Skin

The major mechanical barrier to invading pathogens is the skin. The skin’s protective ability is enhanced by its natural acidic pH, which inhibits growth of some organisms. Also, sebum, the oily secretion of the sebaceous glands, contains long-chain fatty acids that act as a germicide. Antimicrobial peptides, which are small-molecular-weight proteins secreted by epithelial cells, are toxic to some bacteria, fungi, and viruses.⁷ Normal skin flora include coagulase-positive and coagulase-negative staphylococci, streptococci, and diptheroids, which act as a potential reservoir of invading organisms.

In addition to interruption of the skin from injury or surgery, this protective barrier may be disrupted by pressure, shearing, moisture, or friction after patient admission. Pressure from maintaining a body position for a prolonged period, especially when on an unpadded surface (e.g., backboard), retraction by surgical instruments, or therapeutic devices applied to the patient (e.g., traction, braces, splint) can cause tissue ischemia. Any ischemia and subsequent necrosis of the skin provides a rich environment for bacterial growth. Excessive exposure to moisture from secretions, drainage, and incontinence can macerate skin. Friction and shearing created by movement on sheets or against restraints cause mechanical irritation that can abrade skin. Chemical irritation from degerming and defatting agents, adhesive tapes, incontinence, and excoriating exudates can also inhibit innate skin defenses.

Elderly patients have the added burden of the age-related changes that affect the skin’s normal function.⁸ Their skin has less oil secretion, blood flow, innervation, and subcutaneous fat,⁹ which increases the incidence of skin breakdown and wound infection.¹⁰ Similarly, obese patients are also at higher risk for skin breakdown because of impaired mobility and decreased tissue perfusion.

Nursing interventions to enhance the skin’s defense mechanisms include using meticulous aseptic technique, handwashing, handling tissue gently, minimizing the use of adhesive tape, optimizing control of wound drainage with appropriate dressings, alleviating pressure areas, and using the most effective yet least irritating antiseptic solutions. The patient’s risk for skin breakdown should be assessed on admission and regularly during hospitalization. Skin integrity should be evaluated each shift to detect areas with actual or potential breakdown.

Respiratory Tract

The respiratory tract has a complex system of host defense mechanisms. Mucociliated epithelium cleans and protects airway passages to prevent microbial overgrowth. Coughing, sneezing, and deep breathing provide mechanical clearing of the airways. Lung surfactant proteins appear to promote phagocytosis.¹¹

Pathogens can gain access to lower airways during intubation, by inhalation, or from bloodstream infections, aspiration of gastric contents, or spread from nearby areas.¹² The major loss of defenses in trauma patients occurs with placement of an artificial airway. With this intevention, all natural defense mechanisms are circumvented, and microorganisms from the environment can be afforded unobstructed entry into the lungs. Contamination of airway circuits can allow rapid replication of pathogens that are aerosolized into the lungs. Endotracheal tubes allow pooling of oropharyngeal secretions, which contain a variety of pathogens that can pass the inflated cuff and move into distal airways.¹²

Respiratory tract defense mechanisms can be compromised with thoracic or abdominal injury or surgery, after chest tube placement, and when central nervous system (CNS) dysfunction, paralytics, sedatives, or analgesics impair ventilation and effective secretion clearance. Immobility as a result of decreased level of consciousness, neuromuscular blockade, traction and fixation devices, or spinal injury can also contribute to alveolar collapse and secretion retention. Suppression of protective cough and gag reflexes and impaired swallowing associated with traumatic brain injury increase the risk of aspiration and ineffective secretion clearance. Damage from inhalation injuries caused by heat, vaporization of toxic chemicals, and smoke can produce both temporary and permanent destruction of lung defense mechanisms.

Placement of nasal tubes can increase the risk of upper respiratory tract infections. Indwelling nasogastric and nasoendotrachael tubes can obstruct airflow to and drainage from sinuses, resulting in nosocomial sinusitis, or impede flow through the eustachian tubes, resulting in otitis media. The presence of chest tubes and retained hemothoraces are significant factors in the development of nosocomial empyema.

