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CCP 217 Gastrointestinal Emergencies Flashcards

1
Q

most common causes of acute pancreatitis

A
  1. gallstones (pancreatic ductal obstruction)

2. chronic alcohol consumption

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2
Q

pathophysiologic pathway of acute pancreatitis

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. initial inciting event (eg biliary obstruction d/t stone)
  2. Cellular injury triggers the inappropriate activation of digestive enzymes → autodigestion of pancreatic tissue → stimulation of an inflammatory cascade
  3. inflammatory cytokines cause increased vascular permeability → edema, hemorrhage, and/or necrosis
  4. SIRS response promotes translocation of intestinal bacteria → sepsis and septic shock
  5. septic shock → further complications including pleural effusion, ARDS, AKI, MODS, death
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3
Q

two different types of pancreatitis

A
  1. interstitial edematous pancreatitis

2. necrotizing pancreatitis

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4
Q

pancreatic enzymes

A
  1. amylase (more sensitive for pancreatic disease)

2. lipase (more specific for pancreatic disease)

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5
Q

mild pancreatitis definition

A
  1. No organ failure

2. No local or systemic complications

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6
Q

moderate pancreatitis definition

A
  1. Transient organ failure (<48 h)

2. Local or systemic complications

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7
Q

severe pancreatitis definition

A
  1. Persistent organ failure (>48 h)
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8
Q

acute pancreatitis definition

A
  1. Acute inflammatory process of the pancreas

2. pancreas is a retroperitoneal organ with endocrine and exocrine function

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9
Q

Cullen’s sign (define + explain)

A
  1. Ecchymosis/discoloration around the umbilicus due to hemoperitoneum
  2. the sign been associated with a broad range of clinical conditions, notably Hemorrhagic pancreatitis and ruptured ectopic pregnancy
  3. LATE SIGN. typically takes 3-5 days for sign to present
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10
Q

Grey Turner’s sign (define + describe)

A
  1. reddish-brown discolouration around the flanks due to retroperitoneal bleeding
  2. Classically, it correlates with severe acute necrotizing pancreatitis, often in association with Cullen’s sign (periumbilical ecchymosis)
  3. may also be present in other conditions that result in intra-abdominal or retroperitoneal hemorrhage
  4. when Grey Turner’s sign is present in the absence of known direct trauma to the flank, for example, a patient presenting with non-traumatic abdominal pain, it appears to be a marker of severe illness with a potentially high mortality rate (30-40%)
  5. LATE SIGN, >24hrs post bleed
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11
Q

acute pancreatitis treatment algorithm

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

“limit the severity of pancreatic inflammation and provide supportive care”

  1. IV fluid resuscitation (plasma-lyte or LR)
  2. correction of electrolyte and metabolic abnormalities
  3. Antiemetics
  4. Analgesia
  5. Vasopressor support for shock
  6. Nutritional support (enteral nutrition or NG feeds)
  7. Antibiotics (infected necrotizing pancreatitis or extrapancreatic infections)
  8. Management of complications (eg. EtOH withdrawal, infection, ARDS, shock)
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12
Q

Biliary causes of RUQ pain

A
  1. Biliary colic
  2. Acute cholecystitis
  3. Acute cholangitis
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13
Q

Hepatic causes of RUQ pain

A
  1. Acute hepatitis
  2. Liver abscess
  3. Portal vein thrombosis
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14
Q

Splenic causes of LUQ pain

A
  1. Splenomegaly
  2. Splenic infarct
  3. Splenic abscess
  4. Splenic rupture
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15
Q

Differentials for lower abdominal pain

A
  1. Appendicitis (RLQ)
  2. Diverticulitis
  3. Pyelonephritis
  4. Acute urinary retention (suprapubic)
  5. Cystitis (suprapubic)
  6. Infectious colitis
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16
Q

spontaneous bacterial peritonitis (SBP) and Abdominal Sepsis Clinical Presentation

A
  1. Fever
  2. Abdominal pain or discomfort
  3. Altered mental status
  4. Diarrhea or Ileus
  5. Ascites
  6. renal failure
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17
Q

define toxic megacolon (toxic colitis)

A
  1. clinical term for an acute toxic colitis with dilatation of the colon
  2. defined as non-obstructive colonic dilatation larger than 6 cm and signs of systemic toxicity (fever, tachycardia, leukocytosis, AMS, shock)
  3. this is a rare complication of severe inflammatory bowel disease that occurs in approximately 1% of patients
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18
Q

most common presenting symptom for toxic megacolon

A
  1. Severe bloody diarrhea
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19
Q

most serious complication of toxic megacolon

A
  1. colonic perforation leading to abdominal sepsis
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20
Q

treatment pathway for toxic megacolon

A

primarily supportive therapy

  1. ICU monitoring
  2. fluid resuscitation
  3. correction of electrolyte and metabolic derangements,
  4. broad-spectrum ABX
  5. steroids
  6. complete bowel rest
  7. surgical consult for colonic perf, necrosis, full-thickness ischemia, intra-abdominal HTN, ACS, peritonitis
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21
Q

classic case physical exam signs of cirrhosis

🔥🔥🔥MEGA PEARL🔥🔥🔥

A
  1. gynecomastia
  2. spider angiomata
  3. muscle wasting
  4. ascites
  5. palmar erythema
  6. Jaundice
  7. peripheral edema
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22
Q

