Sepsis - Nursing Case Study

Pathophysiology

• Primary mechanism: Sepsis starts with an infection, commonly bacterial, that overwhelms the body's normal immune response. This triggers a systemic inflammatory response syndrome (SIRS), which involves widespread inflammation in the body that can disrupt normal organ function.

• Secondary mechanism: As SIRS progresses, the body's response can lead to severe sepsis, characterized by organ dysfunction due to poor perfusion. This is fueled by the release of inflammatory mediators, causing vasodilation, increased vascular permeability, and clot formation, leading to reduced tissue oxygenation and organ failure.

• Key complication: Septic shock may occur if sepsis is not promptly and effectively treated, leading to dangerously low blood pressure that doesn't respond to fluid replacement. This further exacerbates organ dysfunction and can lead to death.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Diabetes Mellitus Type II, Hypertension, Chronic Obstructive Pulmonary Disease

• Current medications: Metformin, Lisinopril, Salmeterol

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Fever, chills, and difficulty breathing

• Key symptoms: Increased heart rate, confusion, decreased urination, fatigue

• Vital signs: Temperature: 38.8°C (101.8°F), Pulse: 115 bpm, Blood pressure: 90/60 mmHg, Respiratory rate: 28 breaths per minute, Oxygen saturation: 88% on room air

Section 1

Change in Patient Status:

The patient's condition seems to be deteriorating. His blood pressure has dropped further to 85/50 mmHg. His oxygen saturation has also decreased to 82% on room air. He is now more confused, and his skin has become cool and clammy, indicating poor perfusion. He also complains of increasing fatigue and weakness. His urinary output has further decreased, and his urine appears dark and concentrated, indicating possible acute kidney injury secondary to poor perfusion caused by sepsis.

New Diagnostic Results:

Repeat lab work has shown an increase in lactate levels, from 2.5 mmol/L to 4 mmol/L, suggesting a decrease in tissue perfusion. His white blood cell count has spiked to 18,000 cells/µL, indicating an ongoing systemic infection. The blood culture report has come back positive for Staphylococcus aureus, a common bacterial pathogen. His blood glucose level is also elevated at 200 mg/dL, likely due to stress hyperglycemia. The presence of protein and red blood cells in his urine may indicate kidney damage.

These changes signify a progression from severe sepsis to septic shock, necessitating aggressive management and close monitoring. The patient's history of diabetes and hypertension further complicate the situation, as both conditions can impair the body's immune response and make it harder to recover from infections. The patient's COPD can also exacerbate his difficulty breathing and decrease his oxygen saturation. It is crucial to manage these underlying conditions while treating the sepsis to improve his prognosis.

Section 2

Response to Interventions:

Despite aggressive fluid resuscitation and initiation of broad-spectrum antibiotics, the patient's condition continues to worsen. His blood pressure has not responded adequately to the fluid therapy and remains low at 80/45 mmHg, necessitating the commencement of vasopressors. His oxygen saturation has also not improved significantly, fluctuating between 82-85% on room air. Therefore, supplemental oxygen is being delivered through a nasal cannula at 4 L/min, and the healthcare team is considering intubation if his respiratory status does not improve.

New Complications:

The patient's blood glucose levels have further escalated to 250 mg/dL, indicating stress hyperglycemia. This might be due to the body's heightened response to illness, but it could also suggest poor control of his underlying diabetes. His GFR has dropped to 30 ml/min, suggesting worsening renal function. He is now oliguric, and there is an increasing concern for acute kidney injury, which may require renal replacement therapy if it continues to progress. His mental status has also deteriorated, with increasing confusion and decreased responsiveness, raising the concern for septic encephalopathy. These new complications make his clinical situation more complex and precarious, requiring prudent and prompt interventions.