Elderly patients are further compromised by age-related physiologic changes. A gradual decline in many immune functions, including cell-mediated and humoral aspects of acquired immunity, contributes to an increased risk of pneumonia.¹³ Decreased alveolar elasticity, reduced intercostal muscle and diaphragm tone, and diminished vital capacity hinder the elderly patient’s ability to cough and expectorate sputum, increasing the risk of respiratory tract infection.¹⁴

Nurses can promote respiratory tract defense mechanisms by frequently repositioning unconscious and immobile patients and, in awake patients, encouraging the use of incentive spirometry, coughing, and deep breathing to facilitate removal of pulmonary secretions. Chest physiotherapy is vital to critically ill patients, especially those with new pulmonary infiltrates, fever, leukocytosis, or purulent sputum. In a study of critically ill ventilated patients, Joshi et al¹⁵ demonstrated the benefits of vigorous chest percussion. Within 8 hours after chest physical therapy, 80% of patients had partial or complete resolution of pulmonary infiltrates. Another important maneuver that increases coughing and deep breathing to promote aveoli opening and secretion removal is getting patients moved out of bed to a chair and assisting with ambulation as soon as their condition permits. Specific interventions to prevent pneumonia are described later in the chapter.

Gastrointestinal Tract

Heavily colonized by a variety of bacteria, the gastrointestinal tract is a major reservoir of microorganisms that can cause nosocomial infection. An intact mucosal epithelium, the acidic gastric barrier, and continuous peristaltic evacuation throughout the tract constitute the external defenses in the gastrointestinal tract. Lytic enzymes in saliva, secretory antibody immunoglobulin A (IgA), lysozyme, and phagocytic cells work to destroy ingested bacteria. Normally the stomach, duodenum, and jejunum are colonized with low concentrations of mouth flora. However, the trauma patient soon loses this protection because normal gut flora is disrupted by injury, ischemia, decreased gut motility, pH changes, and fasting. Decreased visceral perfusion, seen for example in patients in shock, decreases gut barrier function and raises the potential for “translocation” of bacteria out of the gastrointestinal tract.¹⁶

Drug therapy may have a negative impact on gastrointestinal tract defense mechanisms. Antacids and H₂-blocking agents used to prevent or treat mucosal bleeding elevate the normal gastric pH, eliminating the acidic barrier. Gastric pH greater than 4 facilitates bacterial overgrowth.¹⁷ Muscle relaxants, sedatives, and analgesic agents reduce gastric motility. Last, antibiotics change the composition of the normal gut flora.¹⁸

Genitourinary Tract

Ciliated mucosa lines the normal genitourinary tract, blocking bacterial adherence. The flushing action of the bladder evacuates microorganisms. The acidic pH and hyperosmolar composition of normal urine is bacteriostatic. Therefore, urine is normally sterile because the bladder environment is not conducive to bacterial growth.

Use of an indwelling urinary catheter in any patient breaches normal external defenses, heightening the risk of infection by creating an easy portal of entry for microorganisms. Susceptibility to infection also increases with urinary tract obstruction, renal failure, changes in the chemical composition of urine, and manipulations of the indwelling drainage system. Other factors known to increase the risk of urinary tract infections (UTIs) include increased age, obesity, and length of time an indwelling catheter has been used. Interventions to prevent UTI are addressed later in the chapter.

Fever/Thermoregulation as Part of the Immune Sytem

Under normal conditions, body temperature is determined by the “set point” of the hypothalamic thermoregulatory system and a delicate balance between production and loss of body heat. Heat is produced from food metabolism and body activity. Heat loss occurs by radiation, convection, and vaporization, which are regulated by peripheral blood flow to the skin, sweating, and vaporized loss from the lungs.

