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Ciprofloxacin induced neutropenia icd-9

The pathophysiology of septic shock is not precisely understood but is considered to involve a complex interaction between the pathogen and the host’s immune system (see the image below). The normal physiologic response to localized infection includes activation of host defense mechanisms that result in the influx of activated neutrophils and monocytes, release of inflammatory mediators, local vasodilation, increased endothelial permeability, and activation of coagulation pathways.

Diagram depicting the pathogenesis of sepsis and m Diagram depicting the pathogenesis of sepsis and multiorgan failure. DIC = disseminated intravascular coagulation; IL = interleukin.

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These response mechanisms occur during septic shock, but on a systemic scale, leading to diffuse endothelial disruption, vascular permeability, vasodilation, and thrombosis of end-organ capillaries. Endothelial damage itself can further activate inflammatory and coagulation cascades, creating, in effect, a positive feedback loop and leading to further endothelial and end-organ damage.

Mediator-induced cellular injury

The evidence that sepsis results from an exaggerated systemic inflammatory response induced by infecting organisms is compelling. Inflammatory mediators are the key ciprofloxacin induced neutropenia icd-9 players in the pathogenesis of sepsis (see Table 3 below).

Table 3. Mediators of Sepsis (Open Table in a new window)

induced Type Mediator Activity
Cellular mediators LPS Activation of macrophages, neutrophils, platelets, and endothelium releases various cytokines and other mediators
Lipoteichoic acid
Peptidoglycan
Superantigens
Endotoxin
Humoral mediators Cytokines Activate inflammatory pathways
  • TNF-α and IL-1β

Potent proinflammatory effect
  • IL-6

Acts as pyrogen, stimulates B- and T-cell proliferation
  • IL-8

Neutrophil chemotactic factor, activation and degranulation of neutrophils
  • IL-10

Inhibits cytokine production, induces immunosuppression
  • MIF

Activates macrophages and T cells
  • G-CSF

Promotes neutrophil and macrophage, platelet activation
Complement Promotes neutrophil and macrophage, platelet activation and chemotaxis, other proinflammatory effects
Nitric oxide Involved in hemodynamic alterations of septic shock; cytotoxic, augments vascular permeability, contributes to shock  
Lipid mediators Enhance vascular permeability and contribute to lung injury  
  • Phospholipase A2

   
  • PAF

   
  • Eicosanoids

   
Arachidonic acid metabolites Augment vascular permeability  
Adhesion molecules Enhance neutrophil-endothelial cell interaction, regulate leukocyte migration and adhesion, and play a role in pathogenesis of sepsis; increased levels of VAP-1 activity and anchor protein SDC-1 content have been found in critically ill patients with septic shock [12]  
  • Selectins

   
  • Leukocyte integrins

   
  • High mobility box–1

Late mediator of endotoxin-induced lethality and tissue repair  
G-CSF = granulocyte colony-stimulating factor; IL = interleukin; LPS = lipopolysaccharide; MIF = macrophage inhibitory factor; PAF = platelet-activating factor; SDC-1 = syndecan-1; TNF = tumor necrosis factor; VAP-1 = vascular adhesion protein–1.

Source:  Cinel I, Opal SM. Molecular biology of inflammation and sepsis: a primer. Crit Care Med. 2009 Jan;37(1):291-304. [13]

 
 

Immunologic abnormalities

The following 3 families of pattern recognition receptors are involved in the initiation of the sepsis response:

  • Toll-like receptors (TLRs)

  • Nucleotide-oligomerization domain leucine-rich repeat proteins

  • Cytoplasmic caspase activation and recruiting domain helicases

These receptors trigger the innate immune response and modulate the adaptive immune response to infection. [13]

An initial step in the activation of innate immunity is the de novo synthesis of small polypeptides (cytokines) that induce protean manifestations on most cell types, from immune effector cells to vascular smooth muscle and parenchymal cells. Several cytokines are induced, including tumor necrosis factor (TNF) and interleukins (ILs), especially IL-1. These factors help keep infections localized; however, once the infection progresses, the effects can also be detrimental.

