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Emergency Medicine Clerkship > GI > Flashcards

GI Flashcards

1
Q

Initial actions in a patient with abdominal pain?

A
  1. Primary survey (ABCs, 2 large bore IVs with immediate fluid resuscitation if hemodynamic instability)
  2. Pregnancy test in women of child-bearing age (use Foley to obtain urine if unstable or send blood)
  3. Blood products in unstable patients with suspected hemorrhage
  4. Bedside imaging in patients with concern for pneumo or hemoperitoneum (XR, US)
  5. Order ABX in the setting of sepsis, peritonitis, or perforation
  6. Analgesia
  7. Immediate surgical consultation in the setting of hemodynamic instability or a rigid abdomen
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2
Q

Abdominal pain + hemodynamic instability should alert the physician to what possibilities?

A

Hemorrhage, sepsis, perforated viscus, or necrotic bowel

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3
Q

Life- or organ-threatening diagnoses that must be considered in patients with abdominal pain?

A 
Ectopic pregnancy
Appendicitis
AAA
PID/TOA
Biliary disease
Bowel obstruction
Perforated viscus
Mesenteric ischemia
Testicular
(ACS)
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4
Q

Cholelithiasis occurs as a result of supersaturation of bile with ___ (70%), ___ such as bilirubin (20%), or both (10%), combined with delayed emptying of the gallbladder (stasis).

A

Cholesterol; bilirubin

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5
Q

What is choledocholithiasis?

A

Presence of gallstones within the common bile duct

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6
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder related to the presence of gallstones in 90-95% of cases; acalculous cholecystitis occurs in <10% of cases and are more common in elderly, post-operative, or critically ill patients

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7
Q

What is cholangitis?

A

Inflammation of the bile duct, most often 2/2 polymocrobial bacterial infection

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8
Q

Classic presentation of biliary colic?

A

Episodic/intermittent/colicky burning/pressure-like/heavy RUQ or epigastric pain associated with N/V, may radiate to the back, R flank, or tip of the R scapula

May be related to ingestion of a fatty meal

Most resolve within 4-6 hours

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9
Q

Charcot’s triad?

A

Classic presentation of cholangitis - RUQ pain, fever, jaundice

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10
Q

Physical exam findings of biliary disease?

A

RUQ or epigastric tenderness
Murphy’s sign (good sensitivity, low specificity for acute cholecystitis)
Jaundice if biliary tree obstructed
Elevated temperature suggests cholecystitis and cholangitis

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11
Q

Lab work-up in biliary disease?

A 
WBCs
AST/ALT
Bilirubin (conjugated)
Alkaline phosphatase
Amylase/lipase
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12
Q

Initial diagnostic test of choice for evaluation of biliary tract disease?

A

US

> 95% sensitivity for identification of cholelithiasis (mobile echogenic material casting posterior shadows)

<80% sensitivity for choledocholithiasis

Sensitivity 88-94% and specificity 78-80% for acute cholecystitis (gallstones, GB wall thickening - 5mm or greater, pericholecystic fluid, and/or positive sonographic Murphy’s sign)

Dilation of common bile duct (>6 mm adults, >8 mm in elderly)

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13
Q

Indications for HIDA scan?

A

If US is equivocal or negative for cholecystitis in the presence of a high clinical suspicion (90-94% sensitive for acute cholecystitis)

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14
Q

Positive HIDA study?

A

Lack of visualization of the gallbladder within 4 hours after injection

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15
Q

Indications for CT scan in evaluating biliary disease?

A

If US results are equivocal and HIDA scan is unavailable or if a broad differential is still being considered

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16
Q

Indications for ERCP in suspected biliary disease?

A

Useful for diagnosis and treatment of biliary and pancreatic duct diseases (MRCP or endoscopic US is better for diagnostics alone)

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17
Q

Risk factors for biliary disease?

