Cancer - Nursing Case Study

Pathophysiology

• Primary mechanism: Genetic mutations in oncogenes and tumor suppressor genes disrupt normal cell cycle regulation, leading to uncontrolled cellular proliferation. Mutations can occur due to carcinogens, inherited genetic factors, or random errors during DNA replication.

• Secondary mechanism: Evasion of apoptosis, the programmed cell death process, allows cancer cells to survive despite genetic abnormalities. This is often due to mutations in genes that regulate apoptosis, such as p53, which normally triggers cell death in response to DNA damage.

• Key complication: Metastasis, the spread of cancer cells to distant sites via the bloodstream or lymphatic system, can lead to severe organ dysfunction and is a major cause of cancer-related morbidity and mortality. Metastatic cells often exhibit resistance to conventional therapies, complicating treatment efforts.

Patient Profile

Demographics:

45-year-old female, research scientist

History:

• Key past medical history: Diagnosed with stage IV metastatic breast cancer 2 years ago, hypertension, type 2 diabetes

• Current medications: Paclitaxel, Lisinopril, Metformin, Insulin, Ondansetron

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain and difficulty breathing

• Key symptoms: Intense fatigue, persistent cough, nausea, significant weight loss, jaundice

• Vital signs: Blood pressure 90/60 mmHg, heart rate 120 bpm, respiratory rate 28 breaths/min, temperature 102°F, oxygen saturation 82% on room air

Section 1

Initial Assessment Findings:

Upon arrival at the emergency department, the patient is in acute distress, exhibiting signs of respiratory compromise and hemodynamic instability. Her severe abdominal pain and difficulty breathing necessitate immediate attention. A thorough physical examination reveals decreased breath sounds and dullness to percussion over the right lower lung field, suggesting possible pleural effusion or atelectasis. The abdomen is distended and tender upon palpation, with guarding noted in the right upper quadrant. The patient's skin and sclera are jaundiced, indicating potential liver impairment, likely due to hepatic metastases or obstructive processes.

Initial laboratory investigations reveal critical abnormalities: a complete blood count shows leukocytosis with a white blood cell count of 18,000/mm³, anemia with hemoglobin at 8.5 g/dL, and thrombocytopenia with a platelet count of 90,000/mm³. Liver function tests are significantly deranged, with elevated bilirubin levels at 4.5 mg/dL, AST at 150 U/L, and ALT at 135 U/L, corroborating the clinical suspicion of liver dysfunction. Arterial blood gases show severe hypoxemia with a PaO2 of 55 mmHg and metabolic acidosis with a pH of 7.30 and bicarbonate of 18 mEq/L. These findings suggest a complex interplay of systemic infection, hepatic insufficiency, and possible acute kidney injury, necessitating urgent intervention.

The patient's hemodynamic status and the potential for rapid deterioration demand advanced critical thinking to prioritize interventions. Initiation of supplemental oxygen is crucial to address the hypoxemia, while broad-spectrum antibiotics are considered to cover possible sepsis given the elevated temperature and leukocytosis. Fluid resuscitation is cautiously initiated to support blood pressure, while avoiding exacerbation of potential cardiopulmonary congestion. The need for further imaging, such as a CT scan of the chest and abdomen, is critical to assess the extent of metastatic disease and guide further therapeutic decisions. These initial steps are pivotal in stabilizing the patient and determining the next phase of her complex care journey.

Section 2

Response to Interventions:

Following the initiation of supplemental oxygen via a non-rebreather mask at 15 liters per minute, the patient's oxygen saturation improves modestly from 82% to 88%, though she remains tachypneic with a respiratory rate of 28 breaths per minute. Despite fluid resuscitation efforts with isotonic crystalloids, the patient’s blood pressure remains borderline, fluctuating between 88/52 mmHg and 92/56 mmHg, indicating persistent hemodynamic instability. The addition of vasopressor support with norepinephrine is considered to maintain adequate perfusion pressure.

The administration of broad-spectrum antibiotics is initiated promptly to address the suspected septic process, but the patient's fever persists, with temperatures ranging between 38.5°C and 39.2°C. Repeat blood cultures are drawn to identify the infectious source and guide antibiotic therapy, while lactate levels are monitored closely; an initial lactate level of 4.5 mmol/L underscores the severity of her condition and possible septic shock.

As the team awaits further imaging results, the patient's overall condition remains precarious, with signs of potential multi-organ dysfunction becoming more apparent. The critical care team is consulted for potential transfer to the intensive care unit for advanced hemodynamic monitoring and management. The deteriorating lab values, including a rising creatinine level of 2.1 mg/dL, suggest acute kidney injury, which complicates fluid management strategies. This complex scenario requires ongoing reassessment and adaptive clinical decision-making to address the evolving challenges in this patient's care, as the medical team prepares for further diagnostic insights and therapeutic adjustments.

