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!

 

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 consultaiton

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)

 

 

 

 

 


Some Causes of Perceived Pain in Anatomic Regions

 

Right Upper Quadrant

Duodenal ulcer

Hepatitis

Hepatomegaly

Pneumonia

Fitz-Hugh-Curtis

 

 

 

 

 

 

Periumbilical

Intestinal obstruction

Acute pancreatitis

Early appendicitis Mesenteric thrombosis

Abdominal aortic aneurysm

 

 

 

 

 

 

 

 

 

 

Left Upper Quadrant

Ruptured spleen

Gastric ulcer

Aortic aneurysm

Perforated colon

Pneumonia

Acute pancreatitis

Right Lower Quadrant

Appendicitis

Salpingitis

Ovarian cyst

Ruptured ectopic pregnancy

Renal/ureteral stone

Strangulated hernia

Meckel’s diverticulitis

Regional ileitis

Perforated cecum

Left Lower Quadrant

Sigmoid diverticulitis

Salpingitis

Ovarian cyst

Ruptured ectopic pregnancy

Renal/ureteral stone

Strangulated hernia

Perforated colon

Regional ileitis

Ulcerative colitis

 

 

5.         Character (e.g., colicky or continuous, cramping, or stabbing)

 

Quality and Onset of Abdominal Pain

           

Characteristic

Possible related condition

Burning

Peptic ulcer

Cramping

Biliary colic, gastroenteritis

Colic

Appendicitis with impacted feces

Aching

Appendiceal irritation

Knife-like

Pancreatitis

Gradual onset

Infection

Sudden onset

Duodenal ulcer, acute pancreatitis, obstruction, perforation

 

 

6.         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).

·        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.

 

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)

 

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

 

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

7.         Diagnostic imaging (e.g., flat and upright abdominal films, CXR, abdominal/pelvic U/S or CT, upper and lower bowel contrast studies)

8.         Abdominal paracentesis

9.         Direct visualization by endoscopy, laparoscopy, or surgery

10.       With acute upper abdominal pain, CXR and EKG

 

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.

 

  • Note:    Any evidence suggestive of peritoneal irritation, obstruction, or acute vascular compromise is an indication for immediate hospitalization and surgical consultation.

 

  • Note:    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.

 

Physician consultation is recommended.

 

 

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.
  • 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

 

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.

 

 

Subjective

·        In classic appendicitis, the pain begins as vague and poorly localized, usually felt paraumbilical.  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!

·        Clinical pearl – usually pain proceeds vomiting

·        Characteristics of pain can be highly variable – crampy, to sharp, to dull.  Can easily confuse with PID

 

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

 

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), urinalysis, urine HCG if child bearing age and indicated

·        No imaging necessary in typical appendicitis

  • Imaging (CT of abdomen/pelvis) may be useful in patients in whom the diagnosis is uncertain

  • Abdominal CT:  useful in suspected appendiceal perforation to diagnose a periappendiceal abscess

·        Role of abdominal or transvaginal ultrasound:  diagnostic accuracy of > 85%, useful in the exclusion of adnexal disease in younger women

·        Refer to surgeon for evaluation

 

(Reference:  Papadakis, M.A. & McPhee, S.J. (2005).  2005 Current consult:  Medicine.  New York:  McGraw-Hill, p. 144.)

 

Obstruction

Etiology/Demographics

·        Pain is caused by distention and increased wall tension of affected area

·        Common causes – previous abdominal surgery with adhesions, tumor, constipation

 

Subjective

·        If acute onset of obstruction, the pain is intense, severe and colicky or wavelike, patient is restless.

·        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.

·        Refer for further evaluation.

·        If simple obstruction, may manage medically with decompression by tube insertion.

·        If strangulation – surgically emergent

 

Acute Gall Bladder (Cholecystitis, Cholelithiasis)

Etiology/Demographics

·        Sudden obstruction of the cystic duct

·        Those at most risk are “fair, fat, female, forty”

·        Research suggests that it may be the total calorie intake (i.e. excess) rather than just fatty calorie intake

 

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)

·        Gall Bladder 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

 

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)
 

Older men who are smokers are at higher risk

·        The U.S. Preventive Services Task Force recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men aged 65 to 75 who have ever smoked.