clinical progression of alcoholic-related liver disease

A
  1. Steatosis (alcohol-associated fatty liver)
  2. Fibrosis
  3. Cirrhosis
  4. Hepatocellular carcinoma (HCC)
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23
Q

define Cirrhosis

A
  1. end-stage chronic liver disease
  2. characterized by the destruction of hepatocytes and replacement of normal hepatic architecture with fibrotic tissue and regenerative nodules
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24
Q

liver enzymes

A
  1. alanine aminotransferase [ALT]
  2. aspartate aminotransferase [AST]
  3. alkaline phosphatase [ALP]
  4. gamma-glutamyl transpeptidase [GGT]
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25
Q

liver function tests

MUST KNOW + EXPLAIN PATHO

A
  1. serum albumin
  2. prothrombin time
  3. INR
  4. serum bilirubin level
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26
Q

classic case presentation for severe acute pancreatitis

A
  1. Severe epigastric pain that radiates to the back

2. nausea/vomiting

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27
Q

diagnosis of acute pancreatitis requires 2 out of 3 of these criteria

A

“Atlanta criteria”

  1. “Classic” mid-epigastric abdominal pain
  2. Serum lipase or amylase >3x normal
  3. Confirmatory imaging findings (CT, MRI, or US)
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28
Q

pathophysiology of pancreatitis secondary to pancreatic gallstone

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. gallstones cause pancreatic ductal obstruction
  2. obstruction increases intra-pancreatic duct pressure → acid reflux into the pancreas → trypsin activation → autodigestion of pancreatic tissue
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29
Q

pathophysiology of pancreatitis secondary to alcohol

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. ethyl alcohol sensitizes pancreatic cells to cholecystokinin → increased trypsin production
  2. trypsin activation → autodigestion of pancreatic tissue
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30
Q

cholangitis definition

A

inflammation of the bile duct system

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31
Q

choledocholithiasis definition

A

presence of gallstones within the common bile duct

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32
Q

Cholelithiasis definition

A

The presence of stones in the gallbladder

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33
Q

Amylase vs Lipase sensitivity and specificity for acute pancreatitis

^ must know

A

Lipase has higher sensitivity and specificity

  1. Lipase at 3 times the upper limit of normal is 100% sensitive and 99% specific for acute pancreatitis
  2. Amylase may be elevated in acute pancreatitis but is less sensitive (81%) and specific than lipase. Amylase may also be falsely negative
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34
Q

Cholecystectomy definition

A

surgical removal of the gallbladder

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35
Q

define acute liver failure (aka fulminant hepatic failure, acute hepatic necrosis, fulminant hepatic necrosis, or fulminant hepatitis)

A
  1. Severe acute liver injury with encephalopathy and impaired clotting function (INR ≥1.5) in a patient without underlying cirrhosis or prior liver disease
  2. diagnosed when there is evidence of acute hepatitis with coagulation abnormality (INR ≥1.5) and any degree of encephalopathy in a patient without pre-existing cirrhosis and an illness course <26 weeks in duration
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36
Q

off label use for N-acetylcysteine

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. may be beneficial in any patient with early, non-acetaminophen-related acute liver failure
  2. prospective, double-blind trial of patients with acute liver failure not due to acetaminophen toxicity demonstrated improved transplant-free survival in patients with acute liver failure treated with IV N-acetylcysteine
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37
Q

acute liver failure treatment pathway

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. IV fluid resuscitation
  2. correction of electrolyte and metabolic abnormalities (hypoglycaemia)
  3. Vasopressor support for shock (norepinephrine)
  4. Corticosteroids for refractory shock (hydrocortisone)
  5. Consider administration of N-acetylcysteine
  6. Management of complications (eg. elevated ICP secondary to hepatic encephalopathy, GIB secondary to hepatic coagulopathy)
  7. broad-spectrum ABX for signs of infection
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38
Q

most common causes of acute liver failure in adults

A
  1. acetaminophen overdose (40%)
  2. indeterminate (17%)
  3. idiosyncratic drug reactions (13%)
  4. hepatitis B virus (6%)
  5. ischemic hepatitis (6%)
  6. hepatitis A virus (4%)
  7. autoimmune hepatitis (4%)
  8. Wilson disease (3%)
  9. Budd–Chiari syndrome (2%)
  10. pregnancy (2%)
  11. malignancy (1%)
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39
Q

hepatic encephalopathy grading correlated to asterixis

A
  1. Grade I: mild asterixis
  2. Grade II/III: pronounced asterixis
  3. Grade IV: asterixis is often absent (may exhibit posturing)
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40
Q

asterixis definition

A
  1. sudden loss of muscle tone during sustained contraction of an outstretched limb
  2. associated with a silent period on EMG
  3. referred to as ‘negative myoclonus’
  4. irregular flexion–extension movements at the metacarpophalangeal and wrist joints, which increase during a sustained posture
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41
Q

expected lab abnormalities in the patient with acute liver failure

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Elevated AST/ALT/ALP/GGT/bilirubin
  2. Anemia
  3. Elevated serum creatinine and BUN
  4. Elevated amylase/lipase
  5. Hypoglycemia
  6. Hypophosphatemia
  7. Hypomagnesemia
  8. Hypokalemia
  9. Acidemia or alkalemia
  10. Elevated ammonia
  11. Elevated lactate dehydrogenase (LDH)
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42
Q

cirrhosis definition

A
  1. late stage of progressive hepatic fibrosis
  2. characterized by distortion of the hepatic architecture and the formation of regenerative nodules
  3. irreversible in advanced stages
  4. only treatment option is liver transplantation
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43
Q

most common causes of cirrhosis

A
  1. Alcohol (60-70%)
  2. Chronic viral hepatitis (B or C, 10%)
  3. Non-alcoholic liver disease (10%)
  4. Biliary obstruction (5-10%)
  5. Hemochromatosis (5-10%)
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44
Q

