Module 4: Gastrointestinal and Endocrine Disorders

Acute Gastrointestinal Hemorrhage

• GI Hemorrhage is a critical, life-threatening condition and a common complication in critically ill patients. It accounts for over 300,000 hospital admissions annually in the U.S.

• Mortality Rate: The annual mortality rate remains around 10% in patients with acute GI bleeding.

  Division of GI Tract:

• Upper GI Tract: Bleeding proximal to the ligament of Treitz (e.g., stomach, duodenum, esophagus).

• Lower GI Tract: Bleeding distal to the ligament of Treitz (e.g., colon, rectum).

Common Causes of GI Hemorrhage:

• Peptic Ulcer Disease (PUD): Leading cause of upper GI hemorrhage (40% of cases).

• Esophagogastric Varices: Bleeding due to portal hypertension.

• Stress-Related Mucosal Disease (SRMD): Associated with critically ill patients.

Peptic Ulcer Disease (PUD)

Mechanisms of Protection:

• Mucous barrier, tight junctions between epithelial cells, blood flow, and prostaglandins protect the stomach lining from gastric acid.

Pathogenesis:

• Breakdown of protective mechanisms due to Helicobacter pylori infection or NSAIDs leading to ulceration, autodigestion, and hemorrhage.

Stress-Related Mucosal Disease (SRMD)

Definition:

• ______ is an acute erosive gastritis common in critically ill patients.

Pathophysiology:

• Caused by increased acid production and reduced blood flow to the mucosa, leading to ischemia and degeneration of the mucosal lining.

Risk Factors:

• Mechanical ventilation, burns, trauma, major surgery, shock, sepsis, and coagulopathy.

Management:

• Prophylaxis: Use of H2 antagonists, proton pump inhibitors (PPIs), or cytoprotective agents to prevent further ulceration.

Esophagogastric Varices

Cause:

• Caused by portal hypertension due to hepatic cirrhosis.

Pathogenesis:

• Increased portal pressure leads to diversion of blood into collateral veins (e.g., esophagus, stomach), which become engorged and fragile, making them prone to rupture.

Management:

• Pharmacologic Agents: Vasopressin, somatostatin, and octreotide to reduce portal venous pressure.

• Endoscopic Therapy: Includes endoscopic injection sclerotherapy (EIS) and endoscopic variceal ligation (EVL).

Acute GI Hemorrhage Pathophysiology

• Hypovolemic Shock: Massive GI bleeding leads to blood loss and hypovolemic shock, triggering compensatory mechanisms to maintain organ perfusion.

• Organ Dysfunction: If untreated, it can lead to multiple organ dysfunction syndrome (MODS).

Clinical Implications:

• Underlying Disease Exacerbation: Most deaths from GI hemorrhage occur due to the exacerbation of underlying diseases (e.g., liver disease, cancer).

Diagnostic Procedures for GI Hemorrhage

Urgent Fiberoptic Endoscopy:

• Goal: Identify and treat the source of bleeding.

• Timing: Endoscopy is ideally performed after the patient is stabilized hemodynamically.

Other Diagnostic Options:

• Tagged Red Blood Cell Scanning: Used for localizing active bleeding.

• Angiography: Used if bleeding is not controlled or endoscopy is not feasible.

Management of GI Hemorrhage

Initial Goals:

• Early Identification: Early detection of at-risk patients to reduce mortality.

• Pharmacologic Interventions: Neutralize gastric acid and protect the mucosa using antacids, H2 antagonists, PPIs, and cytoprotective agents.

Stabilization and Initial Management:

• Fluid Resuscitation: Crystalloids, blood, and blood products to restore blood volume and prevent shock.

• Oxygen Therapy: Enhances oxygen delivery to tissues.

• Nasogastric Tube: For active bleeding diagnosis, gastric lavage, and preparation for endoscopic evaluation.

Control of Bleeding in PUD and SRMD

PUD: 

• Endoscopic Injection Therapy: Thermal therapy and injection of agents like epinephrine to induce vasoconstriction and stop bleeding.

SRMD:

• Intraarterial Infusion: Vasopressin or embolization to control bleeding.

Esophagogastric Varices:

• Pharmacologic Agents: Vasopressin, somatostatin, octreotide to reduce bleeding.

• Endoscopic Therapies: Includes Endoscopic Injection Sclerotherapy (EIS) and Endoscopic Variceal Ligation (EVL).

Surgical Interventions for GI Hemorrhage

Peptic Ulcer Disease:

• Surgery: Vagotomy and pyloroplasty to reduce acid production and promote gastric emptying.

Esophagogastric Varices: 

• Shunting Procedures: Portacaval shunt to relieve portal hypertension.

Nursing Management in GI Hemorrhage

At-Risk Populations:

• All critically ill patients are at risk for GI hemorrhage due to factors like mechanical ventilation and stress ulcers.

Prophylaxis:

• Maintain gastric pH between 3.5-4.5 using PPIs, H2 blockers, and antacids.

Signs of Bleeding:

• Hematemesis (vomiting blood), Hematochezia (bright red stools), and Melena (black, tarry stools) should be promptly reported.

IV Access and Volume Replacement:

• Insert two large-diameter peripheral catheters for rapid fluid and blood product administration.

• Gastric Lavage: Use normal saline or room-temperature water to irrigate the stomach for bleeding diagnosis.

Acute Pancreatitis

• Acute pancreatitis is inflammation of the pancreas, often involving surrounding tissues or organs.

• Causes: Most common are gallstones and alcohol consumption, but also trauma, hypercalcemia, toxins, and medications.

Pathophysiology:

• Premature Activation of Digestive Enzymes: Enzymes like trypsin activate other enzymes leading to pancreatic autodigestion, hemorrhage, and fat necrosis.

