Critical Care Nursing Theory: Chapter 10 Gastrointestinal Disorders PDF 2024

Critical Care Nursing Theory Chapter 10 Gastrointestinal Disorders Dr. Rana Al Awamleh 2024 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 1 Hepatic Coma Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 2 ...

Critical Care Nursing Theory Chapter 10 Gastrointestinal Disorders Dr. Rana Al Awamleh 2024 Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 1 Hepatic Coma Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 2  Definition Hepatic Coma, also referred to as Stage IV (4) Hepatic Encephalopathy (HE), is the most severe form of neurological decline due to liver dysfunction. It is characterized by a profound loss of consciousness resulting from the liver's inability to clear toxins, especially ammonia, from the blood. As these toxins accumulate, they affect brain function, leading to progressive mental status changes that culminate in coma. Hepatic coma occurs in patients with acute liver failure or advanced chronic liver disease, such as cirrhosis, and is often triggered by additional factors, including infections, gastrointestinal bleeding, dehydration, or certain medications. It is a medical emergency with high mortality risk, requiring immediate intervention to manage precipitating factors, reduce neurotoxins, and stabilize the patient. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 3  Pathophysiology 1. Ammonia Accumulation Ammonia Production: Ammonia is produced in the intestines by bacterial breakdown of proteins and absorbed into the bloodstream. Liver Dysfunction: In liver disease, the liver fails to convert ammonia into urea, which is normally excreted by the kidneys. As a result, ammonia and other toxins build up in the bloodstream. Blood-Brain Barrier Permeability: Ammonia crosses the blood-brain barrier, leading to direct neurotoxic effects. 2. Neurotransmitter Imbalance GABA and Glutamate Dysregulation: The imbalance of neurotransmitters like gamma- aminobutyric acid (GABA) and glutamate affects brain function. Increased GABA: GABA, an inhibitory neurotransmitter, may increase, causing excessive suppression of neuronal activity and contributing to drowsiness, lethargy, and eventually coma. Altered Glutamate: Changes in glutamate, an excitatory neurotransmitter, disrupt normal brain function and contribute to cognitive and motor symptoms Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 4  Pathophysiology 3. Oxidative Stress and Neuroinflammation Reactive Oxygen Species (ROS): Ammonia and other toxins trigger oxidative stress by increasing ROS, which damages brain cells. Neuroinflammatory Response: Inflammation and activation of brain immune cells (astrocytes and microglia) are common, further impairing brain function. 4. Astrocyte Dysfunction and Cerebral Edema Astrocyte Swelling: Astrocytes, a type of glial cell, take up ammonia and convert it to glutamine. Excessive glutamine within astrocytes causes osmotic imbalances, leading to cell swelling and cerebral edema. Increased Intracranial Pressure: In severe cases (e.g., acute liver failure), astrocyte swelling can result in increased intracranial pressure, which may cause life-threatening brainstem herniation. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 5  Pathophysiology 5. Altered Blood Flow and Brain Metabolism Cerebral Blood Flow Changes: Hepatic encephalopathy can alter cerebral blood flow, potentially decreasing oxygen supply to brain tissues. Energy Metabolism Disruption: Ammonia interferes with the brain’s energy metabolism, impairing ATP production and reducing neuronal function. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 6  Stages/ Signs and symptoms of Hepatic Encephalopathy (HE) ❖ Stage 1: Mild (Minimal) Encephalopathy Symptoms: Mild confusion, slight memory loss, mood changes (e.g., irritability, anxiety) Difficulty with concentration, attention, and performing complex tasks Altered sleep patterns, often with insomnia or hypersomnia Physical Signs: Usually none or very subtle Functional Impact: Patients are usually fully oriented but may have mild cognitive difficulties. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 7  Stages/ Signs and symptoms of Hepatic Encephalopathy (HE) ❖ Stage 2: Moderate Encephalopathy Symptoms: More pronounced confusion and disorientation Personality changes, lethargy, and apathy Asterixis (flapping tremor), an involuntary hand movement, is often present Physical Signs: Slurred speech, slowed reflexes Functional Impact: Tasks requiring concentration and coordination are significantly impaired; patients may need supervision. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 8  Stages/ Signs and symptoms of Hepatic Encephalopathy (HE) ❖ Stage 3: Severe Encephalopathy (Pre-Coma) Symptoms: Marked confusion and agitation, incoherent speech, disorientation to time and place Increased somnolence or lethargy, approaching stupor Severe asterixis and muscle rigidity may be evident Physical Signs: Hyperreflexia, muscular rigidity, potential for bizarre behavior Functional Impact: Patients may be semi-responsive, need assistance for most activities, and may be difficult to arouse. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 9  Stages/ Signs and symptoms of Hepatic Encephalopathy (HE) ❖ Stage 4: Hepatic Coma Symptoms: Unresponsiveness, loss of consciousness, coma Brainstem reflexes may remain initially, but may deteriorate with progression Physical Signs: No response to verbal commands, may have response to painful stimuli in early coma; absence of asterixis Functional Impact: Complete loss of cognitive and physical function; high risk of mortality without intervention. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 10  Causes and Risk Factors Acute Liver Failure (ALF) Common causes: Viral hepatitis, drug-induced liver injury, toxins Chronic Liver Disease and Cirrhosis Most common in patients with advanced liver disease and cirrhosis Precipitating Factors GI bleeding, infections, electrolyte imbalances, sedatives, constipation Additional Risk Factors Dehydration, high-protein diet, hypoxia, renal failure Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 11  Diagnosis 1. Clinical Assessment History: Assess for a history of liver disease or risk factors (e.g., alcohol use, hepatitis, cirrhosis). Identify potential precipitating factors such as gastrointestinal bleeding, infection, electrolyte imbalances, constipation, or recent medications (e.g., sedatives, opioids). Mental Status Evaluation: Evaluate for signs of confusion, disorientation, mood changes, sleep disturbances, and other cognitive impairments. Staging of HE based on the West Haven Criteria, from Stage 1 (mild symptoms) to Stage 4 (coma). Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 12  Diagnosis 2. Physical Examination Neurological Examination: Look for key physical signs, especially asterixis (flapping tremor) in early stages. Reflexes: Hyperreflexia or muscle rigidity may be present in more advanced stages. Systemic Signs: Check for signs of liver disease: jaundice, ascites, edema, and signs of bleeding or bruising. Signs of dehydration, infection, or sepsis if they are suspected as precipitating factors. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 13  Diagnosis 3. Laboratory Tests Serum Ammonia: Elevated levels support the diagnosis but are not definitive alone, as ammonia levels do not always correlate with severity. Liver Function Tests (LFTs): Elevated bilirubin, AST, ALT, and alkaline phosphatase can indicate liver dysfunction. Coagulation Profile: Prothrombin time (PT/INR) may be prolonged in liver failure, indicating a decline in synthetic liver function. Electrolyte Panel: Monitor for electrolyte disturbances like hypokalemia, hypomagnesemia, and hyponatremia, which can precipitate or worsen HE. Complete Blood Count (CBC): Detects infections (leukocytosis), anemia from gastrointestinal bleeding, or other abnormalities. Renal Function Tests: Blood urea nitrogen (BUN) and creatinine levels to assess kidney function, as renal impairment may complicate HE. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 14  Diagnosis 4. Neuroimaging CT Scan or MRI of the Brain: Rule out other causes of altered mental status, such as stroke, brain injury, or infection. MRI is more sensitive in detecting cerebral edema and other structural changes, which may be seen in advanced HE, particularly in acute liver failure. 5. Electroencephalogram (EEG) (if needed) May show diffuse slowing of brain waves, typical of metabolic encephalopathy. Not routinely performed for diagnosis but can be useful in unclear cases or to rule out non-convulsive seizures. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 15  Diagnosis 6. Scoring and Severity Assessment West Haven Criteria: Standard clinical staging system (Stages 1-4) to categorize HE severity based on mental status and physical findings. The Glasgow Coma Scale (GCS): Helpful for assessing consciousness level, particularly in severe cases. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 16 West Haven Criteria Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 17  Treatment and Management 1. Identify and Treat Precipitating Factors Infection: Treat infections (e.g., spontaneous bacterial peritonitis, pneumonia) with appropriate antibiotics. Gastrointestinal Bleeding: Manage GI bleeding promptly with endoscopy, hemodynamic support, and blood transfusions as needed. Electrolyte Imbalance: Correct any electrolyte abnormalities (e.g., hypokalemia, hyponatremia), as these can exacerbate HE. Constipation: Treat constipation with laxatives, as it increases intestinal ammonia production. Medications: Avoid or reduce sedatives, opioids, and other medications that may worsen HE. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 18  Treatment and Management 2. Lower Blood Ammonia Levels Non-absorbable Disaccharides: Lactulose: First-line treatment that works by acidifying the colon and promoting the conversion of ammonia to ammonium, which is less absorbable. Dosage: Adjust lactulose to produce 2-3 soft bowel movements daily. Side effects: Diarrhea, abdominal cramping. Antibiotics: Rifaximin: An antibiotic that reduces the population of ammonia-producing gut bacteria. Often used as an adjunct to lactulose in patients with recurrent HE. Neomycin or Metronidazole: Alternatives when rifaximin is not available, though they may have more adverse effects. L-ornithine L-aspartate (LOLA): This medication can lower ammonia levels by promoting ammonia metabolism in the liver and muscles. Used in some cases, especially in acute liver failure. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 19  Treatment and Management 3. Supportive Care Airway Protection: In patients with severe HE (stages 3-4), airway protection may be necessary. Intubation is considered for those with altered consciousness to prevent aspiration. Fluid and Electrolyte Management: Maintain hydration and electrolyte balance carefully. Avoid over-hydration, especially in patients with cirrhosis who may be at risk for ascites and edema. Monitor sodium levels closely, as hyponatremia is common and can worsen HE. Nutritional Support: Protein Intake: Contrary to previous recommendations, moderate protein intake (1.2-1.5 g/kg/day) is now encouraged, as protein restriction may lead to muscle wasting, worsening HE. Enteral Nutrition: In patients who are intubated, use enteral nutrition with adequate calories and balanced protein. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 20  Treatment and Management 4. Medications to Reduce Neurotoxicity Zinc Supplementation: Zinc is a cofactor in ammonia metabolism, and supplementation may benefit patients with zinc deficiency, common in liver disease. Branched-Chain Amino Acids (BCAA): In some cases, BCAA supplements can support muscle metabolism of ammonia, potentially helping to reduce HE symptoms. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 21  Treatment and Management 5. Monitoring and Follow-Up Neurological Assessment: Monitor mental status regularly using standardized staging criteria (e.g., West Haven Criteria) and Glasgow Coma Scale (GCS) for coma patients. Laboratory Monitoring: Regularly assess ammonia levels, liver function tests, and electrolytes to measure response to treatment. Screening for Recurrent HE: Patients with a history of HE are at high risk for recurrence, and close monitoring can help in the early identification of recurrence or worsening symptoms. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 22  Treatment and Management 6. Consideration for Liver Transplantation Liver Transplant Evaluation: For patients with advanced liver disease (e.g., cirrhosis) and recurrent or refractory HE, liver transplantation offers a potential definitive treatment. Evaluation for transplantation should be considered in eligible patients to improve long-term survival and quality of life. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 23  Preventive Strategies Medication Compliance: Patients and caregivers should understand the importance of adhering to treatment (e.g., lactulose and rifaximin) to prevent recurrence. Patient Education: Educate patients on recognizing early symptoms of HE, avoiding triggers (e.g., alcohol, certain medications), and managing precipitating factors. Regular Follow-Up: Schedule follow-up visits to assess liver function, monitor HE symptoms, and adjust treatment as necessary. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 24  References Critical Care Nursing: A Holistic Approach 11th Edition. Patricia Gonce Morton, Dorrie K. Fontaine Introduction To Critical Care Nursing, Sixth Edition. Mary Lou Sole, Deborah G. Klein, Marthe J. Moseley. Dr. Rana Al Awamleh/ Assistant Professor, Critical Care Nursing 25