Hepatic & GI Study Notes PDF

Hepatic & GI Dr. Jordan Popp, DNP, CRNA, APRN The Liver Introduction Largest internal organ in the body Located in upper quadrant of the ABD Function Processing nutrients from food Protein and other chemical synthesis Energy storage To...

Hepatic & GI Dr. Jordan Popp, DNP, CRNA, APRN The Liver Introduction Largest internal organ in the body Located in upper quadrant of the ABD Function Processing nutrients from food Protein and other chemical synthesis Energy storage Toxin filtration Fights infections Structure The basic structure in the liver is the lobule Lobules are made up of hepatocytes Blood Flow Blood enters the liver through the hepatic artery and portal vein, and then flows, through the sinusoids to the central veins. The central veins empty into the hepatic veins, which carry blood out of the liver to the heart Functions of the Liver Carbohydrate metabolism Bile production Gluconeogenesis Lipid metabolism Glycogenolysis Lipogenesis Glycogenesis Cholesterol synthesis Protein synthesis Coagulation factor synthesis Albumin (maintenance of Production of factors I, II, V, VII, IX, osmolarity) X, and XI Thrombopoietin (platelet Insulin clearance production) Drug metabolism/transformation Amino acid synthesis Bilirubin metabolism Protein metabolism Anesthetics and Liver Blood Flow Inhaled Anesthetics Mainly affect portal blood flow Do not adversely affect liver integrity through blood flow changes Hepatic Artery Buffer Response Regulates total hepatic blood flow Increases hepatic arterial flow when portal flow decreases Liver Function Protein, lipid, and hormone synthesis are maintained despite anesthetic use No artificial substitutes can fully replicate the liver Volatile Anesthetics & Hepatic Blood Flow Volatile Agent Hepatic Artery Blood Flow Portal Vein Blood Flow Desflurane Moderate dose-dependent Moderate dose-dependent decrease decrease Isoflurane Minimal dose-dependent decrease Minimal dose-dependent decrease Sevoflurane Minimal dose-dependent decrease Minimal dose-dependent decrease Carbohydrate Metabolism Glucose Main fuel source Liver Plays a central role in maintaining blood glucose levels Balances supply and demand Gluconeogenesis Makes new glucose from non-carbs Active when glycogen stores are low (fasting) Glycogenolysis Releases glucose from stored glycogen during fasting Protein Synthesis and Clinical Concerns Protein synthesis primarily occurs in the liver Liver disease reduces circulating proteins Decreased plasma oncotic pressure leads to fluid shifts and increased drug distribution volume Highly protein-bound drugs have a greater unbound fraction = more free Muscle Relaxants May need increased dose due to larger distribution volume Succinylcholine and Ester LA Prolonged effects due to reduced plasma cholinesterase Bilirubin A yellow pigment, byproduct of heme breakdown Formation of Unconjugated Bilirubin Reticuloendothelial cells (spleen) break down heme Unconjugated bilirubin is potentially harmful at high levels Transport to the Liver Albumin binds and carries unconjugated bilirubin to the liver Conjugation in the Liver Liver cells attach glucuronic acid, making bilirubin conjugated Excretion int the Intestine Conjugated bilirubin joins bile, and digestive fluid Bacteria further breaks down bilirubin Elimination through feces Most leaves the body through stool however some is reabsorbed and recycled Bile Production Liver Liver Disease Makes bile Steatorrhea Gallbladder Vitamin K Deficiency Stores and concentrates bile Coagulopathy Common Bile Duct (CBD) Coagulopathy in Liver Disease Delivers bile to the small intestine Caused by both Low clotting factor Fat and Protein in Intestine Low Platelets Trigger bile release from gall bladder Treatment Bile Functions Vitamin K FFP Aids fat absorption If coagulopathy is present caution high Helps with fat-soluble vitamins blood loss and invasive procedures Removes drug waste Insulin Clearance The liver is the main site for insulin clearance Removes 50% of insulin during first portal pass Can very widely under different conditions Drug Metabolism/Transformation Drugs undergo chemical changes (metabolism) in the liver before being eliminated Important Enzymes Where Cytochrome P450 (CYP) Mainly the liver Main player in Phase I Drug Interactions Why Can compete for CYP enzymes, affecting metabolism and Make drug excretion easier potentially causing harmful effects Process Tolerance Phase I Some drugs induce enzyme production, leading to Modifies drug structure (oxidation, reduction, hydrolysis) tolerance (needing higher dose for same effect) Phase II Special Cases Attaches molecules to make drug more water-soluble Some drugs rely heavily on liver function for metabolism Elimination Reduced blood flow to the liver can impact their Products excreted in bile or urine clearance First-Pass Effect Orally ingested drugs might be broken down in the liver before entering circulation, reducing their effectiveness. Drug Metabolism in the Liver Phase I Reactions Functionalization reactions Addition or exposure of a functional group (e.g., oxidation, reduction, hydrolysis) Typically result in the loss of pharmacologic activity (excluding prodrugs) Important for metabolizing many of the anesthetic drugs (e.g., midazolam, diazepam, codeine, phenobarbital, inhalation anesthetics, propofol) Phase II Reactions Conjugation reactions Phase I product (substrate) conjugation with a second molecule Lead to the formation of a covalent linkage between a functional group and glucuronic acid, sulfate, glutathione, amino acid, or acetate (e.g., morphine, acetaminophen) Laboratory Evaluation of Liver Function What is the problem Key markers Parenchymal Transferases (ALT & AST) Liver cell dysfunction Sensitive for acute injury, degree of Obstructive elevation helps diagnose type Bile flow blockage Alkaline Phosphatase (ALP), Y-Glutamyl transferase (GGT) Limitations of specific tests Indicate obstructive problems Ammonia Limited usefulness in assessing disease Consider all markers, symptoms, and severity physical exam together Bilirubin Child-Pugh Classification Elevated in many liver diseases Uses albumin, bilirubin, and PT to Albumin assess overall liver function and guide Slow to change, unreliable treatment Grading Liver Function Using the Child-Pugh Classification System Clinical Significance of Liver Biochemical Tests Volatile Anesthetic Selection General Effects of Volatile Anesthetics: Halothane: Reduce hepatic blood flow by 30-50% after Reduces hepatic blood flow most induction. significantly. Halothane causes the largest reduction, Associated with two types of liver injury: followed by desflurane, sevoflurane, and Minor elevation in ALT (10-30% of patients). isoflurane. Severe "halothane hepatitis" (1 in 10,000). May affect liver function, but studies suggest minimal clinical impact with newer agents Largely replaced by newer agents (desflurane, sevoflurane) due to safety Desflurane and Sevoflurane: concerns. Less impact on hepatic blood flow than Viral infections are more likely cause of halothane. jaundice after halothane exposure Sevoflurane may produce fluoride ions, but Other generally below nephrotoxic levels. Preferred for patients with liver