A 
Female
>40 y/o
Family history
Obesity
Multiparity
Rapid weight loss
Sickle cell or other hemolytic disorders (pigmented stones)
DM (increased risk of cholecystitis)
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18
Q

Rx biliary disease

A

Biliary colic - symptom control (NSAIDs, fluids, anti-emetics), elective cholecystectomy

Choledocholithiasis - surgical or ERCP removal of stone

Cholecystitis and cholangitis - symptoms control with fluids, anti-emetics, and analgesics + broad-spectrum parenteral ABX, prompt cholecystectomy

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19
Q

Incidence of appendicitis peaks around which decades?

A

Around the 2nd and 3rd decades

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20
Q

Classic presentation of appendicitis?

A 
Vague epigastric or periumbilical pain
N/V and anorexia
Abdominal tenderness, migrating then localizing to the RLQ
Fever
Leukocytosis
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21
Q

Discuss the sensitivity and specificity of physical exam findings in suspected appendicitis.

A

RLQ pain/guarding - high sensitivity (81%), low specificity
Abdominal rigidity - high specificity (83%), low sensitivity
Psoas, obturator, and Rovsing’s signs are all relatively poor predictors
NO SINGLE EXAM FINDING SHOULD BE USED TO RULE IN OR RULE OUT THE DISEASE

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22
Q

Work-up for appendicitis?

A

CBC (leukocytosis, though 10-20% will have a normal WBC count)
CRP (elevated CRP + elevated WBC has a combined sensitivity of 98%)
BMP
UA

US
CT
MRI

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23
Q

When is US indicated in appendicitis work-up?

A

Preferred imaging in children and pregnant patients

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24
Q

US findings suggestive of appendicitis?

A

Appendix >6-7 mm in diameter, non-compressible, increased wall thickness, periappendiceal stranding, fecalith, increased vascularity on Doppler

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25
Q

When is CT indicated in the work-up for appendicitis?

A

Adult males and non-pregnant females

IV contrast is recommended, though non-contrast is acceptable

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26
Q

When is MRI indicated in the work-up for appendicitis?

A

Pregnant patients with a non-diagnostic US

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27
Q

Rx appendicitis?

A

Prompt appendectomy
NPO, IV ABX (Amp-sulbactam, cefoxitin, combo metronidazole + ciprofloxacin, etc. if uncomplicated, carbapenem with pip/tazo if complicated)

IV fluids
Pain control
Antiemetics

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28
Q

Appendicitis ED dispo options?

A

OR for appendectomy
IR for percutaneous drainage of abscess
Obs in hospital for serial exam
Return in 24 hours for repeat exam

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29
Q

Patients with a rupture AAA may present to the ED with a CC of what?

Common misdiagnoses?

A

Abdominal, back, or flank pain

Renal colic, pancreatitis, bowel ischemia, diverticulitis, cholecystitis, bowel obstruction, MI, and MSK back pain

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30
Q

Classic presentation of ruptured AAA?

A

Pain (acute, severe, constant in the abdomen, back, or flank, can radiate to the chest, thigh, inguinal region, or scrotum)
Hypotension
Pulsatile abdominal mass (at or above the level of the umbilicus)

N/V, near-syncope, syncope, AMS

Continuous abdominal bruit and a palpable abdominal thrill suggest AV fistula; bloody stools can indicate an aortoenteric fistula

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31
Q

Initial actions and primary survey in suspected AAA?

A

If known or suspected ruptured AAA, consider unstable regardless of initial vitals and Hgb.

Manage ABCs -> 2 large bore IVs, type and cross-match blood

Target BP - 90-100 mmHg

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32
Q

Diagnostic testing in suspected AAA?

A

If unstable with known or suspected ruptured AAA - transfer to OR as soon as possible

Labs - H/H, coags, BMP, UA (lipase, LFTs if undifferentiated)

Imaging - US (ideal study), CT (extremely accurate), plain films (if no US/CT)

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33
Q

Rx AAA?

