GASTROENTEROLOGY icterus by mikeholy

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    Upon completion, the student will be able to:
1.   Describe the incidence, morbidity and mortality of
     gastrointestinal emergencies.
2.   Identify the risk factors most predisposing to
     gastrointestinal emergencies.
3.   Discuss the anatomy and physiology of the
     gastrointestinal system.
4.   Discuss the pathophysiology of abdominal
     inflammation and its relationship to acute pain.
5.   Define somatic, visceral, and referred pain as they
     relate to gastroenterology.
6.   Differentiate between hemorrhagic and
     nonhemorrhagic abdominal pain.
7.   Discuss the signs and symptoms and differentiate
     between local, general, and peritoneal inflammation
     relative to acute abdominal pain.
8.   Describe the questioning technique and specific
     questions when gathering a focused history in patient
     with abdominal pain.
9.    Describe the technique for performing a
      comprehensive physician examination on a patient
      complaining of abdominal pain.
10.   Discuss the pathophysiology, assessment findings,
      and management of the following gastroenterological
      a) Upper gastrointestinal bleeding
      b) Lower gastrointestinal bleeding
      c) Acute gastroenteritis
      d) Colitis
e)   Gastroenteritis
f)   Diverticulitis
g)   Appendicitis
h)   Ulcer disease
i)   Bowel obstruction
j)   Crohn’s disease
k)   Pancreatitis
l)   Esophageal varices
      m) Hemorrhoids
      n) Cholecystitis
      o) Acute hepatitis
11.   Differentiate between gastrointestinal emergencies
      based on assessment findings.
12.   Given several scenarios involving patients with
      abdominal pain and symptoms, provide the
      appropriate assessment, treatment, and transport.
   Account for 500,000 emergency visits yearly
   300,000 are due to GI bleeds
   Will increase because of an aging population
   Usually result from an underlying pathologic
    process that is predictable by risk factors:
    a)   excessive alcohol consumption
    b)   excessive smoking           c) increased stress
    d)   ingestion of caustic substances
    e)   poor bowel habits
General Pathophysiology
   Pain is the hallmark of the acute abdominal
   Three main classifications of abdominal pain:
    1) Visceral
    2) Somatic
    3) Referred
Visceral Pain
   Originates in the walls of hollow organs,
   In the capsules of solid organs,
   Or in the visceral peritoneum
   Three separate mechanisms can produce this
    1) Inflammation
    2) Distention (being stretched out or inflated)
    3) Ischemia (inadequate blood flow)
Visceral Pain
   All transmit a pain signal from visceral afferent
    neural fibers back to the spinal column
   Pain is usually not localized to any one specific
   Described as very vague or poorly localized, dull
    or crampy
   Body responds through sympathetic stimulation
    causing N/V, diaphoresis and tachycardia
Somatic Pain
   Sharp type of pain that travels along
    definite neural routes (determined by the
    dermatomes) to the spinal column
   This pain is usually associated with
    perforations or ruptures of hollow organs
   Cause can be bacterial (ruptured appendix
    or gall bladder) or chemical (perforated
    ulcer or inflamed pancreas-leakage of
    acidic juices)
   Resulting peritonitis can lead to sepsis,
    and death
Referred Pain
   Originates in a region other than where it is felt.
   Many neural pathways from various organs pass
    through or over regions where the organ was
    formed during embryonic development.
   Example: inflammation or injury of the
    diaphragm will have a referred pain in their
    necks or shoulders.
   Example: dissecting abdominal aortic aneurysm
    produces pain felt between the shoulder blades
General Assessment
   Similar to a trauma assessment with an
    expanded history.
   Remember scene safety and BSI
   Observe the scene for clues and/or potential
    evidence of your pt’s problem: meds, alcohol,
    ashtrays, emesis buckets, etc..
Scene-Size Up and Initial
   Determine if medical or traumatic cause
   If trauma remember C-spine
   ABC’s as always: With most medical patients,
    you can check responsiveness and airway by
    asking the patient his name and chief complaint.
History and Physical
   History: including SAMPLE
   Then move on to History of Present Illness
History of Present Illness
                                 7.   Associated Symptoms
1.   Onset: when did the
     pain start, was it sudden   8.   Pertinent Negatives
     or gradual?
2.   Provocation/Palliation:
     makes the pain worse
     or better?
