Gastrointestinal - Anatomy, GI Hemorrhage, Pancreatitis, Hepatic Failure

RIGHT UPPER quadrant - abdominal structures?

• pylorus (sphincter connecting stomach to duodenum)

• duodenum (first part of small intestine)

• liver

• right kidney/adrenal gland

• hepatic flexure of colon

• head of the pancreas

LEFT UPPER quadrant - abdominal structures?

• stomach

• spleen

• left kidney / adrenal gland

• splenic flexure of the colon

• body of the pancreas

RIGHT LOWER quadrant - abdominal structures?

• cecum

• appendix

• right ovary/fallopian tube (female)

• right ureter and lower kidney pole

• right spermatic cord (male)

LEFT LOWER quadrant - abdominal structures?

• sigmoid colon

• left ovary and fallopian tube (female)

• left ureter and lower kidney pole

• left spermatic cord (male)

Acute GI hemorrhage - UPPER GI bleed (causes)

• ACCOUNTS FOR 80% OF GI BLEEDING

  • peptic ulcer disease (gastric, duodenal) ~ 50%

  • esophageal ~ 10-20%

  • stress ulcers

  • Mallory-Weiss tear

  • Cancer

Acute GI hemorrhage - LOWER GI (causes)

• ACCOUNTS FOR 20% of acute GI bleeding

  • diverticulosis

  • angiodysplasia (AVMs)

  • tumor

  • radiation

  • colitis

  • inflammatory (Crohn’s disease)

  • infectious (C. diff, E. coli)

Acute GI hemorrhage - Upper vs. Lower bleed → WHICH ONE HAS A HIGHER MORTALITY?

UPPER GI BLEED!!! they are more likely to cause hemorrhagic shock as they involve larger arteries, liver disease (ESOPHAGEAL VARICES), and have an increased risk of aspiration

Acute GI hemorrhage - UPPER GI BLEEDING (general management)

• ADDRESS THE CAUSE

• isotonic fluid resuscitation as for hypovolemic shock; PRBCs

• replace clotting factors (FFP, platelets)

• medications

  • vasopressin constricts splanchnic arteriolar bed, decreases portal venous pressure; watch for chest pain, ST elevation (USED FOR ACUTE VARICEAL BLEEDS)

  • Octreotide (Sandostatin) reduces splanchnic blood flow, gastric acid secretion, and GI motility (USED FOR ACUTE VARICEAL BLEEDS)

  • osmotic laxatives (lactulose) removes nitrogenous materials (blood) out of the gut to prevent ammonia conversion; these are important to administer in the presence of liver disease (NOT GIVEN TO STOP BLEEDING)

  • beta blockers constrict mesenteric arterioles, reducing portal venous flow (HELPS PREVENT RECURRENT VARICEAL BLEEDING)

Acute GI hemorrhage - NORMAL VENOUS DRAINAGE OF GI TRACT

• GI venous drainage

• →portal vein

• →liver

• →hepatic vein

• →inferior vena cava leading to the heart

Acute GI hemorrhage - ESOPHAGEAL VARICES (most common cause?)

• PORTAL HYPERTENSION secondary to LIVER DISEASE

  • liver cirrhosis prevents normal drainage through the liver

    • → pressure backs up into the esophageal vein, like “hemorrhoids of the esophagus”

    • →AND WITH LIVER DISEASE, THERE IS NOT ENOUGH CLOTTING FACTORS TO FIX THE BLEED :(

Acute GI hemorrhage - ESOPHAGEAL VARICES (treatment)

• endoscopy procedure with banding or sclerosing of varices

• esophageal balloon tamponade (Sengstaken-Blakemore tube)

  • a gastric balloon (200-500 mL) is attached to suction and empties the stomach

  • an esophageal balloon (20-40 mmHg) is prescribed by the physician to control bleeding

  • if the esophageal balloon is displaced up, the inflated balloon may occlude the airway

    • CUT THE ESOPHAGEAL BALLOON IF THERE IS RESPIRATORY DISTRESS

EXOCRINE FUNCTIONS OF PANCREAS

• secretion of:

  • bicarbonate to neutralize stomach acid

  • H2O

  • Na, K

  • digestive enzymes →trypsin, amylase, lipase

  • secretion INCREASES by

    • parasympathetic stimulation

    • ingestion of food (secretin and cholecystokinin)

ENDOCRINE FUNCTIONS OF PANCREAS

• Alpha cells → secretes glucagon (INCREASES blood sugar by telling the liver to break down stored glycogen into glucose)

• Beta cells → secretes insulin (TO LOWER THE BLOOD SUGAR)

• Delta cells → INHIBITS the secretion of glucagon and insulin

Acute Pancreatitis - WHAT IS IT?

