turp - Nursing Case Study

Pathophysiology

• Primary mechanism: During Transurethral Resection of the Prostate (TURP), excessive resection or prolonged operation time can lead to significant absorption of irrigation fluids, especially hypotonic solutions, into the systemic circulation, causing dilutional hyponatremia known as TURP syndrome.

• Secondary mechanism: The rapid influx of hypotonic fluids results in fluid overload and electrolyte imbalance, particularly hyponatremia, leading to cellular swelling and neurological effects due to osmotic shifts across the blood-brain barrier.

• Key complication: Severe hyponatremia can cause cerebral edema, manifesting as confusion, seizures, or coma, necessitating prompt recognition and management to prevent permanent neurological damage.

Patient Profile

Demographics:

72-year-old male, retired chemical engineer

History:

• Key past medical history: Benign prostatic hyperplasia, hypertension, type 2 diabetes, chronic kidney disease stage 3

• Current medications: Tamsulosin, Lisinopril, Metformin, Insulin, Aspirin

• Allergies: Penicillin, Shellfish

Current Presentation:

• Chief complaint: Severe lower urinary tract symptoms and inability to urinate

• Key symptoms: Excruciating pelvic pain, hematuria, nausea, dizziness

• Vital signs: Blood pressure 90/60 mmHg, heart rate 120 bpm, respiratory rate 24 breaths/min, temperature 38.5°C, oxygen saturation 88% room air

Section 1

As the nursing team conducts an initial assessment post-TURP, the patient's condition is critical. Upon evaluation, the patient is found to be increasingly confused, with a Glasgow Coma Scale (GCS) score of 10, indicating a significant decline in mental status. His skin is cool and clammy, and he exhibits signs of peripheral cyanosis. The patient is disoriented to time and place, unable to follow simple commands. Neurological examination reveals sluggish pupillary response and a positive Babinski sign bilaterally, suggesting potential cerebral involvement due to severe hyponatremia and possible cerebral edema.

Laboratory results confirm the clinical suspicion of TURP syndrome. Serum sodium level is critically low at 118 mmol/L, indicating severe hyponatremia. Additionally, serum osmolality is decreased, corroborating the dilutional effect of the absorbed irrigation fluids. Renal function tests show elevated blood urea nitrogen (BUN) and creatinine, consistent with the patient's known chronic kidney disease, but now exacerbated by acute kidney injury due to fluid overload. The arterial blood gas reveals metabolic acidosis with a pH of 7.30, further complicating the patient's hemodynamic instability.

The nursing team urgently initiates interventions, administering hypertonic saline cautiously to address the hyponatremia while closely monitoring for signs of rapid sodium correction that could lead to central pontine myelinolysis. Despite these efforts, the patient suddenly develops generalized tonic-clonic seizures, indicating progression of cerebral edema. This acute complication prompts an immediate call for a neurologist consultation and preparation for possible transfer to the intensive care unit for advanced neurocritical care. The patient's deteriorating neurological status necessitates a reevaluation of the treatment plan and continuous monitoring to prevent further complications.

Section 2

As the nursing team continues to manage the patient's critical condition, they observe a rapid decline in his respiratory status. The patient's oxygen saturation drops to 85% on room air, prompting the initiation of supplemental oxygen therapy via a non-rebreather mask. Despite these measures, his respiratory rate increases to 28 breaths per minute, and he begins to exhibit shallow, labored breathing with audible crackles upon auscultation of the lung fields. Review of the patient's fluid balance indicates significant positive fluid status, pointing towards pulmonary edema secondary to fluid overload as a potential cause of the respiratory compromise.

In response to these new findings, the healthcare team orders a stat chest X-ray, which reveals diffuse bilateral infiltrates consistent with acute pulmonary edema. Concurrently, repeat blood gas analysis shows worsening metabolic acidosis with a pH now at 7.28 and a base excess of -6 mmol/L, indicating the need for aggressive intervention. Given the patient's compromised respiratory function and metabolic derangement, the decision is made to initiate non-invasive ventilation to support oxygenation and ventilation while considering diuretic therapy to manage fluid overload, all under close monitoring to prevent further decompensation.

The team remains vigilant for any signs of further deterioration, particularly given the risk of acute respiratory distress syndrome (ARDS) in the context of the patient's complex clinical picture. The interdisciplinary team, including nephrology and pulmonology, is consulted to ensure a comprehensive approach to the patient's worsening condition. This multifaceted scenario demands advanced clinical judgment to balance the correction of electrolyte imbalances, management of fluid status, and support of respiratory function, highlighting the critical nature of the patient's evolving condition and the necessity for coordinated critical care interventions.

Section 3

As the healthcare team implements non-invasive ventilation and administers diuretics, there is a brief improvement in the patient's respiratory status. His oxygen saturation increases to 92%, and his respiratory rate decreases to 22 breaths per minute, offering a momentary reprieve. However, shortly thereafter, the patient begins exhibiting signs of confusion and agitation, suggestive of worsening cerebral perfusion or metabolic imbalance. New lab results indicate a serum potassium level of 5.9 mmol/L and a creatinine level rising to 2.3 mg/dL, suggesting acute kidney injury potentially exacerbated by both the fluid overload and diuretic therapy. The blood pressure, previously stable, now reads at 88/54 mmHg, raising concerns about systemic perfusion and the potential progression to a state of shock.