Circulating levels of IL-6 correlate have a strong correlation with outcome. High levels of IL-6 are associated with mortality, but the role of this cytokine in pathogenesis is not clear. IL-8 is an important regulator of neutrophil function, synthesized and released in significant amounts during sepsis. IL-8 contributes to the lung injury and dysfunction of other organs.

Chemokines (eg, monocyte chemoattractant protein [MCP]-1) orchestrate the migration of leukocytes during endotoxemia and sepsis. Other cytokines thought to play a role in sepsis include the following:

  • IL-10

  • Interferon gamma

  • IL-12

  • Macrophage migration inhibition factor (MIF or MMIF)

  • Granulocyte colony-stimulating factor (G-CSF)

  • Granulocyte macrophage colony-stimulating factor (GM-CSF)

In addition, cytokines activate the coagulation pathway, resulting in capillary microthrombi and end-organ ischemia. [14, 15, 16] (See Abnormalities of coagulation and fibrinolysis, below.)

Gram-positive and gram-negative bacteria induce a variety of proinflammatory mediators, including the cytokines mentioned above, which play a pivotal role in initiating sepsis and shock. Various bacterial cell-wall components are known to release the cytokines, including lipopolysaccharide (LPS; gram-negative bacteria), peptidoglycan (gram-positive and gram-negative bacteria), and lipoteichoic acid (gram-positive bacteria).

Several of the harmful effects of bacteria are mediated by proinflammatory cytokines induced in host cells (macrophages/monocytes and neutrophils) by the bacterial cell-wall component. The most toxic component of gram-negative bacteria is the lipid A moiety of LPS, which leads to cytokine induction via lipoteichoic acid. Additionally, gram-positive bacteria may secrete superantigen cytotoxins that bind directly to the major histocompatibility complex (MHC) molecules and T-cell receptors, leading to massive cytokine production.

The complement system is activated and contributes to the clearance of the infecting microorganisms but probably also enhances the tissue damage. The contact systems become activated; consequently, bradykinin is generated.

Hypotension, the cardinal manifestation of sepsis, occurs via induction of nitric oxide (NO). NO plays a major role in the hemodynamic alterations of septic shock, which is a hyperdynamic form of shock.

In a study that evaluated the role of active nitrogen molecules in the progression of septic shock, investigators found not only that patients with sepsis and septic shock had elevated mean levels of nitrite (NO2)/nitrate (NO3) (sepsis, 78.92 µmol/L; septic shock, 97.20 µmol/L) as well as TNF-α (sepsis, 213.50 pg/mL; septic shock, 227.38 pg/mL) but also that levels of these 3 mediators increased with the severity of the sepsis. [17]

Another factor that contributes to the poor cellular oxygen utilization and tissue organ dysfunction during sepsis is mitochondrial dysfunction. [18] This is associated with excessive generation of peroxynitrates and reactive oxygen species (ROS) in combination with glutathione depletion.

A dual role exists for neutrophils: They are necessary for defense against microorganisms, but they may also become toxic inflammatory mediators, thereby contributing to tissue damage and organ dysfunction. Lipid mediators—eicosanoids, platelet-activating factor (PAF), and phospholipase A2—are generated during sepsis, but their contributions to the sepsis syndrome remain to be established.

Neutrophils are constitutively proapoptotic, a capacity that is essential for the resolution of inflammation and cell turnover. Poor apoptosis is associated with poor cell clearance and a proinflammatory state.

There is a growing body of evidence regarding sepsis-induced immunosuppression, which may culminate in a worse prognosis and a greater predisposition to other nosocomial infections. [19] In addition, there is evidence that patients with sepsis who have previously been infected with cytomegalovirus may have worse outcomes than those who have not. [20] That cytomegalovirus infection can also cause immunomodulation may be another factor contributing to sepsis-induced immunosuppression.

