10. Infectious Disease

  According to the American College of Critical Care and the Infectious Diseases Society of America (IDSA), fever in the ICU can be defined as a temperature >38.3°C (≥101°F)


  A lower threshold should be considered in the immunocompromised host


Epidemiology


  Fever in the ICU is a common phenomenon


  Thirty percent of medical ICU patients become febrile during their hospital stay and about two thirds of patients with severe sepsis become febrile


Common Causes to Remember


Infectious: most common causes of fever in the ICU are due to infection, although not every infectious process results in fever


  The most common ICU acquired infections causing fever include


  VAP (occurs in approx 25% of mechanically ventilated pt)


  Sinusitis (up to 75% of pt after 1 week of mechanical ventilation)


  Catheter-associated bloodstream infections (5.3 per 1,000 catheter days)


  Primary gram-negative septicemia


  Clostridium difficile-related diarrhea


  Abdominal sepsis


  Complicated wound infection


  Candida infection


Noninfectious: noninfectious causes in the ICU often do not exceed a body temperature of >38.9 (exceptions are drug fever and fever 2/2 blood transfusions)


  They are plentiful and include the following:


  Alcohol withdrawal


  Postoperative fever


  Post-transfusion fever


  Drug fever


  Cerebral infarction or SAH


  Adrenal insufficiency


  Myocardial infarction


  Pancreatitis


  Acalculous cholecystitis


  Ischemic bowel


  Aspiration pneumonitis


  ARDS


  Fat emboli


  Transplant rejection


  DVT/PE


  Gout and pseudogout


  Hematoma


  Cirrhosis


  Gastrointestinal bleed


  Phlebitis


  IV contrast reaction


  Neoplastic fever


  Decubitus ulcers


Key Pathophysiology


  A stimulus (such as an infection, injury or drugs) elicits the release of endogenous pyrogens (interleukin [IL]-1, tumor necrosis factor, IL6, and interferons)


  These interact with different cells that produce prostaglandins, which diffuse into the brain


  This leads to up-regulation of the thermostatic set point


  The regions responsible for coordinating the fever response are the hypothalamus and the brain stem


  Through spinal and supraspinal motor systems and the sympathetic system, the body generates heat and reduces heat loss, which increases the body core temperature


Management and Treatment


  Before initiating empiric antibiotic therapy, a thorough history and physical examination should be performed


  Imaging should be reviewed and noninfectious causes should be excluded


  Blood cultures and possibly other specimens should be collected


  Interestingly, the ideal time to draw blood cultures is 1–2 hours before the onset of fever, as the concentration of bacteria in the blood peaks before the onset of fever


  Thus, drawing blood cultures at the time of fever spike might not have the highest yield, and collection of blood cultures at different time points might be helpful in detecting microorganisms by randomly coinciding collection and bacteremia


  Even if there is no obvious source of infection, empiric treatment should be initiated promptly after obtaining cultures if the patient’s condition is deteriorating or in immunocompromised patients


  It should consist of broad-spectrum antibiotic coverage


  Fever itself can be treated either with antipyretic agents (such as acetaminophen) or with external cooling methods (such as hypothermia blankets)


  The benefit of routinely treating fever in the ICU continues to be debated


  Fever is considered a defense mechanism and has been shown to optimize the immune response and to inhibit bacterial and viral growth


  Moreover, the use of cooling blankets is known to be associated with hypermetabolism leading to increased oxygen consumption and elevated levels of catecholamines


  It is, however, generally recommended to control fever >40°C (104°F), in the following patients:


  Those with limited cardiorespiratory reserve


  Hypoxia


  Acute brain injury


Selected Infections (Not Covered Elsewhere)


Central Line Infections


Introduction


  Central line–associated bloodstream infections (CLABSIs) are an important cause of morbidity and mortality


  Infection localized to catheter site or catheter-associated bloodstream infections


Epidemiology


  Infections associated with central lines are one of the leading causes of healthcare-related infections and have been estimated to be the eighth leading cause of death in the United States


  In 2009, the estimated number of ICU CLABSIs in the United States was 18,000


  These infections increase hospital stay by up to 21 days


  Of note, arterial line infections are generally not considered to be a relevant source of infection; however, one study suggests the incidence to be 1.4% in a surgical ICU population


Key Pathophysiology


  CLABSIs within 7 to 10 days of placement occur most commonly from extraluminal bacteria. This is from migration of bacteria from the skin to the blood through the catheter site. Central line infections >10 days occur most commonly from contamination of a hub used to access the catheter


  Common organisms: gram-positive cocci (coagulase-negative staphylococcus, Staphylococcus aureus, and enterococcus species)