Aneurysm may be asymptomatic:

  • If small, risk of having surgery vs. risk of bleeding if does not have surgery must be weighed

  • May do yearly ultrasound to check if getting larger

  • Surgery usually recommended for aneurysms larger than 2 inches (5.5 cm) in diameter and for aneurysms that are enlarging quickly

  • Surgery may be a traditional (open) repair or endovascular stent grafting

If AAA leaking:

·        Patients may complain of tearing pain that radiates to back; pain is severe

·        May feel pulsating mass (approximately 25% of the time)

·        Hypotension present

  • Will need open repair (outcome usually good if repaired before it ruptures; < 40% survive a ruptured AAA.

 

Trauma

 

 

 

Medically Emergent

 

Acute Pancreatitis

Etiology/Demographics

·        Inflammatory breakdown of pancreatic architecture, with release of digestive enzymes into the interstitium of the gland, leading to autolysis (= “autodigestion”)

·        Associated with alcoholism, gallbladder disease, also use of some medications (such as thiazide diuretics, furosemide, and nitrofurantoin), tumor, mumps

 

Subjective

·        Sharp, periumbilical pain

·        History of alcoholism, thiazide diuretics, mumps

·        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, chemistries, including amylase which should be significantly elevated.  Consider lipase in addition to amylase

·        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

·        Diet:  NPO if vomiting; begin diet after pain, tenderness and ileus have resolved

·         Refer

 

Pyelonephritis

Etiology:  Infection of the upper urinary tract/kidney

 

Subjective:

·        Presents with complaints of flank pain, often accompanied by nausea and vomiting (still need to take antibiotics!)

·        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 p.o. 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

 

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

  • 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); also avoid smoking

·        If nausea severe, consider antiemetic such as phenergan or Zofran

·        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.

o       One option is to treat with Pepto Bismol 60 ml QID.  Warn patient that stool will turn dark.

·         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

 

Gastroesophageal Reflux Disease (GERD)

 

Demographics/Etiology

·        Reflux of acid into the esophagus

·        Associated risk factors include obesity, pregnancy, nicotine, caffeine, alcohol

·        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

·        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

·        A large percentage of patients with asthma have GERD (remember, bronchodilators also loosen the LES)

·        GERD is cause of 10-50% of non-cardiac chest pain

 

Subjective

·        Gnawing, burning, reflux sensation up the chest that is worse after large meals, laying down, bending over

·        Pain at least temporarily alleviated with the use of antacids

 

Objective

·        Usually a normal exam

·        May have midepigastric tenderness to palpation

 

Not to be Missed

·        MI, PUD, cholelithiasis, scleroderma, gastric Ca

 

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:

·        Beta-agonists

·        Alpha-adrenergic antagonist

·        Nitrates

·        Calcium channel blockers

·        Anticholinergics

·        Theophylline

·        Morphine

·        Meperidine

·        Diazepam

·        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)

·        Take PPIs 15-30 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)

·        Three 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 medication for symptomatic control and step down once it is achieved

·        Step-in approach – give a PPI as soon as diagnosed with GERD

 

Complications

  • Reflux esophagitis
  • Esophageal ulcers and strictures (Schlotsky's ring)
  • Barrett’s esophagus
    • Replacement of the normal squamous epithelium of the esophagus with a metaplastic columnar epithelium
    • Mechanism:  Barrett’s esophagus linked to repeated and prolonged exposure of the esophageal mucosa to gastric material refluxed into the esophagus
    • Relatively few patients with GERD develop Barrett’s esophagus, however, the condition merits attention because it is a major risk factor for the development of esophageal adenocarcinoma
  • Esophageal adenocarcinoma

 

 

Distinguishing GERD from Peptic Ulcer Disease (Medscape Primary Care 5(2), 2003)

    GERD

  • If a patient complains of a burning sensation rising from the stomach into the chest or towards the neck, it is most likely due to GERD
  • The classic symptoms of GERD of heartburn and/or regurgitation may often be exacerbated by alcohol and certain foods, including those containing caffeine, garlic, and peppermint, as well as fatty foods.

