hepatitis a - Nursing Case Study

Pathophysiology

• Primary mechanism: Hepatitis A virus (HAV) is ingested, typically through contaminated food or water. It then enters the bloodstream through the epithelial lining of the gut and travels to the liver. There, it invades hepatocytes and begins to replicate.

• Secondary mechanism: The immune system responds to the HAV-infected hepatocytes by releasing inflammatory cytokines and cytotoxic T cells. These mechanisms cause hepatocyte death and liver tissue damage, leading to the symptoms of hepatitis.

• Key complication: In severe cases, a massive hepatocyte death can lead to acute liver failure, characterized by coagulation abnormalities, hepatic encephalopathy, and potentially, death. This condition requires immediate medical intervention, often including liver transplantation.

Patient Profile

Demographics:

52-year-old, male, working as a food handler

History:

• Key past medical history: Chronic alcoholism, Diabetes Mellitus Type II, Cirrhosis of the liver

• Current medications: Metformin, Insulin, Furosemide, Spironolactone

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain, yellowing of skin and eyes

• Key symptoms: Fatigue, loss of appetite, dark urine, clay-colored stools, joint pain, unexplained weight loss

• Vital signs: Blood pressure 90/60 mmHg, Pulse rate 110 bpm, Respiratory rate 22 breaths per minute, Temperature 100.4 F, Oxygen saturation 90% on room air.

Section 1

New Diagnostic Results:

Laboratory findings show a significant elevation in Alanine aminotransferase (ALT) and Aspartate aminotransferase (AST) levels, both over 1000 U/L, indicating severe hepatocellular injury. His total bilirubin level is also elevated at 8.6 mg/dL, with direct bilirubin of 6.2 mg/dL, reflecting impaired conjugation and excretion due to liver damage. The prothrombin time (PT) is prolonged to 18 seconds, and the international normalized ratio (INR) is 1.6, showing coagulation abnormalities suggestive of liver dysfunction. The patient's blood glucose level is abnormally high at 250 mg/dL, signifying uncontrolled diabetes, potentially exacerbated by the liver's compromised ability to regulate glucose.

The patient also had positive serologic markers for Hepatitis A, including IgM anti-HAV, confirming acute Hepatitis A infection. An abdominal ultrasound reveals a coarse liver echotexture with irregular borders, consistent with cirrhosis, and ascites. The clinical presentation, together with the lab results and imaging, strongly indicate an acute exacerbation of chronic liver disease due to Hepatitis A infection superimposed on cirrhosis.

The combination of these findings raises concerns about the patient's progression into acute-on-chronic liver failure (ACLF), a syndrome characterized by acute decompensation of chronic liver disease, organ failures, and high short-term mortality. This situation requires advanced critical thinking and clinical judgment to manage the patient's multiple, interacting conditions.

Section 2

The patient's status deteriorates over the next 24 hours, with a significant decline in his level of consciousness. He becomes progressively lethargic, confused, and experiences intermittent bouts of agitation. His Glasgow Coma Scale (GCS) score drops to 11 out of 15. The patient's blood pressure also plummets to 90/60 mmHg, and his heart rate increases to 110 beats per minute. His respiratory rate is slightly elevated at 24 breaths per minute and oxygen saturation drops to 92% on room air. His urine output is also less than 0.5 ml/kg/hr over the past 6 hours, indicating possible renal impairment.

Repeat blood tests reveal further abnormalities. His ALT and AST levels continue to soar, now reaching 1500 U/L and 1200 U/L respectively. Bilirubin levels have also increased to 10.4 mg/dL with direct bilirubin at 7.5 mg/dL. His PT has extended to 22 seconds, and his INR has increased to 1.8. Blood glucose levels remain high at 280 mg/dL. A new onset of lactic acidosis is also noted, with a lactate level of 5 mmol/L, suggesting tissue hypoperfusion.

These findings, along with the patient's deteriorating clinical status, suggest the development of multiple organ failure, including hepatic encephalopathy and possible acute kidney injury. This is a crucial moment in the patient's journey, requiring swift recognition of the serious implications of these changes and the need for immediate, aggressive interventions. The nurse must engage in advanced clinical reasoning to anticipate potential complications and coordinate with the healthcare team to deliver optimal patient care.