disease. Regional anesthesia can also reduce hepatic blood flow due to sympathectomy Isoflurane: Some vasodilatory effects, but may not fully offset its impact on hepatic blood flow Opioid Effects Spasm of the Oddi sphincter is a medical condition that can cause biliary colic, or pain in the upper right abdomen Could cause false-positive on intraoperative cholangiography Causes All opioids have been shown to cause spasm of the Oddi sphincter The more potent the opioid, the greater the resultant increase in biliary pressure Prevention Judicious titration of the anesthetic may help to reduce the occurrence of spasm Even with fentanyl-based anesthesia, the incidence of spams is low Treatment If spasm is suspected, naloxone or nalbuphine can be administered to reverse the effects of opioids Atropine, Glycopyrrolate, Glucagon, & Nitroglycerin Mechanical Ventilation Mechanical ventilation can reduce hepatic blood flow by: Increasing airway pressures, which reduces venous delivery to the right atrium and CO2 Increasing positive end-expiratory pressure Reduced hepatic blood flow can also be caused by: Increased hepatic venous pressure Increased reflex sympathetic tone Hypercapnia and acidosis increase hepatic blood flow, while hypocapnia and alkalosis decrease it. Intraoperative variables like surgical site, ventilation mode, anesthetics, and physiologic responses can affect hepatic blood flow variability. Surgical Site & Hepatic Blood Flow Diseases of the Liver Acute Hepatitis Hepatitis = liver inflammation Can be caused by multiple factors Toxins, Alcohol, Medications, Viral/Bacterial Infections, & Autoimmune Disease Acute hepatitis has variable presentation The cause is usually exposure to an infectious virus Viral Hepatitis Typically, hepatitis A, B, or C Begins with a 1–2-week period of fever, fatigue, nausea, and vomiting Jaundice occurs for the next 2-12 weeks Recovery takes months, symptoms resolve but liver enzymes remain elevated Full Resolution usually takes 4+ months Liver Disease Drug-Related Liver Injury Drug related liver injury can be an idiosyncratic reaction to a substance or an overdose Risk Factors Genetic predisposition is the main risk factor Age, gender, exposure to other substances, and medical conditions Alcohol Hepatitis Alcoholic hepatitis is a common form of drug-induced hepatitis and causes fatty liver Liver Disease Chronic Hepatitis Occurs in 1-10% of acute hepatitis B infections Occurs in 10-40% of hepatitis C infections Does not occur in hepatitis A infections Chronic Persistent Hepatitis Limited to portal areas, benign, hepatic cellular integrity is preserved, and rarely is cirrhosis seen Chronic Lobular Hepatitis Recurrent exacerbations of acute inflammation, cirrhosis is rare Chronic Active Hepatitis Progressive, hepatocyte destruction, cirrhosis and liver failure Hepatic Failure Multiorgan failure, encephalopathy, and esophageal varices Other Symptoms Fatigue, jaundice, thrombocytopenia, glomerulonephritis, myocarditis, arthritis, and neuropathy Plasma albumin levels are usually low and PT is prolonged Liver Disease – Nonalcoholic Fatty Liver Disease Broad spectrum of liver disorders related to fat buildup Most common liver disease worldwide (1/3 of US adults) Causes Unknown but thought to be related to obesity, insulin resistance, and genetics Symptoms Often asymptomatic or may have fatigue, weight loss, and/or RUA pain Treatment No cure Treatment to slow progression include lifestyle changes and medications Hepatitis – Anesthetic Management Chronic mild hepatitis: No increased risk for complications during laparoscopic cholecystectomy. Acute hepatitis: Elective surgery should be delayed until liver function normalizes. Alcohol intoxication: Increased risk of complications, careful anesthetic management needed. Alcohol withdrawal: Surgery associated with higher mortality rate. Urgent/emergent surgery: Manage comorbidities for risk reduction and symptom control. Anesthetic Management of the Patient with Acute Hepatitis Preserve hepatic blood flow: Use isoflurane or desflurane and avoid halothane Maintain normocapnia Avoid PEEP if possible Provide adequate/liberal intravenous hydration Consider regional anesthesia if coagulation is acceptable and the procedure allows Avoid medications with potential for hepatotoxicity or inhibition of CYP450: Halothane Acetaminophen Sulfonamides Tetracycline Penicillin Amiodarone Neuromuscular blocking agents may be prolonged in patients with liver disease because of: Reduced pseudocholinesterase activity Decreased biliary excretion Larger volume of distribution Surgical Recommendations for the Acutely Intoxicated Patient Anesthetic requirement is reduced Acute intoxication reduces MAC Aspiration precautions are needed Full stomach, alcohol-related impaired pharyngeal reflexes Alcohol increases GABA receptor activity Enhanced effects of benzodiazepines, barbiturates, propofol, other CNS depressants Alcohol inhibits NMDA receptors Reduces CNS excitability Cirrhosis Liver disease characterized by scarring and fibrosis = disrupt blood flow Symptoms vary and depend on severity, but common symptoms include: Fatigue, weight loss, ABD pain, swelling, and jaundice Complications: Portal hypertension, ascites, encephalopathy, hepatorenal syndrome, and variceal bleeding Treatment: No cure Lifestyle changes, medications, and liver transplantation. Prognosis Varies depending on severity and casue Causes of Cirrhosis Viral Biliary HBV Atresia HCV Stone HDV Tumor Autoimmune Vascular Autoimmune hepatitis Budd-Chiari syndrome PBC Cardiac fibrosis PSC Genetic Toxic CF Alcohol Lysosomal acid lipase deficiency Arsenic Iatrogenic Metabolic Biliary injury α1-antitrypsin deficiency Drugs: high-dose vitamin A, methotrexate Galactosemia Glycogen storage disease Hemochromatosis Nonalcoholic fatty liver disease and steatohepatitis Wilson disease Laboratory Tests & Findings in Cirrhosis Physical Changes Seen Systemically with Portal HTN Anesthetic Preparation and Management in Cirrhosis Preserve hepatic blood flow. Anticipate relative hypovolemia, worsened by ascites Avoid halothane (isoflurane is the best- Assess for the presence of high cardiac output studied alternative, and better preserves and low peripheral resistance flow). Suspect portal hypertension and/or variceal bleeding, even without history Consider regional anesthesia if procedure Anticipate depressed response to inotropes and and coagulation status allows. vasopressors Consider invasive monitoring Avoid medications with situational Pharmacokinetics and Pharmacodynamics potential hepatotoxicity when possible. Altered volume of distribution may occur Anticipate presence, development, or Decreased serum albumin, increased gamma globulins abnormalities of: Intravascular volume unpredictable, especially Coagulation with ascites Attempt to correct prothrombin time Portosystemic shunted blood bypasses liver Consider cryoprecipitate if fresh frozen plasma is Drugs that are highly extracted by liver are ineffective or fibrinogen abnormality exists especially affected Correct thrombocytopenia Increased sensitivity to sedative medications Anticipate higher than normal blood loss Hemodynamics Perioperative Considerations in Liver Disease Key Factors