Assessment of Metabolic-GI & Liver Disorders

Assessing gastrointestinal and liver disorders requires both subjective data (patient history, with pain being the most common complaint) and objective data (physical examination, diagnostic tests) to form a complete clinical picture.

Invasive assessment techniques are crucial for diagnosis and include several key procedures. Blood glucose monitoring (HbA1C) tracks patterns in diabetes patients, with newer options like Continuous Glucose Monitoring (CGM) providing real-time readings through subcutaneous sensors. The Minimed 770G system even includes a built-in insulin pump for automated delivery.

Esophago-Gastroduodenoscopy (EGD) allows direct visualization of the upper GI tract using a lighted endoscope. Similarly, Endoscopic Retrograde Cholangio-Pancreatography (ERCP) combines endoscopy with X-rays to examine the bile ducts, pancreatic ducts, and gallbladder. ERCP has evolved from primarily diagnostic to therapeutic, enabling procedures like stone removal and biliary stenting.

💡 All endoscopic procedures require patients to remain NPO (nothing by mouth) for approximately 8 hours before the procedure, and patients typically receive sedation and medications to reduce secretions and relax smooth muscles.

Percutaneous Transhepatic Cholangiography (PTC) visualizes the biliary tract by injecting contrast medium directly into a bile duct in the liver. This technique helps distinguish between different causes of jaundice and identify obstructions. While largely replaced by less invasive imaging methods, PTC is still valuable for therapeutic procedures like biliary drainage and stent placement.

Liver biopsy, which removes a small tissue sample via needle aspiration, remains the definitive diagnostic test for many liver conditions. Nursing care focuses on monitoring for bleeding, which may present as severe pain, and positioning patients on their right side after the procedure to apply natural compression.

General Nursing Interventions for Endoscopic Procedures

Nursing interventions for endoscopic procedures fall into two main phases. Pre-procedure care includes ensuring patients are NPO for 8 hours, administering medications like midazolam (for sedation), atropine (to reduce secretions), and glucagon (to relax smooth muscles), and positioning patients in the left lateral position for optimal scope entry.

Post-procedure monitoring is critical and includes checking the level of consciousness, oxygen saturation, pain levels, and watching for signs of perforation (pain, bleeding, swallowing difficulties, fever). After the gag reflex returns, patients may receive lozenges or analgesic gargles. Patients should remain in bed until fully alert and receive both verbal and written discharge instructions.

Liver biopsy involves removing a small amount of liver tissue through needle aspiration, typically to evaluate diffuse disorders or diagnose masses. Following this procedure, nurses must monitor for bleeding signs and position patients on their right side to apply natural compression and stop bleeding. Patients should avoid lifting or bending for 24 hours after the procedure to prevent pressure on the peritoneal cavity.

Acute GI Bleeding

Acute GI bleeding may be obvious or occult (hidden). Upper GI bleeding originates above the ligament of Treitz and presents with symptoms like syncope, hypotension, abdominal tenderness, melena (black stool), or hematemesis (vomiting blood). Laboratory findings often show anemia and an elevated BUN:Creatinine ratio (>20:1).

⚠️ Common causes of upper GI bleeding include peptic ulcer disease (from NSAIDs or H. pylori), erosive esophagitis, stomach varices, arteriovenous malformations, and Mallory-Weiss syndrome (tears from forceful vomiting).

For variceal bleeding (dilated blood vessels from portal hypertension), medications like somatostatin and octreotide reduce splanchnic blood flow, while beta-blockers decrease portal pressure by reducing cardiac output. These pharmacologic interventions are critical in stabilizing patients before definitive treatment.

Management of GI Bleeding

Lower GI bleeding originates below the ligament of Treitz and typically presents as bright red blood in stool (hematochezia). With a mortality rate under 5%, common causes include diverticulosis, hemorrhoids, colorectal cancer, and intestinal ischemia.

Management of acute GI bleeding follows a systematic approach:

1. Hemodynamic stabilization through monitoring cardiovascular status, starting fluid resuscitation with crystalloids, providing supplemental oxygen, and monitoring laboratory values (Hct, Hgb, clotting studies). Blood transfusions are initiated when hemoglobin falls below 7-8 g/dL.

2. Bleeding site identification through history, physical examination, and endoscopic procedures. Prokinetic agents like domperidone may be given to facilitate gastric emptying before endoscopy.

3. Control measures including proton pump inhibitors (PPIs) to stabilize blood clots and endoscopic treatments for non-variceal bleeding.