Abnormalities of coagulation and fibrinolysis

An imbalance of homeostatic mechanisms leads to disseminated intravascular coagulopathy (DIC) and microvascular thrombosis, causing organ dysfunction and death. [21] Inflammatory mediators instigate direct injury to the vascular endothelium; the endothelial cells release tissue factor (TF), triggering the extrinsic coagulation cascade and accelerating thrombin production. Plasma levels of endothelial activation biomarkers are higher in patients with sepsis-induced hypotension than in patients with hypotension from other causes. [22]

The coagulation factors are activated as a result of endothelial damage. The process is initiated through binding of factor XII to the subendothelial surface, which activates factor XII. Subsequently, factor XI and, eventually, factor X are activated by a complex of factor IX, factor VIII, calcium, and phospholipid. The final product of the coagulation pathway is the production of thrombin, which converts soluble fibrinogen to fibrin. The insoluble fibrin, along with aggregated platelets, forms intravascular clots.

Inflammatory cytokines, such as IL-1α, IL-1β, and TNF-α, initiate coagulation by activating TF. TF interacts with factor VIIa to form factor VIIa-TF complex, which activates factors X and IX. Activation of coagulation in sepsis has been confirmed by marked increases in thrombin-antithrombin complexes and the presence of D-dimer in plasma, indicating activation of the clotting system and fibrinolysis. [23, 24] Tissue plasminogen activator (t-PA) facilitates conversion of plasminogen to plasmin, a natural fibrinolytic.

Endotoxins increase the activity of inhibitors of fibrinolysis—namely, plasminogen activator inhibitor (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI). levels of protein C and endogenous activated protein C (APC) are also decreased in sepsis. Endogenous APC is an important inhibitor of coagulation cofactors Va and VIIa. Thrombin, via thrombomodulin, activates protein C, which then acts as an antithrombotic in the microvasculature. Endogenous APC also enhances fibrinolysis by neutralizing PAI-1 and accelerating t-PA–dependent clot lysis.

The imbalance among inflammation, coagulation, and fibrinolysis results in widespread coagulopathy and microvascular thrombosis and suppressed fibrinolysis, ultimately leading to multiple organ dysfunction and death. The insidious nature of sepsis is such that microcirculatory dysfunction can occur while global hemodynamic parameters such as blood pressure may remain normal. [25]

Circulatory abnormalities

As noted (see Shock Classification, Terminology, and Staging), septic shock falls under the category of distributive shock, which is characterized by pathologic vasodilation and shunting of blood from vital organs to nonvital tissues (eg, skin, skeletal muscle, and fat). The endothelial dysfunction and vascular maldistribution characteristic of distributive shock result in global tissue hypoxia or inadequate delivery of oxygen to vital tissues. In addition, mitochondria can become dysfunctional, thus compromising oxygen utilization at the cellular level.

The predominant hemodynamic feature of septic shock is arterial vasodilation. The mechanisms implicated in this pathologic vasodilation are multifactorial, but the primary factors are thought to be (1) activation of adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle cells and (2) activation of NO synthase.

The potassium-ATP channels are directly activated by lactic acidosis. NO also activates potassium channels. Potassium efflux from cells results in hyperpolarization, inhibition of calcium influx, and vascular smooth muscle relaxation. [26] The resulting vasodilation can be refractory to endogenous vasoactive hormones (eg, norepinephrine and epinephrine) that are released during shock.

Diminished peripheral arterial vascular tone may cause blood pressure to be dependent on cardiac output, so that vasodilation results in hypotension and shock if insufficiently compensated by a rise in cardiac output. Early in septic shock, the rise in cardiac output is often limited by hypovolemia and a fall in preload because of low cardiac filling pressures. When intravascular volume is augmented, the cardiac output usually is elevated (hyperdynamic phase of sepsis and shock).

Although cardiac output is elevated, the performance of the heart, reflected by stroke work as calculated from stroke volume and blood pressure, is usually depressed. Factors responsible for myocardial depression of sepsis include myocardial depressant substances, coronary blood flow abnormalities, pulmonary hypertension, various cytokines, NO, and beta-receptor downregulation.

Although cardiac output is elevated, the arterial−mixed venous oxygen difference is usually narrow, and the blood lactate level is elevated. This implies that low global tissue oxygen extraction is the mechanism that may limit total body oxygen uptake in septic shock. The basic pathophysiologic problem seems to be a disparity between oxygen uptake and oxygen demand in the tissues, which may be more pronounced in some areas than in others.