Optimizing Care Disease Severity Address modifiable risk factors Child-Pugh, MELD, and MELD-Na Individualize plan of care predict potential complications Minimize stress Risk Factors Comorbidities Diagnostic Tools Patient History Physical Examination Laboratory Tests LFTs, Coags, Kidney function, CBC, BMP, Glucose, and T&S Cardiovascular Considerations CV complications of cirrhosis: Cardiac dysfunction Abnormal central, splanchnic, and peripheral circulation Hemodynamic changes caused by humoral and nervous dysregulation Increased levels of endogenous vasodilators result in a hyperdynamic circulatory state CV changes associated with liver disease: Increased cardiac output Decreased systemic vascular resistance Decreased arterial blood pressure Systemic collateral circulation Arteriovenous shunting Portal hypertension Esophageal varices Cardiomyopathy Congestive heart failure Fluid Balance and Renal Considerations in Severe Hepatic Disease Complications: Exudative process leads to protein-rich fluid in peritoneum Ascites, Edema, Increased risk of infections, renal failure, poor Misplaced fluids create osmotic gradient and intravascular long-term outcome hypovolemia Fluid Status: Hepatorenal Syndrome (HRS): Relative hypovolemia due to fluid removal and shunting Renal failure in advanced liver disease with portal hypertension Impaired response to blood loss or stress Impaired renal function, abnormal arterial circulation, vasoactive system activity Perioperative Concerns: Triggered by GI hemorrhage, sepsis, surgery, aggressive diuretics Maintain intravascular volume and electrolyte balance Signs: progressive ascites, azotemia, oliguria, multisystem organ Ensure adequate renal perfusion failure Water restriction, controlled IV fluids, potassium replacement Treatment: supportive therapy, liver transplantation Fluid and Electrolyte Disturbances: Goal of HRS Therapy: Hypoalbuminemia Increase renal blood flow through: Renal function decline Renal vasodilation Decreased free water clearance Splanchnic vasoconstriction (reducing blood flow to abdominal organs) Dilutional hyponatremia Hypokalemia Mechanism of Ascites: High pressure in lymphatic and hepatic venous systems Low plasma oncotic pressure (due to hypoalbuminemia) Hematologic Considerations Anemia Hemolysis, folate deficiency, hemorrhage, and bone marrow suppression Thrombocytopenia Splenic platelet sequestration, bone marrow suppression, antiviral therapy, and decreased thrombopoietin Coagulation Deficiencies in clotting factors due to impaired liver synthesis Decreased blood viscosity Enhanced fibrinolysis Excessive transfusion can worsen encephalopathy due to excess protein burden Recommended transfusions FFP, Plt, Cryo Respiratory Complications Arterial hypoxemia is common and is often multifactorial Ascites, hepatic hydrothorax, and COPD in pts with alcoholism) Hepatopulmonary Syndrome (HPS) Triad of liver disease, arterial deoxygenation, and widespread pulmonary vasodilation Causes: Precapillary dilation in lungs Blood shunting Ventilation-perfusion mismatch Increased alveolar-arterial oxygen gradient Preoperative Management Bassline oxygenation levels, address reversable lung issue, pick your drugs carefully Hepatic Encephalopathy Cause: Failing liver can't clear neurotoxins like ammonia from gut bacteria. Ammonia in systemic circulation disrupts brain function. Shunting in cirrhosis bypasses liver, worsening ammonia problems. Effects: Altered mental state (confusion, personality change, coma). Neurotransmitter imbalances and astrocyte injury. Brain swelling and edema. Treatment: Medications to reduce ammonia levels (lactulose, rifaximin). Avoiding sedatives if possible. Intraoperative Anesthetic Consideration: Monitoring ECG 5-lead preferred Monitor ST segments Invasive ART line for cont. BP and blood access Cardiac output Noninvasive monitors are unreliable in cirrhotic patients Other Blood glucose monitoring Temp Coag IV access TEE? Anesthetic Technique: Medications General Less an issue with acute failure Maintain ABP and CO Rocuronium & Vec Consider Regional Prolonged DOA Cisatracurium Volatile Anesthetics Good choice Choose the agent with the least Liver Opioids metabolism Des, Sevo, ISO Caution due to hepatic metabolism Avoid Nitrous if open ABD Fentanyl Careful titration due to CYP3A4 interaction Induction Morphine Caution Benzos Avoid or titrate carefully Neuromuscular Blockers Alfentanil RSI for cirrhotic pts Altered elimination and distribution Succinylcholine Remifentanil Prolonged in chronic liver failure Short ½ life, not affected by liver function Diseases of the Biliary Tract Main symptom: Reduced or stopped bile flow Most common cause: Blockage outside the liver Blockage culprits: Gallstones (most common) Strictures (narrowing) Tumors Infections Reduced blood flow (ischemia) Gallstone composition: 90% cholesterol crystals (radiolucent) 10% calcium bilirubinate (in cirrhosis or hemolytic anemia) Prevalence: Affects 15-20 million adults in the US A&P Overview Cystohepatic Triangle (Calot's Triangle) Gallbladder Function Bile Combination of hepatocyte and biliary tract epithelial secretions Functions include: fat and fat-soluble vitamin absorption, bilirubin excretion, and duodenal alkalization Bile production is 500-1,000 mL/day Bile ducts, gallbladder, and sphincter of Oddi modify, store, and regulate bile flow Absorbed bile returns to the liver via the portal venous system Hepatocytes secrete bilirubin, cholesterol. Bile salts, lecithin, water, and electrolytes Vagal stimulation, secretin, CCK, and gastrin stimulate bile flow. Bile acids increase bile secretion Cholecystitis Inflammation of the gallbladder Caused by obstruction of the cystic duct Symptoms include RUQ pain, fever, and leukocytosis Treatment = Cholecystectomy Pre-op IV fluids, and gastric suction Emergent laparotomy if ruptured Cholelithiasis and Choledocholithiasis Feature Cholelithiasis Choledocholithiasis Location of Gallstones Gallbladder Common Bile Duct Frequency More common Less common Upper abdominal pain, nausea, Similar to cholelithiasis + jaundice, Symptoms vomiting, indigestion fever, chills Treatment Cholecystectomy ERCP, sphincterotomy Severity Less severe More serious Cholelithiasis and Choledocholithiasis Acute obstruction of the CBD can cause similar symptoms to cholecystitis. Recurrent cholecystitis can lead to fibrotic changes in the gallbladder, making it difficult to expel bile. Charcot triad (fever and/or chills, jaundice, right upper quadrant pain) can help diagnose acute ductal obstruction. Other symptoms include weight loss, anorexia, and fatigue. Radiologic evaluation can confirm ductal patency. X-ray, ultrasound, MRI, and CT ERCP is the usual treatment for ductal stones. Endoscopic Retrograde Cholangiopancreatography Anesthetic Considerations in Gallbladder and Biliary Tract Disease Goal NMB Gallstone removal to prevent Monitoring and Management complications Antiemetics for peritoneal irritation, opioid Contraindications to laparoscopic use, and potential volume depletion cholecystectomy Decreased Vt due to CO2 insufflation Coagulopathy Hypotension from retroperitoneal Sever COPD insufflation ESLD Hypercarbia due to CO2 insufflation CHF Hemodynamic compromise from