Pancreatitis/Liver Failure/GI Bleed/DIC

Acute Pancreatitis

You ever make a bad decision and immediately regret it? Like, you take one bite of gas station sushi, and 30 minutes later, you’re bargaining with a higher power on the bathroom floor? That’s how the pancreas feels when it sees alcohol coming—it’s like, 'Oh great, here we go again…

Your pancreas is that friend who just can’t handle their liquor. If they drink too much (alcohol abuse), they totally lose control and start wrecking the place. But instead of just breaking furniture, the pancreas starts digesting ITSELF. That’s right—it’s like a blender that turns on without a lid, spraying enzymes everywhere. Before you know it, the whole house (your abdominal organs) is a disaster zone, and your body is in full-blown inflammation mode.

​Party Animal

PANCREATITIS

• Acute pancreatitis is a sudden inflammation of the pancreas, leading to enzyme activation and pancreatic tissue damage.

• It can range from mild to severe, with severe cases resulting in systemic complications:

  • ARDS

  • Sepsis

  • Multi-organ failure.

Multiple Choice

What is the most common cause of acute pancreatitis?

• Pancreatic Cancer

• Gallstones
• Alcohol consumption
• Diabetes mellitus

Pancreatitis

• Most commonly caused by Gallstones & Alcohol.

• Mild Pancreatitis: Localized inflammation, no organ failure, good prognosis.

• Moderately Severe: Transient organ failure (<48 hours), potential complications.

• Severe Pancreatitis: Persistent organ failure (>48 hours), associated with high mortality due to complications such as sepsis and ARDS.

Multiple Choice

Which two lab values are most indicative of acute pancreatitis?

• glucose and bilirubin

• creatinine and potassium

• AST & ALT

• amylase and lipase

​Severe Abdominal pain (usually epigastric radiating to back)
Nausea & Vomiting
Rigid Abdomen & Guarding
Decreased or Absent Bowel Sounds
Hypotension
Tachycardia
Jaundice

Pancreatitis

Diagnosis

• Diagnosis requires 2 out of 3 criteria:

  1. Epigastric pain radiating to the back

  2. Amylase & Lipase elevated ≥3x upper limit

  3. Characteristic findings on CT imaging

Multiple Choice

A patient presents with severe epigastric pain radiating to the back, nausea, and vomiting. Which additional sign is MOST concerning?

• Cullen's Sign

• Rebound Tenderness

• RLQ Pain

• Rovsing's Sign

Treatment

1. NPO with NG Tube

2. IV Fluids and Albumin

3. PPIs to decrease pancreatic enzymes

4. Antibiotics

5. ERCP Endoscopic Retrograde Cholangiopancreatography

Multiple Choice

A patient with acute pancreatitis develops respiratory distress and requires high levels of oxygen supplementation. What is the most likely complication?

• Pleural effusion

• ARDS

• Pulmonary embolism

• Aspiration Pneumonia

Multiple Choice

A patient with severe acute pancreatitis has worsening hypotension, tachycardia, and decreased urine output despite fluid resuscitation. What is the next best intervention?

• Start Vasopressors

• Increase IV Fluids

• Start Hemodialysis

• Prepare for Emergency laparotomy

​Questions?

Acute Pancreatitis – "Lipase loves to rise when your pancreas fries!"

Liver Failure

Liver Failure

Alright, imagine your liver is like a bouncer at an exclusive club, filtering out troublemakers (toxins, ammonia, and drugs). But one day, the bouncer gets really drunk (liver failure), stops checking IDs, and lets everyone in. Now the place is full of ammonia, the bartenders (clotting factors) are overwhelmed, and security (immune system) is asleep on the job. Next thing you know, people are acting crazy (hepatic encephalopathy), bar fights are breaking out (bleeding issues), and the place is a disaster.

Liver Failure

Acute liver failure is the rapid loss of liver function, leading to toxin accumulation, coagulopathy, hepatic encephalopathy, and multi-organ failure. It has a high mortality rate without intervention.

Multiple Choice

What is the primary mechanism leading to hepatic encephalopathy in liver failure?

• Increased glucose metabolism

• Decreased production of clotting factors

• Accumulation of ammonia and neurotoxins

• Excessive bile production

Liver Failure

1. Hepatocyte Damage → Widespread liver cell destruction

2. Loss of Liver Function → Impaired detoxification of blood

3. Ammonia Accumulation → Hepatic encephalopathy

4. Coagulopathy → Increased bleeding risk

5. Cerebral Edema & Multi-Organ Failure → High mortality risk

Multiple Choice

What is the leading cause of acute liver failure in the United States?

• Acetaminophen overdose
• Chemotherapy drugs

• Viral hepatitis
• Alcohol

Multiple Choice

What is the most life-threatening complication of acute liver failure?

• Hepatic encephalopathy

• Cerebral edema

• Hypoglycemia

• Ascites

​Complications

• Hepatic Encephalopathy: Confusion → Stupor → Coma

• Cerebral Edema: Increased ICP → Brain herniation risk

• Coagulopathy: Bleeding risk from decreased clotting factors

• Hypoglycemia: Liver failure impairs glucose regulation

Multiple Choice

A patient with hepatic encephalopathy develops a flapping tremor when holding their hands outstretched. What is this sign called?

• Myoclonus
• Babinski Reflex

• Grey Turner's sign

• Asterixis

Multiple Choice

What is the most effective treatment for reducing intracranial pressure (ICP) in cerebral edema?

