Metabolic Encephalopathy - Nursing Case Study

Pathophysiology

• Primary mechanism: Metabolic encephalopathy is primarily triggered by systemic metabolic chemical imbalances, affecting the brain's function. These can be due to organ failure (liver, kidney), sepsis, hypoxia, or electrolyte abnormalities like hypernatremia or hyponatremia. The resulting toxins or metabolic products disrupt the brain's neural activity, leading to altered mental status.

• Secondary mechanism: Ischemic injury plays a significant role in worsening the condition. The metabolic imbalances can cause hypoperfusion, leading to inadequate oxygen supply to the brain. This exacerbates neuronal dysfunction and may cause permanent neuronal loss if not rapidly corrected.

• Key complication: Persistent metabolic imbalances can lead to cerebral edema, a severe complication. This is due to an osmotic shift causing water to move into the brain cells, leading to swelling and increased intracranial pressure. The result can be brain herniation, a life-threatening condition requiring imme

Patient Profile

Demographics:

72-year-old male, retired construction worker

History:

• Key past medical history: Diabetes Mellitus Type 2, Chronic Kidney Disease Stage 3, Hypertension, Previous stroke

• Current medications: Metformin, Lisinopril, Aspirin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Progressive confusion and weakness

• Key symptoms: Altered mental status, difficulty speaking, unsteady gait, lethargy, occasional seizures

• Vital signs: Blood Pressure 165/90 mmHg, Heart Rate 110 bpm, Respiratory Rate 24 breaths per minute, Temperature 38.3°C, Oxygen Saturation 88% on room air.

Section 1

New Diagnostic Results:

Despite the initial interventions and correction of his metabolic imbalances, the patient's mental status did not improve significantly. His vital signs were still unstable with Blood Pressure of 170/95 mmHg, Heart Rate 115 bpm, Respiratory Rate 26 breaths per minute, Temperature 37.8°C, Oxygen Saturation 85% on 2L nasal cannula. This prompted further diagnostic tests. Laboratory results revealed a significant increase in his ammonia level to 120 µmol/L (normal range: 15-45 µmol/L), suggestive of hepatic encephalopathy. His kidney function also worsened, with his creatinine increasing to 2.7 mg/dL from a baseline of 1.8 mg/dL, indicating an acute kidney injury. A CT scan of the brain was also performed, revealing cerebral edema and early signs of uncal herniation.

The patient's condition was critical, with multiple organ systems affected. The elevated ammonia level indicated that his liver was not properly detoxifying the blood, and the elevated creatinine showed that his kidneys were failing to filter waste products effectively. Both these conditions could potentially contribute to his encephalopathy. The cerebral edema and early signs of uncal herniation were ominous findings, indicating a severe increase in intracranial pressure that could lead to brain damage if not rapidly and effectively managed. The complex interplay of the patient's existing comorbid conditions (Diabetes, Chronic Kidney Disease, Hypertension, Stroke) along with his current metabolic encephalopathy further complicated the clinical picture, necessitating a very high level of clinical reasoning, judgement and expertise to manage his condition effectively.

Section 2

Change in Patient Status:

Over the next 24 hours, the patient's condition worsened. His Blood Pressure escalated to 190/100 mmHg, Heart Rate rose to 120 bpm, and his Oxygen Saturation fell to 80% on 5L nasal cannula. His level of consciousness also dropped significantly, scoring a 7 on the Glasgow Coma Scale (eye: 2, verbal: 2, motor: 3), indicating a severe decrease in his neurological status. He exhibited decerebrate posturing, a sign of severe brain damage. His verbal responses were incomprehensible and he was only responsive to pain.

New Complications:

The patient's worsening neurological status prompted an emergent repeat CT scan of the brain, revealing progression of the cerebral edema and full-blown uncal herniation. His ammonia level rose further to 150 µmol/L, and his creatinine escalated to 3.5 mg/dL, indicating worsening hepatic and renal function. His arterial blood gas showed a pH of 7.25, PaCO2 of 55 mmHg, and PaO2 of 60 mmHg, suggestive of acute respiratory acidosis, likely due to hypoventilation secondary to his deteriorating neurological status. He also developed new onset atrial fibrillation with rapid ventricular response, likely secondary to his escalating hypertension and possibly contributing to his unstable hemodynamics. These new complications raised the level of complexity of the case, requiring advanced critical thinking and clinical judgement in managing this critically ill patient.