For severe variceal bleeding, esophageal balloon tamponade using a Sengstaken-Blakemore tube or Minnesota tube may be necessary. These devices apply pressure directly on the varices through gastric and esophageal balloons. The gastric balloon is inflated first $verified by X-ray$ and pulled against the gastroesophageal junction, followed by the esophageal balloon if bleeding continues.

💡 Nursing responsibilities with balloon tamponade include close monitoring for complications like gastric balloon rupture (which can cause the esophageal balloon to migrate upward), pulmonary aspiration, or esophageal rupture. Keep scissors at the bedside for emergency tube removal if needed.

Abdominal Compartment Syndrome (ACS) develops when intra-abdominal pressure exceeds 20 mmHg with associated organ dysfunction. It can be primary (from direct abdominal trauma or bleeding) or secondary $from conditions like ascites, sepsis, or large-volume fluid replacement$. ACS affects multiple systems, including cardiovascular function, respiratory capacity, renal function, and intracranial pressure.

Abdominal Compartment Syndrome

Intra-abdominal hypertension (IAH) is defined as sustained pressure above 12 mmHg and is graded from I $12-15 mmHg$ to IV (>25 mmHg). When pressure exceeds 20 mmHg with organ dysfunction, it becomes Abdominal Compartment Syndrome (ACS).

Patients at highest risk for ACS include those with ascites, bowel distention/edema, major trauma, or those requiring massive fluid resuscitation. The condition affects multiple body systems:

• CNS effects: Impaired venous return, increased intracranial pressure
• Cardiovascular effects: Decreased cardiac output, stroke volume, and oxygen delivery
• Respiratory effects: Increased airway pressure, decreased compliance, hypoxemia
• Renal effects: Compression of kidneys, decreased renal blood flow and urine output

Diagnosis typically involves measuring intra-abdominal pressure using an intravesicular catheter (Foley catheter). This trans-bladder technique, considered the gold standard, involves clamping the drainage tubing, connecting to a pressure monitor, and injecting 25cc of sterile saline into the bladder. Measurements should be taken at end-expiration with the patient completely supine.

⚠️ Bladder pressures over 25 mmHg are highly suspicious for abdominal compartment syndrome and require immediate clinical correlation and intervention.

Management initially focuses on non-surgical options to improve abdominal wall compliance, evacuate contents through decompression, drain abdominal fluid, and correct fluid balance. However, the primary treatment for ACS is surgical decompression through emergent laparotomy when conservative measures fail. After decompression, patients typically require continued fluid restriction, diuretics, ambulation, and DVT prophylaxis.

Gallbladder Disorders and Liver Function

Cholelithiasis (gallstones) is the most frequent gallbladder dysfunction. These stones can lead to obstruction, inflammation, and infection. Understanding medical terminology helps: litho (stones), chole $bile/gall$, and cysto $bladder/sac of fluid$.

Jaundice occurs when bilirubin metabolism is disrupted. Normally, when red blood cells are recycled, hemoglobin breaks down into bilirubin, which is processed by the liver and added to bile. Jaundice can be:

• Prehepatic: Excessive RBC breakdown overwhelms normal liver function
• Intrahepatic: Liver dysfunction prevents normal bilirubin processing
• Posthepatic: Obstruction prevents bile from leaving the liver

The liver, the largest organ in the body, performs numerous vital functions:

• Metabolic functions: Synthesizes carbohydrates, fats, proteins, and vitamins; forms bile; produces coagulation factors; converts T4 to T3
• Detoxification: Processes drugs, alcohol, fatty acids, hormones, ammonia, and toxins
• Immune functions: Contains pathogens and maintains immune systems
• Production: Creates cholesterol (precursor to hormones and vitamin D)
• Storage: Houses minerals (copper, zinc, magnesium, iron) and vitamins (A, D, E, K, B12)
• Regulation: Balances blood sugar through glycogen storage
• Synthesis: Produces plasma proteins including albumin and clotting factors

💡 Liver injury typically progresses through a sequence: damage to hepatocytes (hepatitis) → scarring/fibrosis → cirrhosis → liver failure.

Acute liver failure is the rapid deterioration of liver function in a person without prior liver disease, characterized by coagulation abnormalities and encephalopathy within 2-6 weeks of injury. Common causes include viral hepatitis, acetaminophen overdose, thrombosis, and shock.

Liver Failure and Clinical Manifestations

Chronic liver failure develops slowly over years, leading to cirrhosis. Common causes include nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease, chronic hepatitis B and C, and hemochromatosis (iron overload).

Key clinical manifestations of liver failure include:

Jaundice: Results from the liver's inability to process bilirubin, becoming evident when levels exceed 2-3 mg/dL. Patients often experience pruritus (itching) from bile salt accumulation.