This disparity is termed maldistribution of blood flow, either between or within organs, with a resultant defect in the capacity for local extraction of oxygen. During a fall in the oxygen supply, cardiac output becomes distributed so that the most vital organs, such as the heart and brain, remain relatively better perfused than nonvital organs are. However, sepsis leads to regional changes in oxygen demand and regional alteration in the blood flow of various organs.

The peripheral blood flow abnormalities result from the balance between local regulation of arterial tone and the activity of central mechanisms (eg, the autonomic nervous system). Regional regulation and the release of vasodilating substances (eg, NO and prostacyclin) and vasoconstricting substances (eg, endothelin) affect regional blood flow. Increased systemic microvascular permeability also develops, remote from the infectious focus, and contributes to edema of various organs (eg, the lung microcirculation) and to the development of ARDS.

In patients experiencing septic shock, oxygen delivery is relatively high, but the global oxygen extraction ratio is relatively low. Oxygen uptake increases with rising body temperature despite a fall in oxygen extraction.

In patients with sepsis who have low oxygen extraction and elevated arterial lactate levels, oxygen uptake depends on oxygen supply over a much wider range than normal. Therefore, oxygen extraction may be too low for tissue needs at a given oxygen supply, and oxygen uptake may increase with a boost in oxygen supply—a phenomenon termed oxygen uptake supply dependence or pathologic supply dependence. This concept is controversial, however; some investigators argue that supply dependence is an artifact rather than a real phenomenon.

Maldistribution of blood flow, disturbances in the microcirculation, and, consequently, peripheral shunting of oxygen are responsible for diminished oxygen extraction and uptake, pathologic supply dependency of oxygen, and lactate acidemia in patients experiencing septic shock.

Mechanisms of organ dysfunction

Sepsis is described as an autodestructive process that permits the extension of the normal pathophysiologic response to infection (involving otherwise normal tissues), resulting in MODS. Organ dysfunction or organ failure may be the first clinical sign of sepsis, and no organ system is immune to the consequences of the inflammatory excesses of sepsis.

The precise mechanisms of cell injury and resulting organ dysfunction in patients with sepsis are not fully understood. MODS is associated with widespread endothelial and parenchymal cell injury occurring via the following proposed mechanisms:

  • Hypoxic hypoxia – The septic circulatory lesion disrupts tissue oxygenation, alters the metabolic regulation of tissue oxygen delivery, and contributes to organ dysfunction; microvascular and endothelial abnormalities contribute to the septic microcirculatory defect in sepsis; ROS, lytic enzymes, vasoactive substances (eg, NO), and endothelial growth factors lead to microcirculatory injury, which is compounded by the inability of the erythrocytes to navigate the septic microcirculation

  • Direct cytotoxicity – Endotoxin, TNF-α, and NO may cause damage to mitochondrial electron transport, leading to disordered energy metabolism; this is called cytopathic or histotoxic anoxia (ie, inability to use oxygen even when it is present)

  • Apoptosis (programmed cell death) – This is the principal mechanism by which dysfunctional cells are normally eliminated; the proinflammatory cytokines may delay apoptosis in activated macrophages and neutrophils, but other tissues, such as the gut epithelium, may undergo accelerated apoptosis; therefore, derangement of apoptosis plays a critical role in tissue injury in patients with sepsis

  • Immunosuppression – Interaction between proinflammatory and anti-inflammatory mediators may lead to an imbalance and an inflammatory reaction, immunodeficiency may predominate, or both may occur

  • Coagulopathy – Subclinical coagulopathy signified by mild elevation of the thrombin time or activated partial thromboplastin time (aPTT) or by a moderate reduction in platelet count is extremely common, but overt DIC is rare; coagulopathy is caused by deficiencies of coagulation system proteins, including protein C, antithrombin III, and TF inhibitors

Cardiovascular dysfunction

Significant derangement in the autoregulation of the circulatory system is typical in patients with sepsis. Vasoactive mediators cause vasodilatation and increase the microvascular permeability at the site of infection. NO plays a central role in the vasodilation of septic shock. Impaired secretion of vasopressin may also occur, which may permit the persistence of vasodilatation.