Cirrhosis pathophysiology

A
  1. fibrosis of hepatic tissue → elevated Portal pressures due to decreased hepatic venous drainage
  2. decreased hepatic venous drainage → splenomegaly and splanchnic vasodilation
  3. splenomegaly → anemia, hypoalbuminemia, thrombocytopenia, and ascites
  4. splanchnic vasodilation → increased splanchnic blood flow, further elevated portal pressures
  5. feedback loop ensues → decreased blood volume and hypotension/shock/death
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45
Q

major complications of cirrhosis

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. variceal hemorrhage
  2. ascites
  3. bacterial peritonitis
  4. hepatic encephalopathy
  5. hepatorenal syndrome
  6. hepatopulmonary syndrome
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46
Q

leading causes of mortality in patients with cirrhosis

A
  1. Urinary tract infections
  2. bacterial peritonitis
  3. C. difficile colitis
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47
Q

signs of chronic liver disease

A
  1. caput medusae (network of painless, swollen veins around your bellybutton)
  2. ascites
  3. fetor hepaticus
  4. gynecomastia
  5. hepatomegaly
  6. splenomegaly
  7. jaundice/scleral icterus
  8. muscular atrophy
  9. palmar erythema
  10. testicular atrophy
  11. spider angiomas
  12. nail changes (splinter haemorrhages)
  13. parotid gland enlargement
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48
Q

biliary tree anatomical/physiological pathway

A
  1. biliary tree is a series of GI ducts allowing newly formed bile from the liver to be concentrated and stored in the gallbladder prior to release into the duodenum
  2. Bile is secreted from hepatocytes and drains from both lobes of the liver via intralobular ducts and collecting ducts into the left and right hepatic ducts
  3. left and right hepatic ducts join to form the common hepatic duct, which runs alongside the hepatic vein
  4. common hepatic duct descends and is joined by the cystic duct which regulates bile flow in and out of the gallbladder for storage and release
  5. the common hepatic duct and cystic duct combine to form the common bile duct
  6. common bile duct descends and passes posteriorly to the duodenum and head of pancreas
  7. common bile duct now joined by main pancreatic duct, forming the hepatopancreatic ampulla (ampulla of Vater) – which then empties into the duodenum via the major duodenal papilla
  8. major duodenal papilla is regulated by a muscular valve, the sphincter of Oddi
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49
Q

Charcot’s cholangitis triad

A

clinical finding in ascending cholangitis (an infection of the bile duct in the liver)

  1. jaundice
  2. fever (usually with rigors)
  3. right upper quadrant abdominal pain
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50
Q

Murphy’s sign

A

acute cholescystitis

  1. ask the patient to take in and hold a deep breath while palpating the right subcostal area
  2. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive
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51
Q

Acute cholangitis treatment pathway

A
  1. patient NPO
  2. administer IV fluids
  3. analgesics
  4. Empiric IV antibiotics
  5. GI consult
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52
Q

Acute cholecystitis treatment pathway

A
  1. patient NPO
  2. administer IV fluids
  3. analgesics
  4. Empiric IV antibiotics
  5. Surgical consult
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53
Q

Biliary colic pathophysiologic pathway

A

impacted stone or sludge in the cystic duct or the ampulla of Vater → distension and contraction of the gallbladder or biliary tract → an intermittent increase in pressure and pain

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54
Q

Gallstone formation (Cholesterol stones) pathophysiologic pathway

A

The most common type of stone in Western society (80%-90%)

  1. imbalance in biliary cholesterol homeostasis → cholesterol crystallization
  2. Formation is promoted by hepatic hypersecretion, gallbladder hypomotility, and genetic predisposition
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55
Q

Gallstone formation (pigment stones) pathophysiologic pathway

A
  1. Abnormal bilirubin metabolism with excess unconjugated bilirubin
  2. Includes black (uninfected) and brown (infected) stones
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56
Q

Acute cholangitis pathophysiologic pathway

A
  1. biliary tree is normally a sterile environment due to the continuous flow of bile and the immunologic response of the biliary epithelial cells
  2. when an obstruction leads to increased bile duct pressure and the breakdown of these defenses pathology occurs
  3. Bacteria enter the biliary system primarily by ascending from the duodenum into the extrahepatic ducts
  4. The portal venous system and the periportal lymphatic system are also potential routes of entry
  5. E. coli, Klebsiella, and Enterococcus are the most common bugs in patients with acute cholangitis
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57
Q

Acute diverticulitis definition

A

inflammation of colonic diverticula

58
Q

three main types of abdominal pain

A
  1. visceral
  2. parietal
  3. referred
59
Q

visceral pain definition

A
  1. the nerves that run through the walls of an organ get stretched
  2. poorly localized, feels like a dull ache or cramp
  3. comes directly from the organ involved
  4. pain may be dull, hard to locate precisely, and may be either constant or intermittent
60
Q

parietal pain (somatic pain) definition

A
  1. pain caused by irritation of fibres that innervate the parietal peritoneum
  2. sharp, can be localized by pointing to a specific spot
61
Q

