ARDS - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute Respiratory Distress Syndrome (ARDS) primarily involves injury to the alveolar-capillary membrane (air sacs) in the lungs. This can be due to direct (pneumonia, inhalation injury) or indirect (sepsis, trauma, pancreatitis) insults, leading to inflammation and increased permeability.

• Secondary mechanism: Increased permeability allows protein-rich fluid to leak into the alveoli, causing pulmonary edema. This impairs gas exchange, leading to severe hypoxemia (low blood oxygen). Alveolar damage also leads to the release of inflammatory cytokines, worsening lung injury.

• Key complication: The body's response to injury and inflammation can lead to fibrosis (scarring), reducing lung compliance (elasticity). This may result in long-term respiratory complications and decreased quality of life.

Patient Profile

Demographics:

56-year-old male, works as a construction worker

History:

• Key past medical history: Ex-smoker, diagnosed with Chronic Obstructive Pulmonary Disease (COPD)

• Current medications: Symbicort (budesonide and formoterol), Spiriva (tiotropium), albuterol rescue inhaler

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath, fatigue, and fever

• Key symptoms: Persistent cough, chest tightness, difficulty breathing especially with exertion, pale or bluish skin color, decreased appetite, rapid heart rate, disorientation

• Vital signs: Temperature 101.4 F, heart rate 110 bpm, respiratory rate 28 breaths per minute, oxygen saturation 88% on room air, blood pressure 135/85 mmHg.

Section 1

New Diagnostic Results:

The patient's laboratory results showed an increased white blood cell count of 16,000 cells/mm³, indicating an active infection. Blood gas analysis revealed a PaO2 of 54 mmHg and a PaCO2 of 47 mmHg, confirming severe hypoxemia and hypercapnia, respectively. The chest X-ray showed bilateral infiltrates, further supporting the diagnosis of ARDS.

The patient's worsening condition with the development of fever, increased respiratory rate, disorientation, and declining oxygen saturation raised concerns about sepsis, prompting the healthcare team to order a blood culture. The results returned positive for Streptococcus pneumoniae, a common cause of community-acquired pneumonia. This infection, along with the patient's COPD, likely precipitated the onset of ARDS.

Change in Patient Status:

Over the next 24 hours, the patient's condition deteriorated further. His respiratory rate increased to 35 breaths per minute, and his oxygen saturation dropped to 82% despite supplemental oxygen via non-rebreather mask. The patient also became increasingly disoriented, with periods of restlessness and confusion. His blood pressure gradually decreased to 100/65 mmHg, and his heart rate increased to 125 bpm, suggesting signs of septic shock. His worsening condition necessitated transfer to the intensive care unit for closer monitoring and management.

Section 2

New Diagnostic Results:

Over the next few days, the patient's condition continued to worsen. Laboratory results showed an increased creatinine level of 2.5 mg/dL and a decreased glomerular filtration rate, indicating an acute kidney injury likely due to sepsis-induced hypoperfusion. Blood gas analysis depicted a worsening metabolic acidosis with a pH of 7.25 and a bicarbonate level of 18 mEq/L. The patient's coagulation profile was also abnormal, with a prolonged prothrombin time (PT) of 16 seconds and an elevated D-dimer level, suggesting a possible disseminated intravascular coagulation (DIC). Additionally, the patient’s persistently elevated WBC count and positive blood cultures despite antibiotic therapy raised concerns about antibiotic resistance or an ineffective antibiotic regimen.

Change in Patient Status:

Despite aggressive fluid resuscitation and vasopressor support, the patient's blood pressure continued to decrease, reaching 90/55 mmHg. His heart rate further increased to 135 bpm. The patient's respiratory status also deteriorated, with an increased respiratory rate of 40 breaths per minute and a decreased oxygen saturation of 78%. His mental status deteriorated further, progressing from confusion and restlessness to lethargy. His urine output decreased to less than 0.5 mL/kg/hr, indicating decreased renal perfusion and function. His skin became progressively mottled, cold, and clammy, indicative of poor peripheral perfusion. These signs suggested an escalation in the patient's septic shock, requiring further escalation of care and possibly considering advanced life support measures.