Ascites: Develops due to portal hypertension (increased pressure in the portal system) secondary to liver fibrosis. Decreased albumin levels exacerbate the condition, as albumin normally helps maintain oncotic pressure within capillaries, attracting water into the intravascular space.

Hepatic encephalopathy: A spectrum of neuropsychiatric abnormalities caused when ammonia (normally converted to urea by the liver) directly enters the central nervous system. Symptoms range from minor sensory-perceptual changes to profound coma, with asterixis (wrist flapping) being a common sign.

Hepatopulmonary syndrome: Vascular dilation in the lungs leads to impaired gas exchange, causing shortness of breath, cyanosis, and arterial hypoxemia.

⚠️ The most common complications of liver failure include hepatic encephalopathy, esophageal/gastric varices, hepatorenal syndrome, spontaneous bacterial peritonitis, and malnutrition.

Electrolyte imbalances are frequent, including hypokalemia (from inadequate intake or increased losses), hypomagnesemia, hypocalcemia (especially after multiple blood transfusions), hypophosphatemia, and hypoglycemia (from depleted glycogen stores).

Hepatorenal syndrome occurs in up to 40% of patients with advanced cirrhosis and is the most frequent fatal complication. It develops from portal hypertension causing splanchnic vasodilation, leading to renal vasoconstriction and impaired kidney perfusion. The only definitive treatment is liver transplantation.

Management of Liver Failure

Managing liver failure requires careful attention to multiple body systems:

Fluid balance is critical, as patients may experience either fluid volume deficit (from GI bleeding, ascites) or fluid volume excess (from sodium retention and hypoalbuminemia). Daily weight monitoring and measuring abdominal girth help track fluid status. Paracentesis may be performed to relieve ascites and associated dyspnea.

Cardiopulmonary support focuses on monitoring respiratory status and correlating with arterial blood gases. Oxygen administration and positioning to improve oxygenation are essential interventions.

Hematologic and nutritional support includes:

• Monitoring for signs of bleeding (occult blood, petechiae)
• Administering blood products as needed
• Using beta-blockers to prevent variceal bleeding
• Implementing safety measures to minimize tissue trauma
• Preventing infection through sterile technique

💡 Lactulose is the first-line treatment for hepatic encephalopathy, working to decrease gut ammonia production. Combined with reduced dietary protein, this helps manage the neurological complications of liver failure.

Preventing and treating complications requires limiting medications metabolized by the liver (narcotics, sedatives, NSAIDs, certain antibiotics). Keeping the head of the bed elevated helps prevent aspiration, while frequent neurological assessments track mental status changes.

For patients with hepatorenal syndrome, liver transplantation remains the definitive treatment. Similarly, for patients with bleeding from esophageal varices, a combination of pharmacologic therapy, endoscopic procedures, and possibly surgical intervention may be necessary.

Comprehensive management requires an interprofessional approach including nurses, dietitians, nephrologists, pharmacists, physical therapists, and gastroenterologists working together to address the multiple systems affected by liver failure.

Preventing and Managing Liver Failure Complications

Effective management of liver failure requires addressing complications that affect multiple body systems:

Respiratory support continues to be essential as liver failure progresses. Regular monitoring of respiratory status and correlation with arterial blood gases guides oxygen therapy. Positioning the patient to optimize oxygenation can help manage respiratory symptoms associated with ascites and pleural effusions.

Hematologic management remains vigilant for signs of bleeding through regular monitoring of occult blood and watching for petechiae. Blood product administration may be necessary, while preventive measures like beta-blockers can reduce the risk of variceal bleeding. Special attention to oral care and avoiding rectal tubes helps minimize tissue trauma.

Medication management is critical, as the failing liver cannot effectively metabolize or detoxify many drugs. Narcotics, sedatives, NSAIDs, tuberculosis medications, and certain antibiotics should be limited or avoided. When medications are necessary, dosing must be carefully adjusted based on liver function.

Neurological care focuses on managing hepatic encephalopathy. Keeping the head of the bed elevated (reverse Trendelenburg position), monitoring for mental status changes, and implementing safety measures for confused patients are essential. Reducing ammonia levels through lactulose administration and protein restriction in the diet helps control encephalopathy symptoms.

⚠️ Patients with liver failure require comprehensive protocols to manage bleeding risks due to clotting abnormalities and to prevent acute upper GI hemorrhage from variceal rupture.

For patients with hepatorenal syndrome, the definitive treatment remains liver transplantation. The interprofessional team must coordinate care to support renal function while preparing for potential transplantation when appropriate.

Throughout all interventions, maintaining patient comfort, providing emotional support, and educating both patients and families about the condition and its management remain essential components of comprehensive liver failure care.