are nonpalpable) o In advanced stages the liver is often small and hard. Hepatocellular carcinoma should be suspected in patients demonstrating a RUQ bruit or friction rub, especially if blood ascitic fluid is aspirated. Other signs may occur as a result of the primary disorder that caused the cirrhosis. They therefore may be a clue to the cause. They include arthropathy, dermatitis, Dupuytren’s contracture, dysrhythmia, ecchymosis, glossitis, hyperpigmentation, Kayser-Fleisher ring (pigmented ring at the outer margin of the cornea seen in Wilson’s disease), neurologic abnormality, xanthelasma/xanthoma. Laboratory Tests Generally, the following tests are ordered: albumin ALT Alkaline phosphatase 34 | P a g e AST bilirubin globulins 5’-nucleotidase prothrombin time (WHY?) Laboratory abnormalities are often nonspecific. Certain disease processes are associated with more specific laboratory alterations that may suggest the diagnosis (such as checking a hepatitis panel for Hepatitis B, C, D). Liver biopsies may identify histology unique to a given diagnosis. Unfortunately, in late-stage cirrhosis, the histology no longer differentiates the cause. Differential Diagnosis While most cases of cirrhosis occur secondary to alcohol abuse or viral hepatitis, the following are also implicated: Alcohol Biliary obstruction Cardiovascular (right-sided heart failure, tricuspid insufficiency) Drugs and toxins (amiodarone, carbon tetrachloride, isoniazid, methotrexate, methyldopa, oral contraceptives) Infection (Hepatitis B/C/D, schistosomiasis, tertiary syphilis) Malnutrition (gastroplasty, jejunoileal bypass) Metabolic/Inherited (antitrypsin deficiency, hemochromatosis, Wilson’s disease) Treatment Therapy of cirrhosis is usually supportive and aimed at improving nutritional status, treating complications, and avoiding factors that may accelerate hepatic insufficiency. When cirrhosis occurs as a result of a treatable condition, therapy should be directed at the primary disorder. In a limited number of disorders, a drug or therapy of choice does exist. Alcoholic liver disease: Abstinence is the only established therapy. Alpha1-antitrypsin deficiency: Liver transplantation is curative. Hemochromatosis: Iron removal by phlebotomy is the therapy of choice. Chelation therapy with deferoxamine (Desferal) and ascorbic acid is an alternative. Primary biliary cirrhosis: Liver transplantation is curative. Ursodeoxycholic acid (Ursodiol or Actigall) may offer limited benefit. Secondary biliary cirrhosis: Relief of biliary obstruction by endoscopy or surgery serves a preventive and therapeutic role. Wilson’s disease: Penicillamine (Cuprimine) chelates copper and is the drug of choice. Trientine hydrochloride (Cuprid) and zinc sulfate are alternative medications. Transplantation is curative. Diet Patients require a well-balanced diet high in calories. Limiting protein intake is important when encephalopathy is present. 35 | P a g e The use of branched-chain amino acids also may benefit patients with encephalopathy. Appropriate mineral and vitamin (fat-soluble) intake is especially important when cholestasis is present. Sodium restriction is indicated if sodium retention occurs. Copper restriction is important in Wilson’s disease and diseases that involve biliary obstruction. Patients should restrict their intake of copper-rich food such as chocolate, dried beans, organ meat, peas, shellfish, and whole wheat. Patient Education Patients should be made aware of factors (drugs, toxins, infections) that may exacerbate their liver disease. Alcohol counseling benefits patients and family members. Family planning and screening are important in a few diseases such as hemochromatosis and Wilson’s disease. The correct use, need for compliance, and possible side effects of medications should be emphasized. Making patients aware of disease complications encourages them to see prompt medical attention, allowing for early diagnosis and treatment. Follow-Up Monitor medication efficacy and side effects as well as disease progression. Complications include ascites, spontaneous bacterial peritonitis, portal hypertension and variceal bleeding, hepatic encephalopathy, hepatic failure, and hepatorenal syndrome (a life-threatening medical conditions involving rapid deterioration of kidney function in individuals with cirrhosis or liver failure. Usually occurs when liver function deteriorates rapidly due to an acute injury such as infection, GI bleed or overuse of diuretics. Usually fatal without liver transplant. Dialysis may help short term. Occurs in 18% of patients with cirrhosis within 1 year of diagnosis; in 39% within 5 years of diagnosis.) References: Heidelbaugh, JJ, & Bruderly, M. (September 1, 2006). Cirrhosis and chronic liver failure: Part I. Diagnosis and evaluation. American Family Physician, 74(5), 756-762. Heidelbaugh, JJ, & Sherbondy, M. (September 1, 2006). Cirrhosis and chronic liver failure: Part II. Complications and treatment. . American Family Physician, 74(5), 767-776. References for following Hepatitis content: Centers for Disease Control and Prevention, National Center for Infectious Diseases Elgouhari, HM, Abu-Rajb Tamimi, TI, & Carey, W. (January 2009). Hepatitis B: A strategy for evaluation and management. Cleveland Clinic Journal of Medicine, 76(1), 19-35. Gardenier, D. & Alfandre, D. (September 2006). Primary care of the patient with chronic hepatitis C. The Journal for Nurse Practitioners, 517-524. Wilson, TR. (June 2005). The ABCs of hepatitis. The Nurse Practitioner, 30(6),12-21. www.HepatitisFoundation.org 36 | P a g e ************** Case Study #10 ************** The ABC’s of Hepatitis What is it? Incubation Period How is it Spread? Symptoms Treatment of Chronic Disease Hepatitis A (HAV) HAV is a virus that causes inflammation of the liver. It does not lead to chronic disease. Hepatitis B (HBV) HBV is a virus that causes inflammation of the liver. It can cause liver cell damage, leading to cirrhosis and cancer. Hepatitis C (HCV) HCV is a virus that causes inflammation of the liver. It can cause liver cell damage, leading to cirrhosis and cancer. 