    Peptic Ulcer Disease

  • Peptic ulcer disease is typically manifested by symptoms including pain or discomfort localized in the center part of the abdomen
  • PUD is often improved when a patient either has an empty stomach or consumes food to satiety, because eating to fill the stomach may often relieve PUD symptoms

 

 

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

 

Helicobacter pylori

  • 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
    • 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.)
  • Number of different treatment options for H. pylori, some of them include:
    • Amoxicillin or Tetracycline 500 mg QID plus Metronidazole 250 mg QID, plus Pepto Bismol tablets 2 QID for 7-14 days (Cost – approximately $40 for 2 weeks)
    • Metronidazole 500 mg BID plus Omeprazole 20 mg BID plus Clarithromycin 250 mg BID for 7-14 days (Cost – approximately $107-214 for 2 weeks)
    • Clarithromycin 500 mg TID plus Omeprazole 40 mg qd (or 20 mg BID) for 14 days (cost – approximately $148)

 

Problem:  Not everyone that presents with dyspepsia and PUD type symptoms has PUD!  If the individual truly does not have PUD, the benefit of treating for H. pylori (even if lab tests are done and positive) is still an area of great debate.

 

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 think a 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

·        Other medications that are used in refractory cases include proton pump inhibitors and Cytotec (for those with mucous synthesis impairment due to NSAID)

·        Cytotec is contraindicated in pregnancy.

 

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

·        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 CAT 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

  • A common and life-threatening condition
  • 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

 

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

 

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

  • CBC with differential
    • WBC’s may not be elevated
    • Significant left shift
    • Low Hct with perforated peptic ulcer
  • BUN, Creatinine
    • Increased with dehydration, GI bleed
  • Electrolytes
    • Low K from vomiting, diarrhea
    • Low Na with acute illness
  • Liver function
    • Increased with cholelithiasis, hepatitis, cholangitis
  • EKG
    • Inferior wall MI – abdominal pain, intractable vomiting

 

Cholecystitis

  • Most common cause of acute abdominal pain in the older patient
  • Complications
    • Ascending cholangitis
    • Empyema of the gallbladder
    • Perforation of the gallbladder
    • Pancreatitis (high amylase)
    • Indications of gallstone in common duct:  elevated bilirubin

 

Bowel Obstruction

  • Responsible for 25% of acute abdomens in older patients
  • Common causes
    • Incarcerated hernia
    • Carcinoma
    • Adhesions
    • Volvulus
    • Fecal impaction

 

Appendicitis

  • 14% of cases of acute abdomen in elderly
  • Mortality rate up to 15%
    • Late presentation
    • Inaccurate diagnosis
    • High prevalence of perforation at time of presentation
    • Decreased blood flow to appendix
    • Narrower lumen, thinner wall
  • Signs/symptoms
    • Less likely to have classic RLQ pain
    • 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
    • Greater risk of malignant ulcer

 

Diverticulitis

  • Presence increases with age
  • Most commonly affects sigmoid
  • 30% of age 60+ have evidence of diverticulosis
  • Associated with long-term low-fiber diets
  • Common symptoms
    • Classic, but may be absent in older patient:
      • Pain in LLQ
      • Fever
      • Tender mass in LLQ
    • Alternating diarrhea and constipation, rectal bleeding
      • Discomfort decreased after passing stool
    • Malaise, anorexia, N & V
  • Diagnosis:  labs (CBC, ESR), imaging (CT abdomen/pelvis)
  • If has not had a colonoscopy previously, will need one...however cannot scope during acute diverticulitis due to risk of diverticular blowout
  • Treatment
    • If no perforation
      • Rest the bowel
      • Adequate hydration
      • Antibiotics (Flagyl plus fluoroquinoline X 7-10 days OR Augmentin)
    • Surgery if abscess or peritonitis

 

 