Referred abdominal pain definition

A
  1. occurs when the brain is unable to localize the source of discomfort due to nociceptive dorsal horn neurons receiving convergent inputs from different tissues
62
Q

peritoneum definition and anatomy

A
  1. serous membrane that forms the lining of the abdominal cavity
  2. covers most of the intra-abdominal organs
  3. provides support and protection for the abdominal organs
  4. acts as the main conduit for the lymph vessels, nerves, and abdominal arteries and veins
  5. there are two layers of peritoneum; with potential space between those layers
  6. parietal peritoneum (outer layer) is attached to the abdominal wall
  7. visceral peritoneum (inner layer) is wrapped around the intraperitoneal organs
  8. potential space between the two layers is the peritoneal cavity (contains serous fluid)
63
Q

Intraperitoneal Structures

A
  1. stomach
  2. liver
  3. spleen
  4. appendix
  5. transverse colon, sigmoid colon, upper third of the rectum
  6. the first 5cm and the fourth part of the the duodenum
  7. the jejunum, the ileum, the cecum
  8. tail of the pancreas
  9. uterus, fallopian tubes, ovaries, gonadal blood vessels (female)
64
Q

Retroperitoneal Structures

A
  1. main body of duodenum
  2. ascending colon, descending colon
  3. middle third of the rectum
  4. remainder of pancreas (body/neck/head)
  5. kidneys + adrenal glands
  6. proximal ureters, renal vessels
65
Q

Infraperitoneal structures

A
  1. lower 1/3 of rectum

2. urinary bladder

66
Q

Hepatic encephalopathy (HE) definition

A

a reversible syndrome of impaired brain function occurring in patients with advanced liver failure

67
Q

Hepatic encephalopathy (HE) pathophysiology

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. cirrhosis → worsening hepatocyte dysfunction → increase serum NH₃ levels
  2. cirrhosis → systemic inflammation, bacterial translocation, and release of vasoactive mediators → increased BBB permeability
  3. serum NH₃ crosses the BBB → cerebral edema, altered brain glucose metabolism, astrocyte swelling, and neurotransmitter receptor dysfunction (GABA)
  4. Hepatic encephalopathy ensues
68
Q

primary causes of UGIB

A
  1. Esophagogastric varices (alcohol abuse, cirrhosis, ascites, prior UGIB)
  2. Peptic ulcer disease (NSAID use, H pylori infection)
  3. Vascular anomalies (AVM history)
  4. Mallory-Weiss tear (forceful vomiting)
  5. Aortoenteric fistula (history of aortic procedure)
  6. Malignancy
69
Q

primary causes of LGIB

A
  1. Diverticular disease
  2. Colitis
  3. Polyps
  4. Malignancy
  5. UGIB (Hematochezia can be a sign of severe UGIB)
  6. Hemorrhoids
70
Q

esophageal varices pathophysiology pathway

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. cirrhosis → increased intrahepatic flow resistance → portal HTN
  2. portal HTN → the development of a pressure gradient between portal vein and IVC
  3. high portal system pressure → development of venous collaterals to the systemic veins in the esophageal plexus
  4. varicosities form
71
Q

Mallory-Weiss tear definition

A
  1. UGIB secondary to a mucosal tear at the gastroesophageal junction
  2. typically secondary to repeated vomiting episodes
72
Q

primary mechanisms behind acute mesenteric ischemia

A
  1. thrombosis or embolism of the superior mesenteric artery
  2. mesenteric venous thrombosis
  3. non-occlusive mesenteric ischemia due to a low flow state
73
Q

describe the coagulopathy seen in liver failure

A
  1. The liver synthesizes both clotting factors and endogenous anticoagulant factors such as protein C and antithrombin
  2. Both are equally underproduced in cirrhotic patients. 3. This phenomenon leads to “rebalanced hemostasis”
  3. cirrhotic patients may have a close-to-normal clotting tendency, but abnormal routine coagulation studies
  4. INR is not an accurate reflection of hemostasis in cirrhotic patients
74
Q

massive UGIB treatment pathway

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. IV/O2/Monitor
  2. Volume resuscitation (blood products preferred)
  3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets)
  4. promote gastric emptying (NG tube, metoclopramide)
  5. secure airway
  6. control bleeding (Blakemore/Minnesota/Linton tube, octreotide, vasopressin)
  7. prevent further complications (prophylactic ABX, PPI therapy)
  8. STAT GI consult
75
Q

pathophysiologic pathway of acute Mesenteric Ischemia

A
  1. Mesenteric ischemia is classified as arterial vs venous and occlusive vs non-occlusive
  2. Arterial mesenteric ischemia includes SMA embolism, SMA thrombosis, and non-occlusive mesenteric ischemia
  3. Venous mesenteric ischemia is d/t mesenteric vein thrombosis
  4. The abdominal aorta has three branches: the celiac artery, SMA, and IMA
  5. The celiac artery is short and wide, has extensive collateral circulation. rarely involved in acute mesenteric ischemia.
  6. The SMA branches off the aorta at a 45° angle and tapers, making a “funnel” for emboli. SMA is the most common culprit vessel in acute mesenteric ischemia
  7. In acute mesenteric ischemia, ischemia starts at the mucosa and extends toward the serosa
76
Q