• the diffuse inflammation, destruction, and auto-digestion of the pancreas from premature activation of exocrine enzymes (NOT USUALLY CAUSED BY AN INFECTION!!)

  • up to 6L of fluid may be secreted into the interstitial space

  • activation of inflammatory mediators (cytokines, kinins, histamine, clotting factors)

  • →results in systemic inflammatory response syndrome (SIRS)

    • →INCREASED VASCULAR PERMEABILITY

    • vasodilation; vascular stasis; microthrombosis

Acute Pancreatitis - ETIOLOGIES

• alcoholism

• obstruction (gall stones)

• abdominal surgery

• drugs

• hyperlipidemia

• trauma

• infection (ALTHOUGH IT IS RARELY AN INFECTION!!)

Acute Pancreatitis - PULMONARY COMPLICATIONS

• atelectasis, left lower lobe

• left-sided pleural effusion

  • pancreatic inflammation and capillary leak may block the pancreatic duct and cause left diaphragmatic lifting, left atelectasis, and/or left pleural effusion

• bilateral crackles

• ARDS (DUE TO SIRS causing increased capillary permeability → JUICY LUNGS)

Acute Pancreatitis - signs and symptoms

• abdominal pain

  • radiates to ALL quadrants and the lumbar area

• N/V, RIGID ABDOMEN, NO rebound tenderness

• decreased/absent bowel sounds

• low-grade fever

• increased WBCs

• INCREASED AMYLASE (peaks in 4-24 hours, returns to normal in 4 days)

• INCREASED LIPASE (stays elevated longer than amylase)

• DECREASED CALCIUM

• INCREASED BLOOD SUGAR

Acute Pancreatitis - S/S rationales (DECREASED CALCIUM)

• calcium is used up for auto-digestion, precipitating the hypocalcemia → Trousseau’s sign, prolonged QT, seizures

  • Trousseau’s - during inflation of the BP cuff, brachial artery is occluded; absence of blood flow/hypocalcemia and subsequent neuromuscular irritability induces spasms of the muscles of the hand and forearm

Acute Pancreatitis - S/S rationales (BETA CELL INJURY)

• beta cell injury affects the ability of the pancreas to secrete insulin, leading to

  • →HYPERGLYCEMIA

  • →hyperosmolar hyperglycemia state (HHS)

Acute Pancreatitis - S/S rationales (phospholipidase A release)

• Phospholipidase A is released

  • →”kills” type II alveolar cells → DECREASED SURFACTANT → ATELECTASIS and ARDS

Acute Pancreatitis - SIGNS of HEMORRHAGIC PANCREATITIS

• Cullen’s Sign → bluish discoloration and echhymosis of the periumbilical area (Cullen’s….umbilicus)

  • in acute pancreatitis, METHEALBUMIN forms from digested blood and tracks around the abdomen from the inflamed pancreas; this is a sign of intra-abdominal bleeding

• Grey Turner’s Sign → bluish discoloration of the flanks (Turner’s…TURN the patient to see the flank)

  • SIGN OF RP BLEED!!

Acute Pancreatitis - TREATMENT

• FLUID replacement

• Calcium, potassium, and Magnesium replacement

• H2 blockers or PPIs to decrease gastric pH

• NG suction to decrease gastric secretion

• pain management/morphine!!

• glucose control!

• enteral feeding BELOW the duodenum

• MONITOR FOR PULMONARY COMPLICATIONS!!

  • ARDS

  • elevation of diaphragm; bilateral basilar crackles

  • atelectasis (especially left base)

  • left-sided pleural effusion

Hepatic Failure - most common cause of ACUTE? CHRONIC FAILURE?