2 to 25 weeks. Average 7 to 9 wks. Contact with infected blood, contaminated IV needles, razors, and tattoo and body-piercing tools, Infected mother to newborn. Not easily spread through sex. Hepatitis D (HDV) HDV is a virus that causes inflammation of the liver. It only infects those persons with HBV. Hepatitis E (HEV) HEV is a virus that causes inflammation of the liver. It is rare in the U.S. There is no chronic state. 2 to 7 weeks. Average 4 weeks. Transmitted by fecal/oral (anal/oral sex) route, close person to person contact or ingestion of contaminated food and water. Hand to mouth after contact with feces, such as changing diapers. Children may have none. Adults usually have light stools, dark urine, fatigue, fever, nausea, vomiting, abdominal pain, and jaundice. Not applicable 6 to 23 weeks. Average 17 weeks. 2 to 8 weeks. Contact with infected blood, contaminated needles. Sexual contact with HDV infected person. 2 to 9 weeks. Average 40 days. Transmitted through fecal/oral route. Outbreaks associated with contaminated water supply in other countries. May have none. Some persons have mild flu like symptoms, dark urine, light stools, jaundice, fatigue and fever. Same as HBV Same as HBV Same as HEV Interferon and nucleoside/nucleotide analogues (tenofovir, entecavir, adefovir, telbivudine, lamivudine) control replication of virus with varying success. Also vaccinated against hepatitis A if not immune to it. Alcohol rehab Smoking cessation Surveillance for hepatocellular Pegylated Interferon alfa 2a or 2b plus ribavirin with varying success. Interferon with varying success. Not applicable Contact with infected blood, seminal fluid, vaginal secretions, contaminated needles, including tattoo and body-piercing tools. Infected mother to newborn. Human bite. Sexual contact. 37 | P a g e None HBV vaccine prevents HDV infection. None Infants born to infected mother, having sex with an infected person or multiple partners, injection drug users, emergency responders, healthcare workers, persons engaging in anal/oral sex, and hemodialysis patients. Blood transfusion recipients before 1992, healthcare workers, injection drug users, hemodialysis patients, infants born to infected mother, multiple sex partners. Injection drug users, persons engaging in anal/oral sex and those having sex with an HDV infected patient. Travelers to developing countries, especially pregnant women. Vaccination. Vaccination provides Immune protection for 20 plus Globulin within years. Hepatitis B 2 weeks of Immune Globulin exposure. within 1 week of Washing exposure. Clean up hands with soap infected blood with and household bleach and water after wear protective going to the gloves. Do not share toilet. Use razors, household toothbrushes, or bleach (10 parts needles. Safer sex. water to 1 part bleach) to clean surfaces contaminated with feces, such as changing tables. Safer sex. HEPATITIS FOUNDATION INTERNATIONAL 504 Blick Drive, Silver Spring, Maryland 20904-2901 Tel: 301-622-4200 or 1-800-891-0707 Fax: 301-622-4702 Email: [email protected] Website: www.HepatitisFoundation.org Grid 2005 Clean up spilled blood with household bleach. Wear gloves when touching blood. Do not share razors, toothbrushes, or needles with anyone. Safer sex. Hepatitis B vaccine to prevent HBV/HDV infection. Safer sex. Avoid drinking or using potentially contaminated water. Vaccine Who is at Risk? Prevention Two doses of vaccine to anyone over 2 yrs of age Household or sexual contact with an infected person or living in an area with HAV outbreak. Travelers to developing countries, persons engaging in anal/oral sex and injection drug users. carcinoma via liver ultrasound and alpha fetoprotein measurement every 6-12 months. Three doses may be given to persons of any age. 38 | P a g e Serologic Features of Viral Hepatitis Serologic Markers Interpretation IgM anti-HAV Acute disease IgG anti-HAV Remote infection and immunity HBsAg Acute or chronic disease HBeAg Active replication IgM anti-HBc (high titer) Acute disease IgG anti-HBc: - HBsAg positive Chronic disease - HBsAg negative Prior exposure Form of Infection Hepatitis A Hepatitis B Hepatitis C Anti-HCv Acute, chronic, or resolved disease Hepatitis D HBsAg and anti-HDV Acute disease Co-infection Superinfection - IgM anti-HBc positive - IgG anti-HBc positive Hepatitis E None Key: Anti-HAV = antibody to hepatitis A virus Anti-HCV = antibody to hepatitis C virus Anti-HDV = antibody to hepatitis D virus HBeAg = hepatitis B e antigen HBsAg = hepatitis B surface antigen Anti-HBc = antibody to hepatitis B core antigen Anti-HBs = antibody to hepatitis B surface antigen (HBsAg) Serological Interpretation for Hepatitis B (Centers for Disease Control and Prevention, National Center for Infectious Diseases) Tests Results Interpretation Susceptible HBsAg Negative Anti-HBc Negative Anti-HBs Negative HBsAg Negative Immune due to natural infection Anti-HBc Positive Anti-HBs Positive HBsAg Negative Immune due to hepatitis B vaccination Anti-HBc Negative Anti-HBs Positive HBsAg Positive Acutely infected Anti-HBc Positive IgM anti-HBc Positive Anti-HBs Negative HBsAg Positive Chronically infected Anti-HBc Positive IgM anti-HBc Negative Anti-HBs Negative HBsAg Negative Four interpretations (see below) Anti-HBc Positive Anti-HBs Negative Four interpretations: 1. May be recovering from acute HBV infection. 2. May be distantly immune and test is not sensitive enough to detect very low level of anti-HBs in serum. 3. May be susceptible with a false positive anti-HBc. 4. May be an undetectable level of HBsAg present in the serum and the person is actually a carrier. 