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Sepsis syndromes exist on a clinical spectrum with varying prognoses. Septic shock, the most severe complication of sepsis, is fatal. Septic shock occurs due to an inciting agent that activates the pro-inflammatory and anti-inflammatory immune systems. This happens in tandem with the activation of monocytes, macrophages, and neutrophils, which interact with the endothelium via pathogen recognition receptors, resulting in the involvement of cytokines, proteases, kinins, reactive oxygen species, and nitric oxide. The endothelium, as the primary site of this response, not only suffers microvascular injury but also activates the coagulation and complement cascades, exacerbating the vascular injury and leading to capillary leakage. The clinical signs and symptoms of sepsis, as well as the progression from sepsis to septic shock, are caused by this chain of events. The degree of morbidity and mortality of patients with sepsis is ultimately determined by striking a balance between pro-inflammatory responses, which help eradicate the invading microorganism, and anti-inflammatory signals, which keep the inflammatory cascade in check. Antimicrobial judicious and early administration, sepsis care bundle use, and early goal-directed therapies have significantly and positively impacted sepsis-related mortality. Early detection remains the most effective therapeutic tool for sepsis treatment and management. This activity describes the evaluation and management of septic shock and emphasizes the interprofessional team’s role in improving care delivery for affected patients.

Examine the possible causes of septic shock.
Explain septic shock pathophysiology.
Outline the septic shock treatment options.
Explain the significance of improving care coordination among interprofessional team members to improve outcomes for septic shock patients.
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Sepsis syndromes exist on a clinical spectrum with varying prognoses. Septic shock, the most severe complication of sepsis, is fatal. In response to an inciting agent, the immune system’s pro-inflammatory and anti-inflammatory arms work together to activate monocytes, macrophages, and neutrophils, which interact with the endothelium via pathogen recognition receptors to produce cytokines, proteases, kinins, reactive oxygen species, and nitric oxide. [1] The endothelium, as the primary site of this response, not only suffers microvascular injury but also activates the coagulation and complement cascades, exacerbating the vascular injury and leading to a capillary leak. The clinical signs and symptoms of sepsis, as well as the progression from sepsis to septic shock, are caused by this chain of events. The ability to balance pro-inflammatory responses aimed at eradicating the invading microorganism with anti-inflammatory signals aimed at controlling the overall inflammatory cascade ultimately determines the patient’s morbidity and mortality. Antimicrobial judicious and early administration, sepsis care bundle use, and early goal-directed therapies have significantly and positively impacted sepsis-related mortality. Early detection remains the most effective therapeutic tool for sepsis treatment and management.

Visit: Etiology
According to the 2009 European Prevalence of Infection in Intensive Care (EPIC II study), gram-negative bacterial infections are the most common cause of sepsis syndromes (62%), followed by gram-positive infections (47%). An increase in the latter could be attributed to more invasive procedures and increased incidence of nosocomial infections. [2] Staphylococcus aureus (20%), Pseudomonas (20%), and Escherichia coli (16%) are the most common microorganisms isolated from patients. [3] The most common infection sites are respiratory (42%), bloodstream (21%), and genitourinary (10%). [2] These findings must be weighed against the fact that more than one-third of patients never develop positive cultures. [4]
A large meta-analysis demonstrated the impact of bacterial strain and infection site on mortality.

[5] Gram-negative infections were associated with higher mortality in this study. On the other hand, gram-positive bacteremia with Acinetobacter or pneumonia with Staphylococcus had a 40% mortality rate, with Pseudomonal pneumonia having the highest mortality rate at 70%.

Sepsis syndromes caused by multidrug-resistant bacterial strains (MRSA, VRE) are on the rise, with a current incidence of up to 25%; viruses and parasites cause far fewer cases, accounting for 2% to 4% of cases.


The following are risk factors for sepsis:

Kidney and liver disease that is chronic
Corticosteroid use
Immunocompromised state
Significant surgery
Indwelling catheters are present.
Hospitalization for an extended period
Age-related extremes
Visit: Epidemiology
This debilitating condition is increasing at nearly 9% per year.
[7] From 2000 to 2008, sepsis and severe sepsis increased from approximately 600,000 to over 1,000,000 hospitalizations annually. [8] This trend has been accompanied by increased healthcare expenditure, with sepsis becoming the most expensive healthcare condition in 2009, accounting for 5% of total hospital costs in the United States. [9] Because of advances in sepsis management provided by the Surviving Sepsis Campaign, the case fatality rate for patients with sepsis has been decreasing. From 2009 to 2012, the mortality rate in the United States Nationwide Inpatient Sample (NIS) fell from 16.5% to 13.8%. [10] However, severe sepsis remains one of the leading causes of death in hospitalized patients. [11] Furthermore, up to 25% of patients with severe sepsis and 50% with septic shock will die. [2] However, overall mortality from sepsis syndromes can range from 30% to 50% [12] depending on demographic factors such as age, race, gender, co-morbid conditions, and organ dysfunction. [13] For example, inpatient mortality was most strongly predicted by the number and severity of organ injuries, with respiratory, cardiovascular, hepatic, and neurologic failure being the most powerful predictors. [10]