A

Crystalloid, blood products

Emergent surgical repair (vascular surgery)

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34
Q

Dispo AAA?

A

Acutely symptomatic - hospital admission and surgical repair

Unstable - emergent surgery

Stable, not cause of symptoms - refer to surgeon for OP work-up

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35
Q

Initial actions and primary survey in suspected mesenteric ischemia?

A 
Consider in all elderly patients with abdominal pain
Large bore IV access
Fluid resuscitation
Telemetry monitoring
EKG (AFib?)
Surgical consultation early
Address ABCs
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36
Q

Classic presentation of mesenteric ischemia?

A

> 50 y/o
Sudden onset abdominal pain +/- N/V/diarrhea

Pain will initially be severe and diffuse without localization, out of proportion to exam (screaming in pain, benign exam), eventual abdominal distention with guarding, rebound, absence of bowel sounds, bloody diarrhea (late finding)

37
Q

4 different etiologies of mesenteric ischemia?

A

Mesentery artery embolus
Mesentery artery thrombosis
Mesenteric vein thrombosis
Non-occlusive ischemia

38
Q

Most common cause of mesenteric ischemia?

A

Mesenteric artery embolus (50% of cases)

39
Q

Presentation of mesenteric ischemia 2/2 embolus?

A

Classic abdominal pain out of proportion to exam

Risk factors - arrhythmias (AFib), post-MI with mural thrombi, valvular heart disease, structural heart defects (R->L shunts)

40
Q

Most common location of an embolus?

A

SMA due to the oblique angle of the SMA from the aorta

Usually lodges distal to the origin of the middle colic artery, sparing the duodenum and proximal jejunum (vs. thrombosis, which causes a more proximal blockage -> extensive ischemia)

41
Q

Presentation of mesenteric ischemia 2/2 mesenteric artery thrombosis?

A

Patients with systemic atherosclerosis and old age

History of vague and insidious symptoms such as weight loss, abdominal angina (after meals), diarrhea, and fear of food -> chronic mesenteric ischemia, often confused with PUD

Slow progression of atherosclerosis until a certain level of blockage is obtained

42
Q

Vasculature most likely to be involved in mesenteric artery thrombosis?

A

Celiac trunk, SMA

43
Q

Least common cause of mesenteric ischemia?

A

Mesenteric vein thrombosis (10% of cases)

44
Q

Presentation of mesenteric vein thrombosis?

A 
Can occur acutely or over time
Patients may be relatively younger
Risk factors include hypercoagulable states, recent surgery, malignancy, cirrhosis, hx of DVT
May have vomiting, diarrhea
No postprandial pain or food fear
45
Q

Most commonly involved vein in mesenteric vein thrombosis?

A

Superior mesenteric vein

46
Q

Risk factors for mesenteric ischemia 2/2 non-occlusive ischemia?

A

Any condition associated with decreased CO -> cardiogenic shock, CHF, arrhythmias

Hospitalized sick patients

Sepsis, hypotensive states, drugs inducing mesenteric vasoconstriction -> digoxin, cocaine, alpha-agonists, beta-blockers

47
Q

Labs to diagnose mesenteric ischemia?

A

WBC (commonly elevated)
Hemoconcentration
Elevated amylase
Metabolic acidosis
Elevated lactate -> sensitive late in the disease course
D-Dimer -> sensitive (higher than lactate)

48
Q

Imaging to diagnose mesenteric ischemia?

A

Plain films - normal early, subtle signs later (bowel wall thickening, distended bowel loops)

Angiography (gold standard) - lateral view for origins of major vessels, AP views for visualization of distal mesenteric vessels

CTA (93% sensitive, 95% specific) - faster, less invasive, readily available compared to angiography

US, MRA - able to be used, but limitations

49
Q

Initial Rx in mesenteric ischemia?