Fever (defined as core temperature >100.4° F [38° C])²¹ results from any disturbance in the hypothalamic thermoregulatory activity that leads to an increase of the thermal set point. Fever can be an infectious or a noninfectious inflammatory response. The infectious fever response is initiated when exogenous pyrogens, such as lipopolysaccharide complexes in the cell wall of gram-negative bacteria, invade the body. Endogenous pyrogens, fever-causing cytokines, are released by neutrophils and macrophages in response to exposure to bacterial endotoxins or to antigen-antibody complexes. Endogenous pyrogens include interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF), and interferon. These pyrogens act on the preoptic nucleus of the hypothalamus to change the body’s thermostat.²² The hypothalamus and the brainstem signal increased heat production and conservation to raise the body temperature. Peripheral vascular vasoconstriction causes blood to shunt to the body’s core, thereby creating a new temperature level.²²

A febrile response may have beneficial effects by killing temperature-sensitive microbes. Fever also causes decreased levels of iron, zinc, and copper, which are needed for bacterial replication. In addition, elevated body temperature changes metabolism to lipolysis and proteolysis, thereby depriving bacteria of glucose sources. Fever can also increase neutrophil mobility, which increases their killing capability by enhancing their phagocytic capability.²² Because of the beneficial effects of fever, antipyrogenic medications should be used judiciously. Antipyretics can negate the protective fever response and may increase the mortality rate.²¹

Fever may also be harmful by increasing the effects of endotoxins from gram-negative bacteria.¹¹ Also, pyrexia exacerbates ischemic neuronal damage and physiologic dysfunction after acute brain injury.²³ To avoid increasing the cerebral metabolic rate, which can increase the risk for intracranial hypertension and brain ischemia, hyperthermia is typically aggressively treated in patients with acute severe brain injury. Hypermetabolism caused by fever may not be well tolerated by trauma patients in need of nutrients for healing.

In trauma patients, many of the thermoregulatory mechanisms can be compromised by the nature of the injury. Patients sustaining massive burns or extensive soft tissue injury lose the skin’s thermoregulatory functions. Spinal cord injury at the T6 level or above cuts the sympathetic nervous system off from the hypothalmic control center, causing loss of thermoregulatory capability. Patients with these injuries may have a hypothermic set point—that is, a set point below 96° F (35.5° C). Therefore, a sudden increase of temperature to 99° F (37.2° C) may be indicative of fever in these patients. Elderly patients also can have a lower thermal set point, which is attributed to the deterioration of the skin’s normal function. On the other hand, activation and chronic stimulation of the inflammatory response (e.g., rheumatoid arthritis, lupus erythematosus, sarcoidosis) may cause some patients to establish a higher than normal set point. These patients appear to have a persistent fever. Patients sustaining severe brain injury resulting in compromise or injury of the hypothalamus may have irregular, widely variant temperature patterns. Fever resulting from this condition is known as central fever, which is often resistant to antipyretics.

Because fever is a manifestation of both infectious and noninfectious inflammatory responses and its presentation can be modified by many concurrent injuries, its utility for the diagnosis of infection is limited. Therefore, continuous evaluation of the patient’s overall clinical condition compared with the temperature pattern trend is essential.

Acquired Immunity

When a microbe bypasses external defenses and the initial inflammatory cascade system is primed, additional mechanisms are triggered. By this adaptive or acquired immunity, the human body is able to develop powerful specific immunity against invading bacteria, viruses, and toxins. This is often thought of as the humoral or antibody response. The innate and adaptive immune systems are linked. Stimulation of the innate immune system, as described previously, initiates the adaptive immune response, which is slower acting, specific, and very long lived.²⁴ When challenged by substances identified by the body as “foreign,” the adaptive immune system responds with lymphocytes, the WBCs that make antibodies. Foreign antigens include microbial pathogens (bacteria, fungus, virus, or parasites), noninfectious environmental agents (pollen, food, venom), and clinical mediators (drugs, vaccines, transfusions, transplants). Repeated exposure causes the adaptive immunity to “remember” the invader and increase the number of lymphocyte-produced specific antibodies.²⁴ When activated, lymphocytes migrate through lymphoid tissues and become either B lymphocytes, responsible for humoral immunity, or T lymphocytes, responsible for cell-mediated immunity. Although B lymphocytes make antibodies, T lymphocytes are involved in complex cell-mediated responses that provide resistance to infection.²⁵ The human body produces millions of T and B lymphocytes, each capable of recognizing one specific foreign antigen. B cells secrete specialized antibodies that attack antigens. For example, antibodies bind to extracellular microbes and toxins, facilitating elimination of bacteria and viruses. T cells undergo differentiation with maturation and develop into subgroups. Some stimulate leukocytes, whereas others become cytotoxic cells that directly attack and kill antigens. This immunity provides defense against intracellular viruses and bacteria that can live within phagocytes inaccessible to circulating antibodies, thereby eliminating reservoirs of infection.

