A patient with sepsis is showing signs of advancing septic shock, including persistent hypotension and deteriorating mental status. Despite fluid resuscitation, her blood pressure remains low, and her oxygen saturation has decreased to 90%. Which nursing intervention is the highest priority to stabilize the patient’s condition?

B) Start vasopressor therapy as ordered to support blood pressure.

A) Administer a high-flow oxygen therapy to improve oxygen saturation.

B) Start vasopressor therapy as ordered to support blood pressure.

C) Increase the rate of intravenous crystalloids to enhance fluid resuscitation.

D) Monitor urine output closely to assess for acute kidney injury.

A 65-year-old female patient with a history of Type 2 Diabetes is being treated for sepsis secondary to a urinary tract infection caused by Escherichia coli. Despite broad-spectrum antibiotics and fluid resuscitation, her blood pressure remains low, and she is exhibiting signs of confusion. Her creatinine level has risen to 2.1 mg/dL from a baseline of 0.9 mg/dL. Which of the following interventions should the nurse anticipate as a priority to prevent further deterioration?

B) Initiating vasopressor therapy to stabilize blood pressure

A) Administering additional fluids to manage hypotension

B) Initiating vasopressor therapy to stabilize blood pressure

C) Providing antipyretics to manage fever

D) Preparing for dialysis due to rising creatinine levels

A patient in the ICU is receiving norepinephrine for septic shock and has developed acute kidney injury (AKI) with a urine output of 10 mL/hr. Her latest labs indicate a lactate level of 5.2 mmol/L, elevated creatinine, prolonged PT and aPTT, and decreased platelet count. What is the most appropriate nursing intervention to prioritize at this time?

D) Adjust norepinephrine dosage to optimize blood pressure and perfusion.

A) Increase the rate of IV fluids to improve renal perfusion.

B) Prepare for renal replacement therapy to manage AKI.

C) Administer a platelet transfusion to address thrombocytopenia.

D) Adjust norepinephrine dosage to optimize blood pressure and perfusion.

A patient with septic shock is experiencing persistent hypotension, acute kidney injury, and signs of disseminated intravascular coagulation (DIC). Which nursing intervention is the most appropriate to prioritize for this patient?

A) Administering a continuous infusion of norepinephrine to maintain mean arterial pressure.

B) Initiating renal replacement therapy to manage acute kidney injury.

C) Administering fresh frozen plasma to correct prolonged PT and aPTT.

D) Encouraging oral fluid intake to improve hydration status.

A patient in septic shock is experiencing a deteriorating mental status and persistent hypotension despite vasopressor support. The healthcare team is considering the addition of low-dose corticosteroids. What is the primary rationale for this intervention in the context of septic shock?

B) To address potential adrenal insufficiency contributing to refractory shock

A) To directly increase blood pressure by enhancing vascular tone

B) To address potential adrenal insufficiency contributing to refractory shock

C) To reduce the risk of infection by suppressing the immune response

D) To improve renal perfusion by decreasing overall fluid requirements

A patient in septic shock is not responding adequately to increased vasopressor support. Her mean arterial pressure remains around 60 mmHg, and her mental status is deteriorating. Considering the current clinical scenario, which nursing intervention is most appropriate to prioritize at this time?

B) Administer low-dose corticosteroids as ordered by the physician.

A) Increase the rate of intravenous fluids to improve perfusion.

B) Administer low-dose corticosteroids as ordered by the physician.

C) Prepare the patient for immediate renal replacement therapy.

D) Reassess the patient's neurological status and report changes to the healthcare provider.

A patient with acute respiratory acidosis and worsening renal function is being considered for non-invasive ventilation and continuous renal replacement therapy. Which of the following nursing interventions is most critical to address the patient's current clinical status?

B) Monitoring for signs of respiratory fatigue and preparing for potential intubation

A) Administering sodium bicarbonate to correct metabolic acidosis

B) Monitoring for signs of respiratory fatigue and preparing for potential intubation

C) Initiating a fluid restriction to manage acute kidney injury

D) Providing high-flow oxygen therapy to alleviate hypoxemia

A patient with acute respiratory acidosis and worsening metabolic derangement is being considered for non-invasive ventilation or intubation. Considering her elevated potassium levels and renal function decline, which intervention should the nurse prioritize to prevent complications while awaiting nephrology consultation?

C) Administer calcium gluconate to stabilize cardiac membranes

A) Administer sodium bicarbonate to correct acidosis

B) Prepare the patient for immediate intubation

C) Administer calcium gluconate to stabilize cardiac membranes

D) Initiate oxygen therapy at 2 L/min via nasal cannula

A patient with acute kidney injury and respiratory acidosis is receiving non-invasive ventilation and CRRT. She develops hypotension and requires norepinephrine support. Which action should the nurse prioritize to ensure patient stability?

C) Monitor the patient's blood pressure and titrate norepinephrine as needed.

A) Increase the CRRT fluid removal rate to address fluid overload.

B) Adjust the ventilator settings to improve oxygenation.