3.   Quality: dull, sharp,
4.   Region/radiation: pain
5.   Severity: scale 1-10
6.   Time: when and how
Physical Examination
   Patient’s general appearance and
   Complete set of vital signs
   Visually inspect the abdomen before palpation
    (distention, discoloration)
   Cullen’s Sign: periumbilical ecchymosis
   Grey-Turners Sign: ecchymosis in the flank
   Remove clothing as necessary
   Auscultation and percussion are difficult
    techniques in a noisy environment
Physical Examination
    Palpation can give you a large amount of
1.   Can define the area of pain and identify the associated
    Palpate the area of discomfort last
    Palpation should be done with gentle pressure,
     feeling for:
1.   Muscle tension or its absence
2.   Masses, pulsation, tenderness
General Treatment
   Once assessment, focused history and exam have been
    completed you now will make treatment and transport
   Monitor ABC’s, high-flow O2, IV access, cardiac monitor
   Transport in position of comfort
   Provide emotional reassurance
   The use of analgesics could limit further evaluation
   NOTE: persistent abdominal pain lasting longer than 6
    hours is considered a surgical emergency
Specific Illnesses
    Broken down into two broad categories:
1.   Upper Gastrointestinal Diseases
2.   Lower Gastrointestinal Diseases
    Upper GI consists of: mouth, esophagus,
     stomach, and duodenum
    Lower GI consists of: remainder of small
     intestine and the large intestine
Upper GI Bleeding
    Bleeding within the GI tract proximal to the
     ligament of Treitz
    This ligament supports the duodenojejunal
    Accounts for 300,000 hospitalizations yearly
    Mortality of 10%, reasons:
1.   Increasing age of population with associated medical
2.   Over-the-counter treatments, until problem becomes
Upper GI Bleeding
    Six major identifiable causes of upper GI
1.   Peptic ulcer disease
2.   Gastritis
3.   Variceal rupture
4.   Mallory-Weiss syndrome (esophageal laceration,
     usually secondary to vomiting)
5.   Esophagitis
6.   Duodenitis
General Presentation
   Complain of some type of abdominal discomfort
    ranging from a vague burning sensation to an
    upset stomach, gas pain, or tearing pain in the
    upper quadrants
   N/V
   If bleeding is in the upper GI, pt. may have
    Hematemesis (bloody vomitus)
   Bleeding passes in to the lower GI tract, pt. may
    have Melena (tarry, foul smelling stool..partially
    digested blood)
   Bleeding can be light or life-threatening
General Presentation
   Part of your assessment should include the “tilt
    test” (orthostatic hypotension: 10-mmHg change
    in BP or 20-bpm change in HR when pt. goes
    from supine to standing)
   If available the “hematocrit” could be normal in
    early stages but will definitely drop in the latter
   Other general complaints include: malaise,
    syncopal & near-syncopal, tachycardia, and
General Treatment
   Maintain airway, oxygenation and circulatory
   Lateral recumbent position or semi-Fowler’s
   High-flow O2
   Two large bore IV’s when you suspect GI bleed
   Cardiac Monitor
Esophageal Varices
   Swollen vein in the esophagus
   If they rupture mortality is 35%
   Cause is usually a rise in portal pressure, due
    to impeded circulation through the liver.
   This will cause a backup of blood into the left
    gastric vein and into the esophageal veins.
   This will cause the veins to dilate outward, under
    pressure, and as the engorgement continues,
    cause them to rupture
Esophageal Varices
   Primary cause is the consumption of alcohol and
    the ingestion of caustic substances.
   Alcohol consumption can result in cirrhosis of
    the liver.
   This will result in fatty deposits and fibrosis in
    the liver obstructing portal blood flow.
   Caustic substances can erode the esophagus
    from the inside out, causing hemorrhage of a
Esophageal Varices
   Patients usually present initially with painless
    bleeding and signs of hemodynamic instability.
   May complain of hematemesis with bright red
    blood, dysphagia, and a burning or tearing
    sensation as the varices continue to bleed.
   Clotting time increases because the high portal
    pressure backs up blood into the spleen,
    destroying platelets.
   Classic signs of shock are common
Esophageal Varices
   Treatment should focus on aggressive airway
    management (suction!), intravenous fluid
    resuscitation, placing pt. in the shock position,
    and rapidly transporting to the ED.