Trendelenburg position Induction Unknown hemorrhage Standard of RSI with ETT Ventilation Airway Management PCV preferred over VC to minimize alveolar ETT derecruitment and barotrauma with CO2 OG tube insufflation Anesthetic Considerations in Gallbladder and Biliary Tract Disease Laparoscopic Approach: Muscle Relaxants Uses insufflation with CO2, Awake Extubation increasing intraabdominal pressure (IAP). Postoperative Pain 15mm Hg: Routine pressure. Reduced due to small incisions 20-25 cm H2O: Increases cardiac Shoulder pain from output & CVP. pneumoperitoneum 30-40 cm H2O: Decreases cardiac output & CVP. Severe pain management options PCA, Intercostal block, neuraxial Anesthetics opioids All maintenance drugs can be used Avoid Nitrous Oxide Anesthetic Considerations in Gallbladder and Biliary Tract Disease Full Stomach Precautions Jaundice – alert you to hepatic dysfunction and increased risk for: Hemorrhage Exaggerated drug effects Hemodynamic fluctuations Monitoring Depends on pt status CBD Exploration Glucagon Anesthetic Considerations in Gallbladder and Biliary Tract Disease Open Cholecystectomy Indicated for: Emergent cases Infections Technically challenging laparoscopy More complications including pain and resp splinting Patients with comorbidities and prolonged surgery are at increased risk for ischemia and ABD crisis Esophagus Overview Length: Approximately 18-25 cm. Function: Carries food and liquids to the stomach. Structure: Three segments: Cervical, thoracic, and abdominal. Muscular walls: Allow expansion and contraction. Upper esophageal sphincter (UES): Prevents air entry at rest. Lower esophageal sphincter (LES): Controls passage of food into the stomach. Movement: Peristaltic action: Muscular waves push food down. Regulation: Parasympathetic nerves: Control peristalsis. Cranial nerves IX, X, XI: Control muscle contractions and LES relaxation. Sympathetic nerves: Modulate motor activity. Esophageal Disorders Symptoms: Dysphagia, heartburn, chest pain. Primary Motility Disorders: Achalasia: Impaired LES relaxation, can be caused by other diseases. Chronic achalasia: Esophageal dilation, frequent regurgitation. GERD: Failure of antireflux barriers, abnormal reflux of stomach contents. Symptoms: Heartburn Complications: Barrett's esophagus (increased cancer risk). Management: Conservative (most patients): Medications: Antacids, mucosal protectants, H2 blockers, proton pump inhibitors, prokinetics. Surgical (if conservative fails): Mechanically defective LES. Recurring symptoms after stopping medication. Unacceptable medication side effects. Hiatal Hernia Definition: Part of the abdomen (usually stomach) pushes through the diaphragm into the chest. Types: Type I (Sliding): Upper stomach moves through an enlarged opening. (Most common) Type II (Paraesophageal): Stomach moves next to the esophagus, not through the opening. Type III (Combined): Features of both Type I and II. Type IV: Other organs (colon, small bowel) herniate through a large opening. GERD: Contribution to GERD is debated, but important in severe cases. Surgery: Various options, choice is usually made intraoperatively. Anesthesia: Aspiration prophylaxis is important. Cricoid pressure decreases pressure in the lower esophageal sphincter (LES), but its value is debated. Anesthetic Considerations in Esophageal Disease Occult disease (no symptoms) is less concerning than uncontrolled, symptomatic disease. If a patient has a history of reflux symptoms, consider aspiration prophylaxis during anesthesia. While best practices aren't established, modifying stomach acid or volume is common pre-surgery. Rapid sequence induction with cricoid pressure can help protect the airway. Laryngeal mask airway use is controversial due to its lack of complete airway protection. Only consider it if endotracheal intubation is not feasible. Disease of the Stomach: Anatomy Fundus: Thin-walled, upper section for storage. Body: Largest section, contains most digestive cells, curved by the lesser and greater curvatures. Pylorus: Thick-walled, lower section for mixing and controlled release of food into the duodenum. Disease of the Stomach: Function Storage: The fundus relaxes to store food, especially solids, for several hours. Processing: The stomach breaks down large food pieces into smaller particles. Breakdown: Liquids: Pass through the stomach quickly along the lesser curvature. Solids: Churned in the antrum and gradually released into the duodenum through the pylorus. Digestion: Starch: Partially broken down by salivary amylase while in the stomach. Overall: Facilitates digestion by breaking down cell walls for further processing in the small intestine. “Quick” Overview Wall layers: Serosa, muscularis externa (3 Acid and pepsinogen production: Stimulated by layers), submucosa, and mucosa. sight and smell of food. Muscularis externa: Contains a thick circular Gastrin: Major hormonal regulator of acid muscle layer acting as the pyloric sphincter. secretion. Submucosa: Contains blood vessels, lymphatic Acid secretion regulation: vessels, and nerves. Stimulated by: Acetylcholine, gastrin, and histamine. Mucosa: Contains glands responsible for Inhibited by: Somatostatin, duodenal acid, and various functions. negative feedback from gastrin. Glands: Other functions: Fundus: Secrete mucus (protection) and Barrier against pathogens (acidic environment and hydrochloric acid (digestion). immune function). Antrum: Secrete mucus (protection) and gastrin Temperature regulation of ingested substances. (hormone). Secretion of intrinsic factor (vitamin B12 Sphincters: Lower esophageal sphincter (LES) absorption). and pyloric sphincter. Capacity: Stores up to 1.5 liters of fluid. Food storage: Up to 4 hours. Peptic Ulcer Disease Loss of stomach lining due to inflammation, can extend deeper into stomach wall. Types: Acute vs. Chronic (most common) Causes: H. pylori infection (most common) NSAID use Complications: Hemorrhage, perforation, obstruction Duodenal ulcers: More common in men 45-65 and women >55. Caused by excess acid and pepsin. Can involve lower stomach. Gastritis An inflammatory disorder of the stomach Treatment: lining (gastric mucosa) Immediate: Fluid resuscitation, blood Also called stress ulcers, erosive gastritis, or transfusion (if needed) hemorrhagic gastritis Infection control: Antibiotics, source control Stomach protection: Can cause life-threatening bleeding Nasogastric tube (NG) for lavage and decompression Causes: Antisecretory drugs (proton pump inhibitors or Multifactorial: H2 blockers) to reduce acid Physical trauma, shock, sepsis, etc. Complications: Medications, chemicals, or H. pylori infection Increased risk of infection and mortality Reduced blood flow, mucus, or bicarbonate secretion Who is at risk? Reduced prostaglandins Critically ill patients Stress: Hypoxia, sepsis, or organ failure Patients undergoing major surgery Symptoms: Patients with underlying medical conditions (e.g., coagulopathy) Upper GI bleeding Therapeutic Options in Peptic Ulcer Disease Goals: Complications of antacids: Relieve symptoms Acid rebound. Heal the ulcer Milk-alkali syndrome (hypercalcemia, alkalosis, Prevent recurrence elevated blood urea). Treatment: H2-receptor antagonists: H. pylori