C) Monitor the patient's blood pressure and titrate norepinephrine as needed.

D) Administer a bolus of normal saline to increase blood pressure.

A patient is receiving non-invasive ventilation due to respiratory distress, and continuous renal replacement therapy is being used for acute kidney injury. Despite these interventions, the patient develops hypotension and requires vasopressor support. What is the nurse's priority action in response to the patient's hemodynamic instability?

B) Assess fluid status and consider an intravenous fluid bolus as prescribed

A) Increase the rate of norepinephrine infusion to quickly stabilize blood pressure

B) Assess fluid status and consider an intravenous fluid bolus as prescribed

C) Re-evaluate the effectiveness of non-invasive ventilation and consider intubation

D) Monitor renal function tests to evaluate the effectiveness of CRRT

Sepsis - Nursing Case Study

Pathophysiology

• Primary mechanism: Sepsis begins with an overwhelming immune response to infection, where the body releases excessive pro-inflammatory cytokines, leading to systemic inflammation that damages tissues and organs.

• Secondary mechanism: This hyper-inflammatory state causes widespread endothelial dysfunction, increasing vascular permeability, leading to hypotension and inadequate organ perfusion.

• Key complication: The combination of inflammation and vascular changes can trigger disseminated intravascular coagulation (DIC), where small blood clots form throughout the bloodstream, depleting clotting factors and causing both bleeding and further organ damage.

Patient Profile

Demographics:

56-year-old female, school teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Fever and confusion

• Key symptoms: Chills, rapid breathing, decreased urine output, fatigue

• Vital signs: Temperature 102.4°F (39.1°C), Heart rate 110 bpm, Respiratory rate 24 breaths/min, Blood pressure 88/60 mmHg, Oxygen saturation 92% on room air

Section 1

As the healthcare team continues to monitor the patient, new diagnostic results reveal elevated lactate levels of 4.5 mmol/L, indicating significant tissue hypoperfusion and metabolic acidosis. Additionally, her white blood cell count is notably high at 17,000 cells/mm³, suggestive of an ongoing systemic inflammatory response. Blood cultures return positive for Escherichia coli, confirming a bacterial source of infection likely originating from a urinary tract infection, which aligns with her decreased urine output and known history of Type 2 Diabetes. These findings further substantiate the diagnosis of sepsis and underscore the urgency of targeted antimicrobial therapy, given her penicillin allergy.

In response to these results, the medical team initiates broad-spectrum antibiotics, selecting a regimen that avoids penicillin due to her allergy, and begins aggressive fluid resuscitation with intravenous crystalloids to address her hypotension and improve tissue perfusion. Despite these interventions, the patient demonstrates a concerning change in status as her blood pressure remains low at 85/58 mmHg, and her mental status deteriorates with increased confusion, suggestive of advancing septic shock. Her oxygen saturation dips to 90%, necessitating supplemental oxygen to maintain adequate oxygenation.

Given the patient's declining condition, the healthcare team considers the possibility of developing complications such as acute kidney injury (AKI) due to persistent hypotension and hypoperfusion, as evidenced by her low urine output and rising creatinine level, now at 2.1 mg/dL from a baseline of 0.9 mg/dL. The team must now weigh the need for vasopressor support to stabilize her hemodynamics and prevent further end-organ damage while closely monitoring for signs of disseminated intravascular coagulation (DIC), given her predisposition to clotting dysfunctions in the setting of severe sepsis. This critical juncture requires careful clinical reasoning to balance aggressive treatment measures with vigilant monitoring for potential adverse effects and complications.

Section 2

As the healthcare team continues to monitor the patient, they observe her persistent hypotension and deteriorating mental status, raising concerns about her progressing into septic shock. The decision is made to initiate vasopressor therapy, starting with norepinephrine, to stabilize her blood pressure and improve perfusion to vital organs. Despite these efforts, her urine output remains critically low at 10 mL/hr, and her creatinine level has risen further to 2.5 mg/dL, confirming the development of acute kidney injury. Her skin is noted to be cool and mottled, particularly in the extremities, which is a concerning sign of inadequate peripheral perfusion.

In parallel, a repeat set of laboratory tests reveals a further increase in lactate level to 5.2 mmol/L, indicating worsening metabolic acidosis and persistent tissue hypoxia. Her coagulation profile shows a prolongation of her prothrombin time (PT) and activated partial thromboplastin time (aPTT), alongside a decrease in platelet count to 90,000 cells/mm³, suggestive of the early stages of disseminated intravascular coagulation (DIC). These findings necessitate a delicate balance of interventions to manage the complex interplay between improving perfusion, supporting organ function, and mitigating the risk of bleeding due to coagulopathy.

The team adjusts her management plan to address these complications, increasing the dose of her vasopressor support while closely monitoring her coagulation status. They consider the potential need for renal replacement therapy if her kidney function continues to decline. The focus remains on tailoring the antimicrobial therapy effectively against the Escherichia coli infection, all while ensuring that any new interventions do not exacerbate her risk of bleeding. This evolving scenario demands continuous reevaluation of her clinical status and a coordinated, dynamic approach to treatment, highlighting the critical importance of thorough clinical reasoning in managing complex sepsis cases.