   ED management may include the use of a
    Sengstaken-Blakemore tube to tamponade the
    bleed, endoscopic cauterization, or
    sclerotherapy (injection of a thrombus-forming
    drug into the vein itself)
Acute Gastroenteritis
   Inflammation of the stomach and intestines with
    associated sudden onset of vomiting and/or
   Affects 3-5 million people yearly (worldwide).
   20% of all hospitalized patients
   The inflammation causes hemorrhage and
    erosion of the mucosal and submucosal layers
    of the GI tract
Acute Gastroenteritis
   Also can damage the villi inside the intestine,
    which absorb water and nutrients.
   The water will now move through the bowel at
    an increased rate.
   Dehydration secondary to diarrhea is a common
    cause of death.
   Volume replacement is the major prehospital
    intervention to minimize hypovolemia.
Acute Gastroenteritis
   Alcohol and tobacco abusers are at a high risk
    for gastritis and gastroenteritis.
   Also nonsteroidal anti-inflammatory drugs such
    as aspirin can lead to acute gastritis
   Alcohol and tobacco have the same effect on
    the mucosa as aspirin (breakdown the mucosal
    surfaces of stomach and GI tract)
   Other causes include: stress, chemotherapeutic
    agents and the ingestion of acidic or alkalotic
Acute Gastroenteritis
    Infections such as salmonellosis and
     staphylococcus can lead to acute
    Onset is rapid and severe.
    Multiple problems arise:
1.   Diarrhea – leading to dehydration. Especially effects
     pediatric and geriatric patients.
2.   Stool may show melena or hematochezia (bright red
     blood from erosion of the lining of the lower GI tract
Acute Gastroenteritis
3.   Hematemesis
4.   Fever
5.   N/V
6.   General malaise
7.   Patient may complain of widespread and diffuse
     abdominal pain that is not specific to any one region.
Acute Gastroenteritis
   Treatment is mainly supportive and palliative.
   Position to decrease the risk of aspiration
   Oxygenation
   Rehydration
   Antiemetics: prochlorperazine (compazine) or
    promethazine (phenergan)
   Electrolyte replacement may be necessary at
    the hospital
Chronic Gastroenteritis
   Inflammation of GI mucosa marked by long-term
    mucosal changes or permanent mucosal
   Primarily due to microbial infection.
   Most prevalent pathogen in the US is
    Helicobacter pylori bacillus
   Others include: Escherichia coli, Klebsiella
    pneumoniae, Enterobacter, Campylobacter
    jejuni, Vibrio cholerae, Shigella, and Salmonella
Chronic Gastroenteritis
   Viral pathogens include: Norwalk virus and
   Parasitic causes: protozoa Giardia lamblia,
    Cryptosporidium parvum, and Cyclosporidium
   More common in underdeveloped countries
   Transmitted via the fecal-oral route or through
    infected food or water
Chronic Gastroenteritis
   Commonly present with N/V, fever, diarrhea,
    abdominal pain, cramping, anorexia, lethargy
    and if severe, shock.
   The H.pylori presents with heartburn, abdominal
    pain, and gastric ulcers
   Treatment: BSI (protect against cross-
    contamination), monitoring ABCs and transport
   Medical treatment will require identification of
    the offending organism.
Peptic Ulcers
   Erosions caused by gastric acid
   Can occur anywhere in the GI tract
   Location is based on the area of small intestine
    involved (ex. duodenal ulcer); gastric ulcers-only
    in the stomach
   Occurs 4 times more frequently in males
   Duodenal ulcers occur 2-3 times more often
    than gastric ulcers
Peptic Ulcers
   Gastric ulcers more common in patients over 50,
    work in jobs requiring physical activity.
   Pain usually increases after eating or with a full
    stomach and they usually have no pain at night
   Duodenal ulcers are more common in patients
    from 25-50 who are executives or leaders under
    high stress; possible genetic predisposition
   Commonly have pain at night or whenever their
    stomach is empty
Peptic Ulcers
   Nonsteroidal anti-inflammatory medications,
    acid-stimulating products, or Helicobacter pylori
    bacteria are the most common causes.
   GI mucosal lining is irritated by hydrochloric
    acid, and pepsin. Adding any of the above
    agents increases the irritation.
   Treatment is focused on antacid treatment and
    support of any complications (hemorrhage)
Peptic Ulcers
   Blocked pancreatic duct can also contribute to
    duodenal ulcers. This duct releases an alkalotic
    solution in opposition to the high acid contained
    in chyme.