Section 3

New Diagnostic Results:

Despite aggressive medical management, the patient's condition continued to deteriorate. A follow-up arterial blood gas (ABG) showed a pH of 7.15, a PaCO2 of 70 mmHg, and a PaO2 of 50 mmHg, indicating a worsening respiratory acidosis and hypoxia. An emergent electroencephalogram (EEG) was ordered, revealing diffuse slowing and triphasic waves, suggestive of metabolic encephalopathy. A lumbar puncture was performed which yielded normal opening pressure and clear cerebrospinal fluid (CSF). CSF analysis showed an elevated protein level of 80 mg/dL and normal glucose level.

Change in Patient Status:

As the patient's respiratory status worsened, he became increasingly lethargic and unresponsive. His Glasgow Coma Scale dropped further to 5 (eye: 1, verbal: 2, motor: 2). He developed Cheyne-Stokes respiration and his oxygen saturation continued to drop despite being on a non-rebreather mask at 15L. His blood pressure also became labile, fluctuating between 160/90 mmHg and 210/110 mmHg. His heart rate remained elevated at 130 bpm with persistent atrial fibrillation. A repeat abdominal ultrasound revealed new findings of free fluid in the abdomen suggestive of ascites. His total bilirubin rose to 5.2 mg/dL, and his international normalized ratio (INR) escalated to 2.3, indicating further deterioration of his hepatic function. His creatinine also rose further to 4.0 mg/dL, suggesting worsening renal failure.

Section 4

New Complications:

Despite being placed on a continuous renal replacement therapy (CRRT) to manage his renal failure, the patient's creatinine levels continued to rise, peaking at 5.8 mg/dL, and his urine output remained critically low (<0.3 mL/kg/hr). Additionally, he developed frank hematuria, which raised concerns for a possible renal hemorrhage. An urgent renal ultrasound revealed multiple renal cysts and a large perinephric hematoma, suggesting an underlying polycystic kidney disease that had likely led to his renal failure and the present bleeding.

Meanwhile, the patient's liver function continued to deteriorate, with his prothrombin time (PT) extending to 21 seconds and his total bilirubin increasing to 7.0 mg/dL, pointing towards a worsening hepatic failure. He also developed a distended abdomen with shifting dullness on examination, likely due to worsening ascites. A paracentesis was performed, and the ascitic fluid analysis showed a high serum-ascites albumin gradient (SAAG) of 2.0 g/dL and a total protein level of 3.0 g/dL, suggesting portal hypertension as the likely cause. This was further complicated by the development of hepatic encephalopathy, as evidenced by the patient's declining neurological status, asterixis, and an elevated ammonia level of 120 μmol/L. His metabolic encephalopathy had thus taken a complicated turn, with both hepatic and renal factors contributing to his worsening condition.

Section 5

New Complications:

Just as the team was beginning to stabilize the patient's renal and hepatic conditions, he began showing signs of respiratory distress, with labored breathing, decreased oxygen saturation levels to 88% on room air, and an increasing respiratory rate of 28 breaths per minute. His blood gas analysis revealed a pH of 7.28, PaCO2 of 45 mmHg, and HCO3 of 18 mEq/L, indicating a primary metabolic acidosis with respiratory compensation. This suggested the development of a new complication - a possible acute respiratory distress syndrome (ARDS) secondary to sepsis from an unknown source.

To further complicate matters, the patient's blood cultures grew gram-negative bacilli, pointing towards a systemic bacterial infection. His white blood cell count was significantly elevated at 18,000 cells/µL, with 80% neutrophils, and he developed a new fever of 101.5°F. Despite receiving broad-spectrum antibiotics, his condition continued to deteriorate, with his Sequential Organ Failure Assessment (SOFA) score increasing to 15, indicating a high risk of mortality. The team was now faced with managing multiple organ dysfunctions - renal, hepatic, and respiratory - in the setting of a severe systemic infection, testing their clinical acumen and decision-making abilities to the limit.