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    :MATERIAL FOR MIDTERM:
    PACKET ONE:
    ATIEMPTING TO ASSESS PAIN OF ABDOMINAL ORIGIN
    PACKET TWO:
    THE ESOPHAGUS
    PACKET THREE:
    THE STOMACH

    Adapted from: Evidence-Based Physical Diagnosis, McGee
    WB Saunders Co., 2"• edition {April 23, 2007)
    Adapted from: The Rational Clinical Examination: Evidence-Based Clinical Diagnosis,
    Simel & Drummond, McGraw-Hill Professional., 1" edition {August 25, 2008)
    Adapted from: Physical Diagnosis Secrets, Mangione,
    Henley & Belfus, 2000

    ASSESSING PAIN OF ABDOMINAL ORIGIN: 02.
    REVIEW OF PAIN CHARACTERISllCS
    A. REVIEW: COMMON SllMUU OF ABDOMINAL PAIN
    1. Rapid Distention of Hollow Organ Smooth Muscle
    2. Rapid Distention of the capsules of Solid Organs
    a. Note: A more gradual stretch I distention might not produce as much pain
    3. Intense Contraction of the Muscles of Hollow Viscera
    4. Inflammation
    Rectus Abdominis
    Small Intestine
    Aorta
    Visceral Peritoneum
    Not vety pain
    sensitive
    Descending Colon
    B. REVIEW: PAIN THRESHOLDS
    1. Most Sensitive: Parietal Peritoneum (a serous membrane)
    2. Sensitive: Walls of the Hollow Viscera (Gall bladder, bowel, etc.)
    3. Least Sensitive: Parenchymatous Organs (Kidneys, etc.)
    C. HISTORY AS IT RELATES TO ABDOMINAL PAIN: Patient Seated
    1. Pain Location and Character?
    2. When Did the Pain Start?
    3. Is There Anything That Makes it Better or Worse?
    Parietal Peritoneum
    Vety pain sensitive
    Mesentery
    Inf. Vena Cava
    Ascending Colon
    4. Have There Been Any Changes in Location or Character Since the Pain Started?
    )
    )
    ASSESSING PAIN OF ABDOMINAL ORIGIN: 03.
    NON-LOCALIZED VISCERAL PAIN
    A. REVIEW: PAIN OF VISCERAL ORIGIN C'V" for visceral & "V" for "vague'1
    1. Clinical Associations: Visceral pain is usually associated with distension,
    traction or ischemia of a hollow viscus
    2. Visceral Pain is Not Easily Localized
    3. Visceral Pain is Usually Hard to Describe
    a. "Burning", "gnawing", "dull", "colicky", "cramping", "sickening"
    4. Visceral Pain is Often First Noticed Closer to the Midline of the Abdomen
    a. However, visceral pain may also be referred to a distant site
    5. It's Not Usually, Made WotSe by Movement, Coughing, or Deep Respiration
    6. Visceral Pain is Not Usually Made WotSe by Palpation
    7. Visceral Pain is Not Usually Made WotSe by Percussion and Palpation
    8. The Underlving Musculature is Not Tense or Painful
    Because visceral pain fibers are bilateral 8r. can enter the spinal cord at multiple levels,
    visceral pain usually is usually dull, poorly localized, 8r. felt more toward the midline
    y
    ..
    Example:
    The "classic" visceral pain
    associated with passing a
    gallstone has a component
    that involves the midline
    of the upper abdomen
    A referred visceral pain can
    manifest in the area of the
    right trapezius 8r. scapula
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    12-08
    ASSESSING PAIN OF ABDOMINAL ORIGIN:
    LOCALIZED ABDOMINAL PAIN
    Remember, the upper portion of the
    abdomen is surrounded by the lower
    portion of the rib cage
    Remember, all components of the
    abdominal wall share a common
    segmental innervation
    A. POTENTIAL SOURCES OF LOCAUZED ABDOMINAL PAIN
    1. Pain From ~he Parietal Peritoneum I Peritonitis
    a. Parietal: Of or pertaining to the walls of a cavity in the body
    b. Usually well-localized
    c. Might become dermatomal
    2. Nerve Root Pain 1 Intercostal Pain
    a. The patient might complain of a dermatomal pain
    3. Issue: Myofascial Trigger Points /MFTPs
    a. The patient might complain of pain localized to the abdominal wall
    04.
    b. The patient might complain of a diffuse discomfort that mimics visceral pain
    Myofascial Trigger Points I MFTPs
    "A tender trigger point in the abdominal wall is frequently no more than 1 or 2 em in diameter.
    However, it is not unusual for the pain to spread over a wide area or to be referred.
    For instance, pressing on a tender trigger point in the right upper quadrant
    (nerve root T7) can refer pain to the angle of the scapula."
    "Patients are often so preoccupied with the large area of pain spread that they
    do not realize the area of tenderness is extremely localized and superficial.''
    Adapted from The Abdominal Wall: An Overlooked Source of Pain, Suleiman and Johnston
    American Family Phvsician August 1 2001
    )
    )
    6-10
    )
    LOCALIZED ABDOMINAL PAIN: 05.
    PERITONmS: PAIN FROM THE PARIETAL PERITONEUM
    A. REVIEW: PAIN FROM THE PARIETAL PERITONEUM f'P" for Peritoneum & "P" for Point)
    1. The Parietal Peritoneum & the Abdominal Wall Share a Common InneiVation
    a. It is important to differentiate between the two sources
    2. Peritoneal Pain Arises From Noxious Stimulation of the Parietal Peritoneum
    a. The parietal peritoneum is sensitive to mechanical, thermal or chemical stimulation
    3. Peritoneal Pain Tends to Manifest in Oermatomes TS-L2
    4. Peritoneal Pain is Usually Sharper, More Easily Localized, and Easier to Describe
    5. It is Usually Hade WOtSe by Movement, Coughing, or Deep Respiration
    6. Parietal Pain is Hade WotSe by Percussion and Palpation
    7. Peritoneal I"itation can cause Reflexive Contraction of Segmental Muscles
    a. The under/ring muscles are noticeably tense andoainful
    8. Peritoneal Irritation May Also Cause Cutaneous Hyperesthesia
    a. Cutaneous hyperesthesia may also be seen with radiculopathies and neuropathies
    Peritoneal pain associated
    with overt GB inflammation
    Peritoniteal pain may have
    a dermatomal distribution
    Clinical reality:
    Localized pain 8t antalgia
    Clinical axiom: If a visceral pain changes location and starts becoming a parietal pain
    and you can't find evidence of an NMS condition or a Mi=TP as the
    source of the pain, start thinking about peritonitis
    ABDOMINAL EXAM: 06.
    PATIENT SEATED
    A. VITAL SIGNS: BP[TIPIR (Review 5th quarter material on vital signs)
    B. HISTORY REVIEW & GENERAL OBSERVATION OF THE PATIENT
    1. Pain Location &. Character
    a. Where is the pain&. what does it feel like?
    b. When did the pain start?
    c. Has there been a change in the location or character of the pain??????
    2. If the Pain is Localized & Your Are Concerned About Peritonitis:
    a. Ask if the Localized Pain Gets Worse When the Patient Coughs
    b. Ask if the Localized Pain Gets Worse During the Heel Strike Phase of Gait
    Dunphy's sign I positive cough test
    A localized pain that increases with coughing
    Suggestive of peritonitis. PLR: 2.4
    Note: You might be asking the patient to cough again later in the exam
    The "jar" test I "jar" test
    Sudden vibration increases I localizes the pain
    Noticed during the heel strike phase of gait or when the patient stands
    on their tip toes and drops down onto their heels
    Other indicator of peritonitis will be discussed a little later in the course
    C. Additional Exam Components During the Seated Portion of the Exam
    1. Conjunctiva & Sclera:
    a. Yellowing of the conjunctiva overlying the sclera is often the 1" sign of jaundice
    b. Discussed later in the course
    2. Mouth, Thyroid Gland
    3. Cervical 1 Supraclavicular Lymph Nodes (Review 5th quarter PDX-1 lab handout)
    4. Murphy's Percussion I Murphy's Punch if Renal Disease is Suspected
    )
    )
    ABDOMINAL EXAM:
    PATIENT SEATED
    07.
    Supraclavicular lymphadenopathy has the highest risk
    of malignancy, estimated at 90% in patients over 40
    and 25% in those under 40
    The right supraclavicular nodes drain the mediastinum,
    lungs 8r. esophagus. Enlargement suggests
    lung, gastrointestinal or retroperitoneal cancer
    The left supraclavicular nodes drain the thorax and
    the abdomen. Enlargement suggests lymphoma,
    intra-thoradc cancer , or systemic infection.
    Remember Virchow's I Sentinel Node?
    Costovertebral angle tenderness
    and the "thumb pressure test"
    Kidney disease (UTI, kidney stones) may initiate
    a reflexive viscero-somatic pain that manifests
    in the thoracolumbar transitional area
    Palpation near the 12th costovertebral articulation
    might reveal reflexive muscle hypertonicity and
    elicit further pain in such cases
    Murphy's Percussion I Murphy's Punch
    Indirect percussion over the kidney elicits an intense,
    sharp, focal pain in conditions that inflame and/or
    distend the kidney capsule.
    Murphy's percussion is performed when there are indications
    of kidney disease or as a follow-up when costo-vertebral
    angle tenderness is found upon palpation
    ABDOMINAL EXAM:
    PATIENT SUPINE
    08.
    Remember,
    proper patient
    positioning is
    essential
    Note: The patient's hips and knees must be flexed in order to relax the abdominal
    musculature before even thinking of attempting percussion or palpation. And, if
    possible, the head piece of the table can also be brought into flexion.
    Visualizing the four quadrants of the abdomen will be of help during the exam.

    ABDOMINAL EXAM:
    PATIENT SUPINE
    can the patient get comfortable on the exam table?
    If not, why???
    Is there normal abdominal respiration?
    As the patient inhales and the diaphragm moves down
    both the chest wall & the abdominal wall should
    move outward (uoward)
    Does the patient appear anxious?
    Has the patient indicated an area of localized
    abdominal discomfort? If so, address that
    area last as you go through
    the steps of the exam
    Is there any evidence of orthopnea?
    (The need to be upright in order to breathe)
    Abdominal paradox I paradoxical breathing?
    As the patient inhales and the diaphragm moves down both
    the chest wall & the abdominal wall should move outward
    (upward). With paradoxical breathing means the chest moves
    outward but the abdomen moves inward
    09.
    For more on interpreting chest breathing versus diaphragmatic breathing,
    see the section on Posture and Breath Training in the
    CSPE Drotocol Low Back Rehabilitation DI'OQram.
    If appendicitis is suspected: Psoas sign
    Pain upon passive extension of the right psoas muscle
    Hight be associated with "retrocecal" appendicitis
    Mav also be seen with ilioosoas bursitis, psoas abscess, etc.
    If appendicitis is suspected: Obturator sign
    Pain upon internal rotation of the right thigh
    Might be seen with "pelvic" appendicitis
    May also seen with hip disease, etc.
    ACUTE RLQ TENDERNESS, TWO SIGNS OF APPENDICITIS
    Finding: Sensitivity Specificity Positive LR Negative LR
    Psoas sign 13-15% 91-97%
    Obturator sign 8% 94%
    Adapted from: Evidence-Based Physical Diagnosis, McGee, WB Saunders Co., 2001
    ABDOMINAL EXAM: 10.
    PATIENT SUPINE
    A. INSPECTION (In no particular sequence)
    1. Scars, Bulges and Herniations
    "Ventral" or abdominal wall
    scars & hernias often manifest
    in a localized pain. The pain &
    the hernia tend to get worse
    the patient coughs or
    bears down
    Incisional hernia
    Herniation through the scar from
    a past surgery. Can occur months
    or years after the surgery.
    . --·· .
    Epigastric hernia
    Usually seen along the midline and
    results from congenital weakness
    combined with increased intraabdominal
    pressure
    Umbilical hernia
    Occurs in the umbilical "ring"
    surrounding the navel. Result from
    congenital defect, obesity,
    excessive coughing, pregnancy
    Inguinal hernias occur above inguinal ligament and account for
    about 75% of all abdominal wall hernias. They occur up to 25
    times more often in men. There are two sub-types.
    Indirect inguinal hernias
    Can affect both men and women, but is the most common type of
    hernia in men. A loop of intestine and/or fat enters into or through
    the inguinal canal. May be associated with a congenital weakness.
    Direct inguinal hernias
    Typically occurs in men over 40. May result from aging or injury.
    Associated in the
    occur ligament
    Femoral hernias are more common in women and usually
    results as weakness in the tissues I musculature
    surrounding the femoral canal.
    Please review notes
    2. "Swelling" I Abdominal Distension
    Bulging Flanks & Large Volume Ascites (> 500 ml)
    Flank: The fleshy part of the side between the ribs and the hip
    Best observed while standing at the patient's feet.
    The fat of obesity tends to encircle the patient's waist and involve
    the posterior aspect of the patient's torso
    In a supine patient, ascites has a more anterior distribution.
    Posterior spread of the fluid would be limited by the lower
    rib cage and the muscles of the back.
    http://deris.washington.edu/phvsdX/Iiver/tech.htrnl
    )
    )
    '
    )
    ABDOMINAL EXAM: 11.
    PATIENT SUPINE
    A. INSPECTION (In no particular sequence)
    3. Discoloration I Ecchymosis
    Periumbilical ecchymosis that
    is classically associated with
    retroperitoneal hemorrhage
    from pancreatitis. However,
    this is neither sensitive or
    specific for retroperitoneal
    hemorrhage
    Grey- Sign
    Flank ecchymosis that is
    classically associated with
    retroperitoneal hemorrhage
    from pancreatitis. However,
    this is neither sensitive or
    specific for retroperitoneal
    hemorrhage
    4. Veins, Visible Peristalsis 8t Visible Pulsations
    Caput Medusa 8t
    Portal Vein Hypertension
    In Greek mythology, Medusa
    was a monstrous character who
    was often depicted with snakes
    coiled around her arms or legs
    or entwined in her hair. It was
    said that looking into her eyes
    would turn onlookers to stone.
    Inferior Vena Cava Syndrome
    Superficial collateral veins that are distended following an
    obstruction in the inferior vena cava. Often associated with
    thrombosis of the inferior vena cava and might be a subset of
    deep vein thrombosis. May be associated with other conditions.
    Inter-observer Agreement on Collateral Veins is "Moderate": K 0.47
    Peristalsis
    Visible peristalsis from the small intestine seen through the
    abdominal wall of a child who is dying from malnutrition.
    (Think Haiti after the earthquake or Pakistan after the flood)
    ABDOMINAL EXAM: 12.
    PATIENT SUPINE
    A. INSPEcnON (In no particular sequence)
    4. Veins, Visible Peristalsis &. Visible Pulsations, continued
    B. AUSCUL TAllON
    The patient is a 52-year-old man whose esophagus was removed
    and replaced with a section of his jejunum following complications
    of lye ingestion 20 years ago. Currently the patient had a history
    of dysphagia and alchohol abuse. He responded to
    conservative therapy
    Visible Pulsations
    A very large & pulsatile aneurysm of the abdominal aorta
    in a thinner patient. Remember, brief, succinct and small
    pulsations from the abdominal aorta can be seen in healthy,
    young and thin individuals
    1. Auscultation Represents the First Physical Contact With the Patient's Abdomen
    a Note how the patient responds to this contact
    "Classic" Assessment:
    Bowel Sounds in All Four Quadrants
    Abdominal Aorta
    Renal Arteries
    Common Iliac Arteries
    Review: As it relates to bowel sounds, auscultation has a
    relatively minor role in the abdominal exam
    It is performed before percussion or palpation as vigorously touching the abdomen may disturb the
    intestines, perhaps artificially altering their activity and thus bowel sounds. Many physicians will omit
    abdominal auscultation unless there is a symptom or finding suggestive of abdominal pathology
    Adapted from: A Practical Guide to Clinical Medicine, University of california, San Diego
    http:flmeded.ucsd.edu/dinicalmed/abdomen.htm
    )
    )
    ABDOMINAL EXAM: 13.
    PATIENT SUPINE
    B. AUSCULTATION, continued
    Review: Arterial Bruits
    Bruits are best heard when using very light pressure on the
    diaphragm of the stethoscope
    Bruits have a poor localizing value:
    Sounds generated in the abdomen tend to travel throughout the abdomen
    Abdominal bruits are of the greatest significance in cases of renovascular hypertension
    These bruits oa:ur in patients with renal artery stenosis
    These patients usually have severe hypertension that has been resistant to treatment
    (Usually a BP greater than 1601100 in patients older than 55)
    ~ Renal Vascular Hypertension 1 Renal Artery Stenosis
    Are more often systolic-diastolic (ucontinuous")
    jl Often radiate to the patient's side I flank ~ ----"Anterior" bruits near the umbilicus have a higher
    I ~ sensitivity for renal vascular disease
    "Flank" bruits have a higher specificity
    r:
    for renal vascular disease
    Abdominal bruits do not assist in the diagnosis of abdominal aortic aneurysm
    Benign epigastric bruits oa:ur in 4% to 20% of healthy
    persons. They are usually systolic, low-pitched, and
    / usually manifest in the epigastrium
    jl }vY They are often hard to hear in a noisy exam room
    However, they may be heard anywhere between
    ¥' the xiphoid process and the umbilicus
    They rarely radiate to the patient's sides 1 flanks
    Normal bruits apparently originate from the celiac artery
    ABDOMINAL EXAM: 14.
    PATIENT SUPINE
    C. PERCUSSION / UGHT PERCUSSION
    Remember, proper patient positioning
    is important
    Percussion occasionally has a role in the abdominal exam
    Percussion might serve to detect enlargement of solid organs and the presence
    of masses, fluid, or gas in the abdomen
    Percussion might also be of some benefit in the assessment of peritoneal irritation.
    Percussion Tenderness I Direct Percussion
    Light percussion directly over the area of
    tenderness elicits pain
    Rovsing's sign /Indirect Rebound Tenderness
    (Also known as contralateral tenderness)
    Some authors think this to be more accurate than
    direct rebound tenderness
    Acute Appendicitis: Review and Update, Hardin,
    American Family Physician, November 1, 1999
    http://www.aafp.oralafp/991101ap/2027.html
    )
    )
    ABDOMINAL EXAM:
    PATIENT SUPINE
    D. PALPATION
    I f
    Do not use your
    Avoid the temptation to curl the
    finger tips while palpating.
