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Gastroenterology Ambulatory Medicine Clerkship. Scott Grisolano, MD Division of Gastroenterolgy and Hepatology KUMC. Outline. Physical exam History taking Evaluation of abdominal pain Common Clinical Scenarios Differential diagnosis. Physical Exam - Abdomen. Inspection Skin Hernia - PowerPoint PPT Presentation
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GastroenterologyAmbulatory Medicine Clerkship
Scott Grisolano, MD
Division of Gastroenterolgy and Hepatology
KUMC
Outline
• Physical exam
• History taking
• Evaluation of abdominal pain– Common Clinical Scenarios– Differential diagnosis
Physical Exam - Abdomen• Inspection
– Skin– Hernia– Contour– Pulsations, peristalsis
• Auscultation– Bowel sounds– Bruits
• Percussion, Palpation– Liver, spleen, masses, aneurysm– Peritoneal irritation
• Rigid abdomen, guarding, rebound tenderness• How was the ride to the ER?• blunted: elderly, severely ill
• HEENT– Scleral icterus– Conjunctival pallor
• Skin– Jaundice– Spider angiomata– Gynecomastia– Petechiae, bruising– Caput medusae
• Extremities– Palmer erythema
• Abdomen– HSM– Ascites
• Neurological – mentation– Asterixis
• Anorectal– Perianal exam– DRE– Stool
Painful History
• Location • Onset, frequency, duration, severity• Quality • Radiation • Factors that exacerbate or improve symptoms such as
food, antacids, exertion, defecation • Associated symptoms: fevers, chills, weight, N, V,
diarrhea, constipation, hematochezia, melena, jaundice, change in the color of urine or stool, change in the diameter of stool
• Family history of bowel disorders • Medications: OTC (acetaminophen, aspirin, and NSAIDs) • Menstrual history in women
Embryology - Pain - Artery - Organ
• Foregut – Epigastrium – Celiac – S, D
• Midgut – Periumbilical – SMA – J, I, TC
• Hindgut – Hypogastrium – IMA – TC, R
Pain
• Visceral pain (viscus)
– diffuse, poorly localized– gnawing, burning, cramping
• Somatic pain (abdominal wall, parietal peritoneum)
– more intense, better localized
• Referred pain– same dermatome– sharp, well localized; resembles somatic
Abdominal Pain - Triage
• Acute – Sick patient?– High level of suspicion in immunosuppressed,
elderly– Abdominal examination
• Chronic
Abdominal Pain - Triage• History
– differential diagnosis
• Examination– vital signs
• Labs– CBC– CMP– Liver biochemistries– Amylase, lipase– UA– Pregnancy test
• Abdominal x-ray
Ruptured or Perforated Viscus
- PUD, ectopic pregnancy, dissecting aneurysm
Obstruction of Viscus
- adhesions, hernia, volvulus, intussusception
Ischemia
- mesenteric, PE, MI
Inflammation
- pancreatitis, cholecystitis, appendicitis, diverticulitis
Peritonitis
Abdominal Pain - Triage• History
– differential diagnosis
• Examination– vital signs
• Labs– CBC– CMP– Liver biochemistries– Amylase, lipase– UA– Pregnancy test
• Abdominal x-ray
RUQ Pain
• Liver, biliary tree– May radiate to back, epigastrium
• Pancreatitis
• Cardiac
• Pleural/pulmonary
• Nephrolithiasis
Epigastric Pain
• Acute pancreatitis
• PUD
• GER
• Cardiac
• Pleural/pulmonary
Lower Abdominal Pain
• Distal intestinal tract
• Urinary tract
• Pelvic structures
– Colonic, SB source = diarrhea, hematochezia– Rectal source = urgency, tenesmus
Lower Abdominal Pain
• LLQ– Diverticulitis– Colitis
• Infectious, ischemic, IBD
• RLQ– Appendicitis– ileocolitis
Lower Abdominal Pain
• Females– Menses, dysmenorrhea, dyspareunia– Possibility of pregnancy– Vaginal discharge, bleeding
– Adnexal cysts– Ovarian torsion– Ectopic pregnancy– PID
Specific Conditions
• PUD
• Gallbladder disease
• Acute pancreatitis
• Small bowel obstruction
• GI bleeding
Specific Conditions
• PUD
• Gallbladder disease
• Acute pancreatitis
• Small bowel obstruction
• GI bleeding
PUD
• Duodenal ulcer– symptoms of occur when acid is secreted in the
absence of a food buffer– symptoms occur 2-5 hours after meals or on
empty stomach
• Gastric ulcer– more severe pain occurring soon after meals,
with less frequent relief by antacids or food
PUD
• Epigastric pain in 2/3 symptomatic patients– may localize to the RUQ, LUQ – burning, gnawing, or hunger-like in quality, may be
vague
• Sudden development severe, diffuse abdominal pain may indicate perforation
• Vomiting is the cardinal feature in pyloric outlet obstruction