A

Stabilize and resuscitate:
2 large bore IVs with crystalloid fluids if hypotensive
Continuous vital sign monitoring
Insert triple lumen for CVP monitoring if needed to guide IV fluid Rx
Broad spectrum ABX
D/C meds with vasoconstrictive properties

If thrombosis suspected, anticoagulant like heparin can be started to stop propagation of thrombus

If angiography - papaverine during procedure to increase blood flow to bowel (decrease mesenteric vasoconstriction)

Rx ranges from non-operative management with medications, IV thrombolytics, percutaneous angioplasty, operative revascularization, bowel resection, combo of these

50
Q

Rx of choice for mesenteric artery embolus?

A

Embolectomy + bowel visualization to assess for signs of necrosis

Another option - percutaneous treatment with thrombolytics infused into the artery with the embolus during angiography (no peritoneal signs or non-operative candidates)

51
Q

Rx of choice for mesenteric artery thrombosis?

A

Start heparin as soon as diagnosis is made and prior to surgery

Same operative measures as embolectomy

Non-operative patients - percutaneous transluminal angioplasty

52
Q

Rx of choice for mesenteric vein thrombosis?

A

Operative Rx if signs of infarction

Otherwise, thrombectomy with endarterectomy or distal bypass is first line

Anticoagulation to prevent thrombus reoccurrence, usually life-long

53
Q

Rx non-occlusive mesenteric ischemia?

A

Rx undelrying cause
Papaverine to treat vasoconstriction of vessels to the mesentary

OR if peritoneal signs

54
Q

Dispo in mesenteric ischemia?

A

Admitted, usually to ICU

55
Q

Most common causes of SBO? Other causes?

A

Adhesions, followed by tumors and hernias. Strictures, intussusception, volvulus, Crohn disease, gallstones

56
Q

Most common cause of LBO?

A

Malignancy

57
Q

Describe the pathophysiology of SBO.

A

Begins when the normal luminal flow of intestinal contents is interrupted and the small intestine proximal to the obstruction dilates. Secretions are prevented from passing distally. As time progresses, the distention leads to N/V and an inability to take PO. Bacteria may ferment in the proximal intestine and cause feculent emesis. The bowel wall becomes more edematous and leads to a transudative loss of fluid into the peritoneal cavity, increasing the degree of dehydration and electrolyte abnormalities. Decreased urine output, tachycardia, azotemia, and hypotension can also be seen.

58
Q

Define partial bowel obstruction.

A

Gas or liquid stool can pass through the point of narrowing (v. complete, when no substance can pass)

59
Q

History consistent with SBO?

A

Abdominal pain, distention, vomiting, inability to pass flatus, N/V more prevalent in proximal obstruction

Possible diarrhea earlier during obstruction progressing to inability to pass flatus/obstipation

History of prior abdominal surgery, GI disorders like Crohn

60
Q

Physical exam findings in SBO?

A

Abdominal distension (more prevalent in distal obstructions), hyperactive bowel sounds (early) or hypoactive bowel sounds (late)

Fever, tachycardia, peritoneal signs with strangulation

Inguinal hernia

61
Q

Imaging in SBO?

A

Plain radiographs (upright chest - free air/perforation, upright abdominal - air fluid levels, supine abdominal - distended loops of bowel) - diagnosis made when multiple air fluid levels are seen with distended loops of small bowel, absence of air in colon/rectum (complete) vs. presence (partial)

Small bowel series - diagnosis and degree of obstruction (gold standard for determining partial or complete)

CT - replacing small bowel series as study of choice to differentiate partial vs. complete, and to identify strangulation early, can also differentiate between etiologies of SBO and diagnose other causes of abdominal pain (requires PO and IV contrast)

62
Q

Define obstruction on CT.

A

Small-bowel loops >2.5 cm in diameter dilated proximal to a distinct transition zone of collapsed bowel <1 cm in diameter

Smooth beak - simple obstruction
Serrated beak - strangulation

Bowel wall thickening, pneumatosis, and portal venous gas all suggest strangulation

63
Q

Lab work-up in SBO?

