A common and devastating condition, sepsis has significant healthcare implications worldwide. An estimated 1 million cases occur in the United States annually, causing more deaths than prostate cancer, breast cancer, and HIV/AIDS combined. The combined economic toll approaches $17 billion.
As a nurse, you’re undoubtedly aware sepsis can be fatal, but you may not be fully prepared to recognize it early and ensure appropriate emergency care. Early assessment and prompt treatment can improve long-term outcomes. To minimize mortality and morbidity, nurses need to understand the causes, clinical manifestations, and risk factors for sepsis.
The various terms used to describe sepsis and related conditions can be somewhat confusing. Some of the terms have specific diagnostic criteria, which were developed in 1991 and revisited in 2001 at the International Sepsis Definitions Conference.
Systemic inflammatory response syndrome
Systemic inflammatory response syndrome (SIRS) is a clinical syndrome that manifests as an acute, nonspecific illness. It’s the first stage in the underlying progression of sepsis, which ultimately can lead to organ failure. SIRS typically results from surgery, trauma, myocardial infarction, pancreatitis, or burn injury. To meet SIRS criteria, patients must have at least two of the following:
- systemic inflammation
- temperature above 100.4° F (38° C) or below 96.8° F (36° C)
- heart rate faster than 90 beats/minute
- respiratory rate faster than 20 breaths/minute
- partial pressure of arterial carbon dioxide (Paco2) below 32 mm Hg
- white blood cell count above 12,000 cells/mm3 or below 4,000 cells/mm3, or greater than 10% immature (band) forms.
Be aware that a patient can have SIRS even in the absence of clinical sepsis.
A patient who meets SIRS criteria in direct response to a known infection source (bacterial, parasitic, viral, or fungal) is diagnosed with sepsis.
Severe sepsis occurs when a patient with documented sepsis goes on to develop acute organ dysfunction with hypoperfusion and tissue hypoxemia. The most commonly affected organs are the kidneys, lungs, heart, and blood vessels. In some cases, neurologic or hepatic dysfunction may be the primary organ dysfunction. (See Differentiating sepsis-related conditions by clicking the PDf icon above.)
Finally, the patient may develop septic shock (also called distributive shock) from volume loss in the core circulation and poor circulatory support. Typically, septic shock causes a life-threatening blood pressure drop, reduced urine output, and body temperature changes—late signs of inadequate tissue oxygenation. Unless detected and treated early, it can spiral quickly into multisystem failure and death. Severe sepsis is the most common cause of death among patients in noncoronary critical care units.
Sepsis reflects a circulatory dysfunction caused by immunologic overactivity. When a localized inflammatory response becomes systemic, capillaries grow more permeable, hypotension sets in, and fluid and immune mediators are released. These events compromise blood flow to organs and tissues. Intravascular volume decreases and abruptly drops too low to maintain tissue perfusion. Adrenaline release occurs in response to marked vascular dilation and inadequate vascular volume, causing tachycardia. Increased capillary permeability and release of proinflammatory mediators trigger clotting and lysis alterations. These changes, in turn, cause microthrombi to form in the capillaries, restricting oxygen availability to tissues. Cells then switch from aerobic to anaerobic metabolism; the resulting lactic acid buildup causes metabolic acidosis. Lack of circulating volume reduces organ perfusion, leading to organ failure and, without proper treatment, death.
If a patient with SIRS progresses to organ failure, severe sepsis occurs. In the final cascade of sepsis, all major organs suffer. GI peristalsis slows from reduced blood flow, disrupting the protective mechanism of the mucosal barrier. The patient becomes more susceptible to GI ulcers, GI bleeding, and bacterial movement into the bloodstream from the GI tract. Without adequate liver perfusion, drugs can’t be metabolized, impeding metabolism of waste products (such as ammonia and lactate); jaundice may arise from bilirubin accumulation. Severe liver infarction may lead to cell death, causing liver enzyme levels to rise. The kidneys become markedly sensitive to hypoperfusion, resulting in acute renal failure (ARF), which manifests as decreased urine output and elevations in blood urea nitrogen and serum creatinine. Metabolic acidosis arises from lactic acid buildup.
In essence, the body’s normal immune response and the localized inflammatory response go haywire. Identifying exactly when the patient crosses from uncomplicated sepsis to severe sepsis and then septic shock can be a subtle and subjective call.
Sepsis is more common in elderly persons and children. Postoperative patients are 10 times more likely to die from sepsis than from myocardial infarction or stroke. Infection also increases the risk of sepsis and sepsis-related death. Other risk factors include:
- chronic illnesses, such as diabetes and cardiovascular disease
- immunosuppressive diseases (such as HIV/AIDS)
- use of long-term immunosuppressive therapy (such as chemotherapy)
- poor nutrition
Although a patient in severe sepsis may be transferred to the intensive care unit (ICU), medical-surgical nurses must be able to recognize early signs and symptoms of sepsis to ensure prompt treatment before the patient requires ICU admission. Subtle changes, such as an increased respiratory rate (which stems from subtle acid-base changes) are red flags that warrant continued monitoring for additional SIRS criteria. Prompt assessment is crucial to recognizing progression of uncomplicated sepsis to severe sepsis and then septic shock. Keep in mind that a patient with severe sepsis may not look markedly ill because of the body’s ability to compensate for systemic failure to some degree.
The Denver Sepsis Protocol identifies three criteria that warrant a sepsis alert—physical signs of SIRS, a patient history consistent with infection, and signs or symptoms of hypotension or hypoperfusion. So be sure to report even the most subtle changes in the patient’s status.