Section 3

New Diagnostic Results:

The patient's blood work returns, showing a significant increase in lactate levels to 5 mmol/L, reflecting a state of tissue hypoperfusion. This is consistent with his low blood pressure and poor oxygen saturation, suggesting his tissues are not receiving adequate oxygen and nutrients. Furthermore, his white blood cell count has spiked to 20,000 cells/mm3, indicating a worsening infection, and his C-reactive protein is elevated at 180 mg/L, further confirming a systemic inflammatory response. His procalcitonin levels are also raised to 3 ng/mL, which is suggestive of bacterial infection, particularly in the context of his clinical presentation. These findings confirm the severity of the patient's sepsis and the need for immediate, aggressive intervention.

Change in Patient Status:

Despite supplemental oxygen, the patient's respiratory status continues to decline, with his respiratory rate increasing to 28 breaths/minute and his oxygen saturation dropping to 80%. His blood pressure has further decreased to 75/40 mmHg, and his heart rate is tachycardic at 115 beats/minute, indicating his body's struggle to maintain adequate perfusion. His mental status continues to worsen, with increasing lethargy and minimal response to verbal stimuli. His urine output has further decreased to less than 20 mL/hour, suggesting worsening kidney function. These changes in his physiological status indicate a worsening of his septic state, possibly progressing towards septic shock, necessitating urgent reassessment and escalation of his treatment plan.

Section 4

New Complications:

The patient's condition continues to deteriorate, with new signs of end-organ damage. His latest lab results show a serum creatinine level of 2.5 mg/dL, up from 1.0 mg/dL on admission, indicating acute kidney injury likely secondary to poor perfusion. His liver function tests are also abnormal, with an AST of 85 U/L and ALT of 90 U/L, both significantly above the upper normal limit, signifying hepatic involvement. Furthermore, his platelet count has dropped to 90,000 cells/mm3, suggesting possible disseminated intravascular coagulation (DIC), a serious complication of sepsis.

Response to Interventions:

Despite ongoing fluid resuscitation and broad-spectrum antibiotics, the patient shows no significant improvement. His hypotension persists, with a blood pressure of 72/38 mmHg, and his oxygen saturation remains dangerously low at 78% on 4 L of oxygen via nasal cannula. His mental status is increasingly worrisome, as he is now only responsive to painful stimuli. The healthcare team decides to escalate the patient's care to critical status and hastily makes arrangements for his transfer to the Intensive Care Unit (ICU) for closer monitoring, aggressive resuscitation, and consideration for mechanical ventilation. This decision presents an opportunity for further clinical reasoning involving the risks and benefits of intubation and mechanical ventilation in a patient with sepsis.

Section 5

New Diagnostic Results:

Following his transfer to the ICU, a repeat blood culture reveals the presence of gram-negative bacilli, indicating a bacterial infection. The bacteria are identified as Escherichia coli, which is sensitive to the current regimen of broad-spectrum antibiotics. However, his blood lactate level has risen from 2.5 mmol/L at admission to 4.8 mmol/L, an ominous sign of increased tissue hypoxia. An arterial blood gas (ABG) test shows a pH of 7.30, PCO2 of 32 mmHg, HCO3- of 15 mEq/L, and PaO2 of 60 mmHg, indicative of a combined metabolic and respiratory acidosis. These findings suggest ongoing cellular dysfunction and inadequate oxygen delivery despite ongoing interventions.

Response to Interventions:

The ICU team initiates vasopressor therapy with norepinephrine to improve his blood pressure and perfusion to vital organs. The patient is also started on renal replacement therapy (RRT) due to his worsening kidney function. Despite these interventions, his blood pressure remains low at 70/40 mmHg and his urine output is minimal. The healthcare team is also considering the initiation of mechanical ventilation given his progressively worsening hypoxia and altered mental status. However, this decision must be carefully weighed against the potential risks, including ventilator-associated pneumonia, barotrauma, and sedation-related complications. The team's next actions will require intricate clinical reasoning to manage the patient's rapidly unfolding sepsis syndrome.