39 | P a g e Other types of hepatitis: Autoimmune hepatitis Age: 30-60 years of age Sex: F > M Risk factors: associated with autoimmune conditions such as Type 1 DM, thyroid disease, RA, vitiligo, family history, environmental exposure Treatment: Prednisone, Azathioprine o Monitor LFT’s monthly o Therapy for at least 12-18 months o Relapse in 50%; may need lifetime maintenance therapy Alcoholic hepatitis Age: 40-50 years of age Sex: M > F 2:1 Risk factors: Hispanic, poor nutrition, obesity, drinking multiple types of alcohol Associated with 160 g/d ETOH for 10-20 years Treatment: diet, alcohol avoidance, corticosteroids Drug-induced hepatitis Age: middle aged Sex: M = F Risk factors: psych history, history of suicide, dementia, regular ETOH intake Tylenol overdose most common Check toxicology screen Treatment: antidote for medication Nonalcoholic Fatty Liver Disease (NAFLD) Sources: Bayard, M, Holt, J, & Boroughs, E. (June 1, 2006). Nonalcoholic fatty liver disease. American Family Physician, 73(11), 1961-1968. Sublett, L. (August 2007). Deconstructing nonalcoholic fatty liver disease. The Nurse Practitioner, 32(8), 12-17. Formerly called nonalcoholic steatohepatitis (NASH) o Now refers to a spectrum of liver diseases ranging from steatosis (fatty infiltration of the liver) to NASH to cirrhosis Most common cause of elevated liver enzymes in adults in the US Most common cause of cryptogenic cirrhosis, which is cirrhosis that cannot be explained by hepatitis, alcohol abuse, toxin exposure, autoimmune disease, congenital liver disease, vascular outflow obstruction, biliary tract disease Prevalence in US: 16-23% o Prevalence becomes greater with increasing body weight 2/3 of those with BMI of 30 or greater 90% of those with BMI > 39 Two types of NAFLD o Primary NAFLD is related to metabolic syndrome-associated conditions Obesity Diabetes Hypertriglyceridemia 40 | P a g e o Secondary NAFLD occurs after: Bariatric surgery Rapid weight loss in obese patients Total parenteral nutrition Hepatotoxic medications Lipodystrophy Wilson’s disease Increased risk of cardiovascular events Differential diagnosis: diagnosis of NAFLD requires exclusion of alcoholic liver disease and viral hepatitis o Requires that daily alcohol intake be < 2 drinks/day for men, <1.5 drinks/day for women Clinical findings: most are asymptomatic; may complain of fatigue and RUQ abdominal fullness or pain o Up to 50% have hepatomegaly Laboratory evaluation: o Elevated ALT and AST, usually 1-4X the upper limits of normal (although some have normal ALT, AST) o Ratio of AST/ALT usually is < 1 (This ratio is usually >2 in alcoholic liver disease) o Alkaline phosphatase may be elevated X2 the upper limit of normal o GGT may be elevated Imaging: Ultrasound of liver (CT is no more sensitive and is more expensive, but can identify other liver pathology such as masses more effectively) American Gastroenterological Association recommendation for diagnostic approach o Question patient carefully about alcohol use o Obtain ALT, AST, alkaline phosphatase, serum bilirubin, and albumin levels, prothrombin time, and hepatitis panel o Order imaging (ultrasound or CT) Treatment o Focuses primarily on risk factors for atherosclerotic heart disease (Weight loss, exercise) Advise patients to avoid rapid weight loss. A study found that liver histological findings worsened when weight loss exceeded 1.6 kg (3.5 lb) per week. o Treat insulin resistance: metformin o Treat hyperlipidemia: Modest elevation of liver enzyme levels should not preclude the use of statins in patients for whom they are otherwise indicated. The National Cholesterol Education Program states that there is no evidence that statins are harmful in patients with fatty liver caused by obesity. Prognosis: depends upon the extent of liver damage o Steatosis alone generally has a benign course, and progression to cirrhosis is rare. 41 | P a g e Other GI Problems Common anorectal conditions Source: Fargo, MV, & Latimer, KM. (March 15, 2012). Evaluation and management of common anorectal conditions. American Family Physician, 85(6), 624-630. Pruritus ani: perianal itching Most patients self-treat for 12 months before seeking care Many causes (dermatologic, dietary irritants [beer, caffeine, chili peppers, citrus, milk, tomatoes], fecal soilage, infections, malignancy, medications, systemic disease, topical irritants) Treatment: address the underlying cause o Proper hygiene, avoid perfumes, dyes, dietary irritants, and tight clothing o Keep area dry, avoid itch-scratch cycle (scratching exacerbates the inflammation, causing an irresistible urge to scratch even more) o Sedating antihistamine such as hydroxyzine at night o May need topical steroids for 2-4 weeks max (low-potency to minimize skin atrophy) Anorectal pain May be caused by a fissure, an abscess, thrombosed external hemorrhoids, proctitis, perineal sepsis, or proctalia fugax. o Anal fissures: most common site is posterior midline; treat with stool softeners, fiber, sitz baths, topical analgesics o Thrombosed external hemorrhoids: Sudden onset of pain caused by a clot in the external hemorrhoidal vein. Pain is most intensive during the first 24-48 hours after the clot forms and then it resolves rapidly, even with no treatment. If pain is beginning to diminish, treat with topical corticosteroids, warm soaks, and stool softeners. Anorectal masses May be condyloma (anogenital warts), abscess, polyp, prolapse, hemorrhoid, or anal cancer o Risk factors for anal cancer: HPV, 15+ sexual partners during a lifetime, tobacco smoking, long-term corticosteroid use, receptive anal intercourse, and in HIV-infected men and women, age < 30 or male homosexual contact Can do anal pap screening in men with HIV Anorectal fistulas Suspect in any patient with discharge, pain, swelling, or bleeding Treatment: sitz baths, high-fiber diet, analgesics (referral to surgeon for nonhealing or complex fistulas) Anorectal bleeding Due to hemorrhoids, fissures, polyps, diverticular disease, inflammatory bowel disease, or colorectal cancer 42 | P a g e Hemorrhoids Etiology Hemorrhoidal disease may be produced by anything that increases pressure in the hemorrhoidal veins. Common etiologies are thought