Mesenteric Ischemia

  • A disease of old age
    • > 2/3 of cases in those age 70+
  • Mortality rate > 80%
  • Diagnosis is difficult; CT scan and angiography are best for diagnosing this (note:  MRI no better than CT)
  • Suggestive findings
    • Pain more severe than expected
    • History of arteriosclerosis
    • Postprandial abdominal pain
    • Diarrhea (heme +)
    • Leukocytosis

================================================================

 

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
    • Of those diagnosed, 93% are aged 50 and older
  • Although often perceived as a man’s disease, it is an equally important health concern for women
    • 3rd most common non-skin cancer in women (after breast and lung cancers)
    • In 2003, > 66,000 new cases and 28,500 deaths were documented in women in the United States
    • In terms of lifetime risk, approximately 1 in 17 women will develop colorectal cancer and, for those over the age of 65, the risk for developing the disease is equal to the risk of developing breast cancer

 

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
  • 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 5-year survival rate can exceed 90% in men and women
  • If the tumor is not detected early, morbidity and mortality increase rapidly.
    • 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
    • Nonneoplastic polyps include hyperplastic, hamartomatous, inflammatory, and lymphoid polyps
    • 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.
        • 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
    • Overall, fewer than 1% of all polyps progress to cancer
    • However, from 5% to 40% of adenomas are estimated to progress to cancer
      • Generally, the smaller the polyp, the lower the likelihood of cancer
    • 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
    • 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:
    • Appearance of blood on or around the stool
    • Abdominal pain (frequently crampy and intermittent)
    • A change in bowel habits (constipation, diarrhea, or a change in stool caliber or frequency)
    • Iron deficiency anemia secondary to clinically silent GI bleeding
    • 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.
  • Four tests are recommended for colorectal cancer screening
    • Fecal occult blood test (FOBT)
    • Flexible sigmoidoscopy
    • Colonoscopy
    • Double-contrast barium enema
  • Recommend regular screening for all adults aged 50 years or older, including:
    • FOBT every year
    • Flexible sigmoidoscopy every 5 years
    • Double-contrast barium enema every 5 years
    • 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.

 

Chemoprevention

  • In population-based observational studies, people had lower rates of colorectal cancer if they were taking various agents, including NSAIDs, calcium, and folate.
    • Aspirin has shown a modest risk reduction, but is associated with concomitant risks.
    • COX-2 inhibitors are under study as an adjunct to endoscopic surveillance and surgery in patients with familial adenomatous polyposis.
    • Exisulind, the sulfone metabolite of sulindac (NSAID) reduces adenomas in patients with familial adenomatous polyposis.
    • Calcium and folate supplementation have been found to moderately reduce adenoma formation without significant risk.

 

 

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

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.

 

Definition

  • Triad of parenchymal necrosis, regenerating nodules, and fibrosis
  • Cirrhosis:  an irreversible state of chronic liver injury.

 

Epidemiology   

  • The age of onset, incidence, and gender predominance vary among the given causes.
  • Alcohol abuse and viral hepatitis cause most cases.

           

Symptoms

  • Most symptoms are nonspecific and may include:
    • easy bruising
    • fatigue
    • malaise
    • 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, diabetes mellitus, heart failure, hyperpigmentation, hypothyroidism, loss of libido, night blindness, pruritus, and steatorrhea.

 

Clinical Findings

  • Physical examination abnormalities include:

            - clubbing

            - gynecomastia

            - hepatomegaly

            - jaundice

            - lacrimal and parotid gland enlargement

            - muscle wasting

            - palmar erythema

            - spider angioma

            - splenomegaly

            - testicular atrophy

 

  • Portal hypertension is suggested by abdominal collaterals (caput medusae), ascites, encephalopathy, esophageal varices, hemorrhoids, and splenomegaly.