Changes in both systolic and diastolic ventricular performance occur in patients with sepsis. Through the Frank-Starling mechanism, cardiac output is often increased to maintain blood pressure in the presence of systemic vasodilatation. Patients with preexisting cardiac disease are unable to increase their cardiac output appropriately.

Because sepsis interferes with the normal distribution of systemic blood flow to organ systems, core organs may not receive appropriate oxygen delivery. The microcirculation is the key target organ for injury in patients with sepsis. A decrease in the number of functional capillaries leads to an inability to extract oxygen maximally; this inability is caused by intrinsic and extrinsic compression of capillaries and plugging of the capillary lumen by blood cells. Increased endothelial permeability leads to widespread tissue edema involving protein-rich fluid.

Hypotension is caused by the redistribution of intravascular fluid volume that results from reduced arterial vascular tone, diminished venous return from venous dilation, and release of myocardial depressant substances.

Pulmonary dysfunction

The pathogenesis of sepsis-induced ARDS is a pulmonary manifestation of SIRS. A complex interaction between humoral and cellular mediators, inflammatory cytokines and chemokines, is involved in this process. A direct or indirect injury to the endothelial and epithelial cells of the lung increases alveolar capillary permeability, causing ensuing alveolar edema. The edema fluid is protein-rich; the ratio of alveolar fluid edema to plasma is 0.75-1.0, whereas in patients with hydrostatic cardiogenic pulmonary edema, the ratio is less than 0.65.

Injury to type II pneumocytes decreases surfactant production; furthermore, the plasma proteins in alveolar fluid inactivate the surfactant previously manufactured. These enhance the surface tension at the air-fluid interfaces, producing diffuse microatelectasis.

Neutrophil entrapment within the pulmonary microcirculation initiates and amplifies the injury to alveolar capillary membrane. ARDS is a frequent manifestation of these effects.

ALI (mild ARDS in the Berlin Definition) is a type of pulmonary dysfunction secondary to parenchymal cellular damage that is characterized by endothelial cell injury and destruction, deposition of platelet and leukocyte aggregates, destruction of type I alveolar pneumocytes, an acute inflammatory response through all injury phases, and repair and hyperplasia of type II pneumocytes. Migration of macrophages and neutrophils into the interstitium and alveoli produces various mediators that contribute to the alveolar and epithelial cell damage.

If addressed at an early stage, ALI may be reversible, but in many cases, the host response is uncontrolled, and ALI progresses to more severe ARDS. Continued infiltration occurs with neutrophils and mononuclear cells, lymphocytes, and fibroblasts. An alveolar inflammatory exudate persists, and type II pneumocyte proliferation is evident. If this process can be halted, complete resolution may occur. In other patients, progressive respiratory failure and pulmonary fibrosis develop.

The central pathologic finding in ARDS is severe injury to the alveolocapillary unit. After initial extravasation of intravascular fluid, inflammation and fibrosis of pulmonary parenchyma develop into a morphologic picture termed diffuse alveolar damage (DAD). The clinical and pathologic evolution can be categorized into the following 3 overlapping phases [27] :

  • Exudative phase (edema and hemorrhage)

  • Proliferative phase (organization and repair)

  • Fibrotic phase (end-stage fibrosis)

The exudative phase of DAD occurs in the first week and is dominated by alveolar edema and hemorrhage (see the images below). Other histologic features include dense eosinophilic hyaline membranes and disruption of the capillary membranes. Necrosis of endothelial cells and type I pneumocytes occur, along with leukoagglutination and deposition of platelet fibrin thrombi.

Acute respiratory distress syndrome (ARDS), common Acute respiratory distress syndrome (ARDS), commonly observed in septic shock as a part of multiorgan failure syndrome, results in pathologically diffuse alveolar damage (DAD). This photomicrograph shows early stage (exudative stage) DAD.

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Acute respiratory distress syndrome (ARDS), common Acute respiratory distress syndrome (ARDS), commonly observed in septic shock as a part of multiorgan failure syndrome, results in pathologically diffuse alveolar damage (DAD). This is a high-powered photomicrograph of early stage (exudative stage) DAD.

