Upon completion, the student will be able to:
1. Describe the incidence, morbidity and mortality of
2. Identify the risk factors most predisposing to
3. Discuss the anatomy and physiology of the
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
h) Ulcer disease
i) Bowel obstruction
j) Crohn’s disease
l) Esophageal varices
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
Pain is the hallmark of the acute abdominal
Three main classifications of abdominal 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
2) Distention (being stretched out or inflated)
3) Ischemia (inadequate blood flow)
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
Body responds through sympathetic stimulation
causing N/V, diaphoresis and tachycardia
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
Resulting peritonitis can lead to sepsis,
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
Similar to a trauma assessment with an
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
makes the pain worse
3. Quality: dull, sharp,
4. Region/radiation: pain
5. Severity: scale 1-10
6. Time: when and how
Patient’s general appearance and
Complete set of vital signs
Visually inspect the abdomen before palpation
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
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,
1. Muscle tension or its absence
2. Masses, pulsation, tenderness
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
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
3. Variceal rupture
4. Mallory-Weiss syndrome (esophageal laceration,
usually secondary to vomiting)
Complain of some type of abdominal discomfort
ranging from a vague burning sensation to an
upset stomach, gas pain, or tearing pain in the
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
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)
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
Maintain airway, oxygenation and circulatory
Lateral recumbent position or semi-Fowler’s
Two large bore IV’s when you suspect GI bleed
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
Primary cause is the consumption of alcohol and
the ingestion of caustic substances.
Alcohol consumption can result in cirrhosis of
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
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,
Classic signs of shock are common
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)
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
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.
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
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
6. General malaise
7. Patient may complain of widespread and diffuse
abdominal pain that is not specific to any one region.
Treatment is mainly supportive and palliative.
Position to decrease the risk of aspiration
Antiemetics: prochlorperazine (compazine) or
Electrolyte replacement may be necessary at
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
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
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.
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
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
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)
Blocked pancreatic duct can also contribute to
duodenal ulcers. This duct releases an alkalotic
solution in opposition to the high acid contained
Another cause is: Zollinger-Ellison
Syndrome: Where an acid-secreting tumor
provokes the ulcerations; condition causes
stomach to secrete excess HCl acid and pepsin.
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
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
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
IV access, fluid resuscitation
Position of comfort, cardiac monitor
MAST if directed in local protocols
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.
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
10,000 new cases are diagnosed yearly.
Affects patients between the ages of 20-40.
2. Allergic and other immunological
Current research has found that the release of
cytokines can cause an overwhelming
inflammatory response in the submucosa
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
Presents as a recurrent disorder with occasional
bloody diarrhea or stool containing mucus.
Colicky abdominal pain (cramping)
Cramping is usually isolated to the lower
Typically appear restless due to discomfort
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
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
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
Can occur anywhere from the mouth to the
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
Complete intestinal obstruction can also occur
Significant lower bleeding is rare.
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
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
Flareup is usually rapid, requiring a visit to the
Abdominal pain cannot be localized to any
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
Management depends on the patient’s
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
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,
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
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
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
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.
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
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:
Cholesterol-based stones are far more common
and are associated with a specific risk profile:
obese, middle-aged women with more than one
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
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:
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 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
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
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
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
Pain may present in URQ or the right shoulder
Fever may be secondary to infection or to tissue
Treatment is palliative.
Definitive treatment involves antiviral and anti-
inflammatory medications and symptomatic