 

  • Palpation of the liver reveals variable findings:

 

    • Enlarged and easily palpable liver
    • Regenerating macronodules along the liver border (micronodules are nonpalpable)        
    • 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

·        AST

·        bilirubin

·        globulins

·        5’-nucleotidase

·        prothrombin time

 

·        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:

 

1.      Alcohol

2.      Biliary obstruction

3.      Cardiovascular (right-sided heart failure, tricuspid insufficiency)

4.      Drugs and toxins (amiodarone, carbon tetrachloride, isoniazid, methotrexate, methyldopa, oral contraceptives)

5.      Infection (Hepatitis B/C/D, schistosomiasis, tertiary syphilis)

6.      Malnutrition (gastroplasty, jejunoileal bypass)

7.      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.

·        The use of branched-chain amino acids also may benefit patients with ncephalopathy.

·        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, bacterial peritonitis, bleeding varices, encephalopathy, hepatic failure, hepatoma, 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.)
     
  • This is a good time to re-emphasize patient education.

Hepatitis

 

The ABC’s of Hepatitis

 

 

 

Hepatitis A

(HAV)

Hepatitis B

(HBV)

Hepatitis C

(HCV)

Hepatitis D

(HDV)

Hepatitis E

(HEV)

What is it?

 

HAV is a virus that causes inflammation of

the liver. It does not lead to chronic disease.

HBV is a virus that causes inflammation of

the liver. It can cause liver cell damage,

leading to cirrhosis and

cancer.

HCV is a virus that causes

inflammation of the liver. It can cause liver cell damage,

leading to cirrhosis and cancer.

HDV is a virus that causes

inflammation of the liver. It only infects those persons with

HBV.

HEV is a virus that causes

inflammation of the liver. It is rare in the U.S. There is no chronic state.

Incubation

Period

2 to 7 weeks.

Average 4 weeks.

6 to 23 weeks.

Average 17 weeks.

2 to 25 weeks.

Average 7 to 9 wks.

2 to 8 weeks.

 

2 to 9 weeks.

Average 40 days.

How is it

Spread?

 

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.

Contact with infected blood, seminal fluid,

vaginal secretions,

contaminated needles,

including tattoo and body-piercing tools.

Infected mother to newborn. Human bite.

Sexual contact.

Contact with

infected blood,

contaminated IV needles, razors, and tattoo and

body-piercing tools, Infected mother to

newborn. Not

easily spread

through sex.

Contact with

infected blood,

contaminated

needles. Sexual contact with HDV

infected person.

Transmitted

through fecal/oral

route.  Outbreaks

associated with

contaminated water

supply in other

countries.

 

Symptoms

 

Children may have

none. Adults usually

have light stools, dark

urine, fatigue, fever, nausea, vomiting,

abdominal pain, and

jaundice.

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

 

Treatment

of Chronic

Disease

 

Not applicable

Interferon, lamivudine

and adefovir dipivoxil

control replication of

virus with varying

success.

Pegylated

Interferon with

ribavirin with

varying success.

 

Interferon with

varying success.

 

Not applicable

 

Vaccine

 

Two doses of vaccine to

anyone over 2 yrs of

age

Three doses may be

given to persons of

any age.

None

HBV vaccine

prevents HDV

infection.

 

None

 

Who is at

Risk?

 

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.

 

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.

 

Prevention

 

Vaccination. Immune

Globulin within 2 weeks of exposure. Washing

hands with soap and

water after going to the

toilet. Use household

bleach (10 parts water

to 1 part  bleach) to

clean surfaces

contaminated with feces, such as changing

tables. Safer sex.

Vaccination provides

protection for 20 plus years. Hepatitis B

Immune Globulin

within 1 week of exposure. Clean up

infected blood with household bleach and

wear protective gloves. Do not share razors,

toothbrushes, or needles. Safer sex.

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.

 

 

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: hfi@comcast.net

Website: www.HepatitisFoundation.org

Grid 2005

 

 

Serologic Features of Viral Hepatitis

 

Form of Infection

Serologic Markers

Interpretation

Hepatitis A

IgM anti-HAV

Acute disease

 

IgG anti-HAV

Remote infection and immunity

 

Hepatitis B

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

 

Hepatitis C

Anti-HCv

Acute, chronic, or resolved disease

 

Hepatitis D

HBsAg and anti-HDV

Acute disease

 

     - IgM anti-HBc positive

Co-infection

 

     - IgG anti-HBc positive

Superinfection

 

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

 

Tests

Results

Interpretation

HBsAg

Negative

Susceptible

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

Ositive

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.