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The proliferative phase is prominent in the second and third week after the onset of ARDS, but it may begin as early as day 3. Organization of the intra-alveolar and interstitial exudate, infiltration with chronic inflammatory cells, parenchymal necrosis, and interstitial myofibroblast reaction occur. Proliferation of type II cells and fibroblasts, which convert the exudate to cellular granulation tissue, is noted, as is excessive collagen deposition, transforming into fibrous tissue (see the images below).

Photomicrograph showing delayed stage (proliferati Photomicrograph showing delayed stage (proliferative or organizing stage) of diffuse alveolar damage (DAD). Proliferation of type II pneumocytes has occurred; hyaline membranes as well as collagen and fibroblasts are present.

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Photomicrograph showing delayed stage (proliferati Photomicrograph showing delayed stage (proliferative or organizing stage) of diffuse alveolar damage (DAD). Fibrin stain depicts collagenous tissue, which may develop into fibrotic stage of DAD.

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The fibrotic phase occurs by the third or fourth week after the onset of ARDS, though it may begin as early as the first week. The collagenous fibrosis completely remodels the lung, the air spaces are irregularly enlarged, and alveolar duct fibrosis is apparent. Lung collagen deposition increases, and microcystic honeycomb formation and traction bronchiectasis follow.

Gastrointestinal dysfunction

The gastrointestinal (GI) tract may help to propagate the injury of sepsis. Overgrowth of bacteria in the upper GI tract may be aspirated into the lungs and produce nosocomial pneumonia. The gut’s normal barrier function may be affected, thereby allowing translocation of bacteria and endotoxin into the systemic circulation and extending the septic response.

Septic shock usually causes ileus, and the use of narcotics and sedatives delays the institution of enteral feeding. This interferes with optimal nutritional intake, in the face of high protein and energy requirements.

Glutamine is necessary for normal enterocyte functioning. Its absence in commercial formulations of total parenteral nutrition (TPN) leads to breakdown of the intestinal barrier and translocation of the gut flora into the circulation. This may be one of the factors driving sepsis. In addition to inadequate glutamine levels, this may lessen the immune response by decreasing leukocyte and natural killer (NK) cell counts, as well as total B-cell and T-cell counts. [28]

Hepatic and renal dysfunction

By virtue of the liver’s role in host defense, the abnormal synthetic functions caused by liver dysfunction can contribute to both the initiation and the progression of sepsis. The hepatic reticuloendothelial system acts as a first line of defense in clearing bacteria and their products; liver dysfunction leads to a spillover of these products into the systemic circulation.

Acute kidney injury (AKI)—previously termed acute renal failure (ARF)—with remarkably little overt tubular necrosis but markedly impaired renal function often accompanies sepsis. The mechanism for sepsis-induced AKI is poorly understood but is associated with systemic hypotension, cytokinemia (eg, TNF), and activation of neutrophils by endotoxins and other peptides, which indirectly and directly contribute to renal tubular injury.

Central nervous system dysfunction

Central nervous system (CNS) involvement in sepsis produces encephalopathy (septic encephalitis) and peripheral neuropathy. The pathogenesis is poorly defined, but it may involve systemic inflammation from either infectious or noninfectious causes, [29] as well as a combination of the effects of hypoxemia, hypotension, hemorrhage, and medications such as sedatives and analgesics. [29, 30]

Etiology

Most patients who develop sepsis and septic shock have underlying circumstances that interfere with local or systemic host defense mechanisms. Sepsis is seen most frequently in elderly persons and in those with comorbid conditions that predispose to infection, such as diabetes or any immunocompromising disease. Patients may also have genetic susceptibility, making them more prone to developing septic shock from infections that are well tolerated in the general population. [31, 32, 33, 34, 35]

The most common disease states predisposing to sepsis are malignancies, diabetes mellitus, chronic liver disease, and chronic kidney disease. The use of immunosuppressive agents is also a common predisposing factor. In addition, sepsis is a common complication after major surgery, trauma, and extensive burns. Patients with indwelling catheters or devices are also at high risk.

In most patients with sepsis, a source of infection can be identified. The exceptions are patients who are immunocompromised with neutropenia, in whom an obvious source often is not found.

