GASTROENTEROLOGY

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GASTROENTEROLOGY
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OBJECTIVES

• Upon completion, the student will be able to
• Describe the incidence, morbidity and mortality
  of gastrointestinal emergencies.
• Identify the risk factors most predisposing to
  gastrointestinal emergencies.
• Discuss the anatomy and physiology of the
  gastrointestinal system.
• Discuss the pathophysiology of abdominal
  inflammation and its relationship to acute pain.

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OBJECTIVES

• Define somatic, visceral, and referred pain as
  they relate to gastroenterology.
• Differentiate between hemorrhagic and
  nonhemorrhagic abdominal pain.
• Discuss the signs and symptoms and differentiate
  between local, general, and peritoneal
  inflammation relative to acute abdominal pain.
• Describe the questioning technique and specific
  questions when gathering a focused history in
  patient with abdominal pain.

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OBJECTIVES

• Describe the technique for performing a
  comprehensive physician examination on a patient
  complaining of abdominal pain.
• Discuss the pathophysiology, assessment findings,
  and management of the following
  gastroenterological problems
• a) Upper gastrointestinal bleeding
• b) Lower gastrointestinal bleeding
• c) Acute gastroenteritis
• d) Colitis

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OBJECTIVES

• e) Gastroenteritis
• f) Diverticulitis
• g) Appendicitis
• h) Ulcer disease
• i) Bowel obstruction
• j) Crohns disease
• k) Pancreatitis
• l) Esophageal varices

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OBJECTIVES

• m) Hemorrhoids
• n) Cholecystitis
• o) Acute hepatitis
• Differentiate between gastrointestinal
  emergencies based on assessment findings.
• Given several scenarios involving patients with
  abdominal pain and symptoms, provide the
  appropriate assessment, treatment, and transport.

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Introduction

• 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
• Excessive alcohol consumption
• Excessive smoking
• Increased stress
• Ingestion of caustic substances
• Poor bowel habits

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General Pathophysiology

• Pain is the hallmark of the acute abdominal
  emergency.
• Three main classifications of abdominal pain
• Visceral
• Somatic
• Referred

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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 pain
• Inflammation
• Distention (being stretched out or inflated)
• Ischemia (inadequate blood flow)

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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
  area
• Described as very vague or poorly localized, dull
  or crampy
• Body responds through sympathetic stimulation
  causing N/V, diaphoresis and tachycardia

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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

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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.

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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 pts problem meds, alcohol,
  ashtrays, emesis buckets, etc..

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Scene-Size Up and Initial Assessment

• Determine if medical or traumatic cause.
• If trauma remember C-spine.
• ABCs as always With most medical patients, you
  can check responsiveness and airway by asking the
  patient his name and chief complaint.

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History and Physical

• History including SAMPLE
• Then move on to History of Present Illness

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History of Present IllnessOPQRST - ASPN

• Onset when did the pain start, was it sudden or
  gradual?
• Provocation/Palliation makes the pain worse or
  better?
• Quality dull, sharp, constant?
• Region/radiation pain travel?
• Severity scale 1-10
• Time when and how long?
• Associated Symptoms
• Pertinent Negatives

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Physical Examination

• Patients general appearance and posture/position
• Complete set of vital signs
• Visually inspect the abdomen before palpation
  (distention, discoloration)
• Cullens Sign Periumbilical ecchymosis
• Grey-Turners Sign Ecchymosis in the flank
• Remove clothing as necessary
• Auscultation and percussion are difficult
  techniques in a noisy environment

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Physical Examination

• Palpation can give you a large amount of
  information
• Can define the area of pain and identify the
  associated organs
• Palpate the area of discomfort last
• Palpation should be done with gentle pressure,
  feeling for
• Muscle tension or its absence
• Masses, pulsation, tenderness

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General Treatment

• Once assessment, focused history and exam have
  been completed you now will make treatment and
  transport decisions.
• Monitor ABCs, 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

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Specific Illnesses

• Broken down into two broad categories
• Upper Gastrointestinal Diseases
• Lower Gastrointestinal Diseases
• Upper GI consists of mouth, esophagus, stomach,
  and duodenum
• Lower GI consists of remainder of small
  intestine and the large intestine