When obtaining the patient’s history, ask about recent or current bacterial, viral, or other infections (for instance, influenza, pneumonia, or dental abscess). Assess all body systems involved in the sepsis cascade so you can detect minor changes. Be sure to document the patient’s neurologic baseline, as mental status changes can arise early in the sepsis cascade from the brain’s extreme sensitivity to changing oxygen levels. A detailed baseline assessment promotes early identification of subtle changes in the patient’s orientation.
Recognizing sepsis progression
Nursing assessment can prove crucial in identifying signs and symptoms of impending sepsis before the point of septic shock. Assess the patient carefully for even slight changes in oxygenation, heart
rate, tissue perfusion, and mental status. Britain’s National Institute for Health and Clinical Excellence recommends nurses in adult inpatient settings use an early warning system to assess patient status. (See Early warning system for sepsis by clicking the PDF icon above.) Know that the screening tool for severe sepsis can result in a false-positive result in patients with ketoacidosis caused by chest infection and in those with infection-related exacerbation of chronic obstructive pulmonary disease who have worsening heart failure.
When assessing a sepsis patient for progression to septic shock, consider such factors as delayed treatment onset, misdiagnosis, and inappropriate antibiotic use. These may have contributed to a condition that could put the patient on the path to shock.
Oxygenation changes are among the earliest signs of deterioration. The respiratory rate rises as the body tries to compensate for decreased tissue oxygenation. Pulse oximetry values decline, and the patient may need higher levels of administered oxygen to maintain adequate oxygen saturation. The heart rate quickens to maintain cardiac output in an attempt to maintain tissue oxygenation. Prolonged lack of perfusion to vital organs results in organ failure. The heart rate starts to decline when the body can no longer compensate—another sign that the patient’s condition is growing more critical. (See Detecting organ failure by clicking the PDF icon above.)
Be aware that although blood pressure readings are crucial in assessing and planning care for the septic patient, mean arterial pressure more accurately reflects tissue perfusion than does blood pressure. Blood pressure readings can be somewhat deceiving as the body goes through the compensatory process.
Carefully measure the patient’s urine output. Stay alert for low output, which may reflect renal hypo-perfusion. For precise output measurement, an indwelling urinary catheter should be placed.
Hypothermia, another sepsis sign, may not occur because infection sometimes leads to hyperthermia. But with progression to severe sepsis, dehydration may arise, causing poor skin turgor, dry mucus membranes, and decreased urine output. Monitor serum lactate levels, which reflect the body’s metabolic state. Suspect hypoperfusion if the lactate level exceeds 4 mmol/L.
In early stages, most sepsis patients recover with rest, antibiotics, and hydration. But some progress to severe sepsis, with failure of at least one major organ. So stay alert for circulatory problems caused by sepsis, as the major organs become oxygen deprived and begin to fail. At this point, expect the patient to have an increased respiratory rate, a core temperature rise followed by a drop, a faster heart rate, and hypotension.
Fluid resuscitation is crucial in treating severe sepsis. Patients may need 6 to 10 L of fluid during the first 24 hours. Be sure to distinguish fluid given in a fluid challenge from maintenance fluid used for resuscitation. A typical fluid challenge may be given over a brief period, such as 10 minutes, to expand intravascular volume rapidly. Administering maintenance fluid, on the other hand, may take many hours.
As ordered, restore intravascular volume as quickly as possible. Place an indwelling urinary catheter as ordered to help guide volume resuscitation. Strict fluid intake and output measurement guides fluid-replacement therapy in hypovolemic patients receiving vast fluid amounts. Central venous pressure monitoring (with a goal of 8 to 12 cm H2O) provides additional information to guide fluid resuscitation in patients with suspected hypoperfusion. Monitor hemoglobin and hematocrit; as ordered, give transfusions to patients with hemoglobin values below 7 g/dL.
Important: Know that patients who progress to septic shock and receive aggressive fluid resuscitation are still in a state of sustained hypotension. Be sure to monitor hypotensive status, staying alert for lack of blood-pressure response to fluid administration.
Early SIRS detection followed by prompt treatment can reduce sepsis deaths. The Surviving Sepsis Campaign®, created in 2009 by the European Society of Intensive Care Medicine, Society of Critical Care Medicine, and International Sepsis Forum, aims to reduce deaths from severe sepsis. This campaign advocates using the 6-hour resuscitation bundle—a group of evidence-based interventions that are most effective when delivered collectively. To maximize the patient’s outcome, all parts of the bundle must be completed within 6 hours after the patient starts to show sepsis signs and symptoms. (See Using the 6-hour resuscitation care bundle by clicking the PDF icon above.)
Simple prevention strategies
Without proper assessment and early identification, patients with sepsis can deteriorate quickly, suffering compromised tissue oxygenation and organ dysfunction for many hours. Overlooking early signs and symptoms of sepsis and starting treatment late can have catastrophic consequences.
Fortunately, simple strategies can help reduce sepsis and its effects if implemented promptly and appropriately. As a nurse, you can play a crucial role in preventing patients from becoming acutely ill from sepsis. Along with other healthcare team members, take a proactive role in prevention. (See Preventing sepsis by clicking the PDf icon above.) Make sure you’re familiar with early signs and symptoms. Finally, keep in mind the importance of starting aggressive interventions for known infections. Assess the effectiveness of these interventions and adjust accordingly.
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Visit www.AmericanNurseToday.com for a complete list of references.
Meg Bernstein is lead nurse in the division of plastic and reconstructive surgery at the Johns Hopkins Hospital in Baltimore. Shari J. Lynn is a faculty member at the Johns Hopkins University School of Nursing in Baltimore, Maryland.