eradication: Main focus of medical Cimetidine, famotidine, and nizatidine therapy. Block acid secretion and promote healing. Medications: Adjust dosage for kidney function. Antacids: Short-term symptom relief, can cause acid Potential side effects: altered drug metabolism, rebound and milk-alkali syndrome. mental confusion, decreased blood flow. H2-receptor antagonists: Block acid secretion, adjust dosage for kidney function, potential side effects include altered drug metabolism, mental confusion, Proton pump inhibitors: and decreased blood flow. Most effective acid blockers. Proton pump inhibitors: Most effective acid blockers. Sucralfate: Promotes healing and protects the ulcer, Sucralfate: minimal side effects. Promotes healing and protects the ulcer. Misoprostol: Prevents ulcers in NSAID users. Minimal side effects. Antibiotics: Eradicate H. pylori. Surgery: Reserved for: Intractable symptoms despite medication. Complications: bleeding, perforation, obstruction. Therapeutic Options in Peptic Ulcer Disease Gastric Neoplastic Disease Prevalence: Hematemesis (vomiting blood). Gastric outlet obstruction symptoms. Second most common cancer worldwide. Seventh most common cause of cancer Diagnosis: death in the US. Endoscopy with biopsy. Types: Endoscopic ultrasound for staging. 95% adenocarcinoma. Treatment: 4% lymphoma. Early stage: Endoscopic mucosal resection. 1% leiomyosarcoma. Advanced stage: Surgery (most common): Symptoms: Total gastrectomy (proximal or diffuse tumors). Early stage: May have no symptoms. Partial gastrectomy (distal tumors). Advanced stage: Extended lymphadenectomy (may improve staging and survival). Epigastric pain (constant, non-radiating, not Other options: Chemotherapy, radiation therapy. relieved by food). Weight loss. Demographics: Anorexia. More common in men (2:1 ratio). Fatigue. Diagnosed in 5th-7th decades of life. Vomiting. Anesthetic Considerations in Gastric Disease Patients: atelectasis, ileus. Acutely ill (emergency surgery, e.g., bleeding ICU stay may be needed (peritonitis, large ulcer) fluid resuscitation). Stable (elective surgery, e.g., cancer, ulcer) Anesthetic technique: Procedures: May include epidural catheter for pain Often laparoscopic. management. Preoperative considerations: Types of surgery: Correct hypovolemia and anemia. Total/partial gastrectomy Consider invasive monitoring for high-risk Billroth I/II (stomach reconstruction) patients. Laparotomy with ulcer repair Anticipate moderate fluid shift and blood Vagotomy (for ulcers): loss. Reduces acid secretion and promotes Prepare for blood product transfusion. healing. Postoperative complications: Can be truncal (broad) or selective (targeted). Hemorrhage, hypovolemia, hypothermia, Gastrostomy Surgical creation of an opening in the stomach for feeding and decompression. Patients are often neurologically impaired or debilitated with compromised airway reflexes. Increased aspiration risk due to compromised airway reflexes and stomach insufflation. Procedure location: Bedside, endoscopy suite, or operating room. Guiding technique: Percutaneous placement uses endoscopic guidance. Pre-procedure considerations: Stop tube feeding 8 hours prior. Anesthesia: Primary procedure: Sedation and local anesthesia. General endotracheal anesthesia for laparotomy or contraindications to local anesthesia. ETT may need to be held during gastroscope insertion/withdrawal. Pancreatic Exocrine Functions Location: Head: curves around duodenum Body: behind stomach Tail: touches spleen Length: 20 cm Functions: Exocrine (enzymes): Secrete pancreatic juice (neutralizes stomach acid for enzyme activity) Enzymes break down proteins, fats, and carbohydrates Endocrine (hormones): (discussed on next slide) Exocrine juice secretion: Stimulated by hormones (secretin, CCK-PZ) and vagus nerve Neutralizes stomach acid (optimal enzyme activity) Regulation of exocrine secretion: Hormones and nervous system activity Vagolytic agents and vagotomy can decrease secretion Pancreatic Endocrine Functions Cell types: Alpha (A) cells: Secrete glucagon (increases blood sugar). Beta (B) cells: Secrete insulin (decreases blood sugar). Delta (D) cells: Secrete somatostatin (regulates other hormones). Delta-2 (D2) cells: Secrete vasoactive intestinal peptide (VIP). PP (F) cells: Secrete pancreatic polypeptide (PP) (function not fully understood). Main function: Regulate blood sugar levels. Hormone actions: Insulin: Promotes energy storage by lowering blood sugar, increasing protein synthesis, and decreasing breakdown of glycogen and fat. Glucagon: Promotes energy release by raising blood sugar through glycogen breakdown, new glucose production, and increasing fat breakdown. Regulation of insulin secretion: Stimulated by: Parasympathetic nervous system, beta-adrenergic stimulation, and low blood sugar. Inhibited by: Alpha-adrenergic stimulation, stress, and certain medications. Acute Pancreatitis Causes Symptoms Alcohol abuse Pain (severe, radiating) Gallstones Nausea, vomiting, and fever Other factors (trauma, infections, Hypotension medications) Treatment Phases Fluid resuscitation 1st – activation of trypsin in acinar cells Pain management (avoid morphine) 2nd – inflammatory response of the pancreas Nutritional support 3rd – systemic activation of the immune Surgery (for gallstones) system CRP level Culprit enzymes Anesthetic Those activated by trypsin, enterokinase, and bile acids Choice of anesthetic technique depends on pt presentation Pancreatic inflammation, which is caused by vascular breakdown, coagulation necrosis, fat Fluid status necrosis, and parenchymal necrosis Anticipate labile hemodynamics and altered Mimic an MI and can cause ARDS and DIC hepatic function Chronic Pancreatitis Permanent damage to the pancreas with and lungs inflammation, scarring, and tissue destruction. Electrolyte Imbalances: Causes: Hypoalbuminemia: Worsened by treatment with Most common: Alcohol abuse (70% of cases) albumin-free fluids. Other: Smoking, genetics, autoimmune disease, Hypomagnesemia: Common complication. duct obstruction Hypocalcemia: Usually due to low albumin Treatment: Calcium replacement only if ionized calcium Diagnosis: is low. "Classic triad": steatorrhea, pancreatic Endocrine Insufficiency: calcification, diabetes mellitus Steatorrhea only occurs with very low lipase Diabetes: Develops in half of patients after secretion. resection or severe pancreatitis. Increased risk of severe hypoglycemia: Due to Symptoms: combined alpha and beta cell damage. Abdominal pain Other Weight loss and malnutrition Pancreatic abscess: Requires surgical drainage. Potential liver problems (jaundice, ascites, etc.) Fistula formation: Possible, especially to the colon. Malabsorption of fats and proteins Hemorrhage: Possible due to erosion of major Increased risk of fluid buildup around the heart arteries. Pancreatic Pseudocysts Fluid: Watery, rich in pancreatic enzymes. Enzyme levels: Typically elevated in patients with pseudocysts. Resolution: Many resolve spontaneously without intervention. Large (>6 cm) pseudocysts are less likely to resolve on their own. Complications: Symptoms: Tenderness, nausea, vomiting, early fullness, jaundice. Bleeding: Erosion into blood vessels can cause bleeding. Treatment: Not mandatory for all cases. Symptomatic or complicated cases: Drainage preferred. Internal drainage: Endoscopic (preferred for high surgical risk): Transpapillary, cystogastrostomy, cystoduodenostomy. Surgical: Cystogastrostomy, cystoduodenostomy, Roux-en-Y cystojejunostomy. Choice depends on expertise and pseudocyst location. Surgical Therapy for Pancreatitis Endoscopic Therapy (for drainage): Pancreatic duct sphincterotomy Stent placement Pancreatic duct stone removal Open Surgery (for chronic pancreatitis): Intractable pain (failed medical therapy) Complications with nearby organs Failed endoscopic pseudocyst management Internal pancreatic fistulas Pseudocyst Drainage Surgery: Performed after cyst maturation (6 weeks for acute pancreatitis) Cystogastrostomy, cystojejunostomy, cystoduodenostomy, or distal pancreatectomy (depending on location) Percutaneous Drainage (rare): For particularly friable pseudocysts Guided by CT scan Pancreatic Tumors Epidemiology: Imaging (CT, ERCP). 