   Another cause is: Zollinger-Ellison
    Syndrome: Where an acid-secreting tumor
    provokes the ulcerations; condition causes
    stomach to secrete excess HCl acid and pepsin.
Peptic Ulcers
    Findings on exam can vary:
1.   Chronic ulcers can cause a slow bleed with resulting
2.   Visual inspection of the abdomen is only helpful with a
     significant bleed
3.   Palpation, the pain may be localized or diffuse
4.   Patients usually have relief of pain after eating or
     coating their GI tract with a liquid such as milk
5.   Acute, severe pain is probably due to a rupture of the
Peptic Ulcers
6.   Depending on location the patient may have
     hematemesis or may have melena-colored stool
7.   N/V common
8.   Patient will appear ill with signs of hemodynamic
    Treatment is based on severity
1.   Position of comfort, psychological support
2.   Oxygenation, IV access for fluid resuscitation
3.   Pharmacological administration and rapid transport
4.   Meds include: Zantac and Pepcid (histamine blockers)
     and antacids, like Carafate
Lower GI Diseases
   Lower GI tract consists of the jejunum and ileum
    of the small intestine, and the entire large
    intestine, rectum and the anus.
Lower GI Bleeding
   Bleeding in the GI tract distal to the ligament of
   Most frequently occur in conjunction with chronic
    disorders and anatomic changes associated
    with advanced age.
   Most common cause is diverticulosis.
   Other causes: colon lesions, rectal lesions, and
    inflammatory bowel disorders such as ulcerative
    colitis and Crohn’s disease
Lower GI Bleed
   Assessment is identical as with upper GI bleeds
   Ask patient whether this is a new or old problem
   Frequent complaints with lower GI bleeds
    include cramping pain that may be described as
    like a muscle cramp or like gas pain, N/V, and
    changes in stool
   Melenic stool usually indicates a slow bleed
   Bright red blood, bleed is very large or has
    occurred in the distal colon
Lower GI Bleed
   If in the distal colon, hemorrhoids or rectal
    fissures are possible causes.
   Physical presentation is similar to peptic ulcers
   Management is based on physiological status
   ABCs, oxygenation
   IV access, fluid resuscitation
   Position of comfort, cardiac monitor
   MAST if directed in local protocols
Ulcerative Colitis
   An idiopathic inflammatory bowel disorder (IBD),
    that is, one of unknown origin.
   Creates a continuous length of chronic ulcers in
    the mucosal layer of the colon.
   As ulcers heal, granular tissue replaces the
    ulcerations, thickening the mucosa
   Typically involve the rectum or rectosigmoid
    portion of the large intestine.
Ulcerative Colitis
   Usually starts in the rectum and then extends
    proximally into the colon.
   If it spreads throughout the entire colon it is
    called pancolitis; if limited to the rectum it is
    called proctitis.
   10,000 new cases are diagnosed yearly.
   Affects patients between the ages of 20-40.
Ulcerative Colitis
    Contributing factors:
1.   Psychological
2.   Allergic and other immunological
3.   Toxic
4.   Environmental
5.   Infectious
    Current research has found that the release of
     cytokines can cause an overwhelming
     inflammatory response in the submucosa
Ulcerative Colitis
   Acute ulcerative colitis is difficult to differentiate
    from other causes of lower GI bleeds.
   Diagnosing may require hematocrits and
    hemoglobin results, guaiac analyses of the stool
    and endoscopic examinations.
   Severity is based on the extent of the current
    inflammation in the colon.
   Severe presentations usually involve the entire
    colon, instead of one segment
Ulcerative Colitis
   Presents as a recurrent disorder with occasional
    bloody diarrhea or stool containing mucus.
   Colicky abdominal pain (cramping)
   N/V
   Fever
   Weight loss
   Cramping is usually isolated to the lower
   Typically appear restless due to discomfort
Ulcerative Colitis
   Typically are not hemodynamically unstable
   More severe cases may present with bloody
    diarrhea and intense colicky abdominal pain.
   Electrolyte derangements due to fluid loss
    through the colon
   Ischemic damage to the colon itself
   Eventually perforation of the bowel
   These patients will present with S&S of
    hypovolemic shock
Ulcerative Colitis
   Management is based on physiological status.
   If presenting with shock, treat as such.
   Additional management may include antiemetics
    and antispasmodic medications.