Source:  Centers for Disease Control and Prevention, National Center for Infectious Diseases

 

           

 

 


Other GI Problems

 

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 present at the right posterior-lateral, right anterior-lateral, and left lateral positions.  Internal hemorrhoids are graded on the basis of their anatomic presentation:

 

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.

 

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.

 

 

Hernias

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)

 

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 within first 2 years of life)
  • 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

·        Bowel palpable in the scrotum or in the inguinal canal.

 

When examining male:

  • 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.

 

  • 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:

  • 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.

 

·        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.

 

Differential Diagnosis of Inguinal Hernias

·        Hydrocele

·        Varicocele

·        Spermatocele

·        Epididymal cysts

·        Epididymitis

·        Testicular tumor

·        In children, undescended testes

 

Differential Diagnosis of Femoral Hernias

·        Enlarged lymph node

·        Lipoma

·        Direct inguinal hernia

·        Saphenous varix

 

Diagnostic Tests

Often none needed, may order ultrasound after conferring with physician if uncertain about abdominal mass

 

Management

Hernias should have referral to a surgeon.

 

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

 

Irritable Bowel Syndrome (IBS)

Definition

IBS is a functional gastrointestinal disorder attributed to the intestines and associated with symptoms of pain and altered defecation and/or symptoms of bloatedness and distention.

 

Epidemiology

15-20% of patients suffer from IBS; most do not seek medical attention for their symptoms.

 

In Western countries, 75% of patients with IBS seen by a physician are female.

 

Pathophysiology

Certain motility and sensory abnormalities are found in IBS patients as a group, and these distinguish them from healthy individuals:

 

1.         Various stimuli including stress, meals, and peptides alter colonic or small intestinal motor response.

 

2.         It is presumed that pain symptoms in patients with IBS are due to hyperactivity.

 

3.         These patients also have reduced sensory thresholds for stimuli such as rectal and ileal distention.

 

Symptoms

Criteria for IBS include continuous or recurrent symptoms, for at least 3 months of:

 

1.         Abdominal pain or discomfort relieved by defecation or associated with a change in the frequency or consistency of stool and/or

 

2.         An irregular pattern of defecation at least 25% of the time (three or more of the following):

 

            a.         Altered stool frequency

            b.         Altered stool form (hard or loose, watery stool)

c.         Altered stool passage (straining or urgency, feeling of incomplete evacuation)

            d.         Passage of mucus

            e.         Bloating or feeling of abdominal distention

 

Clinical Findings

1.         The physical examination in most IBS patients is generally normal.

 

2.         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.

 

3.         Most patients with IBS are between the ages of 20 and 50.

 

4.         Patients with IBS commonly have a past history of multiple illnesses such as allergies, headache, kidney disease, joint symptoms, and in women dyspareunia.

 

Laboratory Tests

1.         Laboratory studies are generally normal in IBS.  The diagnosis should be suspected based on the patient’s symptoms and by excluding organic diseases.  There are no definitive tests for diagnosis of IBS.

 

2.         A minimal evaluation would consist of a CBC and sed rate.

 

3.         If diarrhea is a predominant symptom, stool samples for leukocytes, culture for enteric pathogens, and examination for ova and parasites should be pursued.

 

4.         A urinalysis should be obtained since urinary tract symptoms can mimic functional GI disease.

 

5.         Sigmoidoscopy offers little diagnostic information unless there is suspicion of inflammatory bowel disease.  In patients with IBS, air insufflation during sigmoidoscopy often reproduces a patient’s symptoms.

 

6.         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 45, a barium enema or colonoscopy should be performed.

 

Differential Diagnosis

1.         Malignancies such as colon cancer

2.         Inflammatory diseases such as Crohn’s disease or ulcerative colitis

3.         Infectious disease such as infectious colitis, diverticulitis, and parasitosis

4.         Ischemic diseases of the GI tract

 

Note:  Diarrhea as the predominant symptom may be due to lactase deficiency, laxative abuse, malabsorption, and hyperthyroidism.