to include: - constipation - straining at stool - Valsalva maneuver during other activities such as lifting - lesions of the rectum and distal sigmoid colon that produce venous obstruction Because the internal hemorrhoidal venous plexus is one of the several areas of anastomosis of the systemic and portal circulation, internal hemorrhoids may also develop secondary to portal hypertension produced by hepatic cirrhosis. Symptoms Internal hemorrhoids are commonly associated with complaints related to: painless rectal bleeding anal pruritus (itching) perianal soiling (secondary to mucosal secretions) Clinical Findings Internal hemorrhoids are graded on the basis of their anatomic presentation: Grade Description Diagram Picture Grade I The hemorrhoidal mass is swollen and projects into the anal canal (do not prolapse) Grade II The hemorrhoidal mass is pendulous (prolapses) on defecation but reduces spontaneously. Grade III The hemorrhoidal mass prolapses on defecation and recedes only following manual reduction. Grade IV The hemorrhoidal mass is permanently prolapsed. Source of above diagrams/photos: http://en.wikipedia.org/wiki/Hemorrhoid 43 | P a g e Tests Before any type of operative hemorrhoidal therapy is undertaken, a digital rectal and flexible sigmoidoscopic examination should be performed and appropriate coagulation studies (PT and PTT) should be obtained if clinically indicated. Treatment Contrary to popular belief, there is no role for suppositories in the management of hemorrhoidal disease. The treatment of grade I and grade II internal hemorrhoids consists of stool softeners and/or surface tension-decreasing agents, warm sitz baths, and improved bowel habits. This noninvasive protocol may reduce the need for more aggressive intervention in the majority of patients. Grade III and IV hemorrhoids usually require surgery. Stubborn itching and inflammation respond well to topical corticosteroids; hydrocortisone cream (1%) is adequate, relatively inexpensive, and available OTC. Should be used 3-4 times/day. Caution with long term use: can permanently damage or cause ulceration of the perianal skin Fecal impaction and incontinence Fecal impaction is a partial or complete blockage of the colon by hard, dry stool; presents as constipation or overflow incontinence Fecal incontinence is the involuntary loss of bowel function Remove physical barriers to the bathroom; institute scheduled defecation schedules for patients with dementia Biofeedback, antidiarrheal medication PT for pelvic floor dysfunction; surgery Hernias Source: Amid, PK, Graham, M, & Selwyn, CA. (May 2005). Abdominal hernia: Emerging trends in diagnosis and management. Patient Care. 43-55. Hernia: a defect in the normal musculofascial continuity of the abdominal wall that permits the passage of structures not normally passing through the wall. Incarcerated hernias are those that cannot be reduced and the contents of the hernial sac cannot be returned to the peritoneal cavity. Strangulated hernias are those which occur when the blood supply to the viscera lying within the hernial sac is obliterated or cut off. Several types: Inguinal hernias (75% of all abdominal hernias are inguinal) Direct: portions of the bowel and/or omentum protrude directly through the floor of the inguinal canal and emerge at the external inguinal ring Indirect: pass through the internal abdominal ring, traverse the spermatic cord through the inguinal canal and emerge at the external inguinal ring (8-10 times more common in men than in women) Femoral hernias (protrusion of omentum through the femoral canal) (3-5 times more common in women than in men) 44 | P a g e Ventral hernias Incisional hernias (develop in the scar of a previous laparotomy or in a drain site) Umbilical hernias (pass through the umbilical ring; often close spontaneously by age 4 or 5 years) Epigastric hernias (occur through the linea alba between the xiphoid process and the umbilicus; may produce symptoms that mimic peptic ulcer disease or biliary colic) History: Ask about: groin pain swelling ability to reduce the hernia circumstances of onset aggravating and alleviating factors, such as exacerbation on standing, straining, or coughing Acute onset of colicky abdominal pain, nausea, and vomiting suggest entrapment and strangulation in a patient with a known hernia. An incarcerated inguinal hernia presents gradually with scrotal pain. Clinical Findings (inspection/palpation/maybe auscultation) Bowel palpable in the scrotum or in the inguinal canal. Bowel sounds may be audible in the scrotum if the hernia is incarcerated. If strangulation has occurred, bowel sounds are not audible in the scrotum, and the abdomen is likely to be tender, distended, and without bowel sounds. When examining male: o With a direct inguinal hernia, when the finger is inserted through the external canal, a bulge will be felt striking the side of the finger. o With an indirect inguinal hernia, when the finger is inserted through the external canal, the bulge will be felt at the fingertip when the client coughs or strains. When examining female: o It is more difficult to establish the diagnosis of inguinal hernia; locate the external inguinal ring by identifying the inguinal ligament and os pubic; place hand over inguinal ring and palpate for bulge when client coughs or strains. Differential Diagnosis of Inguinal Hernias Hydrocele Varicocele Spermatocele Epididymal cysts Epididymitis Testicular tumor In children, undescended testes 45 | P a g e Differential Diagnosis of Femoral Hernias Enlarged lymph node Lipoma Direct inguinal hernia Saphenous varix Diagnostic Tests Often none needed, may order ultrasound if uncertain about abdominal mass Clinical Pearls: If diagnosis is difficult, try having the patient change position from sitting to standing and having him or her cough or strain. The next best diagnostic tool after a thorough history and physical exam is a CT scan, with referral to a surgeon an option at any