TL, A 24-YEAR-OLD woman, is admitted to the ED on a Monday afternoon. She's been sick for 3 days with a fever, productive cough, headache, night sweats, and general malaise. Several family members had recently been treated for Group A streptococcal tonsillopharyngitis (strep throat).
On the morning of her admission, TL's mother calls 911 when TL can't be easily aroused. On admission she doesn't appear very ill, but she's already on a course leading to septic shock. By Wednesday morning, TL will be dead. This article reviews the course of her illness, the treatment she received from admission to her death in 2010, and lessons learned from this experience.
When the emergency medical responders arrive, TL is awake and gets on the stretcher with minimal assistance. She arrives at the ED with a temperature of 101° F (38.3° C), heart rate of 120, respiratory rate of 16, BP of 125/70, and Sao2 of 99% on room air. A chest X-ray reveals bilateral pneumonia.
During the nursing assessment, TL is alert, and her BP and respiratory status are stable. A complete blood cell count and basic metabolic panel (BMP) show normal values except for hypokalemia (2.9 mEq/L; normal, 3.5–5.0 mEq/L) and hyponatremia (129 mEq/L; normal, 135–145 mEq/L). Specimens for blood, urine, and sputum cultures are obtained and rapid antigen detection testing (rapid strep screen) is negative. The ED physician prescribes 1 L of I.V. 0.9% sodium chloride with 40 mEq of potassium chloride to run at 125 mL/hr. TL is diagnosed with community-acquired pneumonia (CAP) and receives stat doses of I.V. ceftriaxone followed by I.V. azithromycin.
Severe sepsis is the 10th leading cause of death in the United States, claiming approximately 200,000 lives each year.1,2 Mortality for severe sepsis is 30% to 50% and may be as high as 50% to 60% for septic shock.3 Fortunately, recent studies have identified some successful evidence-based practices and early goal-directed therapies shown to decrease mortality in patients with sepsis. These studies have led to a better understanding of sepsis, allowing earlier identification and more successful patient outcomes.4 Much of this research is culminated in the Surviving Sepsis Campaign (SSC). This global initiative is an ongoing collaboration between the European Society of Intensive Care Medicine and the Society of Critical Care Medicine.
Following the SSC guidelines is a voluntary commitment. Many hospitals have resisted making changes for various reasons, most commonly because much of the research was funded by pharmaceutical companies.5 Because of this and other financial barriers, many hospitals have taken a “wait and see” approach before acquiring the resources needed to implement the guidelines.5 However, the research is standing up to scrutiny and campaign participation is associated with a reduction in hospital mortality.6
At the time of TL's admission, the hospital didn't have an updated sepsis protocol in place that followed the SSCs early goal-directed guidelines. Due to a lack of awareness and aggressive treatment, the severity of TL's illness wasn't detected early enough to save her.
Sepsis is defined as the presence, probable or documented, of infection together with systemic manifestations of infection.4 It can present in three different stages: uncomplicated sepsis, severe sepsis, and septic shock. Uncomplicated sepsis is the most common form of sepsis and may not even require hospitalization.7 An influenza infection with a fever and general malaise is typically the cause of uncomplicated sepsis. In these cases, the body recognizes an infection and reacts appropriately, initiating an inflammatory and immune response to eliminate the offending pathogen.7,8
Severe sepsis is sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion.4 This inflammatory response is exaggerated and many of the chemical mediators that are released interfere with tissue perfusion.7,8 This dysfunctional response leads to global tissue hypoxia and organ dysfunction. The patient may exhibit hypoxia, hypotension, and coagulation abnormalities.6,9 Severe sepsis with hypotension that doesn't respond to fluid resuscitation is considered septic shock.7,9
The course of sepsis is difficult to predict because nonspecific signs and symptoms can vary from patient to patient. Many can easily be attributed to other causes, delaying diagnosis and appropriate treatment.7
The SSC uses the American College of Chest Physicians and the SCCM criteria for Systemic Inflammatory Response Syndrome (SIRS).10 The guidelines define SIRS as the presence of two or more of the following:
* temperature > 100.4° F (38.0° C) or < 96.8° F (36° C)
* heart rate > 90/min
* respiratory rate > 20/min or a PaCO2 < 32 mm Hg
* white blood cell count > 12,000/mcL or < 4,000/mcL
SIRS may be due to infection or a noninfectious insult such as surgery or trauma. The SSC defines sepsis as SIRS in the presence of a known or suspected infection.10
TL's vital signs are stable when she's admitted to the medical floor at 1600 on Monday evening. Blood work and a repeat chest X-ray are ordered for the next morning. She's treated with acetaminophen for fever and ondansetron for nausea and has an uneventful evening.
At about 0200 Tuesday morning, TL begins complaining of increased shortness of breath and chest pain. Her temperature is 101.3° F (38.5° C), her heart rate has increased to 119, but her BP remains stable. Her Sao2 is 95% on room air but increases to 98% when she's placed on supplemental oxygen at 2 L/minute via nasal cannula (NC). A stat ECG reveals sinus tachycardia without other abnormalities. A repeat chest X-ray shows increasing bilateral infiltrates consistent with infection versus edema. Due to concerns about pulmonary edema, TL's I.V. fluids are discontinued.
By 0800 Tuesday, although her BP remains stable, her heart rate has increased to 130, and her Sao2 is now 95% on oxygen at 2 L/minute NC. A second ECG shows only sinus tachycardia. Her I.V. fluids are restarted at 80 mL/hr.
