Sepsis Overview

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Sepsis Overview

Sepsis

By Shabana Lalji &  Khairunnissa Hooda

Sepsis is a complex syndrome that occurs as a result of the systemic manifestation of infection. Severe sepsis is common; an estimated 750,000 cases occur annually in the United States. The mortality rate for severe sepsis is 30 to 50% and septic shock with multiple organ dysfunctions is as high as 80% to 90%. The Institute for Healthcare Improvement (IHI) has identified sepsis as an area of focus and identified several deficiencies that lead to suboptimal care of patients with severe sepsis. To address these deficiencies, the Surviving Sepsis Campaign and IHI have built upon the Surviving Sepsis Guidelines and created two sepsis treatment bundles to guide therapy for the patient suffering from severe sepsis.

The definition of SIRS, a Systemic Inflammatory Response Syndrome to a variety of severe clinical insults, is characterized by 2 or more of the following conditions:

1. Temperature higher than 38°C or lower than 36°C,

2. Heart rate greater than 90 beats per minute,

3. Respiratory rates greater than 20 breaths per minute or PaCO2 lower than 32 Torr, and

4. White blood cell count higher than 12,000 cells per microliter or lower than 4,000 cells per microliter or the presence of more than 10% immature neutrophils or band cells.

Pathophysiology

The pathophysiology of sepsis begins with the entry of organisms into the bloodstream through the skin or the respiratory, genitourinary, or gastrointestinal tract. The entry organism may include bacteria, yeast, viruses, and/or parasites. This complex syndrome is characterized by simultaneous activation of inflammation and coagulation in response to microbial insult. Cytokines are also released, which play a key role during the inflammatory and immune response. Also, cytokines further the cascade of immune response. As the organisms circulate in the bloodstream, more phagocytes, leukocytes, and cytokines are released or activated. The cytokines and white blood cells trigger vasodilation to increase capillary permeability, neutrophil activation, and adhesion of platelets to the endothelium.

Baroreceptors in the carotid arteries and aorta respond to a drop in the patient’s blood pressure and activate the sympathetic nervous system. This activation stimulates release of potent vasoconstrictors, epinephrine, and norepinephrine to maintain blood flow to the vital organs: the heart and brain. Simultaneously, blood is shunted from the nonvital organs such as lungs, kidneys, gastrointestinal tract, and skin. For example, decreased blood flow to the kidneys activates the renin-angiotensin-aldosterone system. This process eventually affects cardiac output, circulating volume, and blood pressure. This leads to multiple organ dysfunction syndrome (MODS) and, ultimately, death.

Procoagulation induced by sepsis. Sepsis increases expression of tissue factor by the endothelium, activating the coagulation cascade through factors Va and VIIIa. Protein C, protein S, antithrombin III, and tissue factor pathway inhibitor (TFPI) normally maintain hemostasis by downregulating this coagulation process; however, patients with sepsis have a deficiency in these substances. The consequence of these alterations is a procoagulant response leading to microthrombus formation, tissue ischemia, and organ dysfunction

Severe Sepsis

Severe sepsis is defined as sepsis complicated by organ dysfunction. Sepsis may develop into severe sepsis and is associated with organ dysfunction, sepsis-induced hypotension, and hypoperfusion abnormalities such as lactic acidosis, oliguria, and acute alteration of mental status. The hypoperfusion of the circulatory system at this stage may lead to organ dysfunction. For example, dysfunction of the pulmonary system may manifest as acute respiratory distress syndrome. Other organ systems may follow, leading to MODS.

Septic Shock

Septic shock is the presence of sepsis and a state of acute circulatory failure characterized by refractory arterial hypotension unexplained by other causes. Hypotension is defined as a systolic arterial pressure of less than 90 mm Hg or a reduction of more than 40 mm Hg from baseline despite fluid resuscitation, in the absence of another cause of hypotension. The patient is dependent on vasopressors at this point. The transition from sepsis to septic shock occurs most often during the first 24 hours of hospitalization. Septic shock carries with it an increase not only in morbidity but also in mortality.

Sepsis Diagnosis and Diagnostic Testing

The diagnosis of sepsis is difficult, especially in the critical care setting, wherein early signs and symptoms are often superimposed by the patient’s underlying illness. Early organ dysfunction may be the first symptom noted by clinicians. Other diagnostic criteria may include

(1) Hemodynamic instability,                   (2) arterial hypoxemia,

(3) Oliguria (less than 0.5 mL/kg/h),       (4) coagulopathy, and

(5) Altered liver function tests.               (6) Serum lactate level is a diagnostic marker in septic patients.

Lactate is generated by anaerobic cellular metabolism and may reflect the degree of cellular derangements in sepsis. Arterial lactate levels are commonly used as a global indicator of oxygen deficits. Serial lactate levels can reflect adequacy of hemodynamic resuscitation efforts. (PCT), which is a propeptide of calcitonin. In patients with sepsis, PCT levels may increase up to 5,000 to 10,000 times the normal range. Elevated PCT levels in patients with severe sepsis and septic shock have been noted.

Treatment of Sepsis

 Early goal-directed therapy includes (first 6 hours)

(1) Initial Resuscitation: Intravenous fluids, crystalloid-fluid challenge of 20ml per kilogram of body weight over 30-minute period (if lactate 4 mmol/L (36 mg/dL) central venous pressure levels of 8 to 12 mm Hg should be targeted

(2) Vasopressors, (Potential agents include dopamine, norepinephrine, phenylephrine, epinephrine, and vasopressin)

 (3) Packed red blood cells,

(4) Timely administration of antibiotics, (both Gram-positive and Gram-negative bacteria and should be administered intravenously)

(6) Glucose control maintained at or above the lower limit of normal, but 150 mg/dL (8.3 mmol/L).

(5) low-dose steroids for adrenal insufficiency,

(6) Activated protein C, and

(7) Prophylaxis against deep venous thrombosis and stress ulcers.

Examples of Quality Indicators in a Sepsis Protocol

Research suggests initiation of the protocol in 2 steps. First, initiation of treatment measures should begin in the emergency department and second, maintenance therapy. Initial measures include the following:

1. Obtain blood cultures before antibiotic administration,

2. Have an early initiation of antibiotics,

3. Measure serum lactate level,

4. Maintain adequate central venous pressure (greater than 8 mm Hg),

5. If the mean arterial pressure is less than 65 mm Hg, vasopressors were given to maintain a mean arterial pressure of at least 65 mm Hg.

5. Maintain adequate central venous oxygen saturation (greater than 70%),

6. Treat hypotension and/or elevated lactate (greater than 1.5 times the upper limit of normal) with fluids, and

7. Use of vasopressors for ongoing hypotension.

Severe sepsis and septic shock are life-threatening conditions that pose high morbidity and mortality rates for critically ill patients. The critical care nurse plays a leading role in early detection, monitoring, and treatment of patients with these conditions. Thus, with education, use of protocols and healthcare professionals working together should positively impact critically ill septic patients.

References:

1. Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858–873

2. Schlichting D, & McCollam JS., Recognizing and Managing Severe Sepsis: A Common and Deadly Threat Southern Medical Journal June 2007; 100(6).

3. Kleinpell R, Graves B, Ackerman M. Incidence, pathogenesis and management of sepsis: an overview. AACN Adv Crit Care. 2006; 17(4):385-393

4. IHI: Severe Sepsis Bundles. Institute for Healthcare Improvement 2005.

2017-04-26T12:35:51+00:00