    (Possible exception:
    Investigating ilopsoas MFTPs)
    Use the ftflat" of the hand
    Use the full length of the "finger
    Superfidal palpation
    Depress the abdominal wall
    approximately one centimeter
    Deep palpation
    Depress the abdominal wall
    more than one centimeter
    15.
    The examiner may choose to use either one hand or two hands to perform palpation.
    Avoid short, "choppy" movements
    Investigate any area of reported pain last during the steps of the exam
    A. SUPERFICIAL PALPATION: Depress the abdominal wall less than one centimeter
    1. General Introductory Screening Exam: Gently palpate all four abdominal quadrants
    2. Assess Abdominal Muscle Tone &. Areas of Reported Pain or Tenderness
    a .. Compare underlying abdominal muscle tone from side to side which is very
    significant in the assessment of suspected peritonitis
    b. Myofascial trigger points? Evaluation of any scars on the abdomen?
    3. "Classic" Uses: Detecting Huge Masses I Huge Organomegaly I Abnormal Texture of the Liver
    B. DEEP PALPATION: Depress the abdominal wall more than one centimeter.
    1. Follow Abdominal Movement&. Progressively Apply Pressure During Exhalation
    2. Best Use: Evaluation of the Abdominal Aorta
    3. Another Practical Use: Provoking a Suspected Myofascial Trigger Point(MFTP)
    4. Other Applications of Deep Palpation Don't Tell You Much of Anything
    a. Diagnostic ultrasound has become the preferred modality
    ABDOMINAL EXAM:
    PATIENT SUPINE
    D. PALPATION, continued
    Volvulus
    Obstruction due to adhesions
    .--~.·\"··v.·. · ·,- . •I- ' :_
    ' . '
    {
    16.
    Four Abdominal Quadrants I
    Ascending, Transverse and Descending Colon
    Note:
    As it relates to the colon, the sigmoid is the area oF
    the highest intraluminal pressure. In patients with
    initable bowel syndrome (IBS) the sigmoid colon can
    be tender on palpation. Also, sigmoid palpation in IBS
    patients can cause this discomFort to radiate
    To the rectum & anus
    Epigastrium 1 "Stomach" and the Small Intestines
    Note:
    Some degree oF a general epigastric tendemess is
    common in a number oF abdominal conditions,
    especially those involving the stomach.
    There might be palpatory findings with some major
    disorders of the small intestine
    Intussusception Herniation thru abdominal wall
    Mesenteric obstruction Intraluminal obstruction
    www.pedisurg.com
    )
    ABDOMINAL EXAM:
    PATIENT SUPINE
    D. PALPATION, continued
    Liver
    Start deep palpation about
    1 inch 1 2-3 em below the
    costal margin and use the
    patient's respiration to
    work your way in deeper
    17.
    Liver: Deep Palpation
    / /
    !
    \
    Gall Bladder: Superficial
    Gall Bladder
    Palpation of the gall
    bladder is much like
    palpation of the liver.
    Gall Bladder: Deep Palpation
    ----f0
    ./
    You just start the
    palpation a little lower
    _--,,$
    Primary objective: Superficial palpation for assessment of muscle tone (peritonitis)
    Be careful with dee t. tion review Mur h s si n from lecture notes
    Spleen
    Palpation of the spleen
    is much like palpation
    of the liver
    You're just on the other
    side of the abdomen
    You might be able to palpate the spleen in a very thin patient
    Remember mononucleosis is considered a contraindication to s leen al tion
    ABDOMINAL EXAM:
    PATIENT SUPINE
    D. PALPATION, continued
    Appendix: Superficial Palp.
    ~--.. _ ;-:...
    ·~
    18.
    Kidney: VeJY Deep Palpation ????
    Clinically, this is not considered to be worth the effort
    You mightfind massive enlargement of the kidney in young adult
    patients with end-stage polycystic kidney disease (and end-stage
    renal failure) or infants/ toddlers with lots of blood in the urine
    due to a Wilms tumor
    The primary objective in
    superficial palpation over a
    painful appendix is to
    assess for a local increase
    in muscle tone, which can
    be an indication of
    peritonitis
    No Deeo Paloation
    Deep Palpation: Abdominal Aorta
    "Trap" the abdominal aorta between the medial
    aspects of the index fingers
    Normal: A brief, succinct pulse
    Abnormal: An enlarged, pulsatile mass that is
    indicative of an AAA
    Remember, palpation of the abdominal aorta is probably the best use of deep palpation
    "Classically" the normal abdominal aorta is said to be l.S-4.0 em. wide by palpation.
    Do not count on this representing an accurate assessment of aorta size.
    )
    )
    ABDOMINAL EXAM:
    PATIENT SUPINE
    )
    D. PALPATION, continued
    Inguinal Lymph Nodes
    Enlargement is common in a
    number of conditions involving
    the lower abdomen, extemal
    genitalia, and lower extremity
    Urinary Bladder
    19.
    Symphysis pubis & osteitis pubis ·
    Along with adductor tendinitis & "groin strain",
    osteitis pubis can accompany a number
    of sports-related injuries
    (discussed again later)
    Ilio-Psoas MFTPs are common and can be very tender
    MFTPs in the upper portion of the psoas can refer pain to
    the abdominal wall and to the ipsilateral paraspinal area
    MFTPs in the iliacus can refer pain to the overlying
    lower quadrant of the abdomen
    MFTPs in the lower portion of the psoas can refer
    Pain to the ipsilateral groin
    ABDOMINAL EXAM: 20.
    PATIENT SUPINE I CARNETT'S I MFTPs
    Remember, "patients with MFTPs are often so preoccupied with the large area of pain
    spread that they do not realize the area of tenderness is extremely
    localized and superficial."
    Adaoted from The Abdominal Wall: An Overlooked Source of Pain American FamilY Physician Auaust 1 2001
    Example:
    External oblique MFTP in the upper abdomen
    Pa~ient may mistake the pain for "heartburn", etc.
    Adapted from: Myofascial Pain & Dysfunction:
    The Trigger Point Manual, Williams & Wilkens, 1983
    Example:
    External oblique MFTP in the lower abdomen
    Pain may refer to the groin
    Adapted from: Myofascial Pain & Dysfunction:
    The Trigger Point Manual, Williams & Wilkens, 1983
    Example:
    MFTP in the lateral aspect of the
    lower right rectus abdominis
    Pain might "cover" McBurney's point
    Adapted from: Myofascial Pain & Dysfunction:
    The Trigger Point Manual, Williams & Wilkens, 1983
    )
    )
    ABDOMINAL EXAM: 21.
    PATIENT SUPINE I CARNETT'S I MFTPs
    A. CARNETT'S IS USED TO ASSESS A "CHRONIC & UNREMITTING" ABDOMINAL PAIN
    1. The Patient Appears to be Well
    2. The Pain is Usually "Chronic, Nagging and Non-Progressive"
    3. The Pain Usually~ !!Ill Have a Relationship to Eating or Bowel Function
    4. It Often~ Have a Relationship to Movement of the Abdominal Wall
    a. Increased discomfort with voluntary tensing of the abdominal muscles
    b. Increased discomfort with palpation of the abdominal wall
    c. Increased discomfort with posture changes involving the abdominal wall musculature
    d. Increased discomfort with sit-ups or leg-lifts
    e. Increased discomfort with rotation of the trunk
    B. OBJECTIVE:
    1. Determining if the Abdominal Wall is the Likely Source of the Patient's Pain
    Parietal Peritoneum:
    Very pain sensitive
    Rectus abdominis
    muscle
    Visceral Peritoneum:
    Not very pain sensitive
    External oblique
    muscles
    Internal oblique
    muscles
    Transverse
    abdominal muscles
    Carnett's attempts to determine if some condition involving the "non-peritoneal" portions of the
    anterior abdominal wall is responsible for the patient's abdominal pain. The "non-peritoneal"
    components of the anterior abdominal wall include the skin, Camper's fascia, Scarpa's fascia, the
    external oblique muscles, the internal oblique muscles, the transverse abdominal muscles,
    the rectus abdominis muscles, the linea semilunaris, and the fascia tranversalis
    In this scenario the parietal peritoneum is not induded as a component 1 layer
    Carnett's might be helpful in ruling out peritonitis
    Carnett's is notoonsidered to be helpful at ruling in peritonitis
    Arguing against peritonitis, abdominal wall tenderness: sensibvity 1-5%, specificity 32-72%, PLR 0.1, NLR --Adapted
    from: Evidence-Based Physical Diagrtosis, McGee, WB Saunders Co., 2001
    03-09
    ABDOMINAL EXAM:
    PATIENT SUPINE I CARNETT'S I MFTPs
    Step one: Palpation with
    the patient's abdominal
    muscles relaxed
    Step two: Palpation
    in the same spot with
    the patient's abdominal
    muscles contracted
    C. STEP ONE: THE PATIENT IS SUPINE AND RELAXED
    22.
    1. Have the Patient Attempt to Point Out the Site of Their Abdominal Discomfort
    a. Encourage them to use a fingertip in order to do so and to be as specific as possible
    2. Palpate the Site in Question
    a. Apply digital pressure to the suspected locus of the pain
    b. Does this initiate a pain similar to that of which the patient was complaining?
    c. Release the Digital Pressure But Do Not Remove the Finger Contact
    D. STEP lWO: THE PATIENT CONTRACTS I TENSES THE ABDOMINAL MUSCLES
    1. Have Them Perform a Sit-up I Partial Sit-up I Leg Lift
    2. Re-Apply Digital Pressure to the Suspected Site While the Muscles Are Contracted
    3. Does the Discomfort Remain Unchanged When the Abdominal Muscles Are Tensed?
    4. Does the Discomfort Increase When the Abdominal Muscles Are Tensed?
    5. Does the Discomfort Disappear When the Abdominal Muscles Are Tensed?
    E. INTERPRETATION
    1. The Pain Remains UnchangedWhen the Abdominal Muscles Are Contracted
    a. This implies that the pain does originate from the anterior abdominal wall
    2. The Pain Increases in Intensity When the Abdominal Muscles Are Contracted
    a. This also implies that the pain does originate from the anterior abdominal wall
    3. The Pain Decreases in Intensity When the Abdominal Muscles Are Contracted
    a. This implies that the pain does not originate from the anterior abdominal wall
    A PROBLEM WITH TERMINOLOGY
    Most authors use the terms "positive Carnett's" or "Carnett's sign" to indicate that the
    pain originates from the anterior abdominal wall. However, some authors use them
    to indicate that the pain might be originating from the abdominal viscera
    )
    )
    )
    LOCALIZING ABDOMINAL PAIN:
    ALGORITHM
    carnett's positive
    fo< abdomlnr wall pain?
    I
    Surgical scar at
    site of pain?
    I
    Consider an
    incisional hernia
    Pain made worse
    by spinal exam?
    I
    Think involvement
    of a nerve root I
    intercostal nerve
    Pain localized to an
    anatomical site or structure?
    Pain localized common
    sites of abdominal
    or groin hernias?
    I
    No surgical scar
    at site of pain?
    Consider MFTPs I
    sports hernia
    (see pages 9-11)
    Pain localized to the lateral
    aspect of a rectus muscle?
    Possible MFTP?
    Possible rectus ACNES?
    (see page 14)
    23.
    carnett's negative
    for abdominal wall pain?
    I
    Consider a visceral disorder
    (including IBS & NUD)
    Pain notworse
    with spinal exam?
    Pain not necessarily localized
    to an anatomical site?
    Consider rectus
    sheath hematoma
    (see page 13)
    Pain localized to the lower
    costal margin?
    Ribs 8 through 10?
    Think rib tip syndrome I
    slipping rib syndrome
    Adapted from The Abdominal Wall: An Overlooked Source of Pain, Suleiman and Johnston American Family Physician,
    August 1, 2001. For other conditions that might be associated with camett's refer that article and ; Chronic abdominal wall
    pain: a frecuently overlooked problem: Practical approach to diagnosis and management, The American Journal of
    Gastroenterology, Volume 97 Issue 4, Pages 824 - 830
    ABDOMINAL EXAM: 24.
    PATIENT SUPINE I SPORTS HERNIA
    Sports hernia I athletic pubalgia: Groin pain without a clinically-detectable hernia
    Deep I internal inguinal ring Posterior canal wall: Superfidal I external ring
    Fascia transversalis
    Conjoint tendon of internal
    oblique 11 transversus
    Anterior canal wall:
    Aponeurosis of the
    external oblique
    Again, review Gross III notes
    A. SPORTS HERNIA: 'The hernia without a bulge"
    1. "Disruption" of the Inguinal Canal With No Clinically Detectable Hernia
    2. Seen in Sports Requiring Repetitive Twisting and Turning Movements at Speed
    a. May be seen more often in sports requiring sustained forward flexion: hockey, etc.
    b. More often unilateral but may be bilateral
    3. More Common in Male Athletes
    a. This may be due to an increased likelihood that males participate the sports in question
    4. Onset is Most Often Insidious But Can Be Acute
    a. Insidious onset: Pain is more often noted during exercise
    b. Acute onset: Patient may experience a "tearing" sensation during exercise
    5. The Pain May Radiate to the Adductors I Testicles I Perineum
    6. The Pain May be Exacerbated by Coughing, Sneezing, Sudden Movement, etc.
    B. SPORTS HERNIA 11 THE PHYSICAL EXAM
    1. Tenderness Localized to the Conjoint Tendon and I or the Inguinal Canal
    2. Tenderness Exacerbated During a Resisted Sit-Up I Carnett's
    3. A Dilated Superficial 1 External Inguinal Ring
    a. Making this determination would require some experience on the part of the examiner
    Adapted from the "Sports Hernia•: A Common Cause of Groin Pain, Kemp et al,
    The Physician and Sportsmedidne, Vol 26, No. 1, January 1998
    01-09
    )
    )
    ABDOMINAL EXAM: 25.
    PATIENT SUPINE I SPORTS HERNIA
    C. PROBLEM: THE SITE OF PAIN CAN VARY FROM PATIENT TO PATIENT
    1. The Pain May be Well-Localized to the Conjoint Tendon and Its Insertion
    a. A medial pain is felt on the superior aspect of the pubis
    2. In Other Cases the Pain May be Felt Along the Course of the Inguinal Canal
    a. Pain is felt along the lateral aspect of the inguinal canal
    D. PROBLEM: THE DISTINCT POSSIBUTY OF CO-EXISTING CONDffiONS
    1. There Are Other Conditions With More or Less the Same Etiology
    Osteitis pubis
    Inflammation, with possible sclerosis,
    of the symphysis pubis
    Adductor tendinitis I groin strain
    An overload injury due to excessive stretching
    and or contraction of the adductor muscles
    Dr. carnes suggests you review material on adductor
    palpation and testing from 6"' quarter Biomechanics IV
    E. PROBLEM:WHAT TO DO ABOUT A SPORTS HERNIA?
    1. Some Cases Might Respond to ConseiVative Care
    a. Apparently, no treatments other than surgery have been shown to be effective
    b. Rest 1 inactivity might be the best "treatment''
    c. NSAIDs, ice & PT can be tried in an effort to alleviate the patient's symptoms
    2. Cases Resistant to ConseiVative Care May Require Surgery
    3. Surgery Might be Directed to One or More Structures
    a. Pathologic mechanisms can include a torn external oblique aponeurosis, a tom conjoined
    tendon, a "split" that can form between a torn conjoined tendon and the inguinal ligament,
    weakening of the transversalis fascia with separation from the conjoined tendon, tears in
    the internal oblique muscles, or possibly a small tear in the external oblique aponeurosis
    Adapted from the "Sports Hernia": A Common cause of Groin Pain, Kemp et al,
    The Physician and Sportsmedicine, Vol 26, No. 1, January 1998
    http://www.physsportsmed.com/issues/1998/01jan/batt.htm
    Also see: http://www .mayoclinic.org/medical·edge-newspaper-2006/jan-16.html
    http://orthopedics.about.com/od/sportsinjuries/a/hernia.htm
    01-09
    ABDOMINAL EXAM:
    PATIENT SUPINE I SUPPING RIB I RIB TIP SYNDROME
    Slipping rib I rib tip syndrome
    Hypermobility of the anterior
    end of the costal cartilage
    of a "falsen rib
    26.
    Costochondritis I Teitze's
    Inflammation of the
    costochondral junction(s)
    (or costosternal junctions)
    Usually involves ribs 8, 9, 10 Involves ribs 1 through 7
    (Might involve ribs 11 or 12)
    Does not involve the
    costochondral or costostemal
    junctions
    Costochondritis: No swelling
    Tietze's: Swelling
    Remember, Dr. Panzer reviewed this
    material in 6"' uarter NMS I
    A. SUPPING RIB I RIB TIP SYNDROME
    1. The "False" Ribs Are More Likely to be Hypermobile
    a. They're "anchored" by loose I looser connective tissue
    2. The Tip of the Rib Might Actually Move Up Under the Tip of the Superior Rib
    3. Slipping Rib Syndrome May Follow Trauma or Participation in Athletic Events
    4. Typical Pain Pattern: Intermittent Stabbing Pain Followed by a Dull Ache
    5. The Pain Might be Reproduced by a "Hooking" Maneuver
    6. Slipping Rib Syndrome Can be Resistant to Conservative Care
    a. It might require surgical resection of the involved rib
    B. COSTOCHONDRITIS I TIETZE'S SYNDROME
    1. Pain That's Localized to a Costochondral or Costostemal Junction
    2. Usually There is No Swelling
    a. The term "costochondritis" implies there's pain but no swelling
    b. The term "Tietze syndrome" implies there's swelling along with the pain
    3. Most Cases Are Idiopathic
    a. Some cases follow trauma: Tearing I separation at the costochondral junction
    b. Some cases may be associated with systemic inflammation: RA, etc.
    4. Treatment Often Consists of Rest (assuming there's no systemic inflammation)
    Additional reading: The Rib-Tip Syndrome, McBeath and Keene,
    The Journal of Bone and Joint Surgery, Vol. 57-A, No. 6, September 1975
    http://www.ejbjs.org/cgi/reprint/57/6/795
    Slipping Rib Syndrome in a Collegiate Swimmer: A Case Report, Udenmann et al,
    Journal of Athletic Training, Vol. 40, No. 12, June 2005
    http://www.nata.org/jat/readers/archives/40.2/i1062-6050-4Q-2-120.pdf
    01-09
    )
    ABDOMINAL EXAM: 27.