   Transport for diagnostic evaluation
Crohn’s Disease
   The other idiopathic inflammatory bowel
    disorder in humans.
   More common in the Western Hemisphere,
    20,000-30,000 new cases annually in the U.S.
   Tends to run in families, most prevalent in white
    females, those under frequent stress, and in the
    Jewish population.
   Can occur anywhere from the mouth to the
Crohn’s Disease
   35-45% of less severe cases occur in the small
   40% involve the colon
   Severe cases may involve any portion of the GI
    tract, causing a variety of problems ranging from
    diarrhea to intestinal and perianal abscesses
    and fistulas
   Complete intestinal obstruction can also occur
   Significant lower bleeding is rare.
Crohn’s Disease
   It damages the innermost layer of the tissue the
   Affected section of intestinal wall eventually
    becomes rubbery and nondistendable due to
    hypertrophy and fibrosis of the muscles
    underlying the submucosa.
   This will decrease the intestine’s internal
    diameter, resulting in fissures (incomplete tears)
    in the mucosa
Crohn’s Disease
   If a tear extends into the blood vessels in the
    submucosal layer, small bleeds result.
   Clinical presentations vary drastically as the
    disease progresses, and prehospital diagnosis
    is virtually impossible
Signs & Symptoms
   GI bleeding                 Diarrhea
   Recent weight loss          Fever
   Intermittent abdominal
   N/V
Crohn’s Disease
   Flareup is usually rapid, requiring a visit to the
   Abdominal pain cannot be localized to any
    specific quadrant
   Physical exam is also nonspecific, and
    nonlocalized, with diffuse tenderness the most
    commonly found sign.
   Prehospital treatment is palliative because the
    patient is generally hemodynamically stable
Crohn’s Disease
   Management depends on the patient’s
    physiological status
   Additional management may include antiemetics
    and antispasmodic medications
   Relatively common complication of
   Diverticulosis is a condition characterized by the
    presence in the intestine of diverticula, small
    outpouchings of mucosal and submucosal tissue
    that push through the outermost layer of the
    intestine, the muscle.
   Diverticulitis is an inflammation of diverticula
    secondary to infection.
    It is symptomatic, patients complain of lower
     left-sided pain (located in sigmoid colon)
    Exam and testing will show fever and an
     increased WBC count
    Pathogenesis of a diverticulum is twofold:
1.   Stool passes sluggishly through the colon, a condition
     associated with the relatively low fiber diets common in
     developed countries. Colon responds with muscle
     spasms to move the fecal material forward
2.   The outermost layer of colon tissue is made up of
     fibrous bands of muscle wrapped around one another.
     The muscles (teniae coli) become weakened with age,
     and the increased pressure of muscle spasms can
     cause the inner layers of tissue, the mucosa and
     submucosa, to herniate through the openings, forming
    The diverticula then trap small amounts of
     fecal material, including sunflower seeds,
     popcorn fragments, okra seeds, sesame seeds
     etc.. the trapped feces can allow bacteria to
     grow and result in an infection.
   When diverticula become inflamed the result is
   Complications include possible hemorrhage,
    larger perforations of the colon in which the fecal
    matter is spilled into the peritoneal cavity and
    cause peritonitis.
   Most common presentation is colicky pain
    associated with low grade fever, N/V,
    tenderness upon palpation
   If they begin to bleed significantly the
    presentation is similar with any serious lower GI
    bleed (sympathetic response)
   Bleeding diverticula can also result in bright red
    and bloody feces (hematochezia)
   Prehospital treatment is mainly supportive, treat
    for shock as necessary
   Antiemetics (Phenergan or Vistaril) for comfort
   In hospital: antibiotic therapy, endoscopy,
    radiological tests
   Small masses of swollen veins that occur
    in the anus (external) or rectum (internal)
   Frequently develop during the fourth
    decade of life.
   Most are idiopathic, but can result from
    pregnancy or portal hypertension.
   External hemorrhoids often result from
    lifting a heavy object.
    Other causes include:
1.   Straining at defecation
2.   Diet low in fiber
    Internal hemorrhoids most often involve the
     inferior hemorrhoidal plexus and vasculature.
    Commonly bleed during defecation and then
     thrombose into closed state again
    External hemorrhoids result from a thrombosis
     of a vein, often following lifting or straining
   External hemorrhoids cause bright red blood
    with bowel movement.