• IV fluids

• Acetaminophen

• Hypertonic saline (3%) or Mannitol

• Low-protein diet

Cerebral Edema

• Intracranial Pressure Monitoring

• Hypothermia to reduce metabolic demand

• Hypertonic saline (3%) or Mannitol for severe edema

• Head elevation (30°) to reduce ICP

Multiple Choice

What lab finding is most concerning for spontaneous bacterial peritonitis (SBP) in a patient with ascites?

• Albumin <3.5

• PMNs >250 in ascitic fluid

• Elevated ALT/AST

• Hypoglycemia

Questions???

Liver Failure – "Ammonia makes you loopy, clotting factors go poofy."

GI Bleed

GI Bleed

Ever made coffee and then totally forgot about it until the next morning? You go to dump it out, and instead of fresh liquid, it’s this weird, thick, black sludge at the bottom of the pot? Yeah, that’s what happens when blood sits in the stomach—it turns into ‘coffee ground emesis.’ So if you ever hear a patient say ‘it looks like coffee,’ you know that bleed has been there long enough to get a little… aged.



Upper GI bleeds can cause "coffee ground" emesis if blood sits in the stomach and gets partially digested.

GI Bleed

A GI bleed refers to any bleeding that occurs in the gastrointestinal tract, which can be upper (above the ligament of Treitz) or lower GI bleeding (below the ligament of Treitz). It can be overt (visible bleeding) or occult (hidden, detected through testing).

Multiple Choice

What is the mortality rate associated with GI bleeding?

• 1% to 2%

• 5% to 10%

• 10% to 15%

• 15% to 20%

Multiple Choice

Which of the following is NOT a common cause of upper GI bleeding?

• Peptic Ulcer Disease

• Esophageal Varices

• Mallory-Weiss Tear

• Diverticulosis

GI Bleed

• Upper GI Bleed: Peptic ulcers, varices, stress ulcers, gastritis, Mallory-Weiss tears

• Lower GI Bleed: Diverticulosis, AV malformations, ischemic colitis, hemorrhoids

Multiple Choice

What is the most common cause of upper GI bleeding?

• Gastritis
• Esophageal varices
• Mallory-Weiss tear

• Peptic ulcers

Esophageal Varices

• Esophageal varices are dilated veins in the esophagus caused by portal hypertension.

• Treatment:

  • Octreotide (reduces portal pressure)

  • Endoscopic band ligation

  • Sengstaken-Blakemore tube (only for uncontrolled bleeding)

When bleeding is uncontrolled, INTUBATE to protect airway

Sengstaken-Blakemore tube

​

Multiple Choice

Which ICU patients are most at risk for stress-related mucosal disease (SRMD)?

• Patients on anticoagulants

• Critically ill patients on mechanical ventilation

• Patients with GERD

• Patients with chronic constipation

Stree-Related Mucosal Disease

• SRMD = Acute ulcers in critically ill patients

• 75% of ICU patients develop evidence of mucosal injury within 24 hours

• Prevention: PPI prophylaxis, early enteral feeding

Multiple Choice

What is the primary cause of a Mallory-Weiss tear?

• NSAID use

• Severe Vomiting

• H. Pylori Infection

• GERS

Management of GI Bleed

• First priority: ABCs (Airway, Breathing, Circulation)

• Resuscitation: IV fluids, blood transfusion if Hgb < 7 g/dL

• Interventions: Endoscopy, medication therapy, surgery if needed

DIC

​DIC

So imagine you’re at a party, and there's one guest who is just way too extra. At first, they’re throwing glitter everywhere (clotting like crazy), but suddenly, they start sobbing uncontrollably, smudging their makeup and making a huge mess (bleeding out because all the clotting factors are used up). That’s DIC. Your body tries to be fancy and overdoes it, then suddenly crashes because it ran out of resources.

Multiple Choice

What is the initial event in DIC pathophysiology?

• Increased platelet production

• Uncontrolled activation of the clotting cascade

• Spontaneous destruction of RBCs

• Inhibition of thrombin formation

​DIC Patho

• Trigger (sepsis, trauma, etc.) → Excess thrombin production.

• Thrombin converts fibrinogen to fibrin, leading to widespread clotting.

• Microthrombi form, blocking organ perfusion → Multi-organ failure.

• Clotting factors & platelets deplete, leading to uncontrolled hemorrhage.

​Coagulation Cascade & Organ Damage

• Microthrombi impair blood flow → Stroke-like symptoms, AKI, cyanosis.

• Lungs: Pulmonary embolism, hypoxia.

• Kidneys: Acute kidney injury (low urine output).

• Brain: Altered mental status.

​Treatment & Management

• Priority in DIC = Treat the Trigger (Sepsis? Trauma? Obstetric emergency?)

• Supportive Measures:

  • IV Fluids: Maintain perfusion.

  • Blood products: Platelets, FFP, cryoprecipitate as needed.

  • Heparin? ONLY if clotting phase dominates & no active bleeding.

Multiple Choice

A septic patient develops cyanotic fingers, oliguria, and confusion. Labs: ↓ platelets, ↑ D-dimer, ↑ PT/INR, ↓ fibrinogen. What is the priority intervention?

• Start IV heparin to prevent further clots

• Begin aggressive IV fluid resuscitation and broad-spectrum antibiotics

• Transfuse platelets immediately

• Administer fibrinolytics

Multiple Choice

A postpartum patient with placental abruption has widespread petechiae and uncontrolled vaginal bleeding. What is the best treatment approach?

• Administer cryoprecipitate, platelets, and RBCs

• Start IV heparin to prevent further clotting

• Give high-dose corticosteroids

• Perform an immediate exploratory laparotomy