point in the process. Pain does not equal hernia. Pain without a bulge is more likely to be something other than a hernia. Management Hernias should have referral to a surgeon. A hernia that reduced spontaneously could become incarcerated and strangulated Lack of symptoms does not necessarily mean that a hernia is harmless and can be left alone. Unless a defect is very large—with a decreased risk of the herniated sac becoming trapped outside the abdominal wall—it should be surgically repaired. Femoral hernias need to be repaired as soon as possible because of the increased risk of incarceration and strangulation. Follow-Up Examine annually for recurrences Acute Diarrhea Source: Helton, T, & Rolston, DDK (October 2004). One minute consult: Which adults with acute diarrhea should be evaluated? What is the best diagnostic approach? Cleveland Clinic Journal of Medicine, 71(10), 778-785. Definition: An increase in the frequency of stools with a decrease in consistency compared with the patient’s baseline pattern. Acute is diarrhea that has lasted < 14 days; chronic diarrhea has a duration greater than 1 month. (14-29 days = persistent acute diarrhea) For most cases, a brief history and treatment with oral hydration and OTC loperamide, kaopectate, or Pepto-Bismol usually suffice. A full H&P and diagnostic testing is needed for a patient with any of the following: Fever (38.5oC and above) Dysentery (passage of blood and mucus in the stool) 46 | P a g e Symptoms of dehydration, particularly postural lightheadedness, decreased urine output, and excessive thirst) Worsening diarrhea after 48 hours Six or more stools in 24 hours Advanced age (70 years and older) Compromised immune system Age greater than 50 with severe abdominal pain History Travel Sexual practices Antibiotic use within 2 months (concern for Clostridium difficile) Other medications (laxatives, antacids, digoxin, immunosuppressive drugs) Ill contacts Group gatherings after which other attendees also developed similar illness Recent surgeries or procedures Recent meals Water source Pets (particularly turtles) The onset and duration of the illness Diagnostic Testing Stool for occult blood o If (+), obtain stool cultures Consider empiric antibiotics if traveler’s diarrhea is suspected Testing stool for ova and parasites should be done if recent foreign travel, if homosexual who is immunocompromised, if community outbreak of parasite, or if dysentery Fecal leukocyte testing – if (+) suggests an inflammatory cause and would support obtaining stool cultures CBC, BMP, plain film of abdomen Chronic Diarrhea Source: Juckett, G, & Trivedi, R. (November 15, 2011). Evaluation of chronic diarrhea. American Family Physician, 84(10), 11191126. Definition: a decrease in stool consistency continuing for more than 4 weeks. Categories: (may overlap) Watery o Osmotic (water retention due to poorly absorbed substances) o Secretory (reduced water absorption o Functional (hypermotility) Fatty (malabsorption) Inflammatory (with blood and pus) 47 | P a g e History and Physical Examination Determine exactly what the patient means when saying he/she has diarrhea o It may be incontinence due to fecal impaction rather than diarrhea Ask about stool volume, frequency, and consistency Travel history Check regarding recent weight loss Examine eyes, mouth, check lymphadenopathy, abdomen, skin, rectal exam Differential Diagnoses: Includes hundreds of conditions, but most common causes are: Celiac disease Clostridium difficile infection Drug-induced diarrhea Endocrine diarrhea (hyperthyroidism) Giardiasis Infectious enteritis or colitis: bacterial or viral gastroenteritis, amebic dysentery Inflammatory bowel disease Irritable bowel disease Ischemic colitis Microscopic colitis Diagnostic Testing CBC, albumin level, ESR, liver function testing, TSH, electrolytes Fecal leukocyte level and fecal occult blood test Fecal calprotectin (to identify inflammatory bowel disease) If travel risk factors, stool C&S, stool ova and parasite examination, Giardia and Cryptosporidium stool antigen tests. Treatment: Depends on cause found Empiric therapy may be justified if a specific diagnosis is strongly suspected, for example metronidazole for a traveler with possible giardiasis or bile acid resins for bile acid malabsorption. ************** Case Study #11 ************** Chronic Constipation Source: American Gastroenterology Association (2008). Guidelines: Managing chronic constipation. Definition: unsatisfactory defecation resulting from difficult stool passage and/or infrequent defecation Clinical subgroups of constipation Normal transit constipation (functional constipation) o Most common form (59% prevalence rate) o Colonic transit time is normal 48 | P a g e Slow transit constipation (colonic inertia) o 13% prevalence o Delayed colonic transit Pelvic floor dysfunction (disorder defecation) – 25% prevalence Combination (slow transit + pelvic floor dysfunction) Clinical Evaluation History: determine predominant symptom (infrequent defecation, straining, hard stool), duration and severity of symptoms, response to prior or current therapy Source: http://www.bing.com/images/search?q=bristol+stool+form+scale&id=8BFE32FF9B003C09452EAE6D5C814962C88A6276&FORM =IQFRBA#view=detail&id=8BFE32FF9B003C09452EAE6D5C814962C88A6276&selectedIndex=0 Physical exam: rectal exam, check anal reflex, anal sphincter, look for rectocele Diagnostics: colonoscopy if age > 50, alarm signs or additional symptoms present Management Patient education about diet (including fiber and hydration) Lifestyle modifications o Encourage patients to avoid postponing defecation o Monitoring bowel habits with a daily diary o Moderate exercise Choice of therapeutic agent o Polyethylene gycol 3350 o Milk of magnesia o Chloride channel activator (Amitiza [lubiprostone]) o 5-HT4 (tegaserod [Zelnorm]) no longer available Biofeedback for pelvic floor training ************** Case Study #12 ************** 49 | P a g e Irritable Bowel Syndrome (IBS) Source: Wilson, JF (July 3, 2007). In the clinic: Irritable bowel syndrome. Annals of Internal Medicine. ITC7-1 – ITC7-16. Definition IBS is characterized by abdominal pain or discomfort associated with abnormal bowel habits (diarrhea, constipation, or alternation between the two), and associated with symptoms of bloating, distention, straining, feelings of incomplete evacuation, and urgency. Epidemiology Affects as many as 1 in 5 US adults, occurs more often in women than in men, and begins before the age of 35 in about half of all people who develop the disorder Pathophysiology Certain motility and sensory abnormalities are found in IBS patients as a group, and these distinguish them from healthy individuals: Various stimuli including stress, meals, and peptides alter colonic or small intestinal motor response. It is presumed that pain symptoms in patients with IBS are due to hyperactivity. These patients also have reduced sensory thresholds for stimuli such as rectal and ileal distention. IBS, especially in women, overlaps with other GI disorders, non-GI pain disorders, and affective disorders. These include painful menstruation, history of abuse, fibromyalgia and other rheumatologic symptoms, and chronic pelvic pain. Symptom criteria for IBS: Rome III Recurrent abdominal pain or discomfort at least 3 days per month in the past 3 months associated with 2 or more of the following: 1. Improvement with defecation 2. Onset with change in frequency of stool 3. Onset associated with a change in the form and appearance of stool * Criteria must be fulfilled for at least the past 3 months with symptom onset at least 6 months before diagnosis Symptoms History Physical Findings Alarm Features that Suggest Possible Organic Disease Weight Loss Frequent nocturnal awakenings due to gastrointestinal symptoms Fever Blood mixed in stool New onset, progressive symptoms Onset of symptoms after age 50 Recent antibiotic use Family history of colon or ovarian cancer or inflammatory bowel disease Abdominal mass Stool positive for occult blood Enlarge lymph nodes 50 | P a g e Clinical Findings The physical examination in most IBS patients is generally normal. Physical examination may reveal tenderness in the area of the colon in patients with the spastic colon variety of IBS. In patients with small bowel involvement, pressure over the umbilicus or epigastrium may precipitate symptoms. Differential Diagnoses Constipation-predominant symptoms Strictures due to inflammatory bowel disease, diverticulitis, ischemia, or cancer Colonic inertia Pelvic floor dysfunction Neurologic disease (Parkinson disease, MS) Medications (opioids, CCBs, anticholinergics) Hypothyroidism Hypercalcemia Diarrhea-predominant symptoms Crohn’s disease Ulcerative colitis Microscopic colitis Parasites (check on travel, drinking water from streams, etc.) Clostridium difficile Other bacteria Small bowel overgrowth Sprue (gluten-sensitive enteropathy) Lactose intolerance Postgastrectomy syndrome HIV enteropathy GI endocrine tumor (carcinoid, gastrinoma) Laxative abuse Laboratory Tests Laboratory studies are generally normal in IBS. The diagnosis should be suspected based on the patient’s symptoms and by excluding organic diseases. A minimal evaluation would consist of a CBC, CMP, ESR, antibody for celiac disease If diarrhea is a predominant symptom, stool samples for leukocytes, culture for enteric pathogens, and examination for ova and parasites should be pursued. X-ray studies of the small bowel or colon are generally not indicated with typical IBS symptoms. If the patient has had symptoms for more than 3 months or is over age 50, a barium enema or colonoscopy should be performed. 51 | P a g e Treatment Dietary modification Reasonable to consider in cases in which specific foods seems to trigger symptoms Review dietary habits to: o Evaluate for lactose intolerance o Evaluate consumption of caffeine, fructose, or artificial sweeteners (laxative effects) o Inquire about laxative-containing herbal products o Determine whether drinking excess carbonated beverages, drinking with a straw, or chewing gum, all of which can lead to swallowing too much air and result in gas and bloating o Advise against excess intake of fats (cause gas retention) o Advise avoidance of certain carbohydrates such as beans, cabbage, broccoli, and cauliflower, if they trigger symptoms (may be difficult to digest and lead to fermentation and gas in the colon) Fiber is helpful for relief of constipation but not for relief of pain Other nonpharmacologic interventions Reassurance Education with advice about trigger avoidance Stress management o Patients with IBS are more likely to have had early life or current trauma, including losses or abuse, and are more likely to have generalized anxiety disorder and worry. Exercise Pharmacologic therapies Constipation predominant Increase fiber (start with one tablespoon psyllium per day or twice a day). Alternatives include polycarbophil or methylcellulose. Osmotic laxative Stool softener Zelnorm (tegaserod) – binds to 5-HT4 receptors, stimulating GI peristalsis and decreasing visceral sensitivity (Withdrawn from US Market) Amitiza (lubiprostone) -- activates chloride channels, increasing intestinal fluid secretion and motility Diarrhea predominant Antidiarrheals o Loperamide (Imodium), 2-4 mg every 6-8 hours o Diphenoxylate (Lomotil), 2.5-5 mg every 4-6 hours alosetron HCL tablets (Lotronex) – selective 5-HT3 receptor antagonist (inhibits activation of non-selective cation channels which results in the modulation of the enteric nervous system)—Withdrawn from US Market in 2000/Returned to market in 2002. 