    PATIENT SUPINE I ODDS &. ENDS
    A INVOLVEMENT OF AN INTERCOSTAL NERVE I NERVE ROOT
    1. Intercostal Neuralgia: Nerve pain that occurs around the ribs
    a. Often described an intense burning or stabbing pain
    b. Caused by irritation of, or damage to, the intercostal nerve associated with systemic
    disease, inflammation, infection, and compression or physical irritation of a nerve
    2. Intercostal Neuritis: Intercostal neuralgia presumed to be caused by nerve inflammation
    a. The most frequent cause of intercostal neuritis is infection with Herpes Zoster
    B. RECTUS SHEATH HEMTOMA (RSH) (Rectus abdominis)
    1. An Uncommon Cause of Abdominal Pain That's Associated With:
    a. Bleeding into the rectus sheath from damage to the superior or inferior epigastric arteries
    b. A direct tear of the rectus muscle
    c. Ecchymosis I bruising might be visible
    2. Causes of RSH Include:
    a. External trauma to the abdominal wall (including surgical procedures)
    b. Excessively vigorous contractions of the rectus muscle: Strenuous exercise or repeated
    Valsalva maneuvers associated with severe coughing, vomiting, or straining at the stool
    H. ANTERIOR CUTANEOUS NERVE ENTRAPMENT SYNDROME (ACNES)
    1. Nerve Entrapment at the Lateral Border of the abdominis Rectus Muscle
    2. Most Often Localized to the Site of the Linea Semilunaris
    a. Found on the lateral aspect of a rectus abdominis muscle the linea semilunaris is a curved
    tendinous structure that extends from the cartilage of the gth rib to the pubic turbercle. It
    is formed by the aponeurosis of the internal oblique muscle at its line of division to enclose
    the rectus muscle. It is reinforced in front by external oblique and from behind by the
    transversus I fascia transversalis
    3. ACNE is Most Often Seen When People Are More Active (Spring and Summer)
    tp:l lxnet.kp.orglpermanentejournaljsum02lacnes.html
    ABDOMINAL EXAM: 28.
    RED FLAGS
    "Ciassicn signs of peritonitis:
    Abdominal tenderness, fever of l00.5"F or 3B"C or higher, and vomiting
    Abdominal
    Distention
    Red Flag:
    Severe abdominal pain
    of abrupt onset
    Red Flag:
    Acute abdominal pain with
    abdominal "tenderness"
    Red Flag:
    Acute abdominal pain
    with fever
    Red Flag:
    Acute abdominal pain
    before vomiting
    Vety Bright Red Flags: Acute Abdominal Pain and ...
    Palpable
    Masses
    Ecchymosis
    "Bruising"
    Hypotension,
    Shock
    )
    )
    ABDOMINAL EXAM: 29.
    PATIENT SUPINE I PERITONffiS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    A. ACUTE ABDOMINAL PAIN
    1. Onset of Under 6 Hours (+I-)
    2. Abdominal Pain and Tenderness of Less Than 7 Days' Duration
    a. Note: In over 40% of cases the diagnosis is "non-specific abdominal pain"
    B. "THE ACUTE ABDOMEN" ("The Surgical Abdomen")
    1. Abrupt Abdominal Pain and Tenderness Requiring an Urgent Diagnosis
    2. Common cause: Peritonitis
    a. Inflammation: Appendicitis, cholecystitis (over inflammation of the gall bladder)
    b. Perforation of a hollow viscus: Appendix, stomach, duodenum, colon
    3. Common Cause: Bowel Obstruction
    a. Most often involves the small intestine (SI)
    4. Note: Both Peritonitis and Obstruction Can cause Abdominal Tenderness
    In 1,000 patients presenting to an E.R. with acute abdominal pain, 413 had no identifiable cause of
    the pain (non-specific abdominal pain), 377 had causes that were "non-surgical" and were medically
    managed, and 150 were thought to have a "surgical abdomen" and underwent surgery. However,
    20 of the 150 patients who underwent surgery were found to have a non-surgical disease.
    It is important to remember that, at first, the pain of an acute abdomen may not be
    accompanied by any physical exam findings. In most cases surgical abdomen, the physical
    manifestations will occur within 24-48 hours of the onset of the pain.
    Factors that favor a non-surgical diagnosis:
    Pain that is gradual in onset, mild to moderate in intensity, intermittent, recurrent,
    or resolves partially or completely in less than 6 hours
    Factors that favor a surgical diagnosis:
    Pain that is sudden in onset, severe or explosive, progressive, continuous,
    and lasts more than 6 hours
    Bergman, Assessing Acute Abdominal Pain: A Team Physician's Challenge, ,
    The Physician and Sportsmedicine Vol. 24 - No. 4 - April 96
    The most valuable single "test" for a possible acute abdomen is a periodic
    repetition of the physical examination, done by the same physician
    09-05
    ABDOMINAL EXAM: 30.
    PATIENT SUPINE/ PERITONffiS /ACUTE ABDOMINAL PAIN/ ACUTE ABDOMEN
    A. FIRST: Have the Patient Tell You About the Pain When it First Started
    1. Where Was it Located When it First Started
    2. When Did the Pain First Start?
    3. What did it feel like when it first started?
    B. SECOND: Have There Been Any Changes???
    1. Does the Pain Feel Different Than it Did at the OnSet?
    2. Has it Moved to a Different Location?
    C. REVIEW: PERITONffiS / PAIN FROM THE PARIETAL PERITONEUM
    1. The Parietal Peritoneum & the Abdominal Wall Share a Common lnnetvation
    2. Peritoneal Pain Arises From Noxious Stimulation of the Parietal Peritoneum
    3. Peritoneal Pain Tends to Manifest in Dennatomes T5-L2
    4. Peritoneal Pain is Usually Sharper, More Easily Localized, and Easier to Describe
    5. It is Usually Made Wo/S'e by Movement, Coughing, or Deep Respiration
    6. Parietal Pain is Made Wo/S'e by Percussion and Palpation
    7. Peritonea/Irritation can cause Reflexive Contraction of Segmental Muscles
    a. The underlying muscle can noticeably tsnse and painful
    Rectus Abdominis
    Small Intestine
    Aorta
    Visceral Peritoneum
    Not very pain sensitive
    Descending Colon
    Mesentery
    Inf. Vena Cava
    Ascending Colon
    Clinical axiom:
    If a visceral pain changes location and/or starts becoming a peritoneal pain
    and you can't find evidence of an NMS condition or a MFTP as the
    source of the pain, start thinking about peritonitis
    )
    ABDOMINAL EXAM: 31.
    PATIENT SUPINE I PERITONffiS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    FYI: POSSIBLE CAUSES OF ACUTE ABDOMINAL PAIN / THE ACUTE ABDOMEN
    "Surgical" Causes
    Inflammation:
    Inflammatory Bowel Disease
    Acute Appendicitis
    Acute Diverticulitis
    Acute Pancreatitis
    Acute Cholecystitis
    Meckel's Diverticulitis
    Obstruction:
    Intestinal Obstruction
    Acute Cholecystitis
    Ureteric Colic
    Acute Urinary Retention
    Ischemia:
    Mesenteric Ischemia
    Torsion of a Hollow Viscus
    Perforation:
    Perforated Appendix
    Perforated Peptic Ulcer
    Perforated Diverticulum
    Perforated Gallbladder
    Perforated Esophagus
    Perforated Bladder
    Perforation of Bowel
    Rupture of Abdominal Aortic
    Aneurysm
    Medical causes
    Cardiovascular:
    Myocardial Ischemia
    Myocardial Infarction
    Gastrointestinal:
    Gastritis I Gastroenteritis
    Hepatitis
    Hepatic Abscess
    Primary Peritonitis
    Mesenteric Adenitis
    Abdominal Wall Conditions:
    Rectus Sheath Hematoma
    Myofascial Trigger Points, etc.
    Genitourinary:
    Urinary Tract Infection
    Pyelonephritis
    Neurological:
    Tabes Dorsalis
    Hematological:
    Sickle Cell Disease
    Malaria
    Endocrine:
    Diabetes mellitus
    Thyrotoxicosis
    Addison's Disease
    Metabolic:
    Uremia
    Hypercalcemia
    Porphyria
    Infective:
    Herpes zoster
    Gynecological causes
    Ectopic Pregnancy
    Ovarian Cyst Torsion, Rupture,
    Hemorrhage, Infarction,
    Infection
    Pelvic Inflammatory Disease
    Fibroid Degeneration
    Salpingitis
    Mittelschmerz
    Endometriosis
    Adapted from: Smith & Paterson-Brown in, Garden et al, Principles and Practice of Surgery, Churchill Livingston 2002.
    09-05
    ABDOMINAL EXAM: 32.
    PATIENT SUPINE I PERITONmS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    A. INFECTIOUS PERITONmS:
    1. The Most Common Form of Peritonitis
    2. An Infection Spreads to the Abdominal cavity From:
    a. Perforations of the stomach, intestine I gallbladder I appendix, pelvic inflammatory disease
    (infected Fallopian tubes 1 uterus), surgical injury to the gallbladder I ureter I bladder I
    intestine, or the site of drains used for peritoneal dialysis (kidney failure)
    3. The Peritoneum is Actually Resistant to Infection
    4. Peritoneal Lavage: Washing out of the peritoneal cavity for sterilization of the cavity after
    a peritoneal inflammation or the detection of visceral injury following blunt abdominal trauma
    B. INFLAMMATORY I NON-INFEcri:OUS PERITONmS (Common)
    1. The Second Most Common cause of Peritonitis
    2. Peritoneal Inflammation Due to Inflammation of an Adjacent Structure
    a. Peritonitis secondary to acute pancreatitis, acute cholecystitis, etc.
    C. OTHER FORMS OF PERITONmS
    1. Spontaneous Peritonitis 1 "Sterile Peritonitis" (Not common)
    a. Seen with ascites due to liver disease, etc.
    2. Acute "Primary" Peritonitis (Rare)
    a. Blood-borne pathogens lead to infection and peritoneal inflammation
    Reminder: The "classic" signs of peritonitis:
    Abdominal "tenderness", fever of 100.5°F or 38°C or higher, and vomiting
    Unless peritonitis is treated promptly, complications can develop very rapidly
    12-08
    )
    )
    ABDOMINAL EXAM: 33.
    PATIENT SUPINE I PERITONmS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    Review: Auscultation has a relatively minor role in the abdominal exam
    It is performed before percussion or palpation as vigorously touching the abdomen may disturb the
    intestines, perhaps artificially altering their activity and thus bowel sounds. Many physicians will omit
    abdominal auscultation unless there is a symptom or finding suggestive of abdominal pathology
    Adapted from: A Practical Guide to Clinical Medicine, University of california, San Diego
    http:flmeded.ucsd.edulflinicalmed/J!bdomen.htm
    Bowel Sounds: As Classically Taught
    Most bowel sounds originate
    from the small intestine
    Listen in all four abdominal quadrants
    for active bowel sounds
    Normal bowel sounds occur every S to 15
    seconds and are more frequent after
    meals&. less frequent with fasting
    The examiner should auscultate for
    one minute in each quadrant of the
    abdomen before assuming that
    bowel sounds are absent
    Absent bowel sounds: A "functional"
    or "adynamic" ileus is classically
    associated with peritonitis.
    Bowel Sounds: Evidence-Based Findings
    Most bowel sounds actually originate from
    the stomach, followed by the colon and
    then the small intestine
    Bowel sounds originating from one part of
    the GI tract can radiate over the
    entire abdominal wall
    Patients might have no bowel sounds
    for up to 4 minutes and later have
    more than 30 sounds per minute
    Assessing bowel sounds does not help
    in the diagnosis of peritonitis
    Adapted from: Evidence-Based Physical Diagnosis, McGee, WB Saunders, 2001
    D. "CLASSIC" PERITONffiS: DECREASED OR ABSENT BOWEL SOUNDS DUE TO ILEUS
    1. Ileus: The Loss of Normal Peristaltic Action in All or Part of the Intestine
    2. Ileus Leads to Decreased or Absent Bowel Sounds
    3. A "Functional" or "Adynamic" Ileus is Classically Associated With Peritonitis, but ...
    4. Old Clinical Axiom: The examiner should auscultate for one minute in
    each abdominal quadrant before assuming that bowel sounds are absent.
    5. ESP: Assessing bowel sounds does not help in the diagnosis of peritonitis
    ABDOMINAL EXAM: 34.
    PATIENT SUPINE I PERITONmS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    Primarv Obiective: Suoerfidal oaloatjon of the abtfomen in order to afffff
    abt/ominal muscle tone in an area of reoortec/abdominal tendernesc
    (Superficial palpation: Depress the abdominal wall about 1 centimeter)
    E. DIFFERENTIAL: VOLUNTARY "GUARDING"
    Normal variant: Voluntary guarding I "guarding"
    Voluntary contraction of the abdominal wall muscles in
    response to anxiety, cold hands, ticklishness, etc.
    Voluntary guarding can usually be overcome with
    reassurance and gentle light palpation
    F. BEST INDICATOR: RIGIDITY I SPUNTING I INVOLUNTARY OR "TRUE" GUARDING
    1. Guarding That Doesn't Diminish With Reassurance and Continued Palpation
    2. Rigidity I Splinting I Involuntary Guarding I True Guarding: Positive LR S.l
    3. Persistent Guarding: Positive LR 2.6 in one article
    Peritonitis: Rigidity I "true guarding"
    An involuntary contraction of the abdominal wall ms.
    Ught palpation evokes further muscle contraction
    and exacerbates the pain
    Rigidity is considered to be the most reliable indicator
    of oarietal oeritonitis
    G. GOOD INDICA TOR: DUNPHY'S SIGN I POSITIVE COUGH TEST (PLR: 2.4)
    Dunphy's sign I positive cough test
    A localized pain that increases with coughing
    Suggestive of peritonitis. PLR: 2.4
    Adapted from: Evidence-Based Physical Diagnosis, McGee, WB Saunders, 2001
    Adapted From:Practical Strategies in Outpatient Medicine, 2"" ed., W.B. Saunders Co., 1991;
    Assessing Acute Abdominal Pain, Bergman, The Physician & Sportsmedicine, April1996
    Does this Patient Have Appendicitis?, JAMA, November 20, 1996
    )
    )
    )
    ABDOMINAL EXAM: 35.
    PATIENT SUPINE I PERITONmS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    H. GOOD INDICATOR: POSITIVE DIRECT REBOUND TENDERNESS (PLR: 2.1)
    Direct Rebound Tenderness
    "A popular and somewhat unkind way of emphasizing
    what should already be obvious"
    The clinician maintains pressure directly over the area of
    tenderness and then abruptly removes the hand. The
    test is considered positive if the "patient winces"
    Inter-observer Agreement is "Fair": K 0.25
    I. OTHER INDICATORS OF PERITONmS
    .- .--.,....
    The "jar" test
    Sudden vibration increases /localizes the pain
    The patient stands on tip toes and drops down onto their heals
    Rovsing's sign I contralateral tenderness I
    indirect rebound tenderness
    Classically used in cases of acute appendicitis. Percussion in left iliac fossa
    increases the pain felt in the right iliac fossa. Some authors think this
    to be more accurate than direct rebound tendemess
    The psoas sign
    Pain upon passive extension of the right psoas muscle
    Might be associated with "retrocecal" appendicitis
    May also be seen with iliopsoas bursitis, psoas abscess, etc.
    The obturator sign
    Pain upon internal rotation of the right thigh
    Might be seen with "pelvic" appendicitis
    May also seen with hip disease, etc.
    ABDOMINAL EXAM: 36.
    PATIENT SUPINE I PERITONmS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    I. OTHER INDICATORS OF PERITONmS, continued
    I ___ / ,__ \
    ·"- /
    McBurney's sign
    Localized pain at McBurney's point
    Suggests appendicitis
    Murphy's Sign
    Acute pain when palpating the g~llbladder
    The examiner palpates the RUQ while the patient takes a breath
    Acute pain with "a marked inspiratory arrest" is said to
    indicate acute cholecystitis
    KEHR'S SIGN
    Irritation of the left hemidiaphragm, often due
    to splenic rupture, causes a referred pain to
    left shoulder 1 C4 dermatome with
    possible hyperesthesia
    J. PERITONmS & CUTANEOUS HYPERESTHESIA
    1. A Painful Sensation Resulting From a Normally Painless Touch Stimulus
    a. When present, it usually (but not always) overlies the area of peritoneal irritation
    2. Boas' Sign: A "Radiating" Cutaneous Hyperesthesia in Acute Cholecystitis
    a. Pain sometimes radiates to the back when the gallbladder is inflamed. When this happens,
    there might be an area of hyperesthesia at the site to which the pain is radiating.
    b. Some authors describe a site at "inferior angle" of the scapula
    c. Other authors describe a sit "just below" the right scapula
    d. Note: "Boas' sign" has also been described as a "clinical-chemical sign of carcinoma of the
    stomach when there are large amounts of lactic acid the gastric juice."
    ABDOMINAL EXAM: 37.
    PATIENT SUPINE/ PERITONITIS I ACUTE ABDOMINAL PAIN I ACUTE ABDOMEN
    K. OBSTRUCTION OF THE BOWEL
    1. Movement of Material Through the Intestines is Physically Blocked: Causes of "mechanical"
    obstruction are numerous and may include the hernias, post-operative adhesions or scar
    tissue, impacted feces, gallstones, intraluminal tumors, intraluminal tumors, extraluminal
    tumors, granulomatous processes, intussusception, volvulus, and ingested foreign bodies
    2. Exam Findings:
    a. Increased bowel sounds with early mechanical obstruction
    b. Decreased bowel sounds with late mechanical obstruction
    c. Visible peristalsis (An uncommon but very significant finding)
    d. Visceral pain: abdominal pain and cramping
    e. Abdominal distention I fullness I gaseous
    f. Vomiting, constipation, possible diarrhea, possible breath odor
    Bowel Sounds: As Classically Taught Bowel Sounds: Evidence-Based Findings
    Increased, loud, "rushing" bowel sounds
    are classically associated with diarrhea and
    early mechanical obstruction of the bowel
    Decreased bowel sounds (high-pitched
    "tinkling") are classically associated with
    late obstruction of the bowel
    Analyzing bowel sounds has some value in
    diagnosing small bowel obstruction.
    About 40% of patients with SI obstruction
    have hyperactive bowel sounds
    About 25% have diminished or absent
    bowel sounds
    Adapted from: Evidence-Based Physical Diagnosis, McGee, WB Saunders, 2001
    L. VISIBLE PERISTALSIS
    1. Considered to be a Strong Indicator of Small Bowel Obstruction in a
    Patient Presenting With Abdominal Pain and Vomiting
    2. Detecting Obstruction
    a. Visible peristalsis: Positive LR 18.8
    b. Abdominal distention: Positive LR 9.6
    c. Hyperactive bowel sounds: Positive LR 5.0
    d. Abnormal bowel sounds: Positive LR 3.2
    Adapted from: Evidence-Based Physical Diagnosis, McGee, WB Saunders, 2001
    09-05
    ABDOMINAL EXAM: 38.