• Hemorrhage may be heralded by nausea, hematemesis, melena, or dizziness
PUD - Etiology
• Helicobacter pylori
• NSAIDs
< 5%
30-50%
Alarm Symptoms / Red Flags
• Age > 50• Weight loss• Dysphagia• Persistent vomiting• Palpable abdominal mass• Occult gastrointestinal bleeding• Otherwise unexplained anemia• Family history UGI malignancy• Previous gastric surgery
Specific Conditions
• PUD
• Gallbladder disease
• Acute pancreatitis
• Small bowel obstruction
• GI bleeding
Gallbladder
• Biliary colic– Pain reaches crescendo then resolves completely– Pain is visceral in origin (no true gallbladder wall
inflammation) – Pain resolves when the gallbladder relaxes, permitting
stones to fall back from the cystic duct
• Acute cholecystitis– RUQ pain lasting > 4-6 hours should raise suspicion
for acute cholecystitis– Symptoms of malaise, fever more likely
Cholecystitis – Clinical Presentation
• Abdominal pain– RUQ, epigastrium– may radiate to the right shoulder or back
• Pain is steady and severe– nausea, vomiting, and anorexia
• Prolonged RUQ pain (> 4-6 hours), especially if associated with fever, should arouse suspicion for acute cholecystitis as opposed to an attack of simple biliary colic
Differential Diagnosis
• Acute pancreatitis • Appendicitis • Acute hepatitis • Peptic ulcer disease • Diseases of the right kidney • Right-sided pneumonia • Fitz-Hugh-Curtis syndrome
– perihepatitis caused by gonococcal infection
• Sub-hepatic, intra-abdominal abscess • Perforated viscus • Cardiac ischemia
Cholecystitis – Labs
• Bilirubin, AP generally normal in uncomplicated cholecystitis– biliary obstruction is limited to the gallbladder
• If bilirubin, AP elevated this should raise concerns about complicating conditions such as cholangitis, choledocholithiasis– mild elevation in serum aminotransferases and amylase,
and hyperbilirubinemia with jaundice have been reported even in the absence of these complications
• These abnormalities may be due to the passage of small stones, sludge, or pus
Cholecystitis – Physical Exam
• Ill appearing, febrile, and tachycardic• Lie still on exam table because cholecystitis is
associated with local parietal peritoneal inflammation that is aggravated by movement
• Abdominal examination usually demonstrates voluntary and involuntary guarding
• "Murphy's sign" may be a useful diagnostic maneuver
Acute Calculous Cholecystitis
Specific Conditions
• PUD
• Gallbladder disease
• Acute pancreatitis
• Small bowel obstruction
• GI bleeding
Acute Pancreatitis - Etiology
• Gallstones (45%)• Alcohol abuse (35%)• Post-ERCP, medications, metabolic, hereditary,
infectious, connective tissue disease, trauma, congenital anatomic abnormalities, tumors (10%)
• Idiopathic (10%)
• Overall mortality 10 -15%– severe disease as high as 30%
• Males (alcohol) > Females (choledocholithiasis)
80%80%
Acute Pancreatitis – Clinical Presentation
• Mid-epigastric abdominal pain– Steady, boring pain– Radiation to the left upper back
• Anorexia, nausea vomiting diarrhea• Low grade fever• Presentations associated with complications
– Shock– Multi-system failure
• Abdominal tenderness• Fever (76%)• Abdominal guarding (68%)• Abdominal distension (65%)• Tachycardia (65%)• Hypoactive bowel sounds
• Jaundice (28%)• Dyspnea (10%)• Hemodynamic changes (10%)• Melena or hematemesis (5%)• Cullen’s sign• The Grey-Turner sign• Left pleural effusion
Acute Pancreatitis – Physical Exam
• Serum amylase
– Not specific for pancreatitis• intestinal ischemia, renal insufficiency, small bowel obstruction,
macroamylasemia, parotitis– Short half-life: elevates early, returns to normal early (within 2-3 days)
• Serum lipase– More specific to pancreas– Long half-life: levels rise later, stay elevated for longer (7-14 days)
• Liver enzymes– ALT, AST, alkaline phosphatase, total bilirubin– ALT > 150 in patient with cholelithiasis suggests gallstone
pancreatitis
Acute Pancreatitis - Diagnosis
• Ultrasound– Most useful initial test for common bile duct dilation
and gallstones
• Contrast CT Scan– Not necessary for diagnosis of acute pancreatitis– May help identify etiology in rare instances (tumor)– Useful to assess complications - fluid collections or
pancreatic necrosis
Acute Pancreatitis - Diagnosis
Pseudocyst