Section 3

The nurse closely monitors the patient's status, noting a further decrease in his level of consciousness; his GCS score now stands at 7 out of 15. His blood pressure continues to fall, now at 85/50 mmHg, with a heart rate of 120 beats per minute. His respiratory rate increases to 30 breaths per minute, and his oxygen saturation falls to 88% on room air. The patient's urine output further decreases, now less than 0.3 ml/kg/hr over the past 6 hours, and his skin has taken on a yellowish hue, suggestive of jaundice.

Upon reviewing new laboratory results, the nurse notes that the patient's liver function tests have worsened. His ALT and AST levels are now 2000 U/L and 1500 U/L, respectively. His bilirubin levels have risen further to 15 mg/dL with direct bilirubin at 10 mg/dL. His PT has further extended to 25 seconds, and his INR has increased to 2.2. The patient's blood glucose levels remain high at 300 mg/dL. His lactate level has also increased to 6 mmol/L, indicating worsening tissue hypoperfusion.

This significant change in patient status signals the progression of hepatic encephalopathy and acute kidney injury, and potentially, the onset of hepatic coma. Given these critical developments, the nurse must employ advanced clinical reasoning skills to anticipate and mitigate further complications like cerebral edema and coagulopathy. Collaborative action with the healthcare team is crucial to implement aggressive interventions such as potential initiation of renal replacement therapy and management of hyperglycemia.

Section 4

The nurse observes a further decline in the patient's status. His GCS score has dropped to 5, indicating a severe decrease in consciousness. His blood pressure has continued its downward trend to 80/45 mmHg, and he's now experiencing tachycardia with a heart rate of 130 beats per minute. His respiratory rate has increased to 35 breaths per minute, suggestive of possible respiratory distress, and his oxygen saturation is now at 85% on room air, indicating hypoxemia. The patient's urine output remains critically low, now at less than 0.2 ml/kg/hr over the past 4 hours. The icteric color of his skin has deepened, and the nurse also notes a faint flapping tremor in his hands - an early sign of hepatic encephalopathy.

The results of his latest labs show further deterioration in liver function. His ALT and AST levels have risen further to 2500 U/L and 1700 U/L, respectively. His bilirubin levels continue to climb, now at 20 mg/dL, with direct bilirubin at 13 mg/dL. His PT has now extended to 30 seconds, and his INR has risen to 2.5. His blood glucose levels remain persistently high at 320 mg/dL, and his lactate levels have surged to 8 mmol/L.

This alarming change in patient status indicates the rapid progression of hepatic encephalopathy, worsening acute kidney injury, and an increased risk of hepatic coma. The nurse recognizes the need for immediate and aggressive intervention. The healthcare team must be alerted to reevaluate the patient's management plan, which may necessitate renal replacement therapy and intensive management of hyperglycemia. The nurse's advanced clinical reasoning skills will be crucial in effectively managing this critically ill patient and preventing further life-threatening complications.

Section 5

Change in patient status:

Over the next several hours, the patient's condition continues to worsen. His GCS score drops to 3, and he becomes unresponsive to painful stimuli. The nurse notes new onset asterixis – a flapping tremor of the hands when wrists are extended, indicating further progression of hepatic encephalopathy. His blood pressure falls to a concerning 70/40 mmHg, and he remains tachycardic with a heart rate that fluctuates between 130-140 beats per minute. His respiratory rate increases to a dangerous 40 breaths per minute, and his oxygen saturation levels drop further to 80% despite receiving 2 liters of oxygen via nasal cannula.

The patient's urine output remains critically low at less than 0.1 ml/kg/hr over the past 6 hours, indicating acute kidney injury. His icteric skin color has further deepened, and he now also exhibits scleral icterus. The nurse also notices the onset of mild ascites and peripheral edema. The patient's blood glucose levels continue to remain elevated at 340 mg/dL, and his lactate levels have now increased to 10 mmol/L. These alarming clinical signs indicate the accelerating deterioration of the patient's hepatic and renal function, requiring immediate escalation of care. The nurse must alert the healthcare team to reassess the patient's condition and revisit the management plan. In this critical scenario, the nurse's clinical judgment and prompt action are vital in preventing further complications and optimizing patient outcomes.