    PATIENT SUPINE/ ASCITES
    A. ASCITES: Free Fluid in the Abdominal cavity, Most Often Due to Liver Disease
    2. "Large Volume" Ascites: > 500 mL: Relatively easy to detect on physical exam
    3. "Small Volume" Ascites: < 500 mL: Much harder to detect on physical exam
    Inspection & Large Volume Ascites(> 500 mL):
    "Bulging Flanks"
    The fat of obesity tends to encircle the patient's waist
    and involve the posterior aspect of the patient's torso
    In a supine patient, ascites has a more anterior distribution.
    Posterior spread of the fluid would be limited by the lower
    rib cage and the muscles of the back.
    i
    Percussion & Large Volume Ascites(> 500 mL):
    "Percussive Dullness"
    Tympani on Percussion:
    Non-involved Portion of the abdomen
    Dullness on Percussion:
    ---r--Tympani changes to dullness as you start percussing
    Step One:
    Patient supine
    Mark air I fluid interface
    over the area of accumulated ascetic fluid
    Large Volume Ascites
    and Percussion:
    "Shifting Dullness"
    Considered more accurate
    than the fluid wave
    Step Two:
    Patient on side
    Mark air I fluid interface
    )
    )
    ABDOMINAL EXAM:
    PATIENT SUPINE/ ASCITES
    39.
    Percussion, Palpation & Large Volume Ascites(> 500 ml):
    "Fluid Wave"
    An assistant uses his/her hypothenar to attenuate any soft tissue
    abdominal wall movement while the examiner the heel of his/her
    hand to percuss the abdomen on one side and palpates for
    a transmitted fluid wave on the other side
    Percussion, Auscultation & Small Volume Ascites:
    The "Puddle Sign"
    Auscultatory percussion in the prone patient.
    Said to be able to detect ascites in the 120-150 ml range
    but is not considered to be dia nosticall hel ful
    A. THE PUDDLE SIGN: A Form of Auscultatory Percussion
    1. Patient lies prone for 5 minutes
    2. Patient then rises onto elbows and knees
    3. The examiner applies the stethoscope's diaphragm to the patient's near flank at the most
    dependent part of the abdomen
    4. The examiner repeatedly uses one finger to "flick" (percuss) the patient's flank on the near
    side of the patient & continues to "flick" at the same spot throughout the exam procedure
    5. While "flicking, move stethoscope across abdomen away from examiner
    6. The loudness of the sound increases at the edges of the puddle
    7. The loudness of the sound does not change in that area when he/she sits up
    http://www .fpnotebook.comjGI/Exam/PdiSgn. htm
    ASCITES:
    Finding: Sensitivity Specificity Positive LR
    Inspection:
    Psoas sign 73-93% 44-70% 1.9
    Obturator sign 87% 77% 3.8
    Palpation & Percussion
    Flank Dullness 80-94% 29-69%
    Shifting Dullness 60-87% 56-90% 2.3
    Fluid wave 50-80% 82-92% 5.0
    Negative LR
    0.4
    0.2
    0.3
    0.4
    0.5
    Adapted from: Evidence-Based Physical Diagnosis, McGee, WB Saunders Co., 2001
    40.
    )
    )
    )
    CSC 7364 Gastroenterology Dx I Tx, Summer Quarter 2011
    Packet Two: Disorders of the
    Esophagus
    Upper J:sophageal
    Sphincter ---+--~
    Venous return:
    The upper portions the
    esophagus drain into the
    azygos and hemiazygos veins
    Thoracic Duct ---+--11
    Squamo-Columnar
    Junction ----+--
    : ,:
    Thyroid Cartilage &.
    Laryngeal Prominence
    Cricopharyngeus ms.
    Venous return:
    The lower portions of the
    esophagus drain into the
    portal system
    Lower Esophageal
    Sphincter
    Compiled by Peter Shull DC
    Last review I revision: 01-11
    ESOPHAGUS: 02.
    FUNCTIONAL ESOPHAGEAL DISORDERS
    Functional GI disorders:
    Common conditions in otherwise healthy persons.
    Patients with functional bowel disorders comprise the largest subset of
    patients seen in GI outpatient clinics. Functional GI disorders can manifest
    as pain or dysfunction involving the esophagus, stomach, abdomen,
    bowel, urinary bladder and pelvic floor. Up to two-thirds of otherwise
    healthy persons will have one or more symptoms of a functional GI
    disorder at some point in time.
    Adapted from: Yamada & Hasler, in Essentials of Internal Medidne, and;
    Current Diagnosis & Treatment in Gastroenterology, Appleton & Lange, 1996
    Issue: Placebo can be an excellent treatment for IBS
    It is very important to have a placebo arm included in all RCTs that test new therapies for IBS.
    One meta-analysis found that the placebo response was, for the most part, unpredictable and
    varied anywhere from 16% to 71%, with the mean being 44%. The only predictor of
    placebo variability seemed to be the number of office visits.
    Adapted from: Patel SM, Ock SM, Stason W, et al. Placebo effect in irritable bowel syndrome (IBS) trials:
    a meta-analysis. Gastroenterology. 2004;126(suppl 2):A-369, and; Talley NJ. Evaluation of drug treatment in
    irritable bowel syndrome. Br J Clin Pharrnacol. 2003·56:362-369
    Issue: Inconsistencies in diagnostic criteria
    The Rome symptom-based diagnostic criteria for the FGIDs have been the most widely accepted.
    However, there have been three versions of the Rome criteria down through the years. Since these
    criteria don't always "agree", the conclusions from various articles might be "version-dependent"
    Empirically Derived Symptom Sub-Groups Correspond Poorly With Diagnostic Criteria for Functional Dyspepsia and
    Irritable Bowel Syndrome. A Factor and Cluster Analysis of a Patient Sample, Aliment Pharmacal Ther 19(1):133-140, 2004.
    http://www .medscape.com/viewarticle/466789 _print
    )
    )
    ESOPHAGUS: 03.
    FUNCTIONAL ESOPHAGEAL DISORDERS
    A. GLOBUS HYSTERICUS: The Sensation of a ftLump" or ftTightness" in the Throat
    1. Temporarily Relieved by Swallowing
    2. "Classically" Considered to an Emotional/ Psychological Disorder
    a. Note: A globus sensation is now known to occasionally accompany GERD
    B. RUMINATION SYNDROME f'Esophageal" in Rome I & II, "gastroduodenal" in Rome III)
    1. The Involuntary Regurgitation of Recently-Ingested Food Back Into the Mouth
    a. This rumination usually occurs within 15-30 minutes after the meal and is seen in healthy
    people who eat large meals too quickly. It is also seen with bulimia, in severe psychiatric
    disorders, and the severely retarded
    C. FUNCTIONAL HEARTBURN (discussed later)
    1. Heartburn Symptoms With No Pathological Acid Reflux
    D. FUNCTIONAL CHEST PAIN: Non-cardiac Chest Pain (discussed previously)
    1. The Esophagus is a Common Source of Non-cardiac Chest Pain (NCCP)
    Issue: Aspiration
    Aspiration is the passage of food or liquid through the vocal folds.
    People who aspirate are at increased risk for pneumonia.
    However, people without swallowing abnonnalities will still routinely aspirate
    microscopic amounts of food and liquid.
    Gross aspiration, however, is abnormal and may lead
    to respiratory complications
    Dvsohaoia Nam-Jono Paik MD PhD, htto://www.emedidne.com/omr/tooic194.htrn
    Normal adults swallow about 600 times a day:
    200 times while eating or drinking, 350 times while awake but
    not eating or drinking, and 50 times while asleep.
    01-07
    THE ESOPHAGUS: 04.
    ODDS &ENDS
    Side Notes on Peppennint Leaf and Peppennint Oil
    For years, peppennint has been recommended as a "tonic" for the GI system
    and has long_ been used to treat a number of "digestive" disorders.
    Peppennint oil will help relax smooth muscle
    There's some evidence that enteric-coated peppennint oil may be effective in relieving
    some IBS symptoms and that a mixture of peppennint oil and caraway oil might be
    moderately effective in the treatment of non-ulcer dyspepsia.
    There are reports that a topical application of peppennint oil might help
    in the treatment of muscle tension headaches
    There's even a report that peppermint oil enemas might be modestly effective in
    relieving colon spasms that can be associated with barium enemas
    Peppermint oil is well tolerated at the commonly recommended dosages
    Peppermint oil may cause significant adverse effects at higher dosages
    Commonly-reported side-effects include heartbum, allergic reactions,
    perianal burning, blurred vision, nausea, and vomiting
    Rare side-effects include interstitial nephritis, acute renal failure
    Along with grapefruit juice, peppennint oil might inhibit the cytochrome P450 1A2
    system, which means it might lead to complications with statin therapy
    Peppermint oil is contraindicated in patients with symptomatic "hiatal hernia",
    severe GERD, and gallbladder disorders
    (more on these topics later)
    Peppermint Oil, American Family Physician. Kligler and Chaudhary, 2007;75:1027-30
    http://www.aafp.org/afp/20070401/1027.html
    )
    )
    )
    ESOPHAGUS:
    UPPER ESOPHAGEAL SPHINCTER
    l
    A. UPPER ESOPHAGEAL SPHINCTER (UES)
    1. The UES is a 2-4 an. ZOne of Increased Intraluminal Pressure
    a. It is not a "true" sphincter
    OS.
    b. The UES is the most narrow portion of the esophagus. UES resting pressures range from
    40-100 mm Hg and can fall to subatmospheric levels during the act of swallowing.
    However, the pressure in the UES is never lower than the pressure in the esophagus. The
    UES is innervated by cranial nerves IX & X. (Some CN X fibers travel with the internal
    portion of CN XI.) Relaxation of the UES relies on central inhibition of CNS activity.
    2. The UES is Near the Level of the Cricoid cartilage 1 Body of C6
    a. Lesions involving the UES are usually well-localized
    Soft tissue injuries and/or
    dysphagia involving the UES
    (discussed later) are usually
    well-localized by the patient
    The universal choking sign also
    localizes the UES and is of
    extreme significance in a patient
    who can't talk, cough or cry
    Rings and webs are the most common structural abnormalities in the esophagus.
    The terminology, pathogenesis, and treatment of these esophageal lesions remain controversial.
    The terms rings and webs often are used interchangeably in the literature. The pathogenesis and
    treatment of esophageal rings and webs are evolving. Most of these structural lesions are
    asymptomatic but can cause dysphagia. This review attempts to provide a practical update on
    esophageal rings and webs and to discuss their definition, epidemiology, pathophysiology, clinical
    presentation, differential diagnosis, diagnosis, treatment, and follow-up care.
    Esophageal Webs and Rings Zervos emedidne June 27 2006 http://www.emedicine.com/MED/topic3413.htm
    01-Q7
    ESOPHAGUS: 06.
    UPPER ESOPHAGEAL DYSPHAGIA
    A. INTRINSIC OBSTRUCTION: More Trouble With Solids
    1. Oropharyngeal Inflammation: Odynophagia With Solid Food Dysphagia
    2. Esophageal Webs: Intermittent Solid Food Dysphagia
    a. The lumen of the esophagus is narrowed by bands or webs of tissue that may be
    comprised of thickened mucosa, submucosa and/or smooth muscle
    b. Although rarely symptomatic, these webs are sometimes treated by mechanical dilatation
    http:/ /www.emedicine.com/med/topic3413.htm
    3. Plummer-Vinson Syndrome: Anemia (?) 8t Intermittent Solid Food dysphagia
    a. AKA Paterson-Brown Kelly Syndrome
    b. A npost-cricoid" dysphagia, esophageal webs; 8t iron-deficiency anemia
    c. It is classically associated with iron-deficiency anemia, generalized mucosal atrophy,
    koilonychia, etc., especially in females of Scandinavian descent. Some patients with PVS
    have had symptomatic improvement following iron supplementation.
    d. However, the association with iron-deficiency has recently come under fire. For example,
    PVS is rare eastern and central Africa, where chronic iron deficiency is endemic
    )
    e. Other proposed mechanisms include nutritional deficiencies, genetic predisposition, and )
    autoimmune factors.
    http:/ jwww.emedicine.com/medjtopic3431.htm
    4. Zenker Diverticulum: Intermittent solid food dysphagia
    a. Classic Triad: Dysphagia, halitosis 8t regurgitation
    b. ZD is rare and occurs in the elderly
    c. ZD is a 'pulsion' herniation: the esophageal mucosa herniates posteriorly between the
    cricopharyngeus muscle and the inferior pharyngeal constrictor muscles. This false
    diverticulum carries with it a high frequency of food elements retained within its pouch.
    The food elements & secretions lead to halitosis, regurgitation, aspiration, and dysphagia.
    d. ZD has severe complications, including aspiration and pneumonia, & is surgically managed
    Note: The term "cervical dysphagia" can have more than one meaning. Some authors use it to
    describe any dysphagia localized to UES I neck. Other authors use it when describing more
    specific lesions, including those resulting from cervical osteoarthropathy, etc.
    01-07
    )
    ESOPHAGUS: 07.
    UPPER ESOPHAGEAL DYSPHAGIA
    B. EXTRINSIC OBSTRUcnON: More Trouble With Solids
    1. DISH: Possib/elntennittent Solid Food Dysphagia
    a. Note: DISH is "an uncommon cause of dysphagia"
    b. An "oropharyngeal" or "cervical" dysphagia has been reported in some cases of DISH
    c. Although the nature of the dysphagia is usually not reported, it can be presumed to be an
    intermittent solid food dysphagia
    http: I jwww. ijri .erg/articles/ archives/2003-13-1/muscu_79 .htm
    http://www .emedicine.com/Radio/topic218.htm
    2. CeiVical Spondylosis: Possible Intennittent Solid Food Dysphagia
    a. Dysphagia is one of the less common manifestations of cervical spondylosis. Large anterior
    osteophytes involving CS, C6 & C7 can give rise to a "mechanical" dysphagia and/or an
    "annoying awareness of swallowing'
    http://www.emedicine.com/PMR/topic27.htm
    3. CeiVical Acceleration/Deceleration Injuries fWhiplash1
    a. Usually, the type or nature of the dysphagia is not fully described
    b. Dysphagia following a "whiplash" injury can be of serious prognostic significance
    c. A "mild" dysphagia .can result from relatively mild soft tissue trauma.
    d. The early onset of a definite dysphagia can be characteristic of a serious injury.
    The dysphagia might represent the formation of a retropharyngeal hematoma resulting
    from tearing of paravertebral blood vessels or fractures of the vertebrae
    4. Other Considerations: Anterior Mediastinal Masses, Trauma Following Intubation, etc.
    Additional reading: Diagnosis of Bone & Joint Disorders, 3rd ed., Resnick, W.B. Saunders Co., 1995; Cervical FlexionExtension/
    Whiplash Injuries, Teasel! & Shapiro, Hanley & Belfus, 1993; Whiplash Injuries: the Cervical AccelerationDeceleration
    Syndrome, Foreman & Croft, Williams & Wilkins, 1988; The Cervical Spine, 2nd ed. Sherk, et al., J.B. Lippincott
    Co., 1989; Disorders of the Cervical Spine: Diagnosis & Management, Bland, W.B. Saunders Co., 1987
    01-07
    ESOPHAGUS: 08.
    UPPER ESOPHAGEAL DYSPHAGIA
    Injury related characteristics of whiplash daimants stratified by sex
    Characteristic Male* (2926) Female* ( 4533)
    In itia I health care provider
    None 104 (3.6) 124 (2.8)
    MD 1869 (65.2) 2862 (64.3)
    DC 149 (5.2) 256 (5.7)
    MD and DC 405 (14.1) 624 (14.0)
    MD and PT 338 (11.8) 588 (13.2)
    Admitted to hospital overnight 156 (5.3) 158 (3.5)
    Broken bone( s) 96 (3.3) 127 (2.8.) -
    Hit head in collision 976 (33.4) 1169 (25.8)
    Lost consciousness in collision 199 (6.8) 178 (3.9)
    Off work because of collision 1419 (49.0) 2002 (44.5)
    Symptoms after collision
    Neck/shoulder pain 2926(100%) 4533(100%)
    Headache 2291 (78.4) 3902 (86.1)
    Arm/hand numbness/tingling 1104 (37.8) 2103 (46.4
    Leg/foot numbness/tingling 688 (23.5) 1283 (28.3)
    Reduced/painful jaw movement 386 (13.2) 906 (20.0)
    Dizziness/unsteadiness 1210 (41.4) 2183 (48.3)
    Nausea 631 (21.6) 1534 (33.9)
    Vomiting 143 (4.9) 294 (6.5)
    Difficulty swallowing 248 (8.5%) 477 (10.5%)
    Ringing in the ears 625 (21.4) 928 (20.5)
    Vision problems 336 (11.5) 590 (13.0)
    Memory problems 357 (12.2) 570 (12.6)
    Concentration problems 705 (24.1) 1256 (27.8)
    Low back pain 1808 (61.9%) 2926 (64.6%)
    Adapted from: A re-examination of the whiplash associated disorders (WAD) as a systemic illness, Ferrari, Russell, Carroll
    and Cassidy, Annals of the Rheumatic Diseases 2005;64: 1337-1342, Published Online First: 24 February 2005
    http:l/ard.bmjjournals.com/cgijcontent/full/64/9/1337
    01-07
    )
    )
    )
    )
    ESOPHAGUS: 09.
    UPPER ESOPHAGEAL DYSPHAGIA
    There has always been some controversy surrounding the Heimlich maneuver.
    Not all authorities agreed on the proper way to deliver first aid to choking victims
    The recommendations were changed in 2006
    "From 1985-2005, the Heimlich maneuver was the only recommended treatment for choking in
    the published guidelines of the American Heart Association and the American Red Cross.
    In 2006, both organizations drastically changed course and "downgraded the Heimlich
    Maneuver. For conscious victims, the new guidelines recommend first applying backslaps;
    if this method failed to remove the airway obstruction, rescuers were to then apply abdominal
    thrusts. For unconscious victims, the new guidelines recommend chest thrusts, a method first
    recommended in a 1976 study by Charles Guildner MD whose results were duplicated in a
    year 2000 study by Audun Langhelle MD. The 2006 guidelines also eliminated the phrase
    ·"Heimlich maneuver" and replaced it with the more descriptive "abdominal thrust."
    http:/ /en. wikipedia.org/wiki/ Abdominal thrusts
    For infants under one: For children: For adults:
    Many authors recommend a
    series of five "backslaps"
    Five "backslaps" followed by
    five abdominal thrusts.