Causative microorganisms

Before the introduction of antibiotics, gram-positive bacteria were the principal organisms that caused sepsis. Subsequently, gram-negative bacteria became the key pathogens causing severe sepsis and septic shock. Currently, however, the rates of severe sepsis and septic shock due to gram-positive organisms are rising again because of the more frequent use of invasive procedures and lines in critically ill patients. As a result, gram-positive and gram-negative microorganisms are now about equally likely to be causative pathogens in septic shock. [36, 37, 38, 39]

Respiratory tract and abdominal infections are the most frequent causes of sepsis, followed by urinary tract and soft-tissue infections. [36, 37, 38, 39] Each organ system tends to be infected by a particular set of pathogens (see below).

Lower respiratory tract infections cause septic shock in 35-50% of patients. [36, 37, 38, 39] The following are the common pathogens:

  • Streptococcus pneumoniae

  • Klebsiella pneumoniae

  • Escherichia coli

  • Legionella spp

  • Haemophilus spp

  • Staphylococcus aureus

  • Pseudomonas spp

  • Anaerobes

  • Gram-negative bacteria

  • Fungi (see the image below)
    An 8-year-old boy developed septic shock secondary An 8-year-old boy developed septic shock secondary to Blastomycosis pneumonia. Fungal infections are rare causes of septic shock.

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Abdominal and GI tract infections cause septic shock in 20-40% of patients. [36, 37, 38, 39] The following are the common pathogens:

  • E coli

  • Enterococcus spp

  • Bacteroides fragilis

  • Acinetobacter spp

  • Pseudomonas spp

  • Enterobacter spp

  • Salmonella spp

  • Klebsiella spp

  • Anaerobes

Urinary tract infections cause septic shock in 10-30% of patients. [36, 37, 38, 39] The following are the common pathogens:

  • E coli

  • Proteus spp

  • Klebsiella spp

  • Pseudomonas spp

  • Enterobacter spp

  • Serratia spp

  • Enterococcus spp

  • Candida spp

Infections of the male and female reproductive systems cause septic shock in 1-5% of patients. [36, 37, 38, 39] The following are the common pathogens:

  • Neisseria gonorrhoeae

  • Gram-negative bacteria

  • Streptococci

  • Anaerobes

Soft-tissue infections cause septic shock in 5-10% of patients. [36, 37, 38, 39] The following are the common pathogens:

  • S aureus

  • Staphylococcus epidermidis

  • Streptococci

  • Clostridium spp

  • Gram-negative bacteria

  • Anaerobes

  • Fungi

Infections due to foreign bodies cause septic shock in 1-5% of patients. [36, 37, 38, 39]S aureus, S epidermidis, and fungi (eg, Candida species) are the common pathogens.

Miscellaneous infections, such as CNS infections, also cause septic shock in 1-5% of patients. [36, 37, 38, 39]Neisseria meningitidis is a common cause of such infections (see the image below).

Gram stain of blood showing the presence of Neisse Gram stain of blood showing the presence of Neisseria meningitidis.

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Risk factors

Risk factors for severe sepsis and septic shock include the following:

  • Extremes of age (< 10 years and >70 years)

  • Primary diseases (eg, liver cirrhosis, alcoholism, diabetes mellitus, cardiopulmonary diseases, solid malignancy, and hematologic malignancy)

  • Immunosuppression (eg, from neutropenia, immunosuppressive therapy [eg, in organ and bone marrow transplant recipients], corticosteroid therapy, injection or IV drug use [see the image below], complement deficiencies, asplenia)

  • Major surgery, trauma, burns

  • Invasive procedures (eg, placement of catheters, intravascular devices, prosthetic devices, hemodialysis and peritoneal dialysis catheters, or endotracheal tubes)

  • Previous antibiotic treatment

  • Prolonged hospitalization

  • Underlying genetic susceptibility

  • Other factors (eg, childbirth, abortion, and malnutrition)
    A 28-year-old woman who was a former intravenous d A 28-year-old woman who was a former intravenous drug user (human immunodeficiency virus [HIV] status: negative) developed septic shock secondary to bilateral pneumococcal pneumonia.

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Source: http://emedicine.medscape.com/article/168402-overview


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