 

Note:    Constipation as the predominant symptom may be due to hypercalcemia,           hypothyroidism, and medication side effects.

 

Epigastric and periumbilical pain may be due to peptic, biliary, gastric, or pancreatic disease.

 

Treatment

The key to successful management of IBS is a positive diagnosis, which depends on identifying certain symptom patterns.

 

Constipation predominant

1.         Review dietary history

2.         Therapeutic trial

a.         Increase fiber (start with one tablespoon psyllium per day or twice a day).  Alternatives include polycarbophil or methylcellulose.

            b.         Osmotic laxative

            c.         Stool softener

d.         Prokinetic agents (trial of cisapride/Propulsid, 20 mg twice daily—Restricted Access in United States)

3.         Zelnorm (tegaserod) – binds to 5-HT4 receptors, stimulating GI peristalsis and decreasing visceral sensitivity (Withdrawn from US Market)

4.        Amitiza (lubiprostone) -- activates chloride channels, increasing intestinal fluid secretion and motility

 

Diarrhea predominant

1.         Review dietary history.  Eliminate sorbitol products; consider lactose intolerance

2.         Consider lactose H2 breath test

3.         Therapeutic trial

            a.         Loperamide (Imodium), 2-4 mg every 6-8 hours

            b.         Diphenoxylate (Lomotil), 2.5-5 mg every 4-6 hours

4.         Fiber

5.                  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 (now “Restricted Access in US”)

 

Pain/gas/bloat predominant

1.         Review diet history

2.         Plain abdominal radiography

3.         Therapeutic trial

a.         Anticholinergics (dicyclomine[Bentyl], 10-20 mg. 30-45 minutes between meals four times a day; hyoscyamine [Anaspaz, Levbid, Levsin, NuLev])

b.         Antidepressants (amitriptyline HCl/Elavil, or doxepin/Sinequan, starting with 25-50 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.)

            c.         Prokinetic agents, cisapride, 10-20 mg daily

d.         Psychiatric intervention employing biofeedback, psychotherapy, or hypnosis is an alternative for patients with IBS refractory to standard therapeutic measures.

 

Diet

1.         If certain products such as lactose, caffeine, fatty foods, alcohol, sorbitol, or beans are associated with symptoms, they can be eliminated to see if symptoms abate.

2.         Fiber results in improvement of constipation and abdominal pain.

 

Activity

Low physical activity has been reported as an association with constipation.

 

Patient Education

1.         A positive physician-patient interaction is associated with a reduced number of return visits for IBS-related symptoms.

 

2.         Certain acute situations seem to precipitate attacks of IBS.  These include acute illnesses, severe financial demand, loss of a job, a serious family crisis, or death of a close friend or relative.

 

3.         Many patients with IBS come from families in which other members have the syndrome, suggesting that symptoms may be a learned behavior.

 

4.         It is usually helpful to explain that IBS is a real disorder in which the intestine is overly sensitive to various stimuli such as food, hormonal changes (menses), and stress.

 

5.         Make the patient aware that although chronic, the symptoms do not indicate serious illness, require surgery, or shorten life expectancy.

 

6.         Setting realistic goals is extremely important.

 

7.         The patient needs to concentrate on functioning as normally as possible and not on eliminating all symptoms.

 

 

Follow-Up

1.         Prevention

            a.         High-fiber diet and prophylactic use of medications

            b.         Regular exercise

            c.         Avoid products that aggravate symptoms

2.         Monitoring

            a.         Periodic evaluation for a change in symptoms, particularly diarrhea

            b.         Regular visits early in treatment to reassure the patient

3.         Prognosis

a.         A diagnosis of IBS persists over time, and most patients continue to have symptoms several years following the initial diagnosis.

            b.         Up to 30% of patients with IBS resort to alternative medicine.

c.         IBS does not predispose one to more serious diseases or shorten one’s life expectancy.