Superior mesenteric artery thrombosis pathophysiology

A
  1. SMA thrombosis can be considered the “acute coronary syndrome of the gut” (similar pathophysiology)
  2. plaque deposition at the origin of the SMA causes flow-limiting stenosis and pain after eating (“intestinal angina”)
  3. The acute event occurs similarly to MI, with plaque rupture and platelet aggregation
77
Q

classic clinical triad of acute mesenteric ischemia

A
  1. Abdominal pain described as “out of proportion” to exam (patient reports severe pain without peritonitis on exam)
  2. Underlying cardiac disease
  3. “Gut emptying” (N/V/D)
78
Q

abdominal aortic aneurysm definition

A
  1. The normal abdominal aorta (infrarenal) measures 2.0 cm in diameter
  2. AAA is defined as a focal dilation of the abdominal aorta to at least 50% larger than its expected normal diameter
  3. An abdominal aorta measuring >3.0 cm is considered aneurysmal
  4. AAA is a true aneurysm, meaning that the localized dilation involves all three layers of the arterial wall (intima, media, and adventitia)
79
Q

The classic clinical triad of ruptured AAA

A
  1. abdominal pain
  2. hypotension
  3. pulsatile mass in abdomen
80
Q

ruptured AAA treatment pathway

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A
  1. IV/O2/Monitor
  2. Volume resuscitation (target SBP 70-90 mmHg with intact mental status, blood products preferred)
  3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets)
  4. Analgesia
  5. Arterial Line
  6. STAT vascular surgery consult
81
Q

pathophysiology of ruptured AAA (“contained rupture”)

A
  1. loss of elastin and collagen leads to destruction of the aortic media and lamina, allowing for rupture
  2. Aorta ruptures into retroperitoneal space, creates a tamponade effect at the rupture site
  3. Often presents as back pain
  4. Because rupture is contained, it allows the patient’s blood pressure to stabilize temporarily
82
Q

pathophysiology of ruptured AAA (“free rupture”)

A
  1. loss of elastin and collagen leads to destruction of the aortic media and lamina, allowing for rupture
  2. Aorta ruptures into the peritoneum, leading to rapid exsanguination/shock/death
83
Q

nomenclature for classification of bowel obstruction

A
  1. Location (Small bowel vs Large bowel obstruction)
  2. Etiology (mechanical vs functional obstruction)
  3. Severity (complete vs partial)
84
Q

define bowel obstruction

A
  1. the failure to pass intraluminal intestinal contents through the small or large bowel
  2. This obstruction can be mechanical or functional
85
Q

most common causes of large bowel obstruction

A
  1. cancer (60%)
  2. diverticulitis (20%)
  3. stricture
  4. fecal impaction
  5. volvulus (5%)
86
Q

most common causes of Functional bowel obstruction

A
  1. post-operative state
  2. medications
  3. electrolyte abnormalities
87
Q

most common causes of small bowel obstruction

A
  1. Adhesions from a prior abdominal or pelvic surgery (>80% of cases)
  2. hernias (common)
  3. foreign bodies
  4. malignancy (common)
  5. post-radiation strictures or edema
  6. congenital malformations
  7. volvulus
  8. infection
88
Q

volvulus definition

A
  1. Volvulus is a twisting of bowel loops
  2. Volvulus occurs when a part of the colon twists on the mesentery and results in obstruction
  3. Cecal volvulus is due to a mobile segment of the cecum
  4. sigmoid volvulus occurs with redundant sigmoid colon attached to narrow mesentery
89
Q

mechanical bowel obstruction definition

A
  1. Due to a lesion or object that occludes the bowel lumen

2. This can be a result of extraluminal or intraluminal disorders (eg, adhesion, stricture, or mass)

90
Q

functional bowel obstruction definition

A
  1. Due to a lack of propulsive motor activity (eg, post-operative ileus, electrolyte disturbances [hypokalemia]).
91
Q

bowel obstruction pathophysiology

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A
  1. The bowel consists of the small and large intestine
  2. Obstruction causes the failure to pass intraluminal intestinal contents through the small or large bowel
  3. Accumulation of intestinal material proximal to the site of obstruction → bowel dilation
  4. Bowel dilation → increased peristalsis and loose bowel movements early in the disease course as contents distal to the obstruction are evacuated
  5. Further Bowel dilation → Increased intraluminal pressure causing bowel wall edema and distension, nausea, and vomiting
  6. Bowel wall edema → reduced intestinal absorption of intraluminal contents and decreases venous and arterial flow
  7. Bacterial overgrowth d/t stasis → further dilation and increased gas production proximal to the site of obstruction
  8. Bacteria translocate into the bloodstream d/t increased bowel wall permeability
  9. Fluid loss from transudative fluid secretion into the bowel lumen and vomiting → dehydration, metabolic alkalosis, and electrolyte abnormalities
92
Q

define “closed-loop” bowel obstruction

A
  1. occurs when there are multiple sites of obstruction
  2. considered more dangerous than bowel obstruction with a single transition point
  3. Intraluminal pressure in the closed loop increases rapidly → rapid reductions in venous and arterial blood flow → Bowel infarction and necrosis
93
Q

define bowel “Strangulation”