Section 3

New Diagnostic Results:

Despite the ongoing treatment, the patient's condition showed no sign of improvement. Recent laboratory results showed a further increase in creatinine levels to 3.6 mg/dL and a further decrease in glomerular filtration rate, highlighting progressive acute kidney injury. Blood gas analysis now showed a pH of 7.18, indicating a deepening metabolic acidosis. The coagulation profile worsened with a prothrombin time of 21 seconds and an increased D-dimer level, reinforcing the suspicion of disseminated intravascular coagulation (DIC). Furthermore, the patient’s elevated WBC count persisted, and blood cultures remained positive, suggesting the possible need for a change in the antibiotic regimen.

Change in Patient Status:

The patient's vital signs became more concerning over the next few hours. His blood pressure further decreased to 85/50 mmHg, and his heart rate escalated to 145 bpm. Despite maximum oxygen therapy, his oxygen saturation dropped to 72%, and his respiratory rate rose to 45 breaths per minute. The patient's consciousness level worsened, progressing to stupor. His urine output fell to less than 0.3 mL/kg/hr, signaling worsening renal function. His skin was notably cold, mottled, and clammy, indicative of poor peripheral perfusion. The patient's condition indicated an intensification of his septic shock, necessitating a reevaluation of the current treatment plan and consideration of more aggressive interventions.

Section 4

New Diagnostic Results:

The patient's deteriorating condition necessitated further diagnostic tests. A repeat chest X-ray revealed worsening bilateral infiltrates, suggestive of increasing ARDS severity. ABG analysis showed a PaO2/FiO2 ratio of 120 mmHg, below the critical threshold for severe ARDS. A kidney ultrasound showed increased echogenicity and loss of corticomedullary differentiation, supporting the diagnosis of acute kidney injury. In addition, the patient's serum lactate increased to 6 mmol/L, reflecting the severity of his shock state. His platelet count dropped to 50,000/mm3, consistent with DIC. The sputum culture revealed multidrug-resistant Pseudomonas aeruginosa, necessitating a change in antibiotic therapy.

Response to Interventions:

Despite aggressive fluid resuscitation and norepinephrine infusion, the patient's hypotension persisted. Attempts to correct the metabolic acidosis with sodium bicarbonate infusions yielded little improvement, and his acid-base imbalance worsened. His worsening ARDS required escalation to mechanical ventilation with positive end-expiratory pressure (PEEP) settings adjusted to optimize oxygenation. However, his oxygen saturation remained below 90%. Though the antibiotic regimen was switched to Colistin and Meropenem after identifying the Pseudomonas aeruginosa, his fever and leukocytosis persisted, indicating an ongoing severe infection. Renal replacement therapy was initiated due to the unresponsive acute kidney injury. Despite these interventions, the patient's condition continued to decline, prompting consideration of more aggressive life-support measures.

Section 5

New Complications:

Two days following the initiation of renal replacement therapy, the patient's hypotension exacerbated, and his heart rate increased to 135 bpm. His central venous pressure (CVP) showed a decline to 4 mmHg, indicating a decreased preload despite fluid resuscitation. Lab results showed a further drop in his platelet count to 30,000/mm3 along with an increase in D-dimer levels to 2,500 ng/ml, indicating a progression of DIC. Moreover, his liver function tests came back abnormal with a significant elevation in bilirubin levels to 3.8 mg/dL and ALT to 80 U/L, suggesting the development of acute liver injury. A subsequent ultrasound confirmed the presence of hepatomegaly and mild ascites.

Change in Patient Status:

Over the next 24 hours, the patient's condition worsened. He became increasingly confused and agitated, requiring sedation. His Glasgow Coma Scale (GCS) score decreased to 9, indicating a significant decrease in his level of consciousness. His oxygen saturation continued to drop, reaching a low of 85% despite maximum ventilatory support. His arterial blood gas showed a PaO2 of 60 mmHg and PaCO2 of 50 mmHg, suggesting worsening respiratory failure. In addition, his serum creatinine rose to 3.5 mg/dL and his urine output dropped to less than 0.5 ml/kg/hr, confirming the progression of acute kidney injury. The patient's worsening multi-organ failure necessitated a multi-disciplinary approach and a review of his goals of care.