Pathophysiology is an excellent place to start.
Sepsis is a clinical condition that progresses along a pathophysiologic spectrum, beginning with a systemic inflammatory response syndrome (SIRS) and ending with multiorgan dysfunction syndrome (MODS) before death.

The following are the first indications of inflammation:

Fever (higher than 38 degrees Celsius) or hypothermia (temperature less than 36 C)
Tachycardia (a heart rate that exceeds 90 beats per minute), Tachypnea (respiratory rate of more than 20 breaths per minute)
Leukocytosis (white blood cells (WBC) greater than 12,000/cu mm) / leukopenia (WBC less than 4,000/cu mm) with or without the pandemic (more than 10%).
Two of these four clinical signs are required to diagnose systemic inflammatory response syndrome. Following that, the clinical definition of sepsis is systemic inflammatory response syndrome with an infectious source. [14]

With the onset of hypotension, tissue demands are insufficiently met by tissue oxygenation, and the patient is now classified as having severe sepsis.

[14] The decrease in peripheral vascular perfusion and oxygenation causes cellular and metabolic disruptions, most notably a shift from aerobic to anaerobic respiration and lactic acidosis. Signs of end-organ damage, such as prerenal azotemia or transaminitis, can also indicate tissue hypoperfusion. During resuscitation, the difference in oxygen supply and demand can be monitored by trending the mixed venous oxygen saturation from a central line in the superior vena cava (SVC), if one is available. [1]

Septic shock occurs when sepsis-induced hypotension is resistant to initial treatment with fluid resuscitation.

[14] Septic shock differs from other shock states because it is a distributive shock. A combination of inflammatory mediators (histamine, serotonin, super-radicals, lysosomal enzymes) produced in response to bacterial endotoxins increases capillary permeability while decreasing peripheral vascular resistance. This results in a decrease not only afterload but also preload due to a decrease in venous return from third spacing. The resulting reduction in stroke volume is initially accommodated by an increase in heart rate, i.e., compensated septic shock. As a result, the patient is in a hyperdynamic state associated with septic shock. [1]

Patients present with dynamic precordium, tachycardia, and bounding peripheral pulses. They are warm to the touch and have less capillary refill (flash cap refill). This is known as friendly shock. As shock progresses, increased catecholamine production causes an increase in peripheral vascular resistance as the body tries to redirect blood away from non-vital tissues (GI tract, kidneys, muscle, and skin) and toward vital tissues (brain and heart). This is known as cold shock. Understanding the pathophysiology and progression of septic shock is critical for initiating effective treatment measures. [1]

Septic shock is defined functionally as persistent hypotension despite adequate fluid resuscitation of 60 mL/kg to 80 mL/kg of crystalloid or colloid fluid. At this point, starting appropriate vasoactive medications like beta-adrenergic or alpha-adrenergic drugs is critical. The progression of organ dysfunction despite high-dose vasoactive administration defines the condition known as multiorgan dysfunction syndrome (MODS), which has a 75% mortality rate. While determining the exact circumstances predicting poor prognosis and death has been difficult, immunologic dissonance (exaggerated pro-inflammatory response) versus immunologic paralysis (exaggerated anti-inflammatory response) has been suggested to play a role. [15]

Visit the History and Physical Early Signs and Symptoms page.

Sepsis is a systemic inflammatory response syndrome combined with an infectious source. As a result, earlier in the course of sepsis, patients exhibit the following vital sign changes:

Fever (temperature above 38 degrees Celsius) or hypothermia (temperature below 36 degrees Celsius)
Tachycardia is a heart rate greater than 90 beats per minute in adults or less than two standard deviations for age in children.
Tachypnea with a respiratory rate of more than 20 breaths per minute in adults or more than two standard deviations for age in children.
Severe Sepsis Signs and Symptoms Sepsis with end-organ dysfunction is called severe sepsis. Signs and symptoms at this stage may include:

Changes in mental state
Anuria or oliguria
Patients who progress to septic shock will exhibit signs and symptoms of severe sepsis, including hypotension. Notably, blood pressure may be maintained at an early “compensated” stage of wonder, and other signs of distributive shocks, such as warm extremities, flash capillary refill (less than one second), and bounding pulses, also known as friendly shock, may be present. This shock stage can be reversed if treated aggressively with fluid resuscitation and vasoactive support. Hypotension develops as septic shock progresses into the uncompensated stage. Patients may present with cool extremities, delayed capillary refill (more than three seconds), and thready pulses, also known as cold shock. With continued tissue hypoperfusion, shock may become irreversible, rapidly progressing into multiorgan dysfunction syndrome and death.