In response to these alarming changes, the interdisciplinary team urgently reassesses the patient's overall condition. The nephrology consultant recommends cautious fluid management, emphasizing the delicate balance required to alleviate pulmonary edema while ensuring adequate renal perfusion. The pulmonology team evaluates the potential need for escalation to invasive mechanical ventilation, weighing the risks and benefits in the context of the patient's deteriorating mental status and persistent metabolic acidosis, now with a pH of 7.25 and a lactate level of 4.2 mmol/L.

The situation is further complicated when the patient develops hypotension and worsening oliguria, prompting the critical care team to initiate inotropic support to stabilize hemodynamics and maintain end-organ perfusion. As these interventions are enacted, the team remains vigilant for signs of further decompensation, including the possibility of septic shock or multi-organ dysfunction syndrome (MODS), necessitating continuous critical thinking and real-time adaptation of the treatment plan. The evolving case underscores the need for rigorous monitoring and dynamic reassessment, with each decision carrying significant implications for the patient's survival and recovery trajectory.

Section 4

As the healthcare team continues to monitor the patient, new diagnostic results further complicate the clinical picture. A repeat chest X-ray reveals increasing bilateral pulmonary infiltrates, suggestive of worsening pulmonary edema or possible aspiration pneumonia, given the patient's altered mental status. The arterial blood gas analysis now shows a pH of 7.22, PaCO2 of 55 mmHg, and PaO2 of 60 mmHg, indicative of a mixed respiratory and metabolic acidosis. Concurrently, the patient's lactate level has risen to 5.0 mmol/L, raising the alarm for possible progression to septic shock or further deterioration of perfusion status.

In light of these developments, the critical care team re-evaluates the current management strategy, acknowledging the growing complexity of the case. The nephrology consultant expresses concern over the persistent rise in creatinine, now at 2.6 mg/dL, and suggests renal replacement therapy as a potential measure to address both the fluid overload and metabolic derangements. However, the team must carefully weigh this option against the patient's hemodynamic instability. The pulmonology team, faced with the decision to escalate to invasive mechanical ventilation, considers the risk of barotrauma and further hemodynamic compromise in a patient with tenuous blood pressure and increasing reliance on inotropic support.

The patient's condition demands advanced critical thinking and clinical judgment, with the team navigating a precarious balance between aggressive intervention and supportive care. As they deliberate, the patient's heart rate climbs to 125 beats per minute, and he exhibits a further decrease in urine output to less than 10 mL per hour. These changes necessitate immediate action and underscore the importance of a coordinated, multidisciplinary approach to prevent further decompensation and to optimize the patient's chances for recovery. The unfolding narrative sets the stage for a critical decision-making juncture, challenging the healthcare team to adapt dynamically and effectively to the evolving clinical scenario.

Section 5

The critical care team, working under the pressure of the patient's deteriorating condition, decides to prioritize the stabilization of the patient's hemodynamics while preparing for potential renal replacement therapy. The decision is made to initiate continuous renal replacement therapy (CRRT) carefully, to address the severe metabolic acidosis and fluid overload, while minimizing rapid shifts in fluid balance that could precipitate further hemodynamic instability. As the nephrology team prepares for CRRT, the intensivist oversees adjustments to the inotropic support, increasing the dose of norepinephrine to maintain a mean arterial pressure (MAP) above 65 mmHg, recognizing the delicate balance required to support systemic perfusion without exacerbating cardiac stress.

Simultaneously, the pulmonology team initiates high-flow nasal cannula (HFNC) oxygen therapy, a less invasive option aimed at improving oxygenation while reducing the risk of barotrauma associated with mechanical ventilation. Despite this, the patient's oxygen saturation remains stubbornly low at 85%, and his respiratory rate increases to 35 breaths per minute, indicating worsening respiratory distress. The team revisits the decision to intubate, weighing the potential benefits against the risk of further hemodynamic compromise. Meanwhile, the critical care nurse notes new findings during a focused physical assessment: the patient's skin is now notably cool and clammy, with capillary refill time exceeding four seconds, indicating worsening peripheral perfusion and raising suspicions of progressing septic shock.

As the team synthesizes this complex information, a new diagnostic development adds another layer to the clinical picture: blood cultures return positive for gram-negative bacilli, suggesting a source of sepsis that demands urgent antimicrobial intervention. This finding prompts the infectious disease consultant to recommend broadening antibiotic coverage to include meropenem and vancomycin, targeting potential multidrug-resistant organisms. The team must now integrate this new information into the treatment plan, recognizing the need for rapid antimicrobial therapy to address the underlying infection while continuing to manage the patient's critical respiratory and renal challenges. This cascade of events underscores the necessity for continuous reevaluation and dynamic adaptation as the patient's status evolves.