The body’s response to the threat of injury or infection, though usually protective, can be inadequate or excessive and uncontrolled. Understanding how tissue damage can be contained, how infection can be prevented and detected, and how best to treat injuries and promote healing enables nurses to provide optimal patient care.¹¹

Systemic Inflammatory Response Syndrome

SIRS is a complex overall inflammatory response affecting multiple organs with or without infection. It can be precipitated by insults such as trauma, infection, pancreatitis, or surgery. It is seen in almost 70% of patients in critical care and is also common to trauma patients.² SIRS is a massive response of intrinsic mediators and proinflammatory cytokines indicated by the presence of at least two of the following clinical criteria: fever (temperature ≥38° C) or hypothermia (temperature ≤36° C), tachycardia (≥90 beats/min), tachypnea (≥20 breaths/min) or partial pressure of carbon dioxide in arterial blood (PaCO₂) <32 mm Hg, leukocytosis (≥12,000 cells/μL) or leukopenia (≤4000 cells/μL), or a left shift in the immaturation of granulocytes (bands) >10%.²⁹

A SIRS diagnosis does not confirm presence of infection or sepsis but is associated with adverse outcomes.² In trauma patients, the SIRS score on admission is an independent predictor of nosocomial infection and mortality. A SIRS score >2 continues to be predictive of nosocomial infection through 21 days after injury.² SIRS scores have poor specificity, and studies are being done to explore a combination of other biomarkers (e.g., CRP, procalcitonin [PCT]) that can provide a reliable early indicator of infection.

Sepsis

In the United States, sepsis accounts for more than 210,000 deaths each year. It is the leading cause of death among critically ill patients.³⁰ Sepsis has been denoted as a malignant intravascular inflammation because it is uncontrolled, unregulated, and self-sustaining. Extension of the normal local inflammatory response to infection into normal tissue is termed sepsis, an autodestructive process.³¹ Sepsis is a complex, systemic inflammatory response to infection, with or without positive blood cultures. In addition to infection, at least two of the SIRS criteria must be present to meet the definition of sepsis.²⁶ Sepsis is a proinflammatory response and, because it activates the coagulation system, thus altering the procoagulation-anticoagulation balance, it is also a procoagulant response. The activated coagulation system depletes plasmin and antithrombin III and activates protein C, leading to hemorrhage when anticoagulation factors are depleted. Activation of the coagulation cascade and the resultant coagulopathy produce diffuse microthrombi. As microthrombi obstruct flow through capillaries, the tissues become unable to to receive and extract oxygen. Arterial vascular tone decreases and endothelial permeability increases, causing a redistribution of intravascular fluid volume, which fosters progression to severe sepsis. Acute respiratory alkalosis, resulting from stimulation of ventilation, may be seen in early sepsis; however, as deterioration progresses to septic shock, lactic acidosis develops.³²

Severe sepsis is defined as sepsis with organ dysfunction, hypotension, or hypoperfusion.^26,33 It is a leading cause of death in noncoronary intensive care units (ICUs).³⁴ In the United States, patients with severe sepsis have a mortality rate of 28% to 50%.³⁵ Annually, 200,000 patients in the United States die of severe sepsis.³⁶ With an average individual cost of care of $22,000, health care for sepsis accounted for expeditures of $16.7 billion in the United States in 2000.³⁴ It is anticipated that these figures will rise as the population ages, the number of immunocompromised patients increases, more antibiotic-resistant organisms emerge, the use of invasive procedures and monitoring devices expands, and the awareness of severe sepsis criteria increases.²¹