• Acute - acetaminophen (Tylenol) OVERDOSE → which may lead to fulminant hepatitis

• Chronic - ALCOHOL ABUSE!!

Hepatic Failure - LAB abnormalities

• DECREASED serum protein, albumen (ASCITES!!)

• INCREASED AMMONIA (NH3)

• pancytopenia (DECREASED WBCs, RBCs, Platelets)

• coagulopathies (INCREASED PT/PTT)

• INCREASED AST/ALT/Alk Phos, and GGT

• INCREASED serum bilirubin

• DECREASED blood sugar (impaired ability to store glycogen, impaired gluconeogenesis, leading to HYPOGLYCEMIA)

• hyperventilation, respiratory alkalosis → INCREASED LACTATE →metabolic acidosis

• INCREASED creatinine/BUN (LATE sign)

Hepatic Failure - CLINICAL findings

• mental status change (hepatic encephalopathy secondary to elevated ammonia (NH3)

• asterixis (a flapping hand tremor) due to elevated ammonia (NH3)

• ascites (due to low albumin/protein, risk of spontaneous bacterial peritonitis)

• jaundice (due to elevated bilirubin)

• renal failure (hepatorenal syndrome → NOT FULLY UNDERSTOOD, but high mortality (80%); usually due to bleeding or infection

• sepsis (bacterial or fungal) due to decreased immune function (pancytopenia)

• liver becomes ENLARGED/tender during acute inflammatory state

• liver becomes non-palpable as hepatocellular necrosis progresses

Hepatic Failure - STAGES of hepatic encephalopathy (Stage I-IV)

• Stage I - mild confusion, forgetfulness, irritability, change in sleep patterns, EEG is normal

• Stage II - lethargy, confusion, apathy, aberrant behavior, asterixis, EEG is normal

• Stage III - severe confusion, semi-stupor to stupor, hyperactive DTRs, hyperventilation, EEG is abnormal

• Stage IV - NO RESPONSE to stimuli, posturing, positive Babinski, areflexia except for pathologic reflexes, EEG is abnormal

Hepatic Failure - FACTORS THAT INCREASE SERUM AMMONIA (NH3) (that worsen hepatic encephalopathy and may increase ICP)

• HYPOKALEMIA - triggers ammoniagenesis in the kidneys (the mechanism is entirely unclear)

• INCREASED BUN - breakdown of nitrogen

• INCREASED Protein - breakdown of nitrogen

• INCREASE LACTIC ACIDOSIS - may be precipitated by the administration of LR (normally it is converted into bicarbonate by a healthy liver (THIS IS NOT THE CASE IN LIVER FAILURE))

Hepatic Failure - MANAGEMENT

• PREVENT ANYTHING THAT INCREASES AMMONIA LEVELS; attempt to decrease Ammonia levels

• restrict protein ONLY if hepatic encephalopathy is present

• administer clotting factors

• lactulose (TO DECREASE AMMONIA LEVELS)

• neomycin - kills bacteria in the gut that produce ammonia

  • COMPLICATION of neomycin → Vit K deficiency

  • E. coli in the gut helps produce folic acid, riboflavin, and vit K; killing E. coli will drop Vit K

• adjust doses of medications that are metabolized by the liver (sedation, anticoagulants, cardiac meds, etc)

• MONITOR GLUCOSE

• administer acetylcysteine (Mucomist) or Acetadote for ALL SUSPECTED acetaminophen OVERDOSES

• Transjugular Intrahepatic Portosystemic Shunt (TIPS procedure)

Hepatic Failure - what is a TIPS procedure? what is a big complication? why?

• Transjugular Intrahepatic Portosystemic Shunt procedure is done for select patients with cirrhosis to relieve esophageal varices or ascites (helps lower portal vein pressure by diverting blood from the high-pressure portal circulation directly into the low-pressure systemic venous circulation; CONNECTS PORTAL VEIN TO HEPATIC VEIN!)

• hepatic encephalopathy is a big complication! why?

  • stent inserted during the procedure allows shunting of blood directly from hepatic veins into portal vein, BYPASSING THE LIVER (decreasing portal HTN, but DECREASES DETOXIFICATION OF BLOOD)