25,000-30,000 new cases per year in the US. Biopsy. More common in men and older adults (60-80 years old). Treatment: Risk factors: family history, smoking, diabetes. Surgery (if possible): Types: Whipple procedure (head of pancreas, duodenum, etc.). 80-90% are ductal adenocarcinomas. Distal pancreatectomy (tail of pancreas). Location: Other treatments: medication, radiation therapy. Head/uncinate process (70%) - often cause jaundice. Other pancreatic tumors: Body/tail - larger and spread before symptoms appear. Insulinoma (hypoglycemia) - treated with surgery. Symptoms: Gastrinoma (Zollinger-Ellison syndrome) - excess stomach Vague and non-specific. acid, treated with surgery and medication. Jaundice (head tumors). Anesthetic Management Pain (abdomen, back). Fluid and electrolytes Anorexia, fatigue, weight loss. Know the tumor and what it could secrete Nausea, vomiting, diarrhea. New-onset diabetes. Diagnosis: Blood tests (bilirubin, alkaline phosphatase). Anesthetic Considerations in Pancreatic Disease Clinical presentation: Variable, from stable and jaundiced to severely ill with multi-organ involvement. May have severe abdominal pain, possible intestinal obstruction. Preoperative considerations: Aspiration risk: High, requires precautions during anesthesia. Blood sugar: Monitor and manage due to potential diabetes or hypoglycemia. Fluids and blood products: Likely needed for hypotension and hypovolemia, consider invasive monitoring. Electrolytes: Monitor and correct imbalances (calcium, magnesium, potassium, etc.). Coagulation: Monitor regularly (platelets, PT, aPTT, fibrinogen). Kidney function: Assess and monitor (BUN, creatinine, urine output). Lungs: Assess for complications (effusions, mismatching, atelectasis) and risk factors (preoperative state, pain). Heart: Assess for hemodynamic impairment and treat any existing issues. ECG: Monitor for changes (may not indicate actual ischemia). Celiac plexus block: May be used for chronic pancreatitis pain management. Uses combination of glucocorticoid and local anesthetic. Celiac plexus neurolysis can be performed with alcohol injection under imaging guidance. Pancreatectomy Reasons for surgery: Ductal obstruction Pancreatic stones or cysts Trauma Tumors (benign or malignant) Chronic pancreatitis Endocrine tumors Surgery types: Partial pancreatectomy: Removes part of pancreas, duodenum, gallbladder, and bile duct. Total pancreatectomy: Removes part of stomach, gallbladder, bile duct, spleen, lymph nodes, and entire pancreas. Anesthesia: General endotracheal preferred, with muscle relaxants. Avoid nitrous oxide. Epidural or intrathecal morphine for pain control. Postoperative care: May require ventilation and ICU monitoring due to surgery duration and patient health. Small Intestine Layers: Immune function: Serosa: Outermost layer, single layer of cells. Lamina propria has immune cells for protection. Muscularis propria: Composed of smooth muscle IgA antibodies in lamina propria prevent pathogen for contraction. entry. Auerbach plexus: Between muscle layers, controls motility and secretion. Nervous system: Submucosa: Strongest layer, contains connective Autonomic nervous system: tissue and: Parasympathetic: Increases motility and secretions. Meissner plexus: Regulates blood flow, motility, and Sympathetic: Inhibits motility and causes secretions. vasoconstriction. Mucosa: Innermost layer, with folds and villi for Enteric nervous system: increased surface area: Intrinsic neurons within the wall of the small intestine, Muscularis mucosae: Thin muscle layer separating pancreas, and gallbladder, controls local functions like mucosa and submucosa. digestion and peristalsis. Lamina propria: Connective tissue with immune cells Motility: and support functions. Epithelial layer: Covers villi and crypts, contains various Intestinal reflexes regulate movement and cell types for: emptying. Absorption: Absorptive cells take up nutrients. Electrical rhythm and muscle contractions mix and Secretion: Goblet cells secrete mucus, villi secrete move food through the small intestine. enzymes. Hormone production: Endocrine cells release hormones. Small Intestine & Malabsorption Syndromes Function: Protein malabsorption: Largest endocrine gland Peripheral edema (swelling) Digestion and nutrient absorption Ascites (fluid buildup) Absorbs 85-90% of water entering the GI tract Calcium deficiency: Malabsorption syndromes: Vitamin D or calcium malabsorption Disrupt nutrient absorption due to: Fatty acids bind calcium Brush border processing issues Tetany (muscle cramps) Mucosal disruption Osteomalacia (bone softening) Impaired transport Fractures Examples: diverticulosis, radiation enteritis, gastric bypass Symptoms: Treatment for steatorrhea: Unexplained weight loss Pancreatic replacement enzymes (in some cases) Steatorrhea (fatty stool) Causes of malabsorption syndromes: Diarrhea Disruption of intestinal lining (e.g., disease) Other potential issues: anemia, bone loss, menstrual problems Loss of absorptive surface area (e.g., surgery) Affects absorption of: amino acids, carbohydrates, fats Extent of surgery impacts severity of deficiencies Fat malabsorption consequences: Deficiencies in fat-soluble vitamins (A, D, E, K) Vitamin K deficiency: bleeding problems Vitamin B12 deficiency: anemia, nerve problems, tongue inflammation Maldigestion Syndrome Cause: Failure of chemical digestion in the intestines. Common causes: Pancreatic deficiency Lactase deficiency Bile salt deficiency Difference from malabsorption: Maldigestion specifically refers to the breakdown issue, while malabsorption refers to the absorption issue. Key symptom: Steatorrhea (fatty stool) Pancreatic insufficiency: Usually present due to its large functional reserve. Other causes: Cystic fibrosis Fistulas Gallstones Ischemic enteritis Neoplastic diseases Diabetes mellitus Vitamin B6 or B12 deficiency Large Intestine Anatomy: colon), S2-S4 (descending colon, sigmoid colon, Length: 3-5 feet and rectum) Parts: Cecum, appendix, colon, rectum, anal canal Functions: Blood Supply: Store and expel waste Arteries: Superior mesenteric, inferior mesenteric, Absorb water and sodium (mostly in the right internal iliac colon) Veins: Drain into portal venous system (except Efficient absorption: Only 100-200mL out of 1-2L rectum) daily fluid reaches the end Importance: Individuals with ileostomy need extra Lymphatic Drainage: sodium intake Upper rectum and colon: Superior rectal and Electrolyte Balance: inferior mesenteric nodes Lower rectum and anal canal: Inguinal lymph Sodium: Actively reabsorbed, efficient process (5 nodes mEq/day needed for balance) Loss after colectomy can overwhelm small Innervation: intestine's compensatory ability Motor and secretory control: Myenteric plexus Potassium: Passively absorbed/secreted, lost in Sympathetic: T10-T12 (right), L1-L3 (left), presacral mucoid stools (colitis, villous adenoma) nerves (rectum) Chloride: Absorbed with sodium, exchanged for Parasympathetic: Vagus nerve (right & transverse bicarbonate Inflammatory Bowel Disease Types: Crohn's disease: Affects any part of the GI tract, often the distal ileum and proximal colon. Ulcerative colitis (UC): Affects the colonic mucosa, extending proximally. Crohn's Disease: Symptoms: Abdominal pain, diarrhea (with blood and mucus), right lower quadrant tenderness, anemia. Complications: Fistulas, abscesses, kidney stones, nutritional deficiencies, increased cancer risk. Treatment: Medication, surgery (for complications, limited effectiveness). Ulcerative Colitis: Symptoms: Abdominal pain, fever, bloody diarrhea, weight loss. Complications: Toxic megacolon (severe distention and inflammation), arthritis, liver disease, increased cancer risk. Treatment: Medication, surgery (curative for most cases). Similarities: Both are chronic inflammatory bowel diseases. Both can cause anemia and nutritional deficiencies. Both require similar supportive care for systemic issues. Both may require surgery for complications. Differences: Crohn's disease can affect any part of the GI tract, while UC only affects the colon. Crohn's disease often involves deeper layers of the intestine, leading to different complications. Crohn's disease surgery is non-curative, while UC surgery can be curative. UC has a higher risk of toxic megacolon. Anesthetic Considerations in Inflammatory Bowel Disease Preoperative Optimization: Correct anemia, fluid depletion, electrolyte imbalances, and acid-base issues. Assess nutritional status. Consider extracolonic complications (sepsis, liver issues, etc.). Prophylactic steroids for long-term steroid users. Intraoperative Considerations: Avoid nitrous oxide (can cause bowel distention). Many patients require TPN and bowel rest. Be aware of TPN complications (hyperglycemia, electrolyte imbalances, etc.). Maintain existing TPN infusion. Monitor and correct fluid, electrolyte, and blood values regularly. Technique and drug selection depend on severity of extracolonic issues. Anticholinesterases for reversal have no effect on colonic suture lines. Anesthetic Technique: No specific technique required but combined (epidural and general) is common. Combined spinal-epidural may be beneficial for specific cases. Diverticulitis and Diverticulosis Diverticulosis: Outpouchings in the colon wall (most common in the left colon). Usually asymptomatic. Diverticulitis: Inflammation of the diverticula. Symptoms: abdominal pain, nausea, vomiting, diarrhea, dehydration. Complications (requiring surgery): Abscess formation Visceral perforation Bowel obstruction Fistulas Peritonitis Treatment: Initial: IV fluids, antibiotics, corticosteroids. Surgical intervention for severe cases or complications. Bleeding: uncommon but can be difficult to locate. Elective surgery considered for: Recurrent episodes After a second attack (higher complication and mortality rates) Diverticulitis in the right colon can mimic appendicitis, potentially requiring extended surgery. Abdominal Compartment Syndrome High pressure inside the abdomen (>20 mm Hg) that damages organs. Normal pressure is less than 10 mm Hg. Causes: Trauma, bleeding, pancreatitis, bowel obstruction, fluid overload. Pregnancy, ascites, tumors (chronic ACS). Symptoms: Difficulty breathing, decreased urine output, heart problems. Can lead to multiple organ failure and death if not treated promptly. Treatment: Urgent surgery to decompress the abdomen. Anesthesia considerations: Manage existing health problems of the patient. Maintain hemodynamic stability and ventilation. Use drugs cautiously to avoid complications. Complications: Reperfusion syndrome (low blood pressure and acidosis after surgery). Anesthetic Considerations in Elective Colon Surgery Surgeon removes diseased bowel section and connects remaining parts. Intestinal cleaning is crucial to prevent infection: Night before: Oral/NG tube solutions or enemas. Diet: Fluids, low-residue food, clear liquids 24-48 hours before surgery. Antibiotics: Aminoglycosides or cephalosporins + metronidazole. Pre-existing conditions to be aware of: Electrolyte imbalances from aggressive cleaning, especially in elderly/dehydrated patients. Anemia from blood loss. Malnutrition with low protein (albumin). Additional considerations: Drainage tube (NG) might be needed for blocked or inactive colon. Dehydration and electrolyte imbalance may require delaying surgery for correction.  Carcinoma of the Colon Common and treatable: 2nd most diagnosed, 3rd leading cause of cancer death (US). Development: Often starts from polyps. Treatment: Primarily surgery (50% cure rate). Risk factors: Diet (high red meat, low fiber), genetics, inflammatory bowel disease. Screening: Stool tests, rectal exam, colonoscopy. Symptoms: Right-sided: Pain, mass, anemia, dark blood in stool. Left-sided: Abdominal distention, pain, vomiting, constipation, bright red blood in stool, possible obstruction. Prognosis: Worse with deeper tumor penetration and lymph node involvement. Volvulus of the Colon A twisting of the large intestine (colon) that cuts off blood supply and blocks the flow of stool. Most commonly affects the lower part of the colon (sigmoid colon). Symptoms: Sudden and severe abdominal pain, vomiting, and bloating. Fever and low blood pressure can indicate a more serious case. Treatment: Initial: Fluids and a tube inserted through the rectum or colon to decompress the blockage. Surgery: If the tube doesn't work, the affected part of the colon is removed with an opening created in the abdomen (colostomy) or sewn shut (Hartmann procedure). Who gets it? Often affects elderly or people with long-term illnesses or disabilities. May be linked to medications that affect gut movement. Ischemic Bowl Disease What is it? Occurs when blood flow to the intestines is insufficient, damaging tissues. Can be caused by various factors like narrowing of blood vessels, infections, and surgeries. Symptoms: Fever, vomiting, rectal bleeding, and abdominal pain (may last for weeks or months). Sudden bleeding with left-sided pain and signs of infection suggest a serious case. Who gets it? Often affects elderly people with existing conditions like heart disease and high blood pressure. Treatment: Initially focuses on fluids, antibiotics, and managing symptoms. Surgery may be needed to remove damaged tissue (bowel resection) and create an opening in the abdomen (colostomy) in severe cases. In some cases, vascular surgery might be an option to improve blood flow. Notes: Difficult