    Five "backslaps" followed by
    five abdominal thrusts
    Important note: Abdominal thrusts are not recommended in infants.
    If the five backslaps fail, deliver a series of five chestthrusts
    01-07
    ESOPHAGUS: 10.
    UPPER ESOPHAGEAL DYSPHAGIA
    C. NERVOUS SYSTEM DISEASE: Dysphagia With Liquids and Solids
    1. Central Nervous System Diseases: Rapid Onset of Dysphagia For Liquids S. Solids
    a. A medullary swallowing center integrates the activities of cranial nerv~ V, VII, IX, X, &
    XII. Lesions affecting this center lead to dysphagia that is most noticeable with liquids
    b. The patient sputters, gags, chokes, & regurgitates upon swallowing
    c. Stroke is the most common neurologic cause of upper esophageal dysphagia.
    d. Vertebral artery TIAs can also manifest in neurologic dysphagia
    e. The dysphagia is often accompanied by other signs of cranial nerve deficits: dysphonia,
    dysarthria, and weakness of the glossal, palatal and/or pharyngeal musculature
    2. Other Considerations: Parkinson's, brainstem tumors, amyotrophic lateral sclerosis, multiple
    sclerosis, Huntington's chorea, poliomyelitis, syphilis, myasthenia gravis/motor end-plate
    disease, and some peripheral neuropathies
    Stroke is the leading cause of neurologic dysphagia.
    Neurologic swallowing disorders are encountered more frequently in rehabilitation medicine than in )
    most other medical specialties. Approximately 51-73% of patients with stroke have dysphagia, which
    is the most significant risk factor for development of pneumonia; this can also delay the patient's
    functional recovery. Pneumonia accounts for about 34% of all stroke-related deaths and represents
    the third highest cause of death during the first month after a stroke, although not all these cases of
    pneumonia are attributable to aspiration of food. Therefore, early detection and treatment of
    dysphagia in patients who have sustained strokes is very critical.
    Dysphagia Nam-Jong Paik MD PhD http://www.emedicine.com/pmr/topic194.htm
    D. SKELETAL MUSCLE DISEASE: Dysphagia For Liquids S. Solids
    1. UES Achalasia I Cricopharyngeal Achalasia
    a. Incomplete relaxation of the upper esophageal sphincter upon swallowing
    2. Connective tissue disorders
    a. Dermatomyositis & polymyositis and systemic rheumatic processes
    b. Patient also complains of polyarthritis, polyarthralgia, myalgia, myositis, & skin rashes
    Also see: http:ffwww.emedicine.comjpmrjtopic194.htm
    01-07
    )
    ESOPHAGUS:
    ESOPHAGEAL DYSPHAGIA
    Esophageal Dysphagia:
    Poor Localization of Symptoms
    The patient perceives that the obstruction
    is either at or above the level of the lesion?
    http://www.emedicine.comlmedltopic744.htm
    11.
    Remember, the esophagus is commonly implicated
    in cases of non-cardiac chest pain
    Question: Dysphagia with solids only?
    Then consider anatomic obstruction
    Question: Dysphagia with liquids JA solids?
    Then consider neuromuscular disorders
    Are the symptoms
    intermittent?
    Are the symptoms
    progressive?
    Are the symptoms
    intermittent?
    Are the symptoms
    progressive?
    Adapted from: Evaluating the Patient With Dysphagia, Harris, Parkman & Cohen, Hospital Medidne, July 1994, and; The AMA
    Review: Functional Chest Pain I Non-Cardiac Chest Pain
    Functional chest pain f NCCP is characterized by recurrent episodes of unexplained chest pain.
    The pain is usually midline, of visceral quality, and therefore potentially of esophageal origin.
    The pain is often debilitating. The etiology & exact mechanism are often unclear.
    Functional chest pain has a dose association with gastro-esophageal reflux disease.
    Acid reflux and/or abnormal results upon ambulatory pH studies have been implicated in 30%-60%
    of patients with chest pain. Functional chest pain has also been associated with a number of other
    conditions. Esophageal motility disorders have been associated with NCCP. Esophageal
    dysmotility has been found in 12% to 33% of patients with unexplained chest pain.
    Functional chest pain is relatively common in patients with psychiatric I behavioral disorders I
    panic disorders. These patients had a higher incidence of nonspecific, abnormal results upon
    esophageal manometry than did the controls.
    The role of visceral hyperalgesia and enhanced visceral pain perception, first evaluated using
    balloon distention of the esophagus, is under continual investigation.
    The criteria for the diagnosis of functional include at least 12 weeks in the preceding 12 months
    of midline chest pain or discomfort that is not burning in quality, and with an absence of
    pathological gastro-esophageal reflux, achalasia, or other motility disorder with a
    recognized pathologic basis.
    Adapted from: Functional Chest Pain: Nodceptlon and Visceral Hyperalgesia, Chahal and Rao,
    Journal of Oinical Gastroenterology, Vol. 39, Supp. 3 May/June 2005
    01-07
    DYSPHAGIA: 12.
    ESOPHAGEAL DYSPHAGIA
    A. INTERMITTENTDYSPHAGIA FOR SOUDS
    1. Esophageal Rings: Awte, Intermittent &. Recurrent Solid Food Dysphagia
    b. Concentric rings of thickened mucosa which project into the lumen of the esophagus
    c. Rings with an internal diameter > 20 mm are rarely symptomatic
    d. Rings with an internal diameter < 13 mm are almost always symptomatic
    2. Schatzki Ring I "Steakhouse Syndrome": Acute, Recurrent Solid Food Dysphagia
    a. The most common cause of intermittent solid food dysphagia in adults
    b. The ring is usually found near the level of the lower esophageal sphincter (LES))
    c. The dysphagia often occurs during a meal &. is accompanied by chest pain
    d. It is often relieved by the regurgitation of impacted foodstuff.
    e. Treatment: More complete chewing of smaller bites of solid food
    f. Bougienage: Mechanical dilatation of the esophageal ring I web
    A Schatzki ring is a ring composed of mucosa and submucosa located at the esophagogastric junction. The
    exact pathogenesis of lower esophageal rings is not known. Both congenital and acquired origins have been
    proposed for Schatzki rings. The data are not completely conclusive, but the bulk of the evidence indicates
    an acquired etiology. Many patients do not have symptoms before the age of 50 years; hence, a congenital )
    origin is unlikely. Most investigators believe that a Schatzki ring is an annular ringlike stricture '
    caused by scarring as a result of reflux esophagitis.
    Patients also may present with acute food impaction causing an obstruction in the esophagus. These patients
    have acute substernal chest pain or, alternatively, a sense of something stuck in the lower chest. Most
    commonly, a large piece of meat is stuck at the level of the ring, hence the tenm "steakhouse syndrome".
    Schatzki Ring, Vossough, emedicine, April14, 2003, http://www.emedicine.com/Radio/topic620.htm, and;
    Schatzki Ring, Vasudeva April18 2006 http://www.emedicine.com/med/topic2069.htm
    3. Esophageal Diverticula
    a. Diverticula of the mid- to lower esophagus do occur but are rarely symptomatic
    4. Other Considerations With Episodic Dysphagia for Solids
    a. Infectious esophagitis in immuno-c:ompromised patients
    b. Caustic esophagitis can result from the ingestion of drain cleaners, etc.
    c. Mallory-Weiss syndrome: (also see page 32) Longitudinal tearing of the esophageal
    mucosa that can follow large increases in transmural pressure such as that seen with
    vomiting. Accounts for 1% - 15% of cases of upper GI bleeding and often presents with
    hematemesis. The bleeding stops spontaneously in 80% - 90% of cases.
    01-07
    DYSPHAGIA: 13.
    ESOPHAGEAL DYSPHAGIA
    B. PROGRESSIVE DYSPHAGIA FOR SOUDS
    1. Gastro-Esophageal Reflux Disease (GERD)
    a. Up to 40% of patients with GERD experience dysphagia
    b. Dysphagia is considered to be an "alarm symptom" in cases of GERD
    c. "Milder" GERD: The presentation is similar to that seen with esophageal rings. Many
    authors theorize that esophageal rings form in response to chronic GERD
    d. In the more severe forms of chronic GERD, the dysphagia can become slowly progressive.
    Patients might develop esophageal strictures and experience more severe symptoms
    2. Benign Esophageal Strictures: Slowly Progressive, Episodic, Dysphagia For Solids
    a. Strictures manifest in a smooth (and usually tapered), fibrotic narrowing of the distal
    esophagus. Most occur at the gastroesophageal junction.
    b. Stricture formation is often a complication of chronic GERD and is often
    accompanied by a long-term history of heartburn and antacid use
    c. Strictures may be caused by peptic esophagitis
    d. Stricture formation may also be drug-induced: NSAIDs, aspirin, potassium chloride,
    quinidine, some antibiotics and some osteoporosis medications (Fosamax) have been
    implicated. Medication-induced esophagitis may present with acute retro-sternal pain
    e. Endoscopy with biopsy is considered mandatory, so as to rule out malignancy
    f. Strictures often respond to bougienage (mechanical dilatation)
    3. Barrett's Esophagus
    a. Metaplasia in which the squamous epithelium of the distal esophagus is replaced by
    columnar epithelium. It is often due to reflux-induced injury.
    b. Barrett's Esophagus is present in about 10% of GERD patients
    c. Barrett's Esophagus is Indicative of Severe GERD
    d. The involved tissue may form strictures or develop deep, bleeding ulcers
    e. Adenocarcinoma is the most serious complication of Barrett's esophagus and
    is seen in up to 10% of cases
    01-07
    DYSPHAGIA: 14.
    ESOPHAGEAL DYSPHAGIA
    B. PROGRESSIVE DYSPHAGIA FOR SOUDS, continued
    4. Esophageal Cancer: Rapidly Progressive Dysphagia For Solids
    a. Esophageal cancer is one of the least common GI carcinomas
    b. Many patients present with advanced, untreatable disease
    c. It is most often seen in patients between 50-70 years old (Mean 62)
    d. It is more common in males (3:1)
    e. The patient may complain of a substernal pain that can mimic heartburn
    f. The patient may also experience odynophagia (pain upon swallowing)
    g. The patient may experience weight loss: > 10 lb (4.5 kg) in the past 10 weeks
    h. Other complaints include sialorrhea (excessive salivation)
    i. Metastasis may lead to tracheobronchial fistulae that lead to coughing Attacks when
    swallowing and/or aspiration pneumonia
    j. Risk factor: Barrett's esophagus (adenocarcinoma)
    k. Risk factor: Chronic alcohol use (squamous cell carcinoma)
    I. Risk factor: Chronic tobacco use (squamous cell carcinoma)
    5. Other Considerations in Progressive Dysphagia: Dysphagia due to compression of the
    esophagus may occur with mediastinal disorders such as including carcinoma 1 metastasis,
    lymphadenopathy, aneurysms of the aortic arch and left atrial enlargement
    Clinical Axiom: A chronic, progressive dysphagia in an older male smoker
    signals esophageal cancer unless proven otherwise
    Overall, the 5-Year Survival Rate With Esophageal Cancer is 4.8%
    C. INTERN17TENTNEUROMUSCULAR DISORDERS
    1. Esophageal Dysmotility: Non-Cardiac Chest Pain & Dysphagia for Uquids & Solids
    a. Seen in 12% to 33% of patients with unexplained chest pain
    b. nNutcracker esophagus" (30%- 50%): Increased pressure during peristalsis
    (> 180 mm Hg). Nutcracker esophagus is more often seen in patients age 50-60.
    c. Nonspecific motility disorders (Inefficient esophageal motility disorder) (30%)
    d. Diffuse esophageal spasm (15%)
    Adapted from: Esophageal Motility Disorders, Gaumnitz, emedicine, July 6, 2006
    http://wvm.emedicine.com/med/topic740.htm
    01-07
    )
    i
    )
    DYSPHAGIA: 15.
    ESOPHAGEAL DYSPHAGIA
    D. PROGRESSIVE NEUROMUSCULAR DISORDERS
    1.
    2.
    Progressive Systemic Sclerosis (PSS) (Scleroderma)
    a. Severe GERD & progressive dysphagia for solids & liquids
    b. More common in women (2-3:1). The onset can be between the ages 20-40
    c. CREST syndrome
    C: Calcinosis cutis. The skin of the face & hands becomes thick and "hidebound"
    R: Raynaud's phenomenon (often with polyarthralgia) is an early manifestation
    E: Esophageal dysmotility is common, especially in those with Raynaud's
    S: Sclerodactyly (calcinosis of the fingers)
    T: Telangiectasia (With pigmentation changes) of the fingertips & nail folds
    d. Esophageal motility changes are followed by esophageal fibrosis. Atrophy and
    fibrosis of the esophageal musculature leads to weakened peristalsis and/or
    incompetency of the lower esophageal sphincter (LES)
    e. The histopathologic changes seen in the esophagus may involve other parts of
    the GI tract. The patient may show evidence of malabsorption and weight loss.
    f. Esophageal complications include erosive esophagitis, Barrett's and/or peptic stricture
    LES Achalasia: Slow, Progressive Dysphagia For Both Solids & Liquids
    a. Achalasia: The circular muscle is unable to relax
    b. LES achalasia is an idiopathic disease that leads to the loss of peristalsis in the distal
    esophagus and impaired relaxation of the LES
    c. The onset can occur between the ages of 25-60
    d. It's often accompanied by a sensation of substernal "fullness" or discomfort after eating
    e. May be accompanied by decreased eructation, halitosis, & regurgitation of undigested food
    f. The patient may compensate by extending the neck and/or retracting the shoulders so as
    to enhance esophageal emptying
    g. Some degree of weight loss is common
    h. Potential dilation of the distal esophagus:
    "Bird's beak deformity" or "Parrot's beak deformity" upon barium imaging
    i. Treatment includes bougienage, surgery
    01-07
    NON-CARDIAC CHEST PAIN: 16.
    REVIEW, INDIGESTION AND HEARTBURN
    Indigestion and heartburn:
    A descriptive study of prevalence in persons seeking care from chiropractors.
    Bryner & Staerker, Journal of Manipulative and Physiological Therapeutics 1996; 19(5); 317-23.
    Abstract (with emphasis added):
    Objective: To determine the prevalence of indigestion and mid-back pain in persons seeking
    chiropractic care.
    Design: A cross-sectional survey using a self-report questionnaire.
    Setting: Three primary care private chiropractic practices in metropolitan Perth, Australia.
    Subjects: Persons seeking chiropractic care during a 1-month period.
    Intervention: None.
    Outcome measures: Six-month prevalence of indigestion and mid-back pain, rate of
    association between indigestion and mid-back pain, and distribution of thoracic
    dysfunction and manipulation. Proportion who report relief from manipulation.
    Observations: Of 1567 persons who consulted 8 chiropractors on 2974 occasions during
    November 1994, 1494 responses were obtained. There were 119 first-time consultations. The )
    mean age of respondents was 41 yr (rage 10-94); 57% were women. Fifty-seven percent
    reported indigestion infrequently or more and 71% reported mid-back pain during the previous 6
    months. Forty-six percent experienced both symptoms during this time. Of these, 36%
    reported the symptoms together at some time. Twenty-two percent of those with
    indigestion reported some relief after chiropractic care. Compared with those
    reporting no relief, mid-back pain was more common among those reporting
    indigestion. The level at which the manipulation was given was unrelated to relief. No major
    differences were noted between the three clinics in patient demographics or the main outcome
    measures.
    Conclusions: Indigestion and mid-back pain are commonly experienced in this population. A
    person with indigestion is more likely to report mid-back pain. Relief of indigestion by
    manipulation is more common among those who report mid-back pain. Further research is needed
    to understand differences between subgroups and differences compared with other studies. (J.
    Manipulative Physical Ther 1996; 19:317-23).
    03·09
    )
    LOWER ESOPHAGEAL SPHINCTER:
    ) LES OVERVIEW
    17.
    )
    The LES is a zone of increased intra-luminal pressure. The anatomic distinctions between
    the LES and the esophagus are minimal. The physiologic distinctions are considerable.
    A. LES BASAL TONUS (Resting Tonus)
    1. Within certain limits, LES tonus tends to increase as intra-gastric pressures rise
    2. Note: In general, LES smooth muscle has a lower threshold for isometric contraction
    3. Note: The circular muscle in the LES tends to develop more tension upon passive stretching
    4. Basal pressure in the LES tends to vary with respiration. For example, the LES moves axially
    during respiration, cyclically altering the external pressure exerted by the diaphragm. During
    inspiration, pressures are elevated in the lower half of the LES and decreased in the upper half
    B. LES RELAXATION
    1. Relaxation is Initiated by Primary Peristalsis: Peristalsis induced by swallowing
    a. The normal LES relaxes for 3-10 seconds after swallowing so the bolus to pass through
    2. Other, Transient LES Relaxations May Be Stimulated by Gastric Distention
    a. Transient relaxations are not preceded by the normal primary peristaltic sequence and
    may last for up to 30 seconds. LES pressures can fall to zero during a transient relaxation
    Important note: Some degree of esophageal reflux due to these transient LES
    relaxations is considered normal, even in healthy individuals
    LESatrest
    versus
    During a swallow
    Ph reno-esophageal
    ligament
    Mucosal junction with
    abdominal portion of
    the esophagus
    Gastric cardia
    Adapted from: Anatomy,
    5"' edition, Gardner, Gray &
    O'Rahilly, WB Saunders 1986
    01-07
    LES: 18.