Chest computed tomography angiography rules out pulmonary embolism, but shows bilateral moderate pleural effusions suggesting infection. Arterial blood gas (ABG) results show hypoxemia with a Pao2 of 52 mm Hg on 2 L/minute NC.
At 1130 Tuesday morning, TL is transferred to the progressive care unit for closer monitoring. Serum cardiac biomarker results and a repeat BMP are within normal limits. Concerned that pulmonary edema is the cause of her worsening oxygenation status, the healthcare provider discontinues her I.V. fluids once again. Because TL isn't improving with ceftriaxone and azithromycin, I.V. levofloxacin is added.
By 1500 Tuesday afternoon, TL's oxygen flow rate is increased to 5 L/minute NC, which stabilizes her Sao2 at 97%. However, her heart rate is 142 and her BP 96/59. A pulmonologist is consulted to manage her deteriorating respiratory status.
Her sputum Gram stain reveals multiple Gram-positive cocci and Gram-positive rods. For better Gram-positive coverage, her pulmonologist discontinues the ceftriaxone and azithromycin and prescribes I.V. vancomycin stat.11
At this time, TL's platelet count has dropped from 150,000/mm3 on admission to 84,000/mm3, and her BP is decreasing. The pulmonologist prescribes 1 L of 0.9% I.V. sodium chloride solution to infuse over 2 hours and a serum lactate level is obtained.
A serum lactate level 4 mmol/L or more indicates organ dysfunction resulting in tissue hypoxia. The SSC guidelines define hyperlactatemia as more than 1 mmol/L. TL's serum lactate level was 3.9 mmol/L. Hyperlactatemia, in addition to her increasing oxygen requirements, thrombocytopenia, and hypotension, all point to severe sepsis.
Besides serum lactate, central venous oxygen saturation (Scvo2) is another important indicator of tissue hypoxia. A normal Scvo2 value is approximately 70%, which represents the relationship between oxygen consumption and oxygen delivery in the body.12,13 During her time in the hospital, TL's Scvo2 isn't checked.
Thrombocytopenia, a potential complication of sepsis, is one of many coagulopathies that may be seen.14 TL also has an elevated serum fibrin degradation product level. This, combined with thrombocytopenia, is evidence of the beginning of disseminated intravascular coagulation (DIC). This occurs in a patient with sepsis when generalized inflammation activates the coagulation cascade.15 At least one-third of patients with severe sepsis develop DIC.16 Unfortunately, in TL's case, development of DIC isn't recognized or treated at this time.
By 1830 Tuesday evening, TL's BP is the same, but her heart rate is 145. Her Sao2 has dropped to 91% on a 15 L/minute high-flow nasal cannula. Transferred to the ICU, she's endotracheally intubated at 1900 and placed on 100% oxygen. Postintubation ABGs show respiratory acidosis with a pH of 7.25 and severe hypoxemia with a Pao2 of 47 mm Hg.
By 2030, her heart rate is 166 and her BP 94/50, with a mean arterial pressure of 64 mm Hg. A radial arterial line is inserted. At this point, I.V. crystalloids are infusing wide open.
By 2100, despite multiple I.V. vasopressors, TL's BP continues to drop.
Bilateral chest tubes are placed to drain the enlarging pleural effusions. The next ABG value shows that TL's acidosis is worsening with a pH of 7.20 and a critically low Pao2 of 34 mm Hg.
TL suffers cardiac arrest at 2130 Tuesday evening. Following advanced cardiac life support guidelines, the staff notes the return of spontaneous circulation at 2144. The nurse adds an epinephrine infusion to the existing vasopressors for additional BP support.
Several attempts to insert a central venous catheter resulted in steady bleeding from multiple puncture sites, requiring transfusion with 2 units of fresh frozen plasma, 4 units of platelets, and administration of vitamin K.
TL's vital signs remain relatively stable over the next several hours, but by 0345 Wednesday morning her serum lactate level is 14.6 mmol/L, indicating severe organ hypoperfusion.17 Her coagulopathy is worsening, as evidenced by a platelet count of 54,000/mm3 and a partial thromboplastin time of 85.4 seconds (normal, 21 to 35 seconds). She's anuric and her serum creatinine level is elevated at 2.1 mg/dL (normal, 0.6–1.2 mg/dL). Her blood glucose is 871 mg/dL when an insulin infusion is started. Her serum liver enzymes are elevated, showing signs of hypoperfusion and ischemic hepatitis.18 By 0500 her pH is 6.8 and her Pao2 is 47 mm Hg. She's receiving the maximum dose of four vasopressors, yet at 0600 her BP is only 72/44.
At this point, TL's physicians have to explain to TL's parents that nothing more can be done. With her family at her bedside, life support is withdrawn at 0610 and TL is pronounced dead at 0614 Wednesday morning. She was in the hospital a total of 43 hours. (For a discussion of how current SSC recommendations would have improved TL's diagnosis and treatment, see supplemental content on the Nursing2014 iPad app.)
Sepsis campaign awareness and adherence to the SSC bundles remain a challenge for many healthcare providers causing wide-ranging results, but hospitals are consistently reporting reduced sepsis-related mortality associated with adherence to the SSC guidelines.19,20 This case study is likely very similar to many of the other hundreds of thousands of people who died of sepsis in 2010. Would following the SSC guidelines have made a difference for this patient? It's difficult to know for sure, but this case illustrates the importance of remaining informed about the latest research and guidelines in healthcare. Visit www.survivingsepsis.org to learn more about the guidelines for treating sepsis.
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