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Upper GI Bleeding

• Bleeding within the GI tract proximal to the
  ligament of Treitz
• This ligament supports the duodenojejunal
  junction
• Accounts for 300,000 hospitalizations yearly
• Mortality of 10, reasons
• Increasing age of population with associated
  medical problems
• Over-the-counter treatments, until problem
  becomes severe

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Upper GI Bleeding

• Six major identifiable causes of upper GI bleed
• Peptic ulcer disease
• Gastritis
• Variceal rupture
• Mallory-Weiss syndrome (esophageal laceration,
  usually secondary to vomiting)
• Esophagitis
• Duodenitis

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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)

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General Presentation

• 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
• 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)

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General Presentation

• If available the hematocrit could be normal in
  early stages but will definitely drop in the
  latter stages
• Other general complaints include malaise,
  syncopal near-syncopal, tachycardia, and
  indigestion.

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General Treatment

• Maintain airway, oxygenation and circulatory
  status
• Lateral recumbent position or semi-Fowlers
• High-flow O2
• Two large bore IVs when you suspect GI bleed
• Cardiac Monitor

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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

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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 vessel.

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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.

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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).

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Acute Gastroenteritis

• Inflammation of the stomach and intestines with
  associated sudden onset of vomiting and/or
  diarrhea.
• 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.

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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.

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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
  agents

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Acute Gastroenteritis

• Infections such as salmonellosis and
  staphylococcus can lead to acute gastroenteritis.
• Onset is rapid and severe.
• Multiple problems arise
• Diarrhea leading to dehydration. Especially
  effects pediatric and geriatric patients.
• Stool may show melena or hematochezia (bright red
  blood from erosion of the lining of the lower GI
  tract)

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Acute Gastroenteritis

• Hematemesis
• Fever
• N/V
• General malaise
• Patient may complain of widespread and diffuse
  abdominal pain that is not specific to any one
  region.

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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

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Chronic Gastroenteritis

• Inflammation of GI mucosa marked by long-term
  mucosal changes or permanent mucosal damage.
• 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.

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Chronic Gastroenteritis

• Viral pathogens include Norwalk virus and
  rotavirus.
• Parasitic causes protozoa Giardia lamblia,
  Cryptosporidium parvum, and Cyclosporidium
  cayetenis.
• More common in underdeveloped countries.
• Transmitted via the fecal-oral route or through
  infected food or water.

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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.

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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

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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

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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)

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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.

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Peptic Ulcers

• Findings on exam can vary
• Chronic ulcers can cause a slow bleed with
  resulting anemia
• Visual inspection of the abdomen is only helpful
  with a significant bleed
• Palpation, the pain may be localized or diffuse
• Patients usually have relief of pain after eating
  or coating their GI tract with a liquid such as
  milk
• Acute, severe pain is probably due to a rupture
  of the ulcer

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Peptic Ulcers

• Depending on location the patient may have
  hematemesis or may have melena-colored stool
• N/V common
• Patient will appear ill with signs of hemodynamic
  instability
• Treatment is based on severity
• Position of comfort, psychological support
• Oxygenation, IV access for fluid resuscitation
• Pharmacological administration and rapid
  transport
• Meds include Zantac and Pepcid (histamine
  blockers) and antacids, like Carafate

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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.

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Lower GI Bleeding

• Bleeding in the GI tract distal to the ligament
  of Treitz.
• 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 Crohns disease.

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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

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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

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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.

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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.

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Ulcerative Colitis

• Contributing factors
• Psychological
• Allergic and other immunological
• Toxic
• Environmental
• Infectious
• Current research has found that the release of
  cytokines can cause an overwhelming inflammatory
  response in the submucosa.

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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.

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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
  quadrants
• Typically appear restless due to discomfort

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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 SS of
  hypovolemic shock

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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.

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Crohns 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 rectum.

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Crohns Disease

• 35-45 of less severe cases occur in the small
  intestine.
• 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.

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Crohns Disease

• It damages the innermost layer of the tissue the
  mucosa.
• 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 intestines internal
  diameter, resulting in fissures (incomplete
  tears) in the mucosa.

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Crohns 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.