A
  1. Bowel Strangulation occurs with ischemia or twisting of the bowel or mesentery
  2. Bowel infarction and necrosis d/t poor blood flow → perforation, peritonitis, and sepsis.
94
Q

classic CXR finding for perforated bowel

A

free air under the diaphragm

95
Q

Inflammatory bowel disease definition

A
  1. idiopathic immune-mediated intestinal and extraintestinal disease process
  2. caused by a disruption of the natural barriers and protective mechanisms of the gastrointestinal (GI) tract
  3. Two primary inflammatory bowel disease conditions are Crohn’s disease and ulcerative colitis
96
Q

describe Moderate to severe inflammatory bowel disease flare

A
  1. More than 6 bowel movements/day
  2. Moderate to severe rectal bleeding
  3. High local and systemic inflammatory burden
  4. evidence of stricture, deep ulceration, abscesses, obstruction, or perforation
  5. Signs of other significant organ dysfunction
97
Q

pathophysiology of Inflammatory bowel disease

A
  1. mediated by an inappropriate inflammatory response in bowel
  2. Intestinal epithelial cells have ↑ cell permeability → increased invasion by bacteria + cellular destruction
  3. invading bacteria → cellular stress responses from the endoplasmic reticulum d/t ↑ release of inflammatory mediators → GI inflammation
  4. Intestinal epithelial cells have ↓ mucus-production → reduced protective barrier against chemical stress
98
Q

The classic clinical triad (Murphy’s triad) for acute appendicitis

A
  1. RLQ pain
  2. fever
  3. nausea/vomiting/anorexia
99
Q

Complicated appendicitis definition

A
  1. appendicitis with perforation or peritonitis
100
Q

simple/uncomplicated appendicitis definition

A
  1. Nonperforated appendicitis
101
Q

McBurney’s point definition

A
  1. McBurney’s point lies 2/3 of the distance laterally on a line drawn from the umbilicus to the right anterior superior iliac
  2. corresponds to the location of the base of the appendix
102
Q

Rovsing sign definition

A
  1. RLQ pain elicited by palpation of the LLQ in acute appendicitis
  2. If this occurs, it is said to be a positive Rovsing sign.
103
Q

Appendicitis pathophysiology

A
  1. traditionally been thought to result from obstruction of the appendix
  2. Obstruction → increased intraluminal and intramural pressure (due to distention of the appendiceal lumen)
  3. The increase in intraluminal and intramural pressure → inflammation and engorgement of the appendix
  4. Lymphatic stasis and thrombosis + occlusion of the small blood vessels in the wall of the appendix → ischemia and eventual necrosis
  5. Inflammation and necrosis increase the risk of perforation, which can → localized abscess or diffuse peritonitis
  6. Bacterial overgrowth early in the disease process is usually aerobic, while a polymicrobial infection typically occurs later in the disease course
104
Q

define abdominal compartment syndrome (ACS)

A
  1. describes the clinical manifestations of the pathologic elevation of the intra-abdominal pressure (IAP)
105
Q

intra-abdominal HTN vs ACS

A
  1. When the IAP exceeds 12 mm Hg it is referred to as intra-abdominal hypertension (IAH)
  2. When the IAP exceeds 20 mm Hg it is referred to as abdominal compartment syndrome (ACS)
106
Q

effects of abdominal compartment syndrome on the CVS

A

ACS → IVC compression → decreased cardiac preload → decreased CO → tachycardia + elevated afterload → increased MVO2 and decreased coronary perfusion → myocardial dysfunction → cardiogenic shock → death

107
Q

effects of abdominal compartment syndrome on the renal system

A

ACS → increased renal venous pressure → decreased renal perfusion pressure → decreased GFR → decreased urine secretion and decreased buffering capacity → oliguria + metabolic acidosis → renal failure → MODS → death

108
Q

effects of abdominal compartment syndrome on the GI system

A

ACS → decreased abdominal perfusion pressure → gut ischemia → gut barrier failure → bacterial translocation → intra-abdominal sepsis → distributive shock → MODS → death

109
Q

effects of abdominal compartment syndrome on the respiratory system

A
  1. ACS → IAP transmitted across the diaphragm → elevated intra-thoracic pressure, compressive atelectasis, increased alveolar dead space, reduced FRC, VQ mismatch and hypoxic bronchial artery vasoconstriction → increased WOB + accessory muscle use → respiratory fatigue
  2. In MV decreased lung and chest wall compliances result in elevated PIP + PPlat
  3. increased intra-thoracic pressure increases PVR and leads to RV failure
110
Q

effects of abdominal compartment syndrome on the brain/CNS

A
  1. ACS → IAP transmitted across the diaphragm → elevated intra-thoracic pressure → decreased cerebral venous outflow → elevated intracranial pressure (ICP) → decreased cerebral perfusion pressure → cerebral hypoxia → encephalopathy
  2. Neuro ICU patients with elevated ICP should have their IAP monitored closely
111
Q

Intra-abdominal pressure (IAP) definition

A
  1. the steady state pressure concealed within the abdominal cavity
112
Q

Intra-abdominal Hypertension (IAH) definition

A
  1. sustained intra-abdominal pressure (IAP) of > 12mmHg
113
Q

Abdominal Compartment Syndrome (ACS) definition

A
  1. sustained IAP > 20mmHg with new organ failure
114
Q

Abdominal Perfusion Pressure definition

A
  1. (APP) = MAP – IAP
115
Q

Abdominal compliance definition

A
  1. a measure of the ease of abdominal expansion, which is determined by the elasticity of the abdominal wall and diaphragm. It should be expressed as the change in intra-abdominal volume per change in IAP
116
Q

goals in correcting ACS

A
  1. Improve Abdominal Wall Compliance
  2. Evacuate Intra-Luminal Contents
  3. Evacuate Abdominal Fluid Collections
  4. Correct Positive Fluid Balance
  5. Organ Support
117
Q