A

Generally not helpful in diagnosing SBO, but helpful in management (degree of dehydration, operative management) - CBC, BMP, T&S, coags

Lactic acid, LFTs, lipase, UA

64
Q

Rx of SBO?

A

Initial management:

  • Resuscitation and electrolyte replacement
  • Identify severity and cause of obstruction
  • GI decompression
  • Symptomatic Rx
  • Decide surgery or not

If acutely ill/peritoneal signs - emergent surgical consult, aggressive resuscitation (2L wide open with standard O2 and monitoring per protocol), PPx ABX if surgery acutely needed.

If stable, consult surgery to determine if operative management is warranted.

Non-operative: GI decompression with NG tube, IV fluids, bowel rest, symptomatic Rx

Frequent reassessment, IV pain/nausea medication

65
Q

Difference between upper and lower GI bleed?

A

Ligament of Treitz crosses the small intestine at the duodenal-jejunal junction (anatomic dividing line)

66
Q

Initial management of GI bleed?

A

Primary survey (ABCs) - initiate stabilizing care

IV access - minimum of 2 large bore IVs, consider transfusing un-crossmatched blood and IV fluids while type and cross is performed

If severe/uncontrolled, unstable vitals, no ability for emergent endoscopy, consider esophageal tamponade (1 balloon in stomach, 1 balloon in esophagus)

67
Q

Lab evaluation in suspected GI bleed?

A

STAT CBC, BMP, coags, type and cross

68
Q

Primary indication for blood transfusion in GI bleed?

A

Hemorrhagic shock despite IV fluid resuscitation

Subacute bleeding and a Hgb of 7

Symptomatic anemia (dyspnea, lightheadedness, chest pain) at a Hgb of 8 or 9

Massive upper or lower GI bleed (1000 mL maroon-colored thin liquid stools Q20-30 minutes or NG tube with constant output of blood)

Hgb dropping at a rate of 3 g/dL over 2-4 hours in the setting of active bleeding

Hgb <9 in active bleeding

Anemia induced end-organ injury

69
Q

Considerations in a patient with GI bleed who is on anticoagulation or antiplatelet agent?

A

FFP or cryoprecipitate - warfarin, cirrhosis and likely variceal bleeding)

Platelets - ASA or clopidogrel

Consider reason for anticoagulation (risks and benefits)

Newer oral anticoagulations (dabigatran, rivaroxaban, apixaban) are more difficult to reverse

  • Dabigatran can be dialyzed
  • Prhtrombin complex concentrate may be effective with all 3 medications
70
Q

What type of bleed is indicated by the following:

  • Hematemesis
  • Coffee ground emesis
  • Melena
  • Hematochezia
A

Hematemesis/coffee ground emesis - upper GI bleed
Melena (drak/tarry) - 70% upper, 30% lower
Hematochezia - LGIB or UGIB with significant bleeding/increased GI motility

71
Q

How can the source of bleeding be located?

A 
History
NG tube if intractable emesis or if question about upper GI bleed, can be helpful to assess the rate, but is not without risks/vagueness
Bleeding scan (moderate lower GI bleeding, stable patient, especially if recurrent GI bleeding with previously negative colonoscopy and endoscopy)
72
Q

Pharmacologic management of GI bleed?

A

PPIs - first line for acid suppression in upper GI bleed

H2 blockers - second line, used to reduce acid production in outpatient setting as PI; only used in ED when PPIs are contraindicated

Somatostatins (octreotide) - known or highly suspected variceal bleed, causes splanchnic vasoconstriction -> decreased secretion of gastric acid and pepcin

ABX: history of cirrhosis (reduces mortality) - ceftriaxone (first line), ciprofloxacin (second line)

73
Q

How are PPIs administered?