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Signs Symptoms

• GI bleeding
• Recent weight loss
• Intermittent abdominal cramping/pain
• N/V
• Diarrhea
• Fever

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Crohns Disease

• Flare-up is usually rapid, requiring a visit to
  the doctor.
• Abdominal pain cannot be localized to any
  specific quadrant.
• Physical exam is also nonspecific, and
  non-localized, with diffuse tenderness the most
  commonly found sign.
• Prehospital treatment is palliative because the
  patient is generally hemodynamically stable.

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Crohns Disease

• Management depends on the patients physiological
  status.
• Additional management may include antiemetics and
  antispasmodic medications.

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Diverticulitis

• Relatively common complication of diverticulosis.
• 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.

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Diverticulitis

• 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
• 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.

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Diverticulitis

• 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 diverticula.

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Diverticulitis

• 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.

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Diverticulitis

• When diverticula become inflamed the result is
  diverticulitis
• 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.

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Diverticulitis

• 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.
• .

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Hemorrhoids

• 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.

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Hemorrhoids

• Other causes include
• Straining at defecation
• 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.

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Hemorrhoids

• External hemorrhoids cause bright red blood with
  bowel movement.
• Vessels can erode from increased venous pressure,
  causing free bleeding and high risk for
  infection.
• Patients usually call because of bright red
  bleeding and pain on defecation.
• Patients are typically hemodynamically stable
• Treatment is based on patients condition

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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
  treated

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Bowel Obstruction

• Many different causes. Four most frequent are
• Hernia protrusion or organ through its
  protective sheath
• Intussusception part of intestine slips into
  the part just distal to itself
• Volvulus twisting of the intestine
• Adhesions union of normally seperated tissue by
  a fibrous band of new tissue

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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.

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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.

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Bowel Obstruction

• Patients present with diffuse visceral pain,
  usually poorly localized to any one specific
  location.
• Hemodynamically unstable due to necrosis of an
  organ, SS 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.

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Accessory Organ Disease

• These include
• Liver
• Gallbladder
• Pancreas
• Vermiform Appendix

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Appendicitis

• 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.

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Appendicitis

• 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.

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Appendicitis

• 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.

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Appendicitis

• 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 McBurneys point.
• 2/3 the distance from the umblicus to the
  superior illac crest.
• Prehospital care is based on the hemodynamic
  state of the patient.

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McBurneys Point
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Cholecystitis

• 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
• Cholesterol-based
• Bilirubin-based

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Cholecystitis

• 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.

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Cholecystitis

• 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
• Acalculus cholecystitis (no stones)
• Chronic inflamation caused by bacterial
  infection

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Cholecystitis

• Acalculus cholecystitis usually results from
  burns, sepsis, diabetes, and multiple organ
  failure.
• 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
  contraction.

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Cholecystitis

• The pain occurs after a meal that is high in fat
  content because of the secondary release of bile
  from the gallbladder.
• Palpation may reveal either diffuse right-sided
  tenderness or point tenderness under the right
  costal margin, a positive Murphys sign.
• Prehospital treatment is mainly palliative.
• Position of comfort, maintain ABCs, establish IV
• Pain medication meperidine (demerol)
  butorphanol (stadol).

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Pancreatitis

• Inflammation of the pancreas.
• Four main categories, based on cause
• Metabolic
• Mechanical
• Vascular
• Infectious

99
Pancreatitis

• 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.

100
Pancreatitis

• 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.

101
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
  region.
• Most patients experience nausea followed by
  uncontrolled vomiting and retching that can
  further aggravate the hemorrhage.

102
Pancreatitis

• 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.

103
Hepatitis

• 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.

104
Hepatitis

• Any of the viral pathogens, alcoholic exposure,
  or trauma can injure the hepatocytes, causing
  inflammation and, possibly, chronic liver
  disease.
• 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
  death.

105
Hepatitis

• 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.

106
Hepatitis

• 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
  epidemic.
• Effects may be minimal, but can range to severe
  liver ischemia and necrosis.

107
Hepatitis

• 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.

108
Hepatitis

• 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.

109
Hepatitis

• 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.

110
Hepatitis

• Other signs and symptoms include severe N/V,
  general malaise, photophobia, pharyngitis, and
  coughing.
• 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
  necrosis.

111
Hepatitis

• Treatment is palliative
• Secure ABCs
• Establish IV
• Antiemetic administration
• Definitive treatment involves antiviral and
  anti-inflammatory medications and symptomatic
  treatment