CCP Interventions to correct abdominal compartment syndrome

A
  1. sedation + analgesia (↑ Abdominal Wall Compliance)
  2. HOB elevation at 30 degrees (↑ Abdominal Wall Compliance)
  3. neuromuscular blockade (↑ Abdominal Wall Compliance)
  4. nasogastric decompression (Evacuate Intra-Luminal Contents)
  5. avoid excessive fluid (↓ Positive Fluid Balance)
  6. diuretics (↓ Positive Fluid Balance)
  7. maintain an APP > 60mmHg with vasopressors (organ support) APP = MAP - IAP
  8. optimise ventilation strategies (organ support)
118
Q

define Budd-Chiari syndrome

A
  1. congestive hepatopathy caused by blockage of hepatic veins
  2. Two of the hepatic veins must be blocked for clinically evident disease
  3. Liver congestion and hypoxic damage of hepatocytes eventually result in predominantly centrilobular fibrosis
  4. The obstruction may be thrombotic or non-thrombotic anywhere along the venous course from the hepatic venules to junction of the inferior vena cava (IVC) to the right atrium
119
Q

transfusion blood pressure goals in massive GI bleed

A
  1. NOT a goal of “normal” blood pressure.
  2. target a MAP of 65 (although there is nothing wrong with aiming for a blood pressure of 85-90 mmHg systolic)
  3. Do not over resuscitate these patients. This will increase the potential of bleeding. Giving unnecessary blood products can make things worse.
  4. If the patient is a cirrhotic, they live at a lower blood pressure at baseline
120
Q

Volume Resuscitation approach in massive GIB

A

Think of these patients like a bleeding trauma patient (specifically, a bleeding pelvis)

  1. Do not over resuscitate these patients
  2. If you give crystalloid, just give a small amount.
  3. Variceal bleeding is similar to pelvic trauma in that they will need a lot of blood.
  4. If you have a bleed that requires 1-2 units of blood, transfuse PRBC’s with a transfusion target of Hgb of 70. If you need to give the patient 3-4 units of blood in an hour, you should probably initiate MTP with a 1:1:1 ratio
  5. TXA. This is tough. The literature is fairly compelling supporting TXA in a trauma patient who receives blood. GI bleeds are a different situation. The studies available for TXA with GI bleed have been unimpressive. Consider giving it, but it is not a high priority.
121
Q

Indications for blood transfusion in the stable GIB patient (non-cirrhotic)

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A
  1. Hemoglobin <70 g/L
  2. Hemoglobin <90 g/L with ACTIVE acute coronary syndrome (ACS)
  3. Normal hemoglobin with ACTIVE bleeding and hypotension

If giving more than 4 units of blood in the stable patient Transfuse 1 unit FFP

Transfuse for platelets below 50,000/μL [50 x109/L]

122
Q

INR >2 in cirrhotics with GIB

A
  1. Vitamin K 5-10 mg IV

2. Cryoprecipitate 10 bags (approximately 10-15 mL each) OR 1 unit per 10 kg of body weight

123
Q

typical predisposing factors for UGIB secondary to esophageal varices

A

Often a history of alcohol abuse, cirrhosis, ascites, prior UGIB

124
Q

typical predisposing factors for UGIB secondary to Peptic ulcer disease

A

Nonsteroidal anti-inflammatory drug (NSAID) use, Helicobacter pylori infection

125
Q

typical predisposing factors for UGIB secondary to Mallory-Weiss tear

A

forceful vomiting → Longitudinal tear of the esophageal mucosa

126
Q

typical predisposing factors for UGIB secondary to Aortoenteric fistula

A

history of aortic procedure, Massive bleeding

127
Q

typical predisposing factors for UGIB secondary to Vascular anomalies

A 
Arteriovenous malformation (AVM) by history
Angiodysplasia
128
Q

typical causes of Lower GI bleeding

A 
Diverticular disease (Elderly)
Colitis
Polyps
Malignancy
Brisk UGIB
Hemorrhoids
129
Q

Pathophysiology of upper GI bleeding

A
  1. Gastric, duodenal, esophageal, and stomal ulcers are the most common causes of UGIB (d/t ASA, NSAIDs, steroid use, H. pylori infection, and smoking)
  2. Gastric erosion and esophagitis are also common causes of UGIB (alcohol use, NSAIDs/ASA use, stress from severe illness such as sepsis and trauma)
  3. Esophageal and gastric varices result from portal HTN d/t liver cirrhosis
  4. Mallory-Weiss bleeding occurs secondary to a mucosal tear at the gastroesophageal junction, usually secondary to repeated vomiting episodes
130
Q

Hematochezia definition

A

(bright red blood per rectum or maroon-colored rectal bleeding)

131
Q

Pathophysiology of lower GI bleeding

A
  1. LGIB can be classified according to pathophysiologic causes: inflammatory, vascular, oncologic, traumatic, or iatrogenic.
  2. Diverticulosis represents approximately 30% of LGIB
  3. Diverticular bleeding is usually painless and results from a penetrating artery erosion.
  4. AVM and angiodysplasia are the next most common causes of LGIB, followed by ischemic colitis and mesenteric ischemia
  5. Other less common causes of LGIB include colonic polyps, malignancy, anticoagulation side effects, radiation side effects, and inflammatory bowel diseases.
132
Q