Organ dysfunction in severe sepsis results from hypotension and tissue hypoperfusion. Hypotension is defined as mean arterial blood pressure (MABP) <60 mm Hg, systolic blood pressure (SBP) <90 mm Hg, or a decrease in SBP of >40 mm Hg from baseline without other causes.²⁶ Hypoperfusion leads to tissue hypoxia and ischemia. Clinical signs of tissue hypoperfusion may include oliguria, lactic acidosis, or acute alterations in mental status.²⁶

Septic Shock.

Septic shock is sepsis accompanied by hypotension and tissue hypoperfusion, despite adequate fluid resuscitation, with other systemic abnormalities, which may include lactic acidosis, oliguria, and acute mental status changes.^26,29 Infection from a variety of bacteria, fungi, and, rarely, viruses can cause septic shock. These pathogens or exotoxins produced by bacteria interact with the host immune cells to incite a massive inflammatory response. Noncytokine and cytokine mediators (e.g., IL-1, TNF-α, IL-6) are released, activating systemic inflammation and release of mediators (e.g., thromboxane A₂, prostaglandins, and nitric oxide), which causes vasodilation and endothelial damage. Cytokines also activate the coagulation pathway, creating capillary microthrombi.³⁷ The inflammatory and procoagulant responses initiated by bacterial toxins result in capillary leakage, inadequate circulatory volume, circulatory collapse, and potentially profound hypotension despite adequate fluid resuscitation. This leads to impaired tissue perfusion and ischemia. As perfusion of nonvital tissues, and eventually vital organs, decreases and the body shifts to anaerobic cellular metabolism, lactate production increases, leading to metabolic acidosis. To compensate for hypoxia and acidosis, respirations become rapid and shallow. Uncorrected, this respiratory insufficiency can lead to acute respiratory failure. If the shock state is not corrected quickly, the patient’s survival is jeopardized. The mortality rate from septic shock is 50% to 60%.³⁴

As sepsis progresses, organ system function becomes compromised. MODS occurs when organ function is altered and homeostasis cannot be maintained without intervention. The first systems affected are usually the cardiovascular and pulmonary systems, followed by hepatic, gastrointestinal, and renal systems, and, finally, the brain.²¹ As one or more organ systems fail, the mortality rate increases; with failure of three or more systems, the mortality rate reaches 70%.³⁸ Organ system failure is closely linked to a hypercoagulable state.

It is a paradox that progress in the management of severe medical and surgical diseases has increased the patient population now at risk for sepsis. As the population continues to age and more pathogens develop resistance to antibiotic therapy, the number of patients at risk will continue to increase. Therefore, it is extremely important that nurses be able to recognize the early, subtle signs of SIRS and sepsis and re-establish perfusion by instituting optimal supportive care and therapy.

Assessment for Sepsis/Septic Shock.

Critical nursing management includes regular screening of patients for evidence of infection, SIRS critieria, and acute organ dysfunction. Nurses have a crucial role in monitioring for subtle clinical changes to recognize sepsis promptly. Signs and symptoms of specific acute infections affecting various body systems are described later in this chapter.

Vital signs, particulary changing trends in these measures, should be noted.³² Increasing heart and respiratory rates and elevated or reduced body temperature could meet the criteria for SIRS. In early septic shock, the increase in cardiac output offsets low systemic vascular resistance; therefore, systolic blood pressure is maintained. Over time, as circulating blood volume is further depleted and compensatory mechanisms are exhausted, blood pressure will decline. Assessment of WBC count (either leukocytosis or leukopenia) and differential is also important, although leukocytosis is neither sensitive nor specific for infection. As a result of inadequate tissue perfusion, organ dysfunction affecting one or more organs can become apparent. It is important to monitor for signs of altered tissue perfusion, including altered mentation, systemic hypotension, decreased urinary output, prolonged capillary refill time, hypoxemia, respiratory compromise requiring ventilation, and respiratory alkalosis progressing to metabolic acidosis.²⁶ Earliest signs can include increased apprehension, confusion, and decreased sensorium (in a sedated or brain-injured patient, these findings may not be evident).^26,39 Signs of coagulation imbalance, such as decreased platelet count, abnormal coagulation studies, increased bleeding at venipuncture sites, and petechiae, may also indicate sepsis.^26,39 If two or more of the SIRS criteria are met, infection is deemed present or suspected, the patient is hypotensive or has evidence of tissue hypoperfusion, and one or more organs is dysfunctional, severe sepsis is suggested.³⁴