   Vessels can erode from increased venous
    pressure, causing free bleeding and high risk for
   Patients usually call because of bright red
    bleeding and pain on defecation.
   Patients are typically hemodynamically stable
   Treatment is based on patient’s condition
Bowel Obstruction
    Blockages of the hollow space, or lumen, within the
     small and large intestines
    Can be either partial or complete
    Can be catastrophic if not rapidly diagnosed and
    Many different causes. Four most frequent are:
1.   Hernia: protrusion or organ through its protective sheath
2.   Intussusception: part of intestine slips into the part just distal to
3.   Volvulus: twisting of the intestine
4.   Adhesions: union of normally sep. tissue by a fibrous band of
     new tissue
Bowel Obstruction
   Other causes include: foreign bodies,
    gallstones, tumors, adhesions from previous
    abdominal surgery, and bowel infarction.
   Most common location is the small intestine, due
    to its smaller diameter and its greater length,
    flexibility, and mobility
   Obstruction may be chronic, as with tumor
    growth or adhesion progression
   Or acute as with foreign body obstruction
Bowel Obstruction
   Chronic obstruction usually results in a
    decreased appetite, fever, malaise, N/V, weight
    loss, or if rupture occurs (peritonitis).
   Acute-onset pain may follow ingestion of a
    foreign body. Pain may also be due to
    strangulation, possibly leading to infarction.
   Patients frequently vomit, vomitus often
    containing a significant amount of bile.
Bowel Obstruction
   Patients present with diffuse visceral pain,
    usually poorly localized to any one specific
   Hemodynamically unstable due to necrosis of an
    organ, S&S of shock may be present
   Abdominal distention may be obvious (free air)
    from a rupture of the strangulated segment
   Palpation will reveal tenderness
   Treatment is based on physiological status
Accessory Organ Disease
    These include:
1.   Liver
2.   Gallbladder
3.   Pancreas
4.   Vermiform Appendix
   Inflammation of the vermiform appendix
   Occurs in approximately 10-20% of the
    population in the US
   Most common in young adults
   Acute appendicitis is the most common surgical
    emergency you will encounter in the field
   There are no particular risk factors
   Appendix serves no anatomic or physiologic
    function, lymphoid tissue
   It can become inflamed and rupture if left
    untreated, resulting in peritonitis
   Pathogenesis: most often due to obstruction of
    the appendiceal lumen by fecal material.
   Results in inflamed lymphoid tissue and leads to
    bacterial or viral infection
   The inflammation also causes the internal
    diameter to expand, blocking the artery, causing
    infarction and necrosis. Leading to rupture.
   Mild or early appendicitis causes diffuse, colicky
    pain associated with N/V, and low-grade fever.
   Pain is initially located in the periumbilical region
   Patient also loses their appetite
   Continued dilation causes pain to localize in the
    right lower quadrant
   Once the appendix ruptures the pain becomes
    diffuse due to development of peritonitis
   Physical exam shows a patient in discomfort.
   Abdominal exam reveals tenderness or guarding
    around the umbilicus or RLQ
   Common site of pain is McBurney’s point
   Prehospital care is based on the hemodynamic
    state of the patient
    Inflammation of the gallbladder.
    Cholelithiasis (formation of gall stones),
     causing 90% of cholecystitis in the US
    1 million new cases annually.
    Two types of gallstones:
1.   Cholesterol-based
2.   Bilirubin-based
   Cholesterol-based stones are far more common
    and are associated with a specific risk profile:
    obese, middle-aged women with more than one
    biological child
   Definitive treatment of acute cholecystitis include
    antibiotic therapy, laparoscopic surgery,
    lithotripsy (ultrasound) and surgery.
    Gallstones occur because of calculi build up
     lodging in the common bile duct.
    When the movement of bile is obstructed
     gallbladder inflammation and irritation result.
    Over time blood flow to the local epithelium will
     be reduced.
    Other causes of cholecystitis include:
1.   Acalculus cholecystitis (no stones)
2.   Chronic inflamation: caused by bacterial infection
   Acalculus cholecystitis usually results from
    burns, sepsis,diabetes, and multiple organ
   Inflamed gallbladder usually causes an acute
    attack of upper right quadrant abdominal pain,
    with referred pain in the right shoulder.