Mesenteric ischemia common aetiologies

A
  1. thrombosis or embolism of the superior mesenteric artery
  2. mesenteric venous thrombosis
  3. and non-occlusive mesenteric ischemia due to a low flow state.
133
Q

discuss hemostatic evaluation in liver disease

A
  1. In liver disease, the pathophysiology of hemostasis is complex and difficult to assess accurately with the available routine laboratory tests
  2. The liver synthesizes both clotting factors and endogenous anticoagulant factors such as protein C and antithrombin. Both are equally underproduced in cirrhotic patients. This phenomenon leads to “rebalanced hemostasis,” which causes cirrhotic patients to have a close-to-normal clotting tendency but abnormal routine coagulation studies
134
Q

Blood Products Transfusion in Upper GI Bleed (Therapeutic Special Considerations)

A
  1. In most cases, the hemoglobin target is >70 g/L
  2. Actively bleeding patients with thrombocytopenia (<50,000/μL) should receive a platelet transfusion
  3. Non-cirrhotic coagulopathic patients with a prolonged PT and INR >2.0 should receive FFP transfusion (The management of coagulopathy due to cirrhosis is more complicated because the INR is not an accurate reflection of hemostasis in cirrhotic patients)
135
Q

Medications in Upper GI Bleed (Therapeutic Special Considerations)

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A
  1. Proton Pump Inhibitor. The evidence supporting the benefit of PPIs in UGBI is limited. Current guidelines recommend an initial bolus of 80 mg, followed by a continuous infusion at 8 mg/h for 72 h
  2. Prokinetics. Prokinetic agents such as erythromycin and metoclopramide improve gastric visualization at the time of endoscopy
  3. TXA might be useful for cases in which MTP is req’d, in the treatment of patients with complex coagulopathic profiles (DOAC’s), or in patients with evidence of hyperfibrinolysis (cirrhotic’s w/ low fibrinogen levels). The loading dose is 1 g IV followed by continuous infusion of 3g over 24 h.
    4.
136
Q

Medications in Upper GI Bleed (Special Therapeutic Considerations for CIRRHOTICS)

A
  1. Cirrhotic patients are prone to immunocompromise with a tendency toward developing infections secondary to the translocation of intestinal bacteria into the bloodstream.

A meta-analysis concluded that antibiotic prophylaxis for cirrhotics with UGIB was associated with a reduction in overall mortality (NNT was 22 to prevent 1 death)

Ceftriaxone 1 g IV

  1. Somatostatin analogues (octreotide) inhibit the secretion of various gastric hormones and may reduce the risk of bleeding in patients with varices. 20-50 μg IV bolus followed by infusion of 25-50 μg/h.
  2. Vasopressin is thought to be useful in variceal UGIB due to its vasoconstrictive property, reducing portal hypertension by way of vasoconstriction of the splanchnic circulation. Vasopressin might be useful in the management of hemodynamically unstable patients with variceal bleeding.
137
Q

Blakemore tube equipment checklist

A
  • Blakemore tube (BT)
  • OG tube
  • 2 three-way stopcocks
  • 4 dual Luer Lock caps
  • 1 Kelly clamp
  • Insufflating manometer
  • 50 cc syringe
  • Marking pen
  • Lube
  • 1L bag of fluid
  • Rolled gauze for traction
  • Basin of water
138
Q

Blakemore tube INSERTION STEPS

A
  1. Resuscitate & Intubate.
  2. Check for Leaks
  3. Place Stopcocks
  4. Label “G” on OG Tube (Place the OG tube next to the BT with the tip of the OG just above the gastric balloon. At the 50 cm mark on the BT, label the OG tube with “G” for gastric.
  5. Label “E” on OG Tube (Place the OG tube next to the BT with the tip of the OG just above the esophagus balloon. At the 50 cm mark on the BT, label the OG tube with “E” for esophagus.)
  6. Insert Balloon
  7. Partially Inflate Gastric Balloon (50 cc of air)
  8. Get Chest X-Ray (confirm balloon placement in the stomach)
  9. Fully Inflate Gastric Balloon (250cc air)
  10. Apply Traction (1kg traction using 1L NS bag)
  11. Suction the Stomach
  12. Insert the OG (until the “G” is at the 50 cm mark on the Blakemore)
  13. Suction the Lower Esophagus
139
Q

Systemic approach to unstable GIB

A
  1. A-B-C
  2. If unstable assume UPPER GI Bleeding
  3. Intubate early for airway control
  4. Replace blood with blood (permissive hypotension)
  5. Reverse Bleeding disorders
    ○ Vit K if INR high (eg: 10 mg IV),
    ○ DDAVP (0.4mcg/kg IV over 10 minutes) if plt or renal disorder
  6. PPI eg: Pantoprazole 80 mg IV, then 8 mg/hr
  7. Octreotide eg: 50 mcg IV bolus
  8. Call EPOS stat
  9. Consider:
    ○ Antibiotics eg: Ceftriaxone 1 gram IV
    ○ Blakemore Tube or similar
    ○ Transport destination: Is surgery/IR available?
140
Q

anatomical specific location that delineates between an UGIB and LGIB

A
  1. Upper GI bleed: typically originates proximal to the ligament of Treitz in the distal duodenum.
  2. Lower GI bleed: bleeding starts distal to the ligament of Treitz.
141
Q

Most common sources of UGIB (in order of frequency) are:

A

duodenal ulcers, gastric ulcers, gastritis, esophageal varices and esophagitis

142
Q

Most common sources of LGIB (in order of frequency) are :

A

diverticula, arteriovenous malformations, polyps and cancer

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