    GERD
    A. REVIEW: GASTROESOPHAGEAL REFLUX (GER)
    1. Nonnal Asymptomatic Reflux
    a. Spontaneous, passive movements of some gastric contents into the esophagus
    b. Some degree of reflux occurs in almost everyone, several times a day
    2. Symptomatic "Functionaln Heartburn: Reflux symptoms are present, but ...
    a. Acid levels are notelevated
    b. The esophageal mucosa appears normal upon endoscopy
    3. Non-Erosive Reflux Disease: Reflux symptoms are present,. and ...
    a Acid levels are elevated
    b. However ... the esophageal tissue appears nonnal upon endoscopy
    c. Biopsy might reveal some evidence of epithelial keratinization
    4. Gastroesophageal Reflux Disease: Reflux symptoms are present
    a. Acid levels are elevated
    b. There is evidence of esophageal damage on endoscopy I biopsy
    B. REVIEW: THE PHYSICAL ANTI-REFLUX "BARRIERS"
    1. These Are the Weaker Defense Mechanisms
    a. The mucosal "rosettes"
    b. The gastro-Esophageal "angle"
    C. REVIEW: THE PHYSIOLGICAL ANTI-REFLUX "BARRIERS"
    1. These Are the Stronger Defense Mechanisms
    2. The Positive Pressure Gradient Between the LES & the Stomach
    a. Basal LES pressures are normally > 12 mm Hg higher than intra-gastric pressures. Any
    increase in intra-gastric pressure should result in a reflexive increase in LES basal pressure
    3. Positive Intra-Abdominal Pressure
    a. Within limits_ this force is applied equally to the stomach and the infra-diaphragmatic
    portion of the LES, leading to a reflexive increase in LES pressure. As long as this reflex
    mechanism is intact, positive intra-abdominal pressure will act as an anti-reflux barrier
    4. Secondary Peristalsis: Helps "clear'' the esophagus of food & refluxed stomach contents
    )
    )
    )
    )
    LES: 19.
    GERD
    D. REVIEW: "CLASSIC" FACTORS THAT CAN LOWER LES BASAL PRESSURES (1975)
    1. These Factors tan Encourage Reflux & Should be Avoided by Symptomatic Pt:s.
    2. Avoiding These Factors is Considered to be the lot Line in the Treatment of GERD
    3. Note: Making These Changes Might Not be Effective in All Patients
    4. Factors That Decrease LES Basal Pressures & Increase the Risk of Reflux
    a. Gastric acidification, citrus, nicotine, alcohol, fried or fatty foods, caffeine,
    chocolate, peppermint and spearmint.
    b. Some authors include the "nightshade" foods: potatoes, tomatoes, sweet and
    hot peppers, eggplant, tomatillos, tamarios (tamarind?), pepinos, pimentos,
    paprika,-cayenne, and Tabasco sauce
    Important note about lifestyle changes:
    Weight loss and elevating the head of the bed have been shown to be most effective
    Elevating the head of the bed improves esophageal clearance and decreases
    amount of time that the pH in the esophagus is low ( < 4.0)
    Weight loss improved the pH profiles and the symptoms
    Are Ufestyle Measures Effective in Patients With Gastroesophageal Reflux Disease?: An Evidence-Based Approach
    Kaltenbach, Crockett, and Gerson, Arch Intern Med. 2006;166:965-971.
    htto:/iarchinte.ama-assn.om/content/vol166/issue9iindex.dtl
    Along with lying down, LES basal pressure might also be decreased by pregnancy;
    some prescription medications, an a "hiatus hernia" (discussed in GI Dx[fx)
    Factors that are thought to increase LES basal pressure (and therefore decrease the risk of reflux)
    Include gastric alkalinization, meals containing non-fat protein and "reasonable" increases
    in abdominal muscle tone
    Remember, the diagnosis of heartburn I uncomplicated GERD is usually made by the
    absence of alarm symptoms and the presence of heartburn that is exacerbated
    by meals, bending forward or recumbency, and is relieved by the use of antacids
    03-Q9
    LES: 20.
    GERD
    E. REVIEW: HEARTBURN INCIDENCE &. HISTORY
    1. According to One Large SuiVey of US Adults:
    a. Up to 40% complained of having monthly heartburn symptoms
    b. Up to 20% complained of having weekly heartburn symptoms
    c. Up to 10% complained of having daily heartburn symptoms
    Typical Heartburn:
    A substernal uburning"
    pain located anywhere
    from the xiphoid process
    to the episternal notch .1... ;'. ... . ' . . .
    ·. . ~ . :=·
    Referred pain to the
    midthoracic spine is seen
    in about 40% of cases
    Referred pain to the left
    shoulder I arm is seen
    in about 5% of cases
    Possible regurgitation into the back of the throat
    "Acid brash": Acid regurgitation that can "burn" the throat
    "Water brash": Excess salivation
    Implicated in possible ENT complications of GERD
    Heartburn usually occurs 30 to 60 minutes after the offending meal
    Lying down or bending over after meals often provokes it
    The severity of the "heartbum" doesn't always correlate to the degree of damage
    Older I geriatric patients with verified GERD might not experience "heartbum"
    03-Q9
    )
    )
    LES: 21.
    GERD SIGNS & SYMPTOMS
    A. TYPICAL GERD SYMPTOMS (Again): Heartburn & Acidic Regurgitation
    1. More likely to be Seen in Younger I Non-Geriatric Population
    2. Heartburn severity might not wrrelate with the degree of tissue damage
    B. ATYPICAL GERD SYMPTOMS
    1. More likely to be Seen in the Older I Geriatric Population
    2. Hay Manifest in the Absence of Heartburn I Esophageal Inflammation
    a. The absence of heartburn and regurgitation can make the diagnosis difficult
    3. Respiratory Tract Symptoms
    a. Chronic cough 1 asthma (especially nocturnal asthma)
    b. Bronchitis, pneumonitis (and occasionally pneumonia)
    4. ENT Symptoms
    a. Sore throat I hoarseness I pharyngitis I sinusitis
    c. Otalgia (earache)
    d. Halitosis
    5. Dental Erosions 1 Periodontal Disease
    ) C. ONE STUDY: ATYPICAL GERD SYMPTOMS WITH NO"CLASSIC" REFLUX SYMPTOMS
    1. Evidence of GERD Was Found by Measuring pH Levels, etc.
    a .. 40-60% of patients had asthma but denied having classic reflux symptoms
    b. 43-75% of patients had chronic cough but denied having reflux symptoms
    c. 57-94% of patients had ENT symptoms but denied having reflux symptoms
    http://www.medscape.com/viewarticle/579390
    D. ALARM SYMPTOMS: Warning Signs That Suggest Complicated GERD
    1. Chest Pain That can Mimic Angina Pectoris
    a. Motility disorders: Esophageal "spasm", etc.
    2. Dysphagia I Progressive Dysphagia
    3. Odynophagia: Implies a pill-induced or fungal esophagitis
    4. Weight Loss: Implies peptic stricture I esophageal malignancy I LES achalasia, etc.
    5. Anemia 1 Gastrointestinal Bleeding I Blood in the Stool
    Pa'tients with alarm symptoms should undergo prompt endoscopy
    Patients with very chronic GERD but no alarm symptoms should be considered
    for endoscopy because of concerns about a potential Barrett's esophagus
    LES: 22.
    GERD TREATMENT
    A. CONSERVATIVE TREATMENT OF "HEARTBURN" I PRESUMED NON-EROSIVE DISEASE
    1. Enhance the Physical Anti-Reflux Barriers It Improve Esophageal Clearance
    a. Eat smaller meals, stay upright as much as possible, lose weight, don't eat before bedtime
    (allow ~ 3 hours), and consider elevating the head of the bed by 6 inches
    2. Lifestyle Changes: Improve the Function of the Physiologic Anti-Reflux Barriers
    a. Avoid 1 minimize nicotine, alcohol, caffeine, chocolate, peppermint, spearmint, and fat
    3. Lifestyle Changes: Minimize the Use of Gastric Secretagogues
    a. Avoid 1 minimize methylxanthines I caffeine, decaffeinated coffee, alcohol, colas, tobacco,
    red pepper, niacin, and, interestingly enough, calcium
    4. Lifestyle Changes: Minimize the Use of Gastric Irritants
    a. Avoid 1 minimize aspirin, alcohol, caffeine, bile salt extracts, black pepper, chili pepper,
    vinegar, mustard, cloves, nutmeg
    5. Review Medications I Supplements
    a. Anticholinergic agents, beta2-adrenergic agonists, ca++ channel blockers, progestional
    agents & theophylline can all lower L.E.S. basal pressure
    b. NSAIDs (including aspirin) can lead to erosive I peptic esophagitis )
    c. Note: Oral osteoporosis drugs are notorious for damaging the esophagus
    http://www.fda.gov/MEDwatch/safety/1996/fosamax.htm
    Remember:
    Lifestyle modifications have long been considered the first line of treatment
    Studies indicate that some lifestyle changes are not all that helpful in treating GERD
    Losing weight It elevating the head of the bed were shown to have a clear benefit
    Are Lifestyle Measures Effective in Patients With Gastroesophageal Reftux Disease?: An Evidence-Based Approach
    Kaltenbach, Crockett, and Gerson, Arch Intern Med. 2006;166:965-971.
    http://archinte.ama-assn.org/content/vol166/issue9/index.dtl
    )
    )
    LES:
    GERD TREATMENT
    B. THERE ARE VARIOUS ISSUES WITH TREATMENT USING OTCs
    1. Antacids Neutralize I Counteract Stomach Acidity
    a. Antacids: A base or basic salt
    b. Example: Tums®, Rolaids®, etc.
    c. Antacids are not considered to be particularly effective
    d. Their effects are considered "temporary": They will reduce acid levels
    and relieve symptoms for about an hour
    e. There might be an "acid rebound" following their use
    f. Some authors state they have no place in GERD treatment
    2. Demulcents Have Not Been Extensively Studied
    a. Demulcent: An agent that forms a soothing film over a mucous membrane
    b. Most evidence is "C" level: Unclear scientific evidence for this use
    c. Example: Deglycyrrhizinated licorice (DGL):
    d. Example: Gaviscon®
    3. Which Acid Reducer to Use? H2RAs and/ or PPis?
    a. Acid reducers directly or indirectly influence the stomach's "proton pumps"
    23.
    b. Hydrogen-potassium C'proton'') pumps are directly involved in the formation of HCL
    c. H2RAs: Histamine-2 receptor antagonists
    d. PPis: Proton pump inhibitors
    e. Acid reducers are intended for occasional I short-term sse (2 weeks)i
    4. Empiric PPI "Test"?
    a. It's been widely accepted that a rapid symptom response to a normal dose of PPis
    validates the diagnosis of heartburn I uncomplicated GERD.
    b. However, studies confirming this diagnostic test have been inconsistent.
    Response to PPI treatment may not confirm GERD, Sadovsky, American Family Physician, Feb. 2005
    http://findarticles.com/p/artides/mi_m3225/is_jai_n11833484
    4. Empiric Step-up I Step-down?
    a. Step-up: H2RAs followed by PPis if there is no improvement
    b. Step-down: PPis followed by the lowest dose of acid suppression
    5. He/icobacter pylori Has Been Implicated in Some cases of GERD
    a. Test and Treat? Test for H. pylori and treat with PPis if the H. pylori test is negative
    03-09
    FUNCTIONAL ABDOMINAL DISORDERS: 24.
    MILK-ALKAU SYNDROME
    A. MILK-ALKAU SYNDROME / BURNETT'S SYNDROME
    1. ttypercalcemia Due to the Oral Intake of Calcium and an Absorbable Alkali
    a. 1920's: Milk and bicarbonate of soda used in the treatment of peptic ulcer disease. Milk
    represents the calcium source. Bicarbonate is the absorbable alkali
    b. Today: Calcium carbonate for the relief of indigestion and as a calcium supplement.
    Calcium carbonate serves as the source for both.
    c. How oral intake of elemental calcium with absorbable alkali results in hypercalcemia and
    alkalosis is not completely understood
    2. There is a High Individual Variability in the Risk of Milk-Alkali Syndrome
    a. Some individuals with a high calcium intake do not develop the syndrome.
    3. There's Wide Variation in Symptoms, Even With Similar Levels of Serum Calcium
    a. Some patients may be completely asymptomatic, with hypercalcemia found incidentally
    after a multiple chemistry panel. On the other hand, some patients may have severe
    mental status changes that include obtundation and coma, especially as serum calcium
    levels rise to higher than 15 mg/dl.
    4. Milk-Alkali Syndrome Can Follow Either a Very Acute or Very Chronic Course
    5. Milk-Alkali Syndrome Almost Never Results in Death
    a. However, a significant number of patients may be left with permanent renal impairment
    Signs and symptoms of milk-alkali syndrome are those of hypercalcemia of any cause.
    CNS symptoms may include fatigue, depression, malaise, confusion, or changes in mental status. GI
    symptoms may include nausea, vomiting, and constipation, GU symptoms may include changes in
    urinary frequency, renal tubular defects, or renal failure. Cardiac symptoms may include ECG changes
    (short QT interval) or arrhythmias
    With the development of nonabsorbable alkali and histamine-2 blockers for the
    treatment of peptic ulcer disease, milk-alkali syndrome became a rare cause
    of hypercalcemia. However, with increased use and promotion of calcium
    carbonate for dyspepsia and as calcium supplementation, a resurgence
    of milk-alkali syndrome has occurred in the last few years
    Adapted from: Milk-Alkali Syndrome, Scofield http:/lwww.emedicine.com/med/topicl477.htm
    08-05
    )
    LES: 25.
    OTC ACID REDUCERS
    A. HISTAMINE-2 RECEPTOR ANTAGONISTS (H2RA, H2 Receptor Blockers, H2 Blockers)
    1. Ometidine (Tagamet}, Famotidine (Pepcid}, Nizatidine (Axid}, Ranitidine (Zantac)
    2. H2 Blockers Indirectly Affect the Proton Pump
    a. They prevent histamine from stimulating this pump, thereby reducing acid production
    3. OTC H2 Blockers are Usually Half the Dose of the Lowest Available Prescription Strength
    a. They are generally not strong enough to treat and heal ulcers.
    b. One exception: Maximum Strength Pepcid AC contains prescription strength famotidine.
    4. All H2 Blockers Seem to be Similar in Terms of How Well They Work
    5. Cimetidine (Tagamet) Has a Greater Drug Interaction Potential Than the Others
    Note: H2RAs are less effective than PPis at suppressing acid production
    For that reason, H2RAs are no longer recommended as often as PPis
    On the other hand, some clinicians suggest starting treatment with H2RAs,
    followed by PPis if the H2RAs fail to reduce symptoms
    ) ~~--------------------~H~2~B~I~o=ck~e~r~s:~C~o~m~pa~r~is~o~n~o~f~S~id~e~E~ff~e~ct~s~------------------~
    Side Effect
    Breast enlargement
    in males
    Constipation
    Diarrhea
    Dizziness
    Fatigue
    Headache
    Impotence
    Other
    0.3 - 4.0 % Not reported Not reported
    Not reported 1.2% Not reported
    1.0% 1.7% Not reported
    1.0% 1.3% **
    1.0% Not reported **
    1.0% 4.7% Not reported
    1.0% Not reported Not reported
    Hair loss Darkened tongue,
    Darkened stools
    ** Reported, but no mc1dence g1ven
    To Check For Drug Interactions:
    http:f!www.drugdigest.org/DD/Interaction/ChooseDrugs/1,4109,,00.htrnl
    **
    Not reported
    Not reported
    Not reported
    2.4%
    Not reported
    Not reported
    Sweating
    10-08
    LES: 26.
    OTC ACID REDUCERS
    B. PROTON PUMP INHIBITORS (PPis)
    1. Omeprazole (Prilosec), Esomeprazole (Nexium), Lansoprazole (Prevacid)
    2. Proton Pump Inhibitors Directly Affect the Proton Pump
    3. Proton Pump Inhibitors Are Intended for Short-term Use (2 weeks)
    4. The long-term use of PPis has been associated with bile reflux & ''non-addu GERD
    5. Stomach infections have also been reported following long-term use of PPis:
    a. Inhibiting HCI production may decrease the ability to which kill microbes in the stomach
    Highlights of the American Gastroenterological Association 2008 guidelines on the management of
    GERD: Proton pump inhibitors (PPis) are more effective than histamine-2-receptor antagonists,
    twice-daily PPI therapy should be used after inadequate response to once-daily dosing, patients with
    reflux chest pain should receive PPis after careful consideration of cardiac causes, long-term therapy
    with PPis should be titrated down to the lowest effective dose, and PPis are preferable to anti reflux
    surgery, unless the patient is intolerant to the drugs.
    The most common side effects seem to be diarrhea, feeling or being sick, constipation, gas,
    abdominal pain and headaches. Very rarely, PPis may cause allergic reactions, itching, dizziness,
    swollen ankles, muscle and joint pain, blurred vision, depression and a dry mouth. You should use a
    proton pump inhibitor with care if you have liver or kidney problems, are pregnant, or breastfeeding.
    The effects of phenytoin (an epilepsy medicine) and warfarin (for preventing blood clots) are
    increased by some of the proton pump inhibitors. The absorption of the antifungal drugs ketoconazole
    and itraconazole are reduced by proton pump inhibitors. The breakdown of diazepam (Valium) may
    be blocked by some of the proton pump inhibitors so that there is an increased effect of diazepam.
    http://www.bupa.eo.uk/health informationlhtmVmedicine/h2antagonist.html#3
    Side effect
    Abdominal pain Not reported ** Not reported Not reported
    Constipation ** > 1.0% **
    Diarrhea > 1.0% 3.6% Not reported
    Dizziness < 1.0% > 1.0% **
    Gas Not reported ** Not reported Not reported
    Headache > 1.0% < 1.0% 2.4%
    Nausea ** 1.4% Not reported
    Rash < 1.0% > 1.0% **
    Sinusitis Not reported ** Not reported Not reported
    Stomach pain Not reported 1.8% Not reported
    URTI ** > 1.0% Not reported
    Vomitino ** > 1.0% Not reported
    ** Reported, but no mc1dence g1ven
    10-08
    )
    LES:
    HIATAL HERNIA
    "Sliding" hiatal hernia:
    The LES is above the level
    of the diaphragm
    "Rolling" hiatal hernia
    (paraesophageal):
    The LES is at the level
    of the diaphragm, but •••
    27.