   If gallstones are lodged in the cystic duct, the
    pain may be colicky, due to expansion and
   The pain occurs after a meal that is high in fat content
    because of the secondary release of bile from the
   Palpation may reveal either diffuse right-sided
    tenderness or point tenderness under the right costal
    margin, a positive Murphy’s sign.
   Prehospital treatment is mainly palliative.
   Position of comfort, maintain ABCs, establish IV
   Pain medication: meperidine (demerol) & butorphanol
    Inflammation of the pancreas
    Four main categories, based on cause:
1.   Metabolic
2.   Mechanical
3.   Vascular
4.   Infectious
   Metabolic causes, specifically alcoholism,
    account for 80% of all cases
   Mechanical obstructions caused by gallstones or
    elevated serum lipids account for another 9%
   Vascular injuries caused by thromboembolisms
    or shock, along with infectious diseases,
    account for the remaining 11%
   Mortality (30-40%) is due sepsis and shock.
   Acute pancreatitis caused by gallstones that
    obstruct the pancreatic duct.
   Results in backups of digestive enzymes,
    causing inflammation of the pancreas and
    edema, reduction of blood flow, ischemia and
    acinar destruction.
   Acinar tissue destruction causes a second form
    of pancreatitis, chronic pancreatitis.
   Acinar tissue destruction commonly occurs due
    to chronic alcohol intake, drug toxicity, ischemia,
    or infectious diseases.
   Pain can be localized to the left upper quadrant
    or may radiate to the back or the epigastric
   Most patients experience nausea followed by
    uncontrolled vomiting and retching that can
    further aggravate the hemorrhage.
   Patient will appear acutely ill with diaphoresis,
    tachycardia, and possible hypotension.
   Prehospital treatment is supportive and aimed at
    maintaining the ABCs
   Establish IVs
   Definitive treatment involves gastric intubation and
    suctioning for emesis control, diagnostic peritoneal
    lavage, antibiotic therapy, fluid resuscitation, and surgery
    to remove the blockage.
   Involves any injury to hepatocytes associated with an
    inflammation or infection.
   Five viruses: A, B, C, D, and E
   Alcoholic hepatitis, arises from alcoholic cirrhosis, rather
    than an infectious agent.
   Factors that increase the risk of contracting hepatitis
    include: unsanitary living conditions, poor personal
    hygiene that invites oral-fecal transmission, exposure to
    blood borne pathogens, and chronic alcohol intake.
   Any of the viral pathogens, alcoholic exposure,
    or trauma can injure the hepatocytes, causing
    inflammation and, possibly, chronic liver
   Whatever the cause, results are similar:
    enlargement and hypertrophy, fatty changes,
    loss of architecture, and appearance of lesions
    and spontaneous hemorrhages
   Symptoms range from mild to liver failure and
   Hepatitis A is probably the best known.
   Commonly referred to as infectious hepatitis.
   Spreads by oral-fecal route
   Disease is self-limiting
   Lasting between 2-8 weeks.
   Low mortality rate
   Hepatitis B, known as “serum hepatitis”
   Blood borne pathogen that can stay active in
    bodily fluids outside the body for days.
   310 million carriers worldwide, HBV is an
   Effects may be minimal, but can range to severe
    liver ischemia and necrosis
   Hepatitis C caused by the pathogen most
    commonly responsible for spreading hepatitis
    through blood transfusions
   Marked by chronic and often debilitating
    damage to the liver.
   Hepatitis D, less common disorder because its
    pathogen is dormant until activated by HBV.
   Hepatitis E is a waterborne infection that has
    caused epidemics in Africa, Mexico, and other
    third-world nations.
   Mortality rate for pregnant women is high.
   Commonly present with symptoms relative to the
    severity of their disease.
   Complain of URQ abdominal tenderness, not relieved by
    antacids, food, or positioning.
   May lose their appetite and become anorexic, usually
    losing weight.
   Decrease in bile production changes their stool to a clay
    color, and increased bilirubin retention causes jaundice,
    yellow coloring of the skin, and scleral icterus, yellowing
    of the white of the eyes
   Other signs and symptoms include severe N/V,
    general malaise, photophobia, pharyngitis, and
    Exam will reveal a sick patient, possibly with a
    jaundiced appearance.
   Pain may present in URQ or the right shoulder
   Fever may be secondary to infection or to tissue
   Treatment is palliative.
   Secure ABCs
   Establish IV
   Antiemetic administration
   Definitive treatment involves antiviral and anti-
    inflammatory medications and symptomatic

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