Section 3

As the healthcare team continues to manage the patient's complex condition, they observe a notable change in her status. Despite the increased vasopressor support with norepinephrine, her mean arterial pressure remains borderline, hovering around 60 mmHg, which is concerning for inadequate organ perfusion. The patient's mental status further deteriorates, with her Glasgow Coma Scale score dropping to 10, indicating a worsening level of consciousness. This change prompts the team to conduct a thorough neurological assessment, considering both the direct effects of sepsis on the central nervous system and potential metabolic causes related to her acidosis and hypoxia.

In parallel, a new set of diagnostic imaging is ordered to evaluate for potential sources of infection or other complications. A computed tomography (CT) scan of the abdomen and pelvis reveals no evidence of abscess formation or additional infectious foci that could be contributing to her septic state. However, there is a moderate degree of bowel edema, which raises concerns about potential gastrointestinal ischemia. This finding underscores the need for vigilant monitoring of her abdominal status and the careful management of her fluid balance to optimize perfusion without exacerbating edema.

As the team processes these developments, they recalibrate their approach to her care. Given the limited improvement with current interventions, the decision is made to consider adjunctive therapies, such as low-dose corticosteroids, to address potential adrenal insufficiency contributing to her refractory shock. The nephrology team is consulted to assess the timing and modality of renal replacement therapy, should her kidney function continue to decline. These decisions are made in the context of her coagulopathy, weighing the risks and benefits of each intervention carefully. This multifaceted approach highlights the critical need for dynamic clinical reasoning and collaboration across disciplines to navigate the intricacies of her condition effectively.

Section 4

As the healthcare team continues to monitor the patient, they note a concerning change in her respiratory status. The patient's respiratory rate has increased to 30 breaths per minute, with accompanying use of accessory muscles, indicating increased work of breathing. Arterial blood gas analysis reveals a pH of 7.28, PaCO2 of 55 mmHg, and PaO2 of 65 mmHg, suggestive of acute respiratory acidosis with hypoxemia. These findings prompt the team to escalate respiratory support, including consideration for non-invasive ventilation or intubation to correct the gas exchange abnormalities and reduce the risk of respiratory failure.

In addition to her respiratory compromise, the patient's laboratory results indicate a worsening metabolic derangement. Her lactate level has risen to 5 mmol/L, reflecting ongoing tissue hypoperfusion and the severity of her septic state. The comprehensive metabolic panel reveals worsening renal function, with a creatinine level now at 3.5 mg/dL from a baseline of 1.2 mg/dL, and potassium elevated to 5.8 mmol/L. These findings highlight the need for urgent nephrology intervention to mitigate the risk of hyperkalemia and prevent further renal damage. The nephrology team discusses the potential initiation of continuous renal replacement therapy (CRRT), given the patient's hemodynamic instability and electrolyte imbalances.

These developments necessitate a rapid reassessment of the patient's treatment plan. The healthcare team must balance the need for aggressive intervention to stabilize her respiratory and renal functions against the backdrop of her coagulopathy and existing cardiovascular challenges. This situation underscores the importance of dynamic clinical reasoning and the integration of multidisciplinary expertise to tailor interventions that will best support the patient's recovery while minimizing potential complications. The team remains vigilant, ready to adjust their strategies as the patient's condition evolves.

Section 5

As the healthcare team initiates non-invasive ventilation to support the patient's compromised respiratory status, they closely monitor her for any signs of improvement or further deterioration. Within the first hour of intervention, her respiratory rate stabilizes to 24 breaths per minute, and the use of accessory muscles diminishes slightly, indicating a partial response to the increased respiratory support. However, arterial blood gas analysis shows minimal improvement, with a pH of 7.32, PaCO2 of 50 mmHg, and PaO2 of 70 mmHg. While these changes are encouraging, the patient's respiratory acidosis and hypoxemia remain concerning, prompting the team to maintain vigilance and consider intubation if further improvement does not occur.

Meanwhile, the nephrology team proceeds with continuous renal replacement therapy (CRRT) to address the patient's acute kidney injury and hyperkalemia. Within the first few hours of CRRT initiation, her potassium level decreases to 5.2 mmol/L, reflecting a positive trend in managing her electrolyte imbalance. However, her creatinine level remains elevated at 3.3 mg/dL, indicating ongoing renal impairment. The team continues to monitor her fluid balance and renal function closely, aware that her hemodynamic instability could complicate fluid management and necessitate adjustments in therapy.

Despite these interventions, the patient's condition remains precarious, and new complications arise. She develops hypotension, with blood pressure readings dropping to 85/50 mmHg, necessitating the initiation of vasopressor support with norepinephrine to maintain adequate perfusion. This development highlights the delicate interplay between her septic state and cardiovascular function, prompting the multidisciplinary team to reassess her overall treatment plan continuously. The healthcare team's ability to adapt and respond to these evolving challenges is critical as they strive to stabilize the patient and prevent further deterioration.