    Hiatal hernia: A portion of the infra-diaphragmatic esophagus I stomach
    prolapses through the diaphragmatic esophageal hiatus
    Sliding hiatal hernias are common. By themselves they do not cause symptoms
    Most people with hiatal hernias are asymptomatic
    "Hiatal hernia" and "gastroesophageal reflux disease" are not synonymous terms
    Hiatal hernias mightworsen reflux symptoms in a minority of patients
    Hiatal Hernia, Qureshi, emedicine, Feb 28, 2006
    ) L-------------------~h~ttp,~:::~~~www~~.e~m~ed~ia~·n~e=.c~om~~/~rm~ed~j~~<O~P~IC~1~0~12~.H~TM~------------------~
    A. "SUDING" HIATAL HERNIA: The Much More Common Type (99%?)
    1. The LES and A Small, "Bell-shaped" Portion of the Infra-Diaphragmatic Esophagus
    Are Elevated Above the Level of the Diaphragm
    2. Sliding Hiatus Hernias Are Most Often Asymptomatic
    3. When "Symptomatic", the Clinical Presentation is the Same as That of GERD
    B. "ROLUNG" / PARAESOPHAGEAL HIATAL HERNIA
    1. Marked Widening of the Diaphragmatic Crurae Allows the Infradiaphragmatic
    Esophagus and the Proximal Stomach to Herniate Up Into the Thorax
    2. GERD is Usually Not Partofthe Clinical Presentation
    3. "Rolling" Hiatus Hernias Are Most Often Seen in the Elderly
    4. Symptoms of an Uncomplicated 'Rolling' Hiatus Hernias Include Belching
    (Eructation), a Sensation of Chest "Heaviness" and Occasional Chest Discomfort
    5. Complicated "Rolling" Hiatus Hernias Have Been Called the "Great Mimic"
    a. Symptoms often develop suddenly
    b. Symptoms often relate to incarceration and/or hemorrhage of the stomach
    10-08
    28.
    )
    )
    )
    CSC 7364 Gastroenterology Dx I Tx, Summer Quarter 2011
    Packet Three: Selected Disorders of the
    Stomach
    For starters:
    Neither clinical impressions nor computer models that incorporated patient
    demographics, risk factors, history items, and symptoms adequately
    distinguished between organic disease process and functional
    disorders in patients referred for endoscopic evaluation of dyspepsia.
    In the emergency department setting, the initial dinical presentations of
    complicated acute gastritis, chronic gastritis, and peptic ulcer disease
    (PUD) are usually are indistinguishable
    ,.
    }L-------------------~~~::/~/www~~·e~m~~~ic~in~e~.co~m~/ee~m~e~,~~~~~O~~~C~82~0~.HT~M~------------------~
    Cardia
    Some parietal cells, mucous
    cells, chief cells, stem cells
    Pylorus
    More mucous neck cells and G
    cells that secrete gastrin
    Fundus
    Corpus I Body
    Mucous cells, mucous neck
    cells, parietal cells,
    chief cells
    Antrum
    The antrum is notable as the
    potential home of H. pylori
    Compiled by Peter Shull DC
    Last review I revision: 01-11
    STOMACH: 02.
    DYSPEPSIA
    Dyspepsia refers to nondescript, nonspecific upper abdominal symptoms:
    Discomfort, bloating, early satiety, unusual postprandial fullness, nausea,
    loss of appetite, heartburn, regurgitation of food or acid, and belching
    In 1862, a French writer called dyspepsia "the remorse of a guilty stomach."
    Contrary to the implication of this derivation, there is little evidence that
    digestion is adversely affected in cases of dyspepsia
    http://www.medterms.com/script/main/art.asp?articlekey=8285
    A. THE MOST COMMON CAUSES OF DYSPEPSIA INCLUDE:
    1. Non-Ulcer Dyspepsia 1 Functional Dyspepsia: "'60% of cases
    a. Due to an augmented perception of visceral pain?
    b. Patients with NUD are more likely to have symptoms of anxiety or depression
    2. Peptic Ulcer Disease: 15-25% of cases
    3. GERD I Reflux Esophagitis: 5-15% of cases
    4. Gastric cancer 1 Esophageal cancer: < 2% of cases
    5. There Are Several Other Potential Causes, All of Them Considered Rare
    B. EVEN IN COMPLICATED CASES THE EXAM FINDINGS ARE USUALLY NON-SPECIFIC
    1. A Mild Epigastric Tenderness is Usually Present
    2. Bowel Sounds Are Usually Intact
    In the absence of alarm symptoms, the initial treatment of dyspepsia is usually
    empirical. Trials involving acid reducers are the first line of treatment
    In cases with documented H. pylori infection an "antibiotic cocktail" will be added
    C. ROME III: FUNCTIONAL DYSPEPSIA/ FD I NON-ULCER DYSPEPSIA
    1. At Least 3 Months (With Onset > 6 months Previously) of One or More:
    a. Bothersome postprandial fullness, and/or;
    b. Early satiety, and/or;
    c. Epigastric pain I epigastric burning
    d. No evidence of structural I organic disease that is likely to explain the
    symptoms (including findings on upper GI endoscopy)
    )
    )
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    STOMACH:
    DYSPEPSIA
    .
    Other than using a common sense approach, the treatment of
    FD I NUD remains a major challenge. There is no clear evidence
    on the best treatment of functional dyspepsia 1 NUD
    Pharmacological inte!Ventions for non-ulcer dyspepsia. Cochrane review updated 08-23-06
    http://www.cochrane.org/reviews/en/ab001960.html
    03.
    Most of the agents used in practice have limited or no evidence of efficacy,
    and the results typically are short-lived once therapy is ceased. Appropriate
    therapy currently is based on a consideration of putative (supposed)
    pathophysiologic mechanisms.
    Functional dyspepsia: A new Rome III paradigm, Current Treatment Options in Gastroenterology,08-07
    http://www.springerlink.com/content/Bg5615n71m400w68/
    Antacids (and bismuth) seem tO be no better than placebo.
    Empiric treatment with PPis?
    (Proton pump inhibitors that decrease acid production)
    Empiric treatment with prokinetic agents?
    (Medications that enhance gastric emptying)
    Test and treat?
    (Test for Helicobacter infection and then treat for it, as needed.)
    Dyspepsia alarm symptoms
    (which increase the likelihood of gastric cancer &. complicated peptic ulcer disease)
    Overt anorexia
    Rectal bleeding
    Age: > 45 years
    Jaundice
    Dysphagia
    Melena
    Family Hxof gastric ca
    Abdominal mass
    Weight loss > 10%
    Anemia
    Personal Hxof peptic ulcer
    Am Fam Physician 1999;60:1773-88
    Endoscopy should be performed promptly in patients who have "alarm symptoms"
    Management remains controversial in young patients with no alarm symptoms
    A cost-effective initial approach is to test for Hellcobacter pylori and treat the infection
    if the test is positive. If the H. pylori test is negative, empiric therapy with a
    gastric acid suppressant or prokinetic agent is recommended
    Am Fam Phvsidan 1999·60: 1773-88 hti:Q:Lfwww.ai)fQ.Cl_rg/afi>L20020401/1327 .html
    STOMACH: 04.
    DYSPEPSIA
    CLINICIAN'S CORNER: Can the Clinical History Distinguish Between Organic and
    Functional Dyspepsia?, Paul Moayyedi, MD, et al, lAMA. 2006;295:1566-1576.
    Context Upper gastrointestinal symptoms occur in 40% ofthe population. An accurate
    diagnosis would help rationalize investigation and treatment.
    Objective To systematically review the literature of the accuracy of primary care
    physicians, gastroenterologists, or computer models in diagnosing organic dyspepsia.
    Data Sources A search of Cochrane Controlled Trials Register (December 2003),
    MEDLINE (1966-December 2003), EM BASE (1988-December 2003), and CINAHL (1982-
    December 2003) for studies that reported on cohorts of patients attending for endoscopy
    that had symptoms, clinical opinion, or both recorded before investigation.
    Study Selection Studies that prospectively compared the diagnosis reached by a
    clinician, computer model, or both with results of upper gastrointestinal endoscopy in
    adult patients with upper gastrointestinal symptoms.
    Data Extraction Two authors independently assessed studies (n = 79) for eligibility and
    abstracted data for estimating likelihood ratios (LRs) of clinical opinion, computer models,
    or both in diagnosing an organic cause for dyspepsia.
    Data Synthesis Fifteen studies were identified that evaluated 11 366 patients, with 4817
    patients (42%) classified as having organic dyspepsia. The computer models performed
    similarly to the clinician; therefore, the 2 approaches were combined. The diagnosis
    reached by the clinician or computer model suggesting organic dyspepsia had an LR of
    1.6 (95% confidence interval [CI], 1.4-1.8), and a negative result decreased the
    likelihood of organic dyspepsia (LR, 0.46; 95% CI, 0.38-0.55). A diagnosis of peptic ulcer
    disease performed similarly with an LR of 2.2 (95% CI, 1.9-2.6), but an evaluation that
    suggested the absence of peptic ulcer disease had an LR of 0.45 (95% CI, 0.38-0.53). A
    clinical history suggesting esophagitis had an LR of 2.4 (95% CI, 1.9-3.0) vs a negative
    history that had an LR of 0.50 (95% CI, 0.42-0.60).
    Conclusion Neither clinical impression nor computer models that incorporated
    patient demographics, risk factors, history items, and symptoms adequately
    distinguished between organic and functional disease in patients referred for
    endoscopic evaluation of dyspepsia.
    Author Affiliations: Department of Medicine, McMaster University, Hamilton, Ontario (Dr
    Moayyedi); Center for Enteric Neurosciences and Translational Epidemiological Research,
    Rochester, Minn (Dr Talley); Oregon Health and Science University, Portland (Dr
    Fennerty); and University of Wisconsin Medical School and College of Health Sciences,
    Marquette University, Milwaukee (Dr Vakil).
    )
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    DYSPEPSIA 05.
    Dyspepsia: What It Is & What to Do About It, American Family Physician, October 1999
    Please note: This information was as current as we could make it on the date given above. But medical
    information is always changing, and some information given here may be out of date. For regularly updated
    information on a variety of health topics, please visit familydoctor.org, the AAFP patient education Web site.
    What is dyspepsia? Dyspepsia is a pain or an uncomfortable feeling in the upper middle part of your stomach.
    The pain might come and go, but it's usually there most of the time. People of any age can get dyspepsia. Both
    men and women get it. About one of every four persons gets dyspepsia at some time.
    What are the signs of dyspepsia? Here are some of the signs of dyspepsia: A gnawing or burning
    stomach pain, bloating (a feeling of fullness in your stomach), Heartburn (stomach contents
    coming back up into your throat), upset stomach (nausea), vomiting, and burping. If you have
    these signs, or any kind of stomach pain or discomfort, talk to your family doctor.
    What causes dyspepsia? Often, dyspepsia is caused by a stomach ulcer or add reflux disease. If you have add
    reflux disease, stomach add backs up into your esophagus. (The esophagus is the tube leading from your
    mouth to your stomach.) This causes pain in your chest. Your doctor may do some tests to find out if you have
    an ulcer or acid reflux disease. If you have dyspepsia, your doctor will ask If you take certain medicines. Some
    medicines, like anti-inflammatory medicines, can cause dyspepsia. Rarely, dyspepsia is caused by stomach
    cancer, so you should take this problem seriously. Sometimes no cause of dyspepsia can be found.
    Is dyspepsia a serious condition? Most often, medicine can take care of this condition. Sometimes dyspepsia can
    be the sign of a serious problem--for example, a deep stomach ulcer. If you have dyspepsia, talk to your family
    doctor. This is especially important if any one of the following is true for you: You're over 50 years of age, you
    recently lost weight without trying to, you have trouble swallowing, you have severe vomiting, you have black,
    tarry bowel movements (this means blood in your stools), you can feel a mass in your stomach area
    How is dyspepsia treated? If you have a stomach ulcer, it can be cured. You may need to take an acid-blocking
    medicine. If you have an infection in your stomach, you may also need to take an antibiotic. If your doctor
    thinks that a medicine you're taking causes your dyspepsia, you might take another medicine. A medicine that
    cuts down on the amount of acid in your stomach might help your pain. This medicine can also help if you have
    acid reflux disease. Your doctor might want you to have an endoscopy exam if: You still have stomach pain after
    you take a dyspepsia medicine for 8 week or if t he pain goes away for a while but comes back again.
    In an endoscopy exam, a small tube with a camera inside it is put into your mouth and down into your stomach.
    Then your doctor can look inside your stomach to try to find a cause for your pain.
    Do the medicines for dyspepsia have side effects? The medicines for dyspepsia most often have only minor side
    effects that go away on their own. Some medicines can make your tongue or stools black. Some cause
    headaches, nausea or diarrhea. If you have side effects that make it hard for you to take medicine for
    dyspepsia, talk to your family doctor. Your doctor may have you take a different medicine or may suggest
    something you can do to make the side effects less bothersome. Remember to take medicines just the way your
    doctor tells you. If you need to take an antibiotic, take all of the pills, even when you start feeling better.
    Can I do anything else to avoid dyspepsia? You can do quite a bit to help yourself feel better: If you smoke,
    stop smoking. if some foods bother your stomach, try to avoid eating them, try to reduce the stress in your life,
    if you have acid reflux, don't eat right before bedtime. Raising the head of your bed with blocks under two legs
    may also help. Unless your doctor tells you otherwise, don't take a lot of anti-inflammatory medicines like
    ibuprofen, aspirin, naproxen (brand name: Naprosyn) and ketoprofin (brand name: Orudis). Acetaminophen
    (brand name: Tylenol) is a better choice for pain, because it doesn't hurt your stomach.
    This handout provides a general overview on this topic and may not apply to everyone. To find out if this
    handout applies to you and to get more information on this subject, talk to your family doctor. Copyright©
    1999 by the American Academy of Family Physicians. Permission is granted to print and photocopy this material
    for nonprofit educational uses. Written permission is required for all other uses, including electronic uses.
    STOMACH: 06.
    OVERVIEW OF CUNICAL ANATOMY
    Mucosa and the gastric pits:
    Diffuse mucosal erosion can lead to
    significant bleeding
    Muscularis mucosa: 2 thin layers
    Penetrating ulcers "invade" the
    muscularis mucosa
    Submucosa with larger blood vessels
    "Invasion" of the sub mucosa can
    lead to significant bleeding
    Oblique muscularis
    Circular muscularis
    Longitudinal muscularis
    Serosa: 2 thin layers
    Side Notes on Gastrointestinal Bleeding
    Normal: The average person will lose 1-3 ml of blood per day due to the transudation
    of RBCs across the GI mucosa and "slight" bleeding from tiny abrasions
    Occult blood in the stool may occur with as little as 15-20 ml of blood per day
    Melena (dark, tarry stools stained with blood pigments) occurs when there is
    a blood loss of 50 ml or more of blood per day
    Hematemesis (the regurgitation of blood) "classically" results in "coffee ground vomitus"
    (gastric acid alters the composition of hemoglobin). Hematemesis indicates a much more
    brisk rare of bleeding and most likely indicates upper GI bleeding
    Hematochezia is the passage of red blood from the rectum. It usually indicates
    bleeding from the lower tract. However, it may also result from
    profuse I massive upper GI bleeding
    Adapted from: Core Textbook of Gastroenterology, Eastwood, J.B. Lippincott Co., 1984
    ···· ..
    )
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    STOMACH: 07.
    INTER-RELATED MUCOSAL DEFENSE MECHANISMS
    Old clinical axiom: "No add, no ulcers"
    Many ulcer therapies focus on reducing acid secretion.
    However, increased add secretion alone is not likely to produce ulcers.
    Many patients with ulcers have been found to have normal rates of acid secretion.
    Even when the luminal pH is low, the pH of the surface epithelium
    can remain neutral
    Adapted from: The cellular and molecular basis of gastric mucosal defense, Wallace & Granger.
    Federation of American Societies for Experimental Biology Joumal, VollO, May 1996
    http://www.fasebj.oeg/cgi/reprint/10/"'l/731.pdf
    Note: Coffee and ethanol are stimulants of gastric secretion
    A. EXTRA-MUCOSAL DEFENSE MECHANISMS
    1. Gastric Acid as a Defense Mechanism
    a. Acid's primary role in defense is to kill ingested microorgansims
    b. Acid may also help limit the amount of antigenic material that enters the small intestine
    ) 2. The "Mucus-Bicarbonate Barrier" (Apparently a somewhat controversial topic)
    a. Gel-forming mucus from the neck cell is an important defense mechanism
    b. Mucus traps bacteria, limiting bacterial movement to the surface epithelium
    c. Mucus also traps the bicarbonate ions that are secreted by the epithelium,
    which helps neutralize luminal acid that migrates toward the epithelium
    Evidence indicates that chronic alcohol ingestion can dramatically decrease
    the delivery of mucus glycoprotein to the gastric epithelial surfaces.
    Evidence also indicates that smoking dgarettescan significantly reduce mucus
    synthesis and eventually the thickness of the mucous secreting layer
    http:flwww.ncbi.nlm.nih.gov/pubmed/9161600
    http:flgut.bmj.com/cgi/content:/abstrad:/47/2/170
    3. Surface-active Phospholipids (secreted I stored by organelles in the surface epithelium)
    b. These phospholipids are hydrophobic and tend to "repel" luminal acid
    Bile acids and "non-selective" NSAIDs (especially aspirin) tend to dissipate these
    surface-active phospholipids, allowing acid to contact the epithelium
    STOMACH: 08.
    INTER-RELATED MUCOSAL DEFENSE MECHANISMS
    B. THE EPITHEUUM AS A DEFENSE MECHANISM
    1. Studies Indicate That the Epithelium is More Resistant to Acid Than Once Thought
    a. Apparently, the epithelial cell membranes can resist acid damage in a manner that is
    independent of "contributions" by mucus, bicarbonate ions, or mucosal blood flow
    2. Epithelial Cell Repair I Regeneration
    a. The human gastric epithelium has a tum-over time of 2-4 days
    b. Apparently, new cells are "extruded" in a manner that does not break the cell "barrier"
    If given a chance, the gastric mucosa can repair itseff in a short period of time
    C. MUCOSAL BLOOD FLOW & SENSORY AFFERENT NERVES
    1. The Mucosal "Microcirculation" (capillary beds under the surface epithelium)
    a. Arteriolar tone and mucosal blood flow are modulated by submucosal sensory afferents
    b. Mucosal blood flow is also modulated by several endogenous substances
    c. The microcirculation removes, dilutes, and help neutralize toxic substances
    d. The microcirculation also facilitates delivery of bicarbonate ions to surface epithelium
    Normally, there's a profound and rapid increase in mucosal blood flow when
    the gastric mucosa is exposed to gastric acid or other irritants
    Decreases in mucosal blood flow can lead to hemorrhagic necrosis
    An intact microcirculation in needed in order to start the repair process, which might
    include development of new blood vessels (angiogenesis)
    "Stress ulcers" are associated with decreased mucosal blood supply
    Associated with the physiologic stress of a severe illness
    Not associated with psychological stress
    For more on the mucosal immune system and both the good and bad attributes of the acute
    inflammatory response as it relates to the stomach, go to:
    http://WNW.fasebj.org/o;Ji/reprint/10/7/731.pdf
    )
    10-08 )
    STOMACH: 09.