to differentiate from other conditions like inflammatory bowel disease. Definitive diagnosis involves endoscopy and biopsy. X-rays or ultrasounds help rule out bowel perforation. Diseases of the Rectum and Anus Types: Rectal cancer: Treated with surgery (abdominal-perineal resection) or chemotherapy/radiation (squamous cell). Rectal prolapse: Eversion of rectal wall, repaired with surgery (rectosigmoidectomy or proctopexy). Perirectal abscess: Pus collection, treated with drainage (inpatient or outpatient). Perirectal fistula: Connection between an abscess and skin, treated with drainage and delayed surgery. Hemorrhoids: Swollen veins in the rectum/anus, treated with rubber band ligation, surgical excision (internal) or surgical excision (external). Anesthesia: Regional anesthesia (spinal, epidural) or local anesthesia with sedation are common. General anesthesia may be needed in some cases. Anesthesia considerations include patient positioning and its impact on cardiovascular and respiratory systems. Radiation Enteritis Inflammation of the small intestine caused by radiation therapy for abdominal and pelvic cancers. Causes: Radiation damaging healthy cells along with cancer cells. Factors increasing risk: Amount of radiation used. Amount of small bowel exposed to radiation. Previous intestinal surgery. Concurrent chemotherapy. Symptoms: Acute (short-term): Diarrhea Abdominal pain Malabsorption (difficulty absorbing nutrients) Chronic (long-term): Caused by blood vessel damage Develops years after radiation therapy Treatment: Acute: Supportive care (fluids, medication) Chronic: Surgery (bypass, resection) if complications like obstruction, fistula, perforation, or bleeding occur. Complications: Increased risk of bleeding and tissue damage during surgery due to adhesions and weakened tissues. Relentless disease course with potential need for multiple surgeries. Up to 25% mortality rate from complications. Appendicitis Inflammation of the appendix, a small finger-shaped organ attached to the large intestine. Most common reason for emergency abdominal surgery. Who gets it? Typically affects people between 10-30 years old, slightly more common in males. Symptoms: Early: Vague upper abdominal pain that moves to the lower right abdomen. Later: Nausea, vomiting, loss of appetite, fever, localized tenderness in the lower right abdomen (McBurney's point). Complications of a perforated appendix: Peritonitis (infection of the abdominal lining) Abscess (collection of pus) Thrombus in the portal vein Treatment: Appendectomy: Surgical removal of the appendix. Laparoscopic (minimally invasive) surgery preferred for simple cases. Open surgery may be needed in some cases. Anesthesia: General, regional, or local anesthesia with sedation may be used depending on the situation. Preoperative fluids and antibiotics may be needed. Splenic Disease Location and Size: Spleen Removal (Splenectomy): Upper left abdomen, behind the stomach and ribs. Can be done for various reasons, including: Normal weight: less than 250g. Blood disorders (e.g., sickle cell disease, thalassemia). Not usually palpable. Cancers (e.g., lymphoma). Spleen infections or cysts. Structure: Enlarged spleen (splenomegaly). Capsule divided into 3 zones by connective tissue. People without a spleen are more susceptible to White pulp (lymphoid tissue), red pulp (blood filtration), infections. and marginal zone (interface). Blood Supply: Splenic artery supplies blood. Splenic vein drains blood to the portal system. Functions: Filters blood: removes old/damaged red blood cells and debris. Immune system: helps fight infections and produces antibodies. Minor storage: platelets and red blood cells (in emergencies). Splenectomy Minimally Invasive Surgery: Avoiding nitrous oxide to prevent bloating. Laparoscopy is the preferred approach for most Maintain blood pressure and hydration. splenectomies. Monitor all labs (BMP, CBC, Coag) Benefits: faster recovery, lower risk of complications. Patients with Past Chemotherapy: May have weakened organ systems requiring careful assessment. Potential complications: heart problems, lung damage, nerve damage, liver damage, kidney problems. Preoperative Preparation: Lab tests to assess blood cell counts, clotting function, kidney function, and liver function. Blood typing and crossmatching for potential transfusion. Steroid administration if previously used in treatment. Anesthesia: General endotracheal anesthesia with or without epidural for pain management is common. Specific considerations: Rapid sequence intubation for certain situations. Carcinoid Tumors What are they? Diagnosis: Slow-growing cancers arising from hormone- Elevated levels of hormone breakdown producing cells. products in urine. Most common in the gastrointestinal tract, but can occur elsewhere (lung, pancreas, etc.). How do they cause problems? Release hormones that can affect various body functions. Serotonin: flushing, diarrhea, heart problems. (Elevated 5-HIAA found in the urine) Histamine: bronchospasm, flushing. Bradykinin: severe hypotension, flushing, bronchospasm. Carcinoid Syndrome and Crisis Carcinoid Syndrome A group of symptoms caused by hormones released from tumors, especially those that have spread to the liver. Symptoms can include: Flushing Diarrhea Heart problems Wheezing Abdominal pain Low blood pressure or high blood pressure Octreotide has improved patient prognosis Carcinoid Crisis A life-threatening form of carcinoid syndrome that can be triggered by surgery or other procedures. Surgery can be an effective treatment for carcinoid tumors. Important Note: Carcinoid syndrome can cause complications during surgery, so careful management is needed. Carcinoid Tumors and Carcinoid Syndrome: Anesthetic Management Main Goal: Prevent the release of hormones from tumors that can cause complications (carcinoid crisis). Medications: Octreotide and lanreotide (long-acting) are used to control symptoms before and after surgery. Anesthesia: General anesthesia is most common to avoid complications from neuraxial anesthesia. Spinal anesthesia might be an option with careful monitoring and medication use. Preoperative tests: standard blood work, ECG, and heart function assessment are crucial. Monitoring: invasive monitoring (arterial line, CVP) is often needed due to potential blood pressure changes. Induction: Drugs that avoid triggering hormone release are preferred (propofol might be best). Avoid drugs that cause histamine release (morphine, thiopental, some muscle relaxants). Pain Management: Opioids are used, but avoid those causing histamine release. Vecuronium or rocuronium are preferred muscle relaxants for their cardiovascular stability. Ventilation and Anesthetic Agents: Balanced anesthesia with inhalation agents, muscle relaxants, opioids, and positive pressure ventilation is common. Inhalation agents with low blood-gas solubility (desflurane) are preferred. Nitrous oxide is safe to use. High-dose opioids might be needed due to potential heart problems in these patients. Blood Pressure Management: Hypotension is a concern. Use medications that avoid further hormone release (alpha-receptor agonists like phenylephrine). Enhanced Recovery After Surgery The End! You made it!