  Predisposing host factors include chronic illness, BMT, immune deficiency, malnutrition, TPN administration, previous BSI, extremes of age and loss of skin integrity (e.g., burns), prolonged hospitalization before insertion of catheter, catheter type, catheter location (increased infection rate of internal jugular (IJ) vs subclavian catheter), conditions of insertion, catheter-site care, skill of the catheter inserter


Clinical Manifestations


  Fever is the most common presenting sign


  Signs of infection include erythema, induration, tenderness, or purulent discharge


  Diagnosis


  IDSA definition: Isolation of the same organism from a quantitative blood cx drawn through the CVC and from a peripheral vein with the single bacterial colony count at least threefold higher in the CVC as compared to the peripheral culture


  A shorter time to positivity (>2 hours earlier) in the CVC culture as compared to the peripheral culture has also been shown to be sensitive as well as specific for diagnosis


  CDC Definition: “recovery of a pathogen from a blood culture (a single blood culture for organisms not commonly present on the skin and two or more blood cultures for organisms commonly present on the skin) in a patient who had a central line at the time of infection or within the 48-hour period before development of infection. The infection cannot be related to any other infection the patient might have and must not have been present or incubating when the patient was admitted to the facility.”


Management and Treatment


  If CLABSI is suspected, empiric therapy should be based on the most likely organism and take into consideration host factors and the overall clinical picture


  For short-term catheters, removal/replacement is recommended if the infection is caused by S. aureus, Enterococcus spp., gram-negative bacteria, fungi and mycobacteria


  Salvage of the catheter with antibiotic lock therapy can be attempted if the organism colonizing the central line is coagulase-negative staphylococcus


  For long-term CVC catheter salvage can only be attempted in a few circumstances:


  Uncomplicated CLABSI caused by organisms other than S. aureus, Pseudomonas aeruginosa, Bacillus spp., Micrococcus species, propionibacteria, fungi, or mycobacteria)


  Restricted to patients with limited vascular access or those who need central access for survival


  Salvage therapy should include antibiotic lock as well as systemic therapy


  Prevention guidelines during insertion include:


  Selection of site —subclavian vein catheters are thought to have the lowest risk of infection


  Recent evidence reveals no difference in the infection rate based on catheter site except in patients with BMI > 40


  No difference in infection rate in all three sites (subclavian, IJ, and femoral) if the following is instituted:


  Aseptic technique


  Hand hygiene


  Maximal sterile barrier precautions including full body drape


  Use of 2% chlorhexidine skin prep


  Ultrasound for placement


  Use of a checklist


  Prevention guidelines during maintenance include:


  Disinfecting catheter hubs, injection ports, and connectors before accessing the catheter


  Replacement of administration sets other than sets used for lipids or blood products every 96 hours


  Daily reassessment of need for the central line


Outcome


  The mortality of CLA BSI has been reported to be as high as 12% to 25%


Necrotizing Soft Tissue Infections


Introduction


  Necrotizing soft tissue infections (NSTI) (“flesh eating bacteria syndrome”) is a rare but life threatening infection of the soft tissues that is associated with a high mortality rate


  It is characterized by subtle onset and rapid spread leading to necrosis spreading from fascia through muscles and subcutaneous fat tissue causing necrosis of the adjacent skin


  If localized to the perineum or the scrotum, this infection is also known as Fournier’s Gangrene


  If localized to the submandibular space, it is also known as Ludwig’s angina


  NSTI can be classified into three types based on microbiology:


  Type 1 (55%to 75%): polymicrobial infection which includes at least one anaerobic species and usually four or more organisms


  Most commonly caused by Bacteroides streptococci, staphylococci, enterococci, and gram-negative rods


  Type 2: Mono or bi-microbial


  Most commonly caused by invasive group A Streptococcus pyogenes, occasionally S. aureus


  Affects healthy patients but has also been associated with nonsteroidal anti-inflammatory drugs


  Occurs after minor injuries of skin or muscle


  May present in the setting of streptococcal toxic shock syndrome


  Type 3: Caused by clostridial infections


  Other causes include marine Vibrio species from marine exposure


Epidemiology


  The incidence of NSTI has been estimated at 500 to 1,000 cases per year in the United States


Key Pathophysiology


  The mechanisms leading to tissue necrosis depend on the bacteria involved


  Necrosis can develop either directly from the toxins produced by the bacteria or from invasion and destruction of the vascular system


  Predisposing factors in adults include diabetes mellitus, immune suppression ESRD, liver cirrhosis, pulmonary disease, malignancy, and IVDU


  Other authors also mention advanced age, obesity, peripheral vascular disease, alcoholism, and malnutrition


Clinical Manifestations

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Jul 13, 2016 | Posted by in ANESTHESIA | Comments Off on 10. Infectious Disease

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