    HOW TO REALLY "BREAK" THE MUCOSAL DEFENSE MECHANISMS
    Prostaglandins help establish the acute inflammatory response. NSAIDs can interfere
    with prostaglandin synthesis by inhibiting the enzyme cyclooxygenase
    There are two types of cyclooxygenase: COX-1 and COX-2.
    COX-11eads to the production of prostaglandins involved in the inflammatory response,
    supports platelet function and helps maintain healthy tissue. COX-1 inhibition can
    lead to stomach irritation I bleeding and decreased kidney function
    COX-2 is only involved the pathway of the acute inflammatory response
    The bad news: The "non-selectiven OTC NSAIDs inhibit both COX-1 and COX-2,
    thereby increasing the likelihood of stomach irritation I stomach bleeding
    More bad news: Rx "'SAIDs inhibit only COX-2, which sounds good on paper.
    However, Rx COX-2 inhibitors were found to have serious side-effects
    A. NSAIDs: Non-Steroidal Anti-Inflammatory Drugs
    1. NSAIDs Can Adversely Impact Both the Inflammatory Pathways and
    the Layer of Surface-Active Phospholipids
    2. "Traditional"/ "Non-Selective" NSAIDS Inhibit Both COX-1 and COX-2
    a. Blocking COX-1 promotes bleeding and encourages ulcer formation
    3. "Selective" NSAIDS Inhibit Only COX-2
    a. Celebrex: FDA approval12-31-98. Remains on the market
    b. Vioxx: FDA approval 05-21-99. Recalled 09-30-04
    4. Salicylates: OTC Aspirin and RxSalsalate
    a. Aspirin is the only NSAID that inhibits prolonged blood clotting
    b. Aspirin is considered to be the most "ulcerogenic" non-prescription drug
    1995: Gastrointestinal toxicity resulting from NSAID use is the major type of adverse drug reaction
    reported to the FDA. The FDA estimates that 2% to 4% of chronic NSAID users will develop upper GI
    bleeding, a symptomatic ulcer, or an intestinal perforation each year, and that as many as 20,000
    deaths will occur annually as a result of NSAID-induced GI injury.
    Fifteen percent or more of chronic NSAID users have upper GI ulcers on endoscopy,
    many of them with no symptoms of dyspepsia at the time.
    1999: Introduced in January, 1999, Celebrex has become the fastest-selling new drug ever.
    Sales totaled $600 million (6.86 million prescriptions) for the first 6 months of 1999.
    Celebrexprotects the stomach by inhibiting cyclooxygenase-2.
    At the same time, it does not inhibit the cyclooxygenase-1.
    STOMACH: 10.
    HOW TO "BREAK" THE MUCOSAL DEFENSE MECHANISMS
    Non-steroidal anti-inflammatory drugs (NSAIDs):
    The adverse effects of NSAIDs can occur at any time.
    The most common NSAID side effects include nausea, vomiting, diarrhea, constipation, decreased
    appetite, rash, dizziness, headache, and drowsiness. They may lead fluid retention and edema.
    The most serious side effects are kidney failure, liver failure, ulcers and prolonged bleeding
    Some people are allergic to NSAIDs and may develop shortness of breath when using NSAIDs.
    Asthmatics are apparently at a higher risk of experiencing serious allergic reactions to NSAIDs.
    People with an allergy to one NSAID are likely to have similar reactions to a other NSAIDs.
    The antipyretic & anti-inflammatory effects of NSAIDs can mask the signs and symptoms of infection.
    Some NSAID users experience adverse drug reactions with other medicationss
    Long-term use of NSAIDs may have a damaging effect on chondrocyte (cartilage) function.
    http://arthritis.about.com/cs/nsaids/a/factsofnsaids.htm
    htt : www.medicinenet.com nonsteroidal antiinflammato dru s article.htm
    Steroidal anti-inflammatory drugs
    Rxprednisone reduces inflammation, however it has a lengthy, lengthy
    list of side effects, including stomach ulcers
    Prednisone can suppress the immune system, increase the risk of infection, decrease the
    effectiveness of antibiotics and vaccines, cause liver damage as it is synthesized to its active form,
    cause atrophy of the adrenal glands when used for a prolonged period of time, increase the likelihood
    of osteoporosis, increase the likelihood of some birth defects if taken during pregnancy, interact
    adversely with some drugs and supplements, and increase the risk of primary open-angle glaucoma
    Also, withdrawal from long-term prednisone use can be about as much fun as shaving
    your head with a cheese grater or chewing the fingers off your right hand
    http:/ /arthritis.about.com/od/prednisone/a/prednisonefacts.htm
    Remember, rapid healing of superfidal, non-complicated stomach lesions
    can take place in as little as 24-48 hours if any ''noxious agents" are
    removed and the add is neutralized
    10-08
    )
    )
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    STOMACH: 11.
    HOW TO REALLY "BREAK"THE MUCOSAL DEFENSE MECHANISMS
    B. CHRONIC ALCOHOL INGESTION ADVERSELY IMPACTS MUCUS SECRETION
    1. Alcohol is Rapidly Absorbed in Acidic and Neutral Environments
    a. Alcohol stimulates gastric secretion a. decreases mucus delivery
    b. Alcohol can lead to gastric inflammation I erosion of superficial cells
    2. Remember, Cigarette Smoking Also Adversely Impacts the Gastric Mucus Layer
    C. BILE REFLUX ADVERSELY IMPACTS THE SURFACE-ACTIVE PHOSPHOUPIDS
    1. Bile Reflux Was Once Considered an Uncommon cause of Stomach Irritation
    2. Current Evidence Indicates Bile Reflux is More Common Than Once Thought
    "GERD may occur with acid, non-acid bile or in a mixed form."
    Bile reflux has been linked to long-term use of proton-pump inhibitors (PPis)
    (PPis decrease acid production by interfering with W delivery in the stomach)
    Acid and bile reflux in erosive reflux disease, non-erosive reflux disease and Barrett's esophagus, Hak, et a\,
    Hepatogastroenterology. 2008 Mar·Apr;55(82-83):442-7.
    httP://wvm.ncbi.nlm.nih.gov/pubmed/18613384
    During the fasting phase, regular episodes of increased peristalsis sweep
    undigested solids from the stomach into the small intestine.
    httfJ".}/wvm.ncbi.nlm.nih_.g_ov:BO/bookshelf/br.fgji?book=ciT@lilrt=A2779
    With liquids: The resting tone of the fundus establishes a pressure gradient
    that promotes emptying of liquids into the duodenum
    With Solids:
    Following the ingestion of solids
    the pressures at
    both the LES and the pylorus
    increase
    Next, antral "pumping" will
    macerate solids until the
    particles are less than
    1 mm in diameter
    Last, coordinated actions
    of the antrum and pylorus allow
    small aliquots of the particles to
    be emptied
    into the duodenum
    Disruption of these coordinated activities can lead to both GERD and the reflux of bile
    http://wvm.ncbi.nlm.nih.gov:SO/bookshelf/br.fcgl?book=cm&part=A2779
    STOMACH: 12.
    HOW TO REALLY "BREAK"THE MUCOSAL DEFENSE MECHANISMS
    Helicobacter is considered by some to be the most common bacterial infection
    in humans, infecting more than 1 billion people world-wide. However, only
    a small number of infected subjects ever develop one of the
    diseases associated with Helicobacter infection
    Therefore, there are other factors that determine which asymptomatic but infected
    individuals will ultimately develop an Helicobacter pylori-related disease.
    Once thought to be a member of the campylobactergenus,
    Helicobacteris a gram-negative spiral-shaped bacterium with 4-6
    unipolar flagella. Its helical shape and flagella assist in its
    ability to move through the mucus layer
    Helicobacter resides beneath the mucous layer,
    but does not invade the gastric mucosa
    Helicobacter produces a urease enzyme that hydrolyzes urea
    into ammonia. This ammonia the buffers the gastric acid,
    helping protect the organism
    D. HELICOBACTER PYLORI CAN INDIRECTLY IMPACT THE GASTRIC MUCOSA
    1. H. Pylori Prefers to Colonize in the Gastric Antrum
    a. There might be a concurrent but less intense infection in the gastric fundus
    2. The Mechanism by Which H. Pylori Damages the Mucosa is Not Fully Understood
    a. Damage to the surface-active phospholipids and/or the lipids in the epithelial cell walls?
    3. H. pylori Infection is Associated With:
    a. GERD and dyspepsia
    b. Peptic ulcer disease
    c. Chronic active superficial gastritis I Antral gastritis f Type B gastritis
    d. An increased risk of gastric cancer
    Helicobacter treatment involves 10- to 14-day multidrug regimens including antibiotics and acid
    suppressants, combined with education about other ulcer-causing factors and the need for follow-up
    http://www .aafp.org/ afo/2002040 1/1327. hbnl
    )
    Adapted from: Feldman's GastroA~as Online, Vol. 3: Stomach and Duodenum, Ch. 6: Helicobacter Pylori, Cryer & Lee,
    http://www.gastroatlas.com, and; Lancet 2001;357:1738-1742, and; Lancet 2000;356:455-460, and; JAm Board Fam Pract
    13(6):449-450, 2000, Am J Gastroenterol 2000;95:2206-2211. )
    10-08
    )
    STOMACH:
    DYSPEPSIA, AGAIN
    A NON-ULCER DYSPEPSIA / FUNcnONAL DYSPEPSIA ( ~60% of cases)
    B. DYSPEPSIA 8t GERD (~5-15% of cases)
    a. Heartburn? Regurgitation? Non-cardiac chest pain 1 esophageal spasm?
    C. DYSPEPSIA 8t DYSMOTILITY I GASTROPARESIS (incidence not stated)
    a. Early satiety? Bloating? Abdominal distention? Flatulence? Nausea?
    D. DYSPEPSIA 8t "GASTRITIS" (incidence not stated)
    1. "Gastritis" is Now Considered to be an OVer-Used, Non-Specific Term
    2. There is No General Agreement on the Classification of Gastritis
    13.
    a. Endoscopic "gastritis": Endoscopic findings of mucosal erosions and/or focal hemorrhagic
    lesions, often with no microscopic evidence of histiologic·inflammation
    b. Histologic "gastritis": Microscopic evidence of inflammatory cells
    c. The "Sydney system" , which combines topographical, morphological and etiologic i
    information, was introduced in 1990 as an attempt to reconcile some of these differences
    in taxonomy and classification
    E. ACUTE GASTRITIS
    1. Acute Gastritis: Superficial lesions most often due to exogenous causes
    a. Used by some to describe a gastric pain of sudden onset I short duration
    b. Used by others to describe an inflammation that's limited to the gastric mucosa
    c. In either case, acute gastritis is most often due to exogenous causes:
    NSAIDS 1 aspirin I alcohol, etc.
    d. NSAID-induced ''gastritisH is often "clinically silent" until complications occur
    e. Significant bleeding can mask the symptoms of acute gastritis
    Acute gastritis: Focal, superficial erosions limited to the
    mucosa and the lamina propria. The lesions do not
    extend into the submucosa
    Up to 30% of cases of acute GI hemorrhage
    are due to acute gastritis
    Additional reading: Gastritis and Peptic Ulcer Disease, Shayne, emedidne, Aug 21, 2008
    http://WNW.emedidne.com/emerg{fOPIC820.1fTM
    Gastritis, Chronic, Sepulveda & Dore, emedidne, October 15, 2007
    http://WNW.emedidne.com/med{fOPIC852.1fTM
    STOMACH: 14.
    DYSPEPSIA
    F. "CHRONIC" GASTRITIS
    1. Chronic Gastritis: A potential of deeper lesions that may lead to gastric atrophy
    a. Used by some to describe a gastric pain of longer duration
    b. Used by others to describe a bunch of different, unrelated disease processes
    c. Note: The lesions in chronic gastritis can be either superficial or deep
    d. Note: Some forms of chronic gastritis can lead to gastric atrophy
    Type A chronic gastritis involves the proximal acid-secreting stomach
    Type A is implicated in cases of hypochlorhydria and achlorhydria
    To a lesser extent, Type A has been implicated in gastric cancer
    Type B chronic gastritis involves the gastric antrum
    Type B is most often the result of an H. pylori infection
    Tyoe B is directly linked to an inqeaseclrisk of gastric cancer
    G. DYSPEPSIA &. PEPTIC ULCER DISEASE (PUD)
    Classic definition:
    Peptic ulcers extend through the muscularis mucosa
    and are larger than Smm in diameter
    (The erosions seen with acute gastritis would not meet this definition)
    Complication: "Penetrating ulcers" I "bleeding ulcers"
    Implies the lesion has extended into the deeper layers of the gut
    Bleeding is the most common complication of PUD
    "Perforating" ulcers:
    Lesion extends through the serosa into the abdominal cavity,
    resulting in inflammation of surrounding organs or peritonitis
    )
    )
    STOMACH:
    DYSPEPSIA, AGAIN
    Peptic ulcer disease can occur in the esophagus
    where it is often medication-induced
    Gastric ulcers are less common than duodenal ulcers
    Gastric ulcers were once considered to be uncommon. As compared
    to duodenal ulcers, the incidence of gastric ulcers
    has been steadily increasing
    Duodenal ulcers are still the most common type
    As compared to gastric ulcers, the incidence of duodenal ulcers
    has been steadily decreasing
    Peptic ulcers typically tend to heal and then recur
    G. DYSPEPSIA 8r. PEPTIC ULCER DISEASE, continued
    1. "Classic" PUD Questions
    a. A history of NSAID use?
    b. Current cigarette smoking?
    c. A family history of ulcers?
    d A personal history of ulcers and a possible recurrence?
    2. Common Cause: Helicobacter pylori infection
    a. Often seen in combination with other "aggressive" risk factors
    3. Common Cause: NSAID I aspirin-induced injury
    15.
    a. NSAID-induced PUD is often "clinically silent" until complications occur
    4. "Classic" Duodenal Ulcers Have a Symptom "Pattern" (seen in about 50% of DU pts)
    a. The pain is usually associated with an empty stomach
    b. A steady gnawing, burning, aching, epigastric soreness or a feeling of hunger
    c. Usually absent on awakening but appears by mid-morning
    d. Milk I food I antacids usually relieve the pain for 1-3 hours
    e. Night pain is common
    5. "Classic" Gastric Ulcers Might Not Have a Symptom Pattern
    6. Bleeding is the Host Common Complication of PUD
    a. Hematemesis 8r. Melena
    STOMACH: 16.
    DYSPEPSIA, AGAIN
    G. DYSPEPSIA &. PEPTIC ULCER DISEASE, continued
    "Classic" associations in peptic ulcer disease
    (which are variable to the point they have limited diagnostic value)
    I Factor:
    Acid secretion:
    Pain:
    Pain pattern:
    Effects of food:
    Weight change?
    Effects on sleep?
    Duodenal ulcers
    Normal to increased
    Gnawing, epigastric
    Predictable:
    1-3 hours after a meal
    Relieves the pain
    Weight gain common
    May awaken pt. at night
    Gastric ulcers
    Low to normal
    Variable
    Unpredictable
    Unpredictable
    Weight gain uncommon
    Remember the dyspepsia alarm symptoms
    (which increase the likelihood of complicated PUD and gastric cancer
    Overt anorexia
    Rectal bleeding
    Age: > 45 years
    Jaundice
    Dysphagia
    Melena
    Family Hxof gastric ca
    Abdominal mass
    Weight loss > 10%
    Anemia
    Personal Hxof peptic ulcer
    Am Fam Physician 1999;60:1773-88
    10-QB
    )
    )
    STOMACH: 17.
    DYSPEPSIA
    H. DYSPEPSIA 8r. GASTRIC CANCER (90-95% of which are adenocarcinomas)
    .
    The incidence of gastric cancer in North America and Western Europe
    has been steadily declining for the past 50 years
    In Asia and some developing countries the incidence of stomach cancer is high
    and is 2nd only to lung cancer in the rate of cancer-related mortality
    Early diagnosis is difficult. Most patients are asymptomatic in the earlier stages
    It is not possible to detect early stomach cancer on physical examination
    The pathogenesis of gastric cancer is probably multifactorial
    1. Definite Risk Factors for Gastric cancer
    a. Certain genetic I hereditary I familial syndromes: "' 10% of cases
    b. Chronic atrophic gastritis 1 Type A chronic gastritis I Type B chronic gastritis
    c. Helicobacter pylori infection
    2. Probable Risk Factors for Gastric cancer
    a. Tobacco smoking (adenocarcinoma of the gastric cardia)
    b. Pernicious anemia
    c. History of gastric surgery I subtotal gastrectomy
    3. Possible Risk Factors for Gastric Cancer
    a. Excess alcohol ingestion
    b. Diet (see below)
    c. Growths and tumors of various sorts: Hamartoma, Menetrier's disease, etc.
    A diet rich in pickled vegetables, salted fish, excessive dietary salt, and smoked
    meats has been associated with a higher incidence of gastric cancer
    A diet rich in fruits and vegetables rich in vitamin C has been associated
    with a /ower incidence of gastric cancer
    Adapted from: Gastric cancer: Diagnosis and Treatment Options, Layke & Lopez, American Family Physidan, March 1, 2004
    http://WWW .aafp.org/afp/20040301/1133.html
    Gastric carcinoma, Hassan, emedidne, October 19, 2006
    http://www.emedidne.com/RADIO/topic787.htm
    Gastric cancer, cabebe, Mehta & Fisher, emedicine, July 21, 2008
    http://www.emedidne.com/MED/topic845.htm
    STOMACH: 18.
    DYSPEPSIA
    Remember the dyspepsia alarm symptoms
    (which increase the likelihood of complicated PUD and gastric cancer
    Dysphagia
    Melena
    Weight loss > 10%
    Anemia
    Overt anorexia
    Rectal bleeding
    Age: > 45 years
    Jaundice
    Family Hxof gastric ca
    Abdominal mass
    Personal Hxof peptic ulcer
    Am Fam Physician 1999:60:1773-88
    H. DYSPEPSIA & GASTRIC CANCER, continued
    4. Signs of Advanced 1 Late-Stage Gastric cancer
    a. A palpably enlarged stomach
    b. An enlarged liver
    c. Virchow's node 1 Sentinel node (left supraclavicular fossa)
    d. Sister Mary Joseph's nodule I periumbilical nodule
    e. Blumer's shelf (a metastatic tumor felt on rectal examination)
    5. Esophagogastroduodenscopy is the Diagnostic Procedure of Choice
    10-08
    ' .

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