Clinical Manifestations:

• Abdominal Pain: Often severe, located in the epigastric region, radiating to the back.

• Signs of Hypovolemic Shock: Tachycardia, hypotension, fever, diaphoresis.

• Grey Turner and Cullen Signs: Rare, but indicate pancreatic hemorrhage.

Management of Acute Pancreatitis

Fluid Management:

• Crystalloids and colloids are given for hypovolemic shock and hemodynamic stability.

Nutritional Support:

• Enteral feeding is preferred over parenteral nutrition (TPN) to maintain gut integrity and reduce infection risks.

Complications:

• Hypovolemic shock, acute kidney injury (AKI), and ARDS are common complications.

• Infected Pancreatic Necrosis requires surgical intervention like necrosectomy.

Acute Liver Failure (ALF)

Definition and Etiology:

• Acute liver failure (ALF) is characterized by rapid liver dysfunction, coagulopathy, and hepatic encephalopathy.

• Causes: Massive hepatocyte necrosis due to viral infections, toxic drugs (e.g., acetaminophen overdose), or autoimmune hepatitis.

Pathophysiology:

• Impaired bilirubin conjugation, clotting factor production, and glucose synthesis lead to jaundice, coagulopathy, and hypoglycemia.

Management:

• Liver Transplantation: The only definitive treatment for ALF.

• Ammonia Reduction: Lactulose and antibiotics (neomycin, metronidazole) are used to reduce ammonia production.

Diabetic Ketoacidosis (DKA)

• Etiology: Common in Type 1 Diabetes, usually triggered by infection or stress.

• Management: Includes fluid resuscitation, insulin therapy, and electrolyte correction.

Hyperglycemic Hyperosmolar State (HHS): 

• Occurs in: Type 2 Diabetes, characterized by extreme hyperglycemia (>600 mg/dL) and dehydration without significant ketosis.

• Management: Similar to DKA, but with slower insulin infusion rates.

Total Parenteral Feeding (TPN)

• It is a way of supplying all the nutritional needs directly into blood stream bypassing gastrointestinal tract.

• It is administered outside the digestive tract, intravenously.

Indications

1. When individuals cannot or should not get nutrition through eating.

2. When the intestines are obstructed, when the small intestine is not absorbing nutrients properly or a gastrointestinal fistula (abnormal connection) is present.

3. When the bowels need to rest and not have any food passing through them. Bowel rest may be necessary in Crohn’s disease, pancreatitis, ulcerative colitis, and with prolonged bouts of diarrhea in young children.

4. Individuals with severe burns, multiple fractures, and in malnourished individuals to prepare them for major surgery, chemotherapy, or radiation treatment.

5. Individuals with aids or widespread infection (sepsis).

Composition of Ingredients in Bag for IV Delivery

• Usual fluid volume is 1.5 - 2.5L over a 24 hours period for most people.

• Actual infusion depends on:

  1. Site of infusion; and

  2. Patient’s fluid and nutrient requirements.

Carbohydrate

• Dextrose provides the _____ content of PN, up to 75% of the total energy of the solution. It provides 3.4 kcal/g.

• Glucose is the body’s main source of energy.

• Concentration is 12.5% (maximum for peripheral introduction) to 25% (total parenteral nutrition)

• Restricted in ventilator patients because oxidation of glucose produces more carbon dioxide than does oxidation of fat.

Protein

• Mixture of essential and non-essential amino acids

• Concentration 3.5 – 15%

• Quantity of amino acids depends on patients estimated requirements and hepatic and renal function.

Fat

• Lipid emulsion is a soluble form of fat that allows it to be infused safely into the blood.

• Safflower and soybean oil with egg lecithin used as an emulsifier.

• Isotonic

• Significant source of calories.

• Usual dose is 0.5 to 1 g/kg/day to supply 20- 30% of total kcal requirement.

• IV fat contraindicated for severe hepatic pathology, hyperlipidemia or severe egg allergies.

• Used cautiously with atherosclerosis, blood coagulation disorders.

Micronutrients

• Standard multi-vitamin and trace mineral preparations added to parenteral solutions to meet micronutrient needs.

Electrolyte

• It is dictated by patient’s blood chemistry values and physical assessment findings.

Peripheral vein

• Must be isotonic and therefore low in dextrose and amino acids to prevent phlebitis and increased risk of thrombus formation.

• The need to maintain isotonic solutions of dextrose and amino acids while avoiding fluid overload limits the caloric and nutritional value of PPN

Advantages:

1.Delivers complete but limited nutrition.

2. The final concentration cannot exceed 12.5% dextrose – lower concentrations of amino acids.

3. Vitamins and minerals are added.

4. Lipid emulsion may be added to supplement calories depending on the patients’ tolerance.

5. Provides temporary nutritional support.

6. Short - term: 7 – 10 days and do not require more than 2000 to 2500 kcal per day.

7. May be used for a post surgical ileus or anastomotic leak or for patients who require nutritional support but are unable to use TPN because of limited accessibility to a central vein.

8. Sometimes used to supplement an oral diet or tube feeding or transition from TPN to enteral intake. Total Parenteral Nutrition (TPN)

Superior vena cava

• Hypertonic solutions provide more dextrose and/or protein but they must be delivered centrally in a large diameter vein so that they can be quickly diluted,

• Higher concentration is used for TPN due to more rapid dilution in superior vena cava.

• It is used when nutritional requirements are high and anticipated need is relatively long 3 litres of 10% dextrose provides only 1020 kcal.

Indications:

1. Severe malnutrition

2. GI abnormalities: due to obstruction, peritonitis, severe acute pancreatitis

3. After surgery or trauma especially that involving extensive burns, sepsis

4. Need for supplementation of inadequate oral uptake in patients who are being treated aggressively for cancer

5. Bone marrow transplantation