- - takes > 4 weeks to takes > 4 weeks to develop pseudocystdevelop pseudocyst
Acute Pancreatitis - Severity Staging
Ranson Criteria - > 3 indicates severe AP
• At Admission– Age > 55; WBC > 16K; Glucose > 200; LDH >350; AST > 250
• During first 48 hours– Hct decrease by > 10% with hydration– BUN increase > 5 mg/dL– Calcium < 8 mg/dL– pO2 < 60 mm Hg– Evidence of fluid sequestration (> 6L replacement
needed)
Specific Conditions
• PUD
• Gallbladder disease
• Acute pancreatitis
• Small bowel obstruction
• GI bleeding
Small Bowel Obstruction
• Post-operative adhesions
• Hernia
• Tumors
SBO - Symptoms• Abdominal distention, vomiting, crampy pain
• Abdominal pain– Periumbilical, crampy– paroxysms of pain every 4-5 minutes– presence of constant abdominal pain or change of pain
from colicky to constant suspect strangulation
• Patients may or may not complain of obstipation and inability to pass flatus since colon requires 12-24 hours to empty after the onset of bowel obstruction
SBO – Physical Exam• Fever, tachycardia: associated with strangulation• Inspection
– surgical scars, degree of distention
• Auscultation– may reveal high-pitched or hypoactive bowel sounds
• Percussion, Palpitation– Tenderness to percussion, rebound, guarding, and localized
tenderness suggests peritonitis– Tympany usually present due to air-filled loops of bowel or stomach– abdominal mass may indicate an abscess, volvulus, or tumor– Search for inguinal, femoral, and incisional hernias
• Rectal examination– gross or occult blood can be found with neoplasm, ischemia, and
intussusception.
SBO – Labs
• Leukocytosis: may indicate presence of strangulation
• Metabolic alkalosis: seen with frequent emesis
• Metabolic (lactic) acidosis: ischemic bowel
SBO – X-rays• Upright chest film to rule out the presence of free air
• Supine and upright abdominal films– Multiple air-fluid levels with distended loops of small bowel are seen
in small bowel obstruction, although occasionally can be seen in setting of paralytic ileus
• Presence of air in the colon or rectum makes the diagnosis of complete obstruction less likely, particularly if symptoms have been present for more than 24 hours
• Plain films:– equivocal in 20-30% of patients– normal, nonspecific in 10-20%
SBO – CT scan
• Presence, level (transition point), severity, and cause may be identified
• Other abdominal pathology can be detected• Absence of air, fluid in distal small bowel or colon
denotes complete obstruction• Intestinal pneumatosis and hemorrhagic mesenteric
changes can be seen in advanced strangulation • In most cases of SBO, no obvious source of
obstruction is seen, since adhesions cannot be detected by CT scan
SBO - Management
• "never let the sun rise or set on a small bowel obstruction"
Specific Conditions
• PUD
• Gallbladder disease
• Acute pancreatitis
• Small bowel obstruction
• GI bleeding
All bleeding is not the same…
• Where is it coming from?
• Pace of bleeding?
• Volume of bleeding?
• Associated symptoms?
• Color of blood?
What color blood?
• Melena
• Hematochezia
• Occult blood positive
Acute GI Bleeding
UPPER > LOWER
75-80% vs. 20-25%
Acute GI Bleeding
• Assessment, stabilization, resuscitation
• Medication review– Anticoagulants (Coumadin)– Antiplatelet agents (Plavix)– Aspirin, NSAIDs
Clinical Prognostic Factors
Older age (>60)Severe comorbidityAltered hemodynamics
- Tachycardia > 100 bpm- Orthostasis > 20 mg Hg systolic
> 10 mg Hg diastolicTransfusion
- 4 - 6 units/resuscitation eventSevere coagulopathyInpatient status at time of bleed
UGI Bleeding
• EGD– Diagnosis
• identifies bleeding site (90-95%)• prognostic value
– Endoscopic Therapy
• Medical Therapy– IV Proton Pump Inhibitors (PPIs)– octreotide
Active Bleeding - Dieulafoy Lesion
90%
Esophageal Varices
LGI Bleeding
• LGIH accounts for 20-25% of all GI bleeds
• Definition: distal to the ligament of Treitz
• Colonic lesions account for vast majority
• Majority cease without intervention
• 15-20% require intervention
LGIB - Etiology
* post-polypectomy bleeds
LGI Bleeding
• Urgent Colonoscopy– After rapid oral purge
– Diagnosis• identifies bleeding site 54-80%
– Treatment• epinephrine, heater probe, bipolar, hemoclips
Diverticular Bleed
Post-polypectomy - NBVV
Ischemic Colitis
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