AK - Nursing Case Study

Pathophysiology

• Primary mechanism: Kidney ischemia - Decreased blood flow to the kidneys due to conditions like shock or severe dehydration leads to renal hypoperfusion. This induces tubular cell death and acute tubular necrosis, which is the most common cause of AKI.

• Secondary mechanism: Nephrotoxic injury - Exposure to certain drugs, toxins, or contrast media can damage renal tubular cells, leading to intratubular obstruction or direct tubular cell injury.

• Key complication: Fluid overload - Reduced glomerular filtration rate (GFR) in AKI prevents the kidneys from properly excreting fluids and electrolytes, leading to volume overload, edema, hypertension, and potentially, heart failure and pulmonary edema.

Patient Profile

Demographics:

63 years old, male, retired construction worker

History:

• Key past medical history: Diagnosed with chronic obstructive pulmonary disease (COPD), hypertension, type 2 diabetes, and previous history of heart disease

• Current medications: Metformin, Lisinopril, Advair Diskus, and Aspirin

• Allergies: Penicillin and Sulfa drugs

Current Presentation:

• Chief complaint: Fatigue, decreased urine output, and confusion

• Key symptoms: Severe fatigue, decreased urine output, dizziness, vomiting, confusion, shortness of breath, swelling of legs and ankles

• Vital signs: Blood Pressure: 180/110 mm Hg, Heart Rate: 110 beats per minute, Respiratory Rate: 24 breaths per minute, Temperature: 37.8°C, Blood Oxygen Saturation: 88%

Section 1

Change in Patient Status:

Over the next 24 hours, AK's condition deteriorated. His blood pressure increased to 190/115 mm Hg and his heart rate escalated to 120 beats per minute. His blood oxygen saturation dropped to 82%, necessitating supplemental oxygen. His respiratory rate also increased to 28 breaths per minute and his temperature spiked to 38.5°C, suggesting a possible infection. His confusion also worsened, and he became increasingly disoriented.

His swelling of legs and ankles intensified, indicating worsening fluid overload. Additionally, his urine output continued to decrease, with only 200 mL recorded over the last 24 hours. His skin appeared pale and dry, and he complained of excessive thirst, possibly indicating severe dehydration. Despite an increase in his fluid intake, his symptoms did not improve.

New Diagnostic Results:

Lab results showed a significant increase in his serum creatinine level from 1.2 to 3.5 mg/dL and a decrease in his estimated glomerular filtration rate (eGFR) to 15 mL/min/1.73 m², suggesting severe kidney function impairment. His blood glucose was 250 mg/dL, indicating poorly controlled diabetes. His BUN (Blood Urea Nitrogen) level was also elevated at 60 mg/dL. His complete blood count showed a high white blood cell count of 15,000 µL, indicating a possible infection. A urinalysis revealed proteinuria and microscopic hematuria. An ECG showed signs of left ventricular hypertrophy, possibly due to chronic hypertension and fluid overload. These findings point to an escalation in AK's acute kidney injury and the potential onset of kidney failure.

Section 2

New Complications:

AK began to exhibit sudden restlessness and a decrease in consciousness. His Glasgow Coma Scale (GCS) plummeted to 9. He also developed Cheyne-Stokes respiration, a pattern of rhythmic oscillation of ventilation between apnea and hyperpnea. His blood pressure dropped dramatically to 85/50 mm Hg, and his heart rate rose to 130 beats per minute. His blood oxygen saturation further declined to 75% despite the supplemental oxygen. He also complained of severe headache and blurred vision.

A stat CT scan of the head was ordered, which revealed signs of a cerebral infarction. This suggested that AK may have had a stroke, likely due to a combination of his hypertension, dehydration, and the potential thromboembolic risk associated with his kidney failure. Additionally, his lab results showed a significant increase in his D-dimer level to 5000 ng/mL, indicating a high likelihood of thrombosis. His platelet count also dropped to 100,000 µL, suggesting possible disseminated intravascular coagulation. This new complication adds to the complexity of AK's condition, necessitating immediate and aggressive interventions to prevent further deterioration.

Section 3

Change in patient status:

AK's condition continued to deteriorate rapidly. He developed a fever of 39.5°C, and his respiratory status worsened, with crackles heard on auscultation and his oxygen saturation dropping further to 70% despite high-flow oxygen. He became increasingly somnolent and unresponsive, with his GCS decreasing to 6. Additionally, he started to exhibit signs of right-sided weakness, indicating a possible extension of his stroke.

His blood pressure further dropped to 80/40 mm Hg, and his heart rate increased to 140 beats per minute. His urine output also decreased significantly to less than 20 mL/hour. Repeated lab tests showed a further rise in his D-dimer levels to 6000 ng/mL, a decrease in his platelet count to 85,000 µL, and an increase in his serum creatinine to 4.5 mg/dL, indicating worsening kidney function. These changes in AK's status demand an immediate reassessment of his treatment plan and the need for more aggressive interventions.

Section 4

New complications:

As AK's condition worsened, a sudden bradycardia of 40 beats per minute was noted, accompanied by widening of the QRS complex on his ECG, suggestive of severe hyperkalemia. Furthermore, his arterial blood gas showed a pH of 7.25, PaCO2 of 55 mmHg, and HCO3 of 20 mEq/L, indicating severe respiratory acidosis with partial metabolic compensation. He also developed a distended abdomen with decreased bowel sounds, raising the suspicion of an acute abdominal condition.

A rapid bedside ultrasound confirmed the presence of free fluid in his abdomen, consistent with spontaneous bacterial peritonitis (SBP). His serum potassium level came back at 6.5 mEq/L, and his serum lactate was significantly increased at 7 mmol/L, indicative of tissue hypoperfusion. These new complications necessitate immediate medical attention and a shift in the treatment plan. The team must manage his hyperkalemia, respiratory acidosis, potential SBP, and deteriorating hemodynamics while continuing to address his ongoing stroke and kidney issues.

Section 5

Change in Patient Status:

Despite immediate interventions, including the administration of calcium gluconate for hyperkalemia and non-invasive ventilation for respiratory acidosis, AK's condition continued to deteriorate. Within the next few hours, his heart rate dropped to 35 beats per minute, and his respiratory rate increased to 30 breaths per minute. His oxygen saturation levels were fluctuating between 85-90% despite being on high-flow oxygen. The repeat arterial blood gas showed a worsening respiratory acidosis with a pH of 7.20, PaCO2 of 60 mmHg, and HCO3 of 22 mEq/L, suggesting inadequate ventilation and worsening metabolic acidosis.

Furthermore, his level of consciousness declined, with a Glasgow Coma Scale (GCS) of 9 (E2, V3, M4), compared to the previous GCS of 12. His blood pressure also dropped to 90/60 mmHg from the previous reading of 110/70 mmHg, indicating possible septic shock secondary to SBP. Repeat labs revealed potassium of 7.0 mEq/L and lactate of 9 mmol/L, suggesting persistent hyperkalemia and tissue hypoperfusion, respectively. This rapid deterioration in AK's condition raises concerns about the potential failure of the initial interventions, and the need for advanced critical care measures, including possible intubation and the initiation of inotropic support.