A

Low-risk patient who is likely to be admitted: empiric IV PPI (40 mg IV BID), continue until source identified

More severe/active bleed or with comorbidities that increase risk: IV bolus followed by continuous protonix infusion (80 mg bolus, 8 mg/hr drop)

74
Q

Dispo GI bleed?

A

Mild (mild anemia, no active bleeding beside positive stool guaiac or blood-streaked emesis) - home with prompt follow-up for Hgb monitoring and GI referral as appropriate

Severe/acute - admission to floor or ICU based on vital signs, rate of bleeding, need for transfusion, potential for decompensation, comorbidities, need for procedures/sedation only available in ICU

75
Q

DDx - GI bleed (upper)?

A 
Gastric ulcer
Duodenal ulcer
Gastritis
Esophagitis
Gastroesophageal varices
Mallory-Weiss tear
Aortoenteric fistula
Malignancy
76
Q

DDx - GI bleed (lower)?

A 
Diverticulosis
Meckels diverticulum
Angiodysplasia
Malignancy
Colitis (infection, ischemia, IBD)
Anorectal (hemorrhoids, fissures)
77
Q

DDx - perforated viscus (broad categories)

A
  1. Foreign body perforation
  2. Extrinsic bowel obstruction
  3. Intrinsic bowel obstruction
  4. Loss of GI wall integrity
  5. GI ischemia
  6. Infection
78
Q

DDx - perforated viscus (foreign body perforation)

A

Penetrating trauma
Endoscopy/iatrogenic
Ingestion of foreign bodies

79
Q

DDx - perforated viscus (extrinsic bowel obstruction)

A 
GI stromal tumors
Lymphoma
Surgical adhesions
Hernia
Volvulus
80
Q

DDx - perforated viscus (intrinsic bowel obstruction)

A 
Phytobezoar
Crohn's stricture
Diverticulitis
Appendicitis
Intraluminal neoplasm
81
Q

DDx - perforated viscus (loss of GI wall integrity)

A
  1. Peptic ulcer
  2. Crohn disease
  3. Tumor lysis syndrome
82
Q

DDx - perforated viscus (GI ischemia)

A
  1. Shock/hypotension
  2. Thromboembolic event
  3. Visceral arterial sclerosis
  4. Portal vein thrombosis
83
Q

DDx - perforated viscus (infection)

A
  1. Salmonella typhosa
  2. C. difficile
  3. CMV
84
Q

Initial actions and primary survey in suspected perforated viscus?

A
  1. Cardiac monitoring, continuous pulse ox, large bore IV access
  2. Fluid resuscitation
  3. Focused H&P
  4. Broad spectrum ABX
  5. Rapid surgical consultation
85
Q

Presentation of perforated viscus?

A

Severe sudden onset abdominal pain with rapidly worsening overall condition

May have a history of prior abdominal pain that is less severe due to the underlying cause

SIRS (fever, tachycardia, tachypnea, hypotension, septic shock) due to leakage of air, GI contents, and bacteria toxins into the peritoneal cavity

Ill/toxic

Presentation may be altered in patients with delayed presentation, immunocompromise, or elderly

86
Q

Labs indicated in suspected perforated viscus?

A 
CBC with diff
CMP
Lipase
UA
Urine pregnancy test
Lactic acid
VBG
T&amp;S/T&amp;C
Coags
EKG
87
Q

Imaging in suspected perforated viscus?

A

Plain radiograph - rapid, bedside, ideal for unstable patients, limited as it can miss free air in many patients

CT A/P - best test for free air, limited by longer time and if unstable

US - reliable for intra-abdominal fluid and AAA, free air if experienced operator

88
Q

Rx perforated viscus

A
  1. Resuscitation
  2. Early ABX (common regimens include cipro + metronidazole, Pip/Tazo, or imipenem)
  3. Early surgical consult

Emergency Medicine Clerkship (18 decks)

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