Section 3

As the critical care team prepares for the patient's transfer to the intensive care unit, new diagnostic results from the imaging studies reveal the presence of extensive bilateral infiltrates on the chest X-ray, consistent with acute respiratory distress syndrome (ARDS). Additionally, an abdominal ultrasound indicates splenomegaly and possible hepatic congestion, suggestive of underlying complications such as portal hypertension or hepatic involvement due to metastatic disease. These findings necessitate further refinement of the treatment plan, as the respiratory compromise now appears multifactorial, involving both infectious and possible neoplastic processes.

In response to these developments, the medical team initiates a trial of lung-protective ventilation strategies upon the patient's arrival in the intensive care unit, aiming to improve oxygenation while minimizing further lung injury. The decision is also made to escalate antimicrobial therapy based on the latest culture sensitivities, as preliminary blood culture results indicate a gram-negative bacteremia. Concurrently, nephrology is consulted regarding the rising creatinine and potential need for renal replacement therapy, given the patient's worsening kidney function and oliguria, which now complicates fluid management decisions further.

Despite these interventions, the patient's condition remains tenuous. Her mental status begins to fluctuate, with episodes of confusion and disorientation, raising concerns about encephalopathy possibly related to hepatic dysfunction or sepsis-associated delirium. The team must now integrate these new complexities into the overall care strategy, balancing aggressive treatment of the underlying infection and cancer while mitigating the risk of further organ system compromise. This dynamic situation demands constant vigilance and adaptation, as each new piece of clinical data may significantly influence the trajectory of the patient's treatment and prognosis.

Section 4

As the critical care team continues to closely monitor the patient, a significant change in her status is observed. Overnight, her respiratory parameters deteriorate, with a drop in oxygen saturation to 85% despite being on high-flow nasal cannula. Further assessment reveals increased work of breathing and the development of coarse crackles throughout both lung fields on auscultation. Arterial blood gas analysis shows a pH of 7.28, PaCO2 of 58 mmHg, and PaO2 of 55 mmHg, indicating worsening hypoxemia and respiratory acidosis. These findings suggest progression of the ARDS and necessitate intubation and mechanical ventilation with a lung-protective ventilation strategy.

In conjunction with the respiratory decline, her hemodynamic status becomes more labile. The patient's blood pressure fluctuates, with systolic readings ranging from 80 to 100 mmHg, requiring the initiation of vasopressor support with norepinephrine to maintain adequate perfusion. Meanwhile, her urine output remains scant despite fluid resuscitation, and her creatinine continues to rise, now at 3.5 mg/dL. The nephrology team recommends the initiation of continuous renal replacement therapy (CRRT) to address the worsening acute kidney injury and to aid in fluid management.

As these interventions are implemented, the patient's neurological status also warrants attention. Her episodes of confusion and disorientation have become more pronounced, with periods of lethargy interspersed with agitation. A CT scan of the brain is performed to rule out acute intracranial pathology, which returns unremarkable, reinforcing the likelihood of metabolic encephalopathy. The team considers adjusting the antimicrobial regimen in light of the patient's renal status and potential neurotoxicity while ensuring adequate coverage for her gram-negative bacteremia. This delicate balance of managing respiratory support, hemodynamics, and neurological status highlights the complexity of her care, requiring ongoing multidisciplinary collaboration and reassessment to navigate the intertwined challenges of her critical condition.

Section 5

As the critical care team closely monitors the patient's response to the interventions, a notable change in her status emerges. Despite the initiation of mechanical ventilation with lung-protective strategies, her oxygenation only modestly improves. The patient's oxygen saturation hovers around 89%, with persistent respiratory acidosis on follow-up arterial blood gases revealing a pH of 7.31, PaCO2 of 55 mmHg, and PaO2 of 60 mmHg. Meanwhile, vasopressor support with norepinephrine is titrated upwards to maintain a mean arterial pressure above 65 mmHg, highlighting ongoing hemodynamic instability. Her blood pressure now oscillates between systolic readings of 75-95 mmHg, further complicating the clinical picture.

In parallel, the CRRT is initiated, yet urine output remains negligible, and fluid overload becomes a growing concern. Her creatinine has risen to 4.0 mg/dL, and serum potassium levels have increased to 5.8 mmol/L, necessitating careful electrolyte management to prevent arrhythmias. In the context of these challenges, the patient's neurological status deteriorates further. She becomes increasingly unresponsive, failing to awaken to verbal stimuli, with a Glasgow Coma Scale score dropping to 7. Repeat laboratory tests reveal a bicarbonate level of 18 mmol/L, and lactate has risen to 5.0 mmol/L, suggesting a worsening metabolic acidosis and possible septic encephalopathy.

The interdisciplinary team faces a critical juncture in the patient's care. They must reassess the adequacy of current antimicrobial therapy, considering the potential need for broader-spectrum coverage or alternative agents due to her renal insufficiency. Additionally, the team explores the possibility of other contributing factors such as adrenal insufficiency or an undisclosed source of infection, prompting further diagnostic testing including cortisol levels and echocardiography to evaluate cardiac function. These developments underscore the complexity of her case, requiring meticulous coordination across specialties to adjust the treatment plan and address emerging complications with precision.