Investigations continue in attempting to identify a biologic marker that would provide early, accurate detection of sepsis with good specificity and sensitivity. As mentioned earlier, the host response in sepsis is modulated by a cascade of proinflammatory cytokines or mediators (e.g., TNF, IL-1, IL-6, and interleukin-8 [IL-8]) followed by immunomodulators that down-regulate the response (e.g., anti-inflammatory mediators include interleukin-4 and interleukin-10). Markers of interest include IL-6 and IL-8, which may correlate with patient outcome. High IL-6 levels are associated with death in septic patients. However, the cytokines are not specific and are also induced by various noninfective stimuli, including surgery, viral infections, and autoimmune disorders.⁴⁰ There is great clinical interest in using these markers for predicting patients most at risk for sepsis.

Currently available markers include PCT, CRP, and the erythrocyte sedimentation rate (ESR). PCT is a propeptide produced in the thyroid gland. Usually at low systemic levels (<0.1 ng/ml), the PCT concentration rises dramatically in sepsis to more than several hundred nanograms per milliliter. PCT levels seem to reflect increasing severity of the systemic inflammatory response.² Another early marker is CRP, a liver-produced protein released after inflammation or tissue damage. It has both proinflammatory and anti-inflammatory actions and is frequently used to detect the presence and severity of infection or sepsis. However, multiple-trauma patients and elective surgery patients may show an increase of PCT, CRP, and other biomolecules, indicating inflammation during the early postoperative or posttraumatic period independent of the diagnosis of sepsis or infection.^41–43

The ESR is a nonspecific blood test used to detect inflammation. Normal erythrocytes are negatively charged and repel each other. In the presence of positively charged plasma proteins, the surface charge of the erythrocytes is neutralized and they are able to aggregate. Sedimentation rate testing demonstrates the ability of the red blood cells (RBCs) to settle to the bottom of a glass tube. This rate is increased in the presence of infection, rheumatoid arthritis, lupus erythematosus, leukemia, and cancers.

Recent investigations have identified a new potential sepsis biomarker, sTREM-1. This soluble triggering receptor expressed on myeloid cells has a sensitivity of 96% and a specificity of 89% in determining the presence of infection.⁴⁴ Other biomarkers being studied for their potential prognostic ability include endotoxin (a component of gram-negative cell walls), brain natriuretic peptide (a myocardial dysfunction indicator), and endogenous protein C.⁴⁵ Much research is under way to determine the accuracy of these biomarkers in identifying and guiding the treatment of sepsis.

Management of Sepsis and Septic Shock.

In 2003, critical care and infectious disease experts convened at an international conference to develop evidenced-based guidelines for the management of sepsis and to launch an initiative to encourage use of these interventions to improve patient outcomes from sepsis—the Surviving Sepsis Campaign. Key recommendations focus on the need for early syndrome recognition. New monitoring and therapy developments place great importance on the early identification and aggressive management of the septic patient. Meta-analysis of sepsis resuscitation trials showed that early interventions before organ dysfunction provide better outcomes.⁴⁵ Rivers et al⁴⁶ showed that the timeliness of treatment significantly improves the mortality rate when hemodynamic optimization is achieved within the first few hours after disease presentation. Patients with septic shock have a significantly greater risk of death when antibiotics are started more than 1 hour after initial presentation or diagnosis of septic shock.⁴⁷ These and other recommendations for managing sepsis are included in the established guidelines. The guidelines continue to evolve, and the reader is referred to the latest published recommendations for up-to-date suggestions for the management of sepsis.