52 | P a g e o Now “Restricted Access in US”: In order to prescribe, you must enroll in GlaxoSmithKline’s Prescribing Program for Lotronex (www.lotronex.com) Pain/gas/bloat predominant Antispasmodics (Anticholinergics) (dicyclomine[Bentyl], 10-20 mg. 30-45 minutes between meals four times a day; hyoscyamine [Anaspaz, Levbid, Levsin, NuLev]) Antidepressants (amitriptyline HCl/Elavil, or doxepin/Sinequan, starting with 2550 mg at hour of sleep and gradually increased to 75-150 mg at hs as tolerated. Fluoxetine/Prozac, 20 mg, as single daytime dose is less sedating.) Referral Consultation with gastroenterology is warranted when patients do not fit Rome criteria, when patients have alarm symptoms, and when patients do not respond to initial management. Celiac Disease Source: Crowe, SE (2011). In the clinic: Celiac disease. Annals of Internal Medicine. ITC5-2 – ITC5-16. Also known as gluten-sensitive enteropathy, celiac sprue, nontropical sprue Affects 1% of U.S. population Results from an inappropriate T-cell-mediated immune response to ingested gluten that causes inflammatory injury to the small intestine in genetically predisposed persons. Damage to the proximal small intestinal mucosa results in the malabsorption of nutrients. Source: Harrison, MS, Wehbi, M., & Obideen, K. (March 2007). Celiac disease: More common than you think. Cleveland Clinic Journal of Medicine, 74(3), 209-216. Strong genetic component: 90-95% of patients with celiac disease possess the HLA-DQ2 allele, and the other 5-10% possess the HLA-DQ8 allele. Classic GI manifestations: diarrhea, flatulence, abdominal distention, weight loss, malaise, steatorrhea, and recurrent aphthous ulcers Associated conditions o Dermatitis herpetiformis, a skin disorder exclusive to celiac disease Photo source: http://www.bing.com/images/search?q=dermatitis+herpetiformis&id=4F0A2782A9719743B8A9529FA7F4AB2BA549D03D&FOR M=IQFRBA#view=detail&id=AB818BA0D1D7D736E482BB13FBC64E5E053EDDD8&selectedIndex=36 o Enteropathy-associated T-cell lymphoma 53 | P a g e o Other malignancies (small-bowel adenocarcinoma, oropharyngeal and esophageal adenocarcinoma, liver cancer, melanoma, non-Hodgkin’s lymphoma) o Autoimmune disorders (type 1 diabetes mellitus and autoimmune thyroiditis) o Down syndrome, Turner syndrome, Williams syndrome Source: Presutti, RJ, Cangemi, JR, Cassidy, HD, & Hill, DA (December 15, 2007). Celiac disease. American Family Physician, 76(12), 1795-1802. Testing: o Anyone with chronic diarrhea, malabsorption, weight loss, and persistent abdominal distention should be tested. Also consider in patients with premature osteopenia or osteoporosis, unexplained iron deficiency anemia or unexplained liver abnormalities o Testing must be done while on a gluten-containing diet o Serology: IgA endomysial antibodies and IgA tissue transglutaminase antibodies o Because serologic markers may have false-positive or false-negative results, they cannot be relied on for the diagnosis of celiac disease. However, positive serologic markers can indicate the need for further evaluation with small bowel biopsy, particularly in patients at increased risk. o A small bowel biopsy is required to confirm the diagnosis of celiac disease for most patients. Treatment o Avoidance of food products that contain gluten proteins (wheat, rye, barley) Can be extremely difficult May produce considerable psychological, emotional, and economic stresses Need formal consultation with dietician o Correction of nutritional deficiencies associated with malabsorption (iron, folic acid, vitamin B12, and fat-soluble vitamins o Check thyroid function, DEXA Follow-up o Serologic markers may be used to monitor compliance with a gluten-free diet Antibody levels typically return to normal within 3-12 months of starting a gluten-free diet Inflammatory Bowel Diseases (IBD): Crohn’s Disease & Ulcerative Colitis Source: Abraham, C & Cho, JH. (November 19, 2009). Mechanisms of disease: Inflammatory bowel disease. N Engl J Med, 361(21), 2066-2078. Evidence suggests that IBD results from an inappropriate inflammatory response to intestinal microbes in a genetically susceptible host. At risk for primary sclerosing cholangitis, ankylosing spondylitis, and psoriasis IBD affects 1.4 million Americans 54 | P a g e Peak onset is in persons 15-30 years of age Source of following table: Buch, KE (July 2007). Inflammatory bowel disease: A clinical review of Crohn’s disease and ulcerative colitis. Advance for Nurse Practitioners, 57-60. Location Common symptoms Crohn’s Disease Anywhere in GI tract, usually ileocecal region RLQ pain, diarrhea, weight loss, low-grade fever Radiologic appearance Skip lesions, strictures, fistulas Colonoscopic appearance Ulcers separated by normal mucosa, fistulas, strictures Rare Common Common Less common Smokers at increased risk Rectal Involvement Fistulas Strictures Bleeding Cigarette smoking affect* Ulcerative Colitis Rectum and colon, beginning distal and extending proximal Bloody diarrhea, crampy LLQ abdominal pain, fecal urgency, tenesmus, weight loss Fine, granular mucosa, pseudopolyps, ulceration Continuous proximal extension of mucosal inflammation Always Rare Rare Common Former smokers and nonsmokers at greater risk ++++ Colon Cancer Risk** ++ * Source: Abraham, C & Cho, JH. (November 19, 2009). Mechanisms of disease: Inflammatory bowel disease. N Engl J Med, 361(21), 2066-2078. ** Source: Wilkins, T, Jarvis, K, & Patel, J. (December 15, 2011). Diagnosis and management of Crohn’s disease. American Family Physician, 84(12), 1365-1375. Crohn’s disease Source: Wilkins, T, Jarvis, K, & Patel, J. (December 15, 2011). Diagnosis and management of Crohn’s disease. American Family Physician, 84(12), 1365-1375. Diagnostic testing o Initial: CBC, BUN, creatinine, liver enzymes, C-reactive protein, ESR, stool culture and testing for C. difficile o Subsequent testing: iron, ferritin, TIBC, vitamin B12, folate, albumin, prealbumin, calcium, vitamin D o Colonoscopy with ileoscopy and biopsy Treatment o Traditional “step-up” approach begins with corticosteroids or mesalamine products and advances to immunomodulators or anti-tumor necrosis factor (TNF) agents based on severity of disease Mesalamine products: sulfasalazine (Azulfidine) and 5aminosalicylic acid (5-ASA) Immunomodulators: 6-mercaptopurine, azathioprine (Imuran), budesonide (Entocort EC), methotrexate, prednisone TNF agents: adalimumab (Humira), infliximab (Remicade), certolizumab pegol (Cimzia) o A “top-down” approach begins with anti-TNF agents 55 | P a g e Ulcerative Colitis (UC) Source: Langan, RC, Gotsch, PB, Krafczyk, MA, & Skillinge, DD. (November 1, 2007). Ulcerative colitis: Diagnosis and treatment. American Family Physician, 76(9), 1323-1330. Diagnostic testing o Stool examinations for ova and parasites, stool culture, and testing for C. difficile toxin o ESR and C-reactive protein may be elevated o CBC (may show anemia), BMP (may show electrolyte abnormalities such as hypokalemia from persistent diarrhea) o Colonoscopy and biopsy = tests of choice to diagnose UC Treatment o Therapeutic approach determined by severity of symptoms and degree of colonic involvement Proctitis: 5-ASA suppositories Mild to Moderate UC Left-sided: 5-ASA suppositories Extensive: Oral 5-ASA and if no response, oral steroids Moderate to Severe UC Oral steroids If no response hospitalize to receive IV corticosteroids If no response to IV steroids, consider referral for therapy with cyclosporine (Sandimmune) or infliximab (Remicade) Steroids are tapered when possible and 5-ASA used as prophylaxis/maintenance o Increased risk of developing colon cancer American Cancer Society guidelines: Initial colonoscopy 8 years after disease onset of pancolitis, 12-15 years for left-sided disease Follow-up colonoscopy every 1-2 years (risk of colon cancer increases the longer patient has UC) Obesity Source: Meires, J, & Christie, C. (September 2011). Contemporary approaches to adult obesity treatment. The Nurse Practitioner, 36(9), 37-46. A transdisciplinary approach to adult obesity including NP, MD, and RD (registered dietician) Assess anthropometrics (RD) o Wait-to-hip ratio o Waist circumference o Height and weight o Calculate BMI o Frame size Screen to rule out organic causes and make appropriate referrals (NP/MD) o Pituitary dysfunction o Thyroid disease o Polycystic ovary disease o Hypothalamic disorders 56 | P a g e o Genetic disorders o Others Assess comorbid conditions (NP/MD) o Hypertension o Dyslipidemia o CVD o Hyperinsulinemia o Diabetes o Metabolic syndrome o Sleep apnea o GERD o Osteoarthritis o Breast, endometrial, and/or colon cancer o Depression o Others Assess health risk (NP/MD/RD) BMI < 25 25-<27 27-<30 30-<35 35-<40 40 and above No comorbidities Minimal Low Moderate High Very high Extremely high One or more comorbidities Low Moderate High Very high Extremely high Extremely high R/O weight loss contraindications (NP/MD) o Pregnancy/lactation o Medical/mental conditions such as eating disorders, psychosis, bipolar disorder, severe depression Assess readiness for weight loss (RD/NP/MD) o Is client ready? If not, discuss prevention of further weight gain; reevaluate readiness at future visits Discuss treatment options (RD/NP/MD) Implement weight loss protocol – Goal is to lose 5-10% body weight o Individualized lifestyle changes including sleep recommendations (RD/NP/MD) o 500 calorie deficit below calculated need to result in one pound weight loss/week Personalized meal plan (RD) Self-management training (RD/NP/MD) Exercise prescription (NP/MD) Reinforce physical activity (RD/NP/MD) When goal weight is achieved, implement weight maintenance protocol Personalized meal plan (RD) Self-management training (RD/NP/MD) 57 | P a g e Exercise prescription (NP/MD) {See below} When goal weight is NOT achieved, discuss possible adjunctive therapy (NP/MD) o Pharmacotherapy (BMI > 27 with high health risk and no contraindications) Medical surveillance required (NP/MD) Personalized meal plan and lifestyle change (RD) o Bariatric surgery (BMP > 30 with comorbidities) Medical surveillance required (NP/MD) Preoperative lifestyle change (NP/MD) Postoperative personalized meal plan and lifestyle change (RD) Guidelines for activity prescription: Source: Mcinnis, KJ, Franklin, BA, & Rippe, JM. (March 15, 2003). Counseling for physical activity in overweight and obese patients. American Family Physician, 67(6), 1249-1256. Frequency Intensity Time Type of exercise The FITT Principle 3-5 days/week. More frequent exercise is desirable, but care should be taken to first establish a regular exercise habit before recommending levels that may not be sustainable in the long term To avoid musculoskeletal injuries and promote compliance, start at a low to moderate intensity and gradually progress over the course of several weeks or months to more vigorous efforts (if desired by the patient) 30-60 minutes, using a gradual progression Multiple short bouts produce similar benefits as a single long bout of the same total duration Low-impact activities (e.g., walking, cycling, low-impact aerobics, water exercise) that are convenient, accessible, and perceived as enjoyable by the participant Also: American Society of Bariatric Physicians (ASBP) Obesity Algorithm: Adult Adiposity Evaluation and Treatment 2013 available at: http://www.asbp.org/images/ADV-COPY_ASBPObeistyAlgorithmOctober2013.pdf Overall management goals o Improve patient health o Improve quality of life o Improve body weight and body composition 5 A’s of Obesity Management o Ask Ask for permission to discuss body weight Explore readiness for change o Assess Assess body mass index, waist circumference, and obesity stage Explore drivers and complications of excess weight o Advise Advise the patient about the health risks of obesity, the benefits of modest weight loss, the need for a long-term strategy, and treatment options o Agree Agree on realistic weight-loss expectations, targets, behavioral changes, and specific details of the treatment plan 58 | P a g e o Arrange/Assist Assist in identifying and addressing barriers Provide resources Assist in finding and consulting with appropriate providers Arrange regular follow-up ************** Case Study #13 ************** ***Additional case studies to be discussed in class as time permits***