The key recommendations of the evidence-based guidelines for management of sepsis and septic shock are highlighted in Box 15-1. Many instituations have developed treatment algorithms on the basis of these evidence-based recommendations. An example of an algorithm is found in Figure 15-1.

BOX 15-1 Guideline Recommendations for Management of Sepsis and Septic Shock

• Initial resuscitation

• Resuscitation should begin immediately upon recognition of sepsis-induced tissue hypoperfusion

• During the first 6 hours, the desired therapeutic end points for initial resuscitation of hypoperfusion caused by sepsis include:

– Central venous pressure (CVP) 8 to 12 mm Hg

– Mean arterial pressure ≥65 mm Hg

– Urine output ≥0.5 mL/kg¹/hr¹

– Central venous (superior vena cava) (ScvO₂) or mixed venous oxygen saturation (SvO₂) ≥70% or ≥65% respectively

• During the first 6 hours of severe sepsis or septic shock resuscitation, if the ScvO₂ or SvO₂ does not reach 70% or 65%, respectively, once fluid administration achieves a CVP of 8 to 12 mm Hg, transfuse red blood cells to obtain a hematocrit of ≥30% and/or administer dobutamine to reach SvO₂ goal

• Diagnosis

• Obtain appropriate cultures (e.g., urine, cerebrospinal fluid, wound, respiratory secretions, body fluids, at least 2 blood cultures [one percutaneously and one from each vascular access in place over 48 hours]) before antimicrobial therapy is begun if not associated with a significant delay in starting antibiotics

• When possible, promptly perform diagnostic/imaging/ultrasound studies to identify infection source and causative organism

• Antibiotic therapy

• Initiate intravenous antibiotics within 1 hour of severe sepsis or septic shock recognition

• Consider combination antibiotic therapy with Pseudomonas infections

• Consider empiric combination antibiotic therapy for neutropenic patients

• Do not continue combination antibiotic therapy given empirically >3 to 5 days

• Initial empiric intravenous antibiotics should have activity against likely pathogens and should penetrate in sufficient concentrations to the probable septic source

• Duration of antibiotic therapy is typically 7 to 10 days, although longer courses may be necessary in certain patients

• Reassess antimicrobial selection daily; optimize to narrowest effective spectrum

• Discontinue antibiotics if noninfectious source is discovered

• Source control

• Identify a specific site of infection as soon as possible

• Remove potentially infected devices, drain abscess or local infection, debride necrotic tissue. If a suspected source of infection, promptly remove vascular access after new site is established

• Choose the source control intervention least likely to cause physiologic upset

• Once identified, perform the intervention to control the source as soon as possible (except delay surgical intervention for infected pancreatic necrosis)

• Fluid therapy

• Resuscitate with colloids (300 to 500 mL) or crystalloids (≥1,000 mL) over 30 min. Provide additional fluid at perhaps a faster rate based on patient’s condition and response (e.g., blood pressure, urine output, heart rate, CVP)

• Reduce fluid administration when cardiac filling pressures increase without improving hemodynamics

• Vasopressors

• Maintain mean arterial blood pressure ≥65 mm Hg

• Norepinephrine or dopamine are first-choice vasopressor agents; vasopressin (0.03 units/min) may subsequently be administered with norepinephrine

• Epinephrine is the first alternative in treating hypotension from septic shock that is refractory to norepinephrine or dopamine

• Low-dose dopamine should not be used for renal protection

• If vasoactives are needed, an arterial line should be placed as soon as possible

< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

EVOLUTION OF THE TRAUMA CYCLE TRAUMA IN THE ELDERLY MASS CASUALTY INCIDENTS THE ORGAN AND TISSUE DONOR WOUND HEALING AND SOFT TISSUE INJURIES SPINAL CORD INJURIES

Stay updated, free articles. Join our Telegram channel

Join