Go to: Laboratory Results Evaluation

The following are the findings in sepsis, severe sepsis, and septic shock [16]:

Hyperglycemia (glucose levels greater than 120 mg/dL)
Leukopenia (WBC less than 4000/mm3) or leukocytosis (WBC greater than 12,000/mm3)
More than 10% bandemia
C-reactive protein or procalcitonin levels that are more than two standard deviations above normal
More than 70% mixed venous saturation
PaO2: FiO2 levels less than 300
Azitemia prerenal
Coagulopathy, INR greater than 1.5, or PTT greater than 60 seconds
Thrombocytopenia (less than 100,000 platelets/mL)
Hyperbilirubinemia (more than 4 mg/dL total bilirubin)
Lactic acidosis (levels greater than 2 mmol/L)
Patients should be placed on continuous cardiopulmonary monitoring so that vital signs can be closely monitored. End-organ function and peripheral perfusion should be thoroughly evaluated to determine where they may fall on the pathophysiologic continuum of sepsis. A Glasgow Coma Scale (GCS) or mental status assessment, urine output measurement, or lactate/mixed venous saturation determination should all be included (with central lines). All patients, regardless of where they are on the continuum, should have a complete blood count with differential (CBC-d), source cultures (blood, urine, tracheal (if intubated), wound), and a urinalysis. A lumbar puncture may be indicated depending on the presentation’s severity and the patient’s age, for example, patients with signs of encephalitis or meningitis or febrile pediatric patients under six weeks of age. C-reactive protein or procalcitonin, both acute-phase proteins, may help distinguish viral from bacterial sepsis, with the latter showing steeper elevations in these proteins. Additional labs that may provide crucial information on the severity of sepsis syndrome in a patient include a complete chemistry panel with liver function tests, a disseminated intravascular coagulation (DIC) board, and arterial blood gas.

Before administering antibiotics, at least two sets of blood cultures are recommended. However, only about 40% of blood cultures are positive.

An x-ray of the chest may reveal signs of pneumonia or ARDS. If the patient has necrotizing fasciitis, plain x-rays of the extremities may indicate the presence of gas in the tissues. The gallbladder can be evaluated using ultrasound. A CT scan looks for abscesses, bowel perforation, or ischemia in the abdomen.

Please visit Treatment / Management.
The guidelines below are adapted from the Surviving Sepsis Campaign Guidelines. [17][18]

Control of the Source

All patients should be given broad-spectrum antibiotics within one hour of being diagnosed. Initial empiric anti-infective therapy should be active against all likely pathogens and penetrate source tissue sufficiently.
Infected/necrotic tissue should be removed if it is the source of septic shocks, such as in patients with cellulitis, abscesses, infected devices, or purulent wounds.
Shock Management [19]

Measures are most effective if implemented within six hours of diagnosis.
Restore central venous pressure (CVP) between 8 and 12 mmHg.
Restore mean arterial pressure (MAP) above 65 mmHg.
Restore 70% superior vena cava saturation or 65% mixed venous saturation.
Up to 80 ml/kg fluid resuscitation with crystalloid (NS or albumin) and colloid (blood products).
Mechanical ventilation is used to lower metabolic demand.
First-line vasoactive agents (epinephrine in cold shock versus norepinephrine in warm shock) are used when fluid-refractory.
Dopamine has fallen out of favor as a first-line agent due to its inhibitory effect on the HPA axis, specifically prolactin and growth hormone, which can cause immunologic dysfunction [20].
Improving Host Response

Corticosteroids indicated in vasoactive-refractory shock and or in patients with low (unstimulated) basal cortisol levels less than 150 ug/L) [21] [22]
The addition of vasopressin was indicated in vasoactive-refractory shock.
While central lines are not required to renew patients with septic shock, they provide an accurate means of monitoring CVP and mixed venous oxygen. Remember that CVP and MVO2 are most accurate from a central line within the right atrium; lower extremity significant lines do not provide the most accurate data for monitoring these indices of resuscitation. Regarding the need for primary venous access for vasoactive agents, a recent study showed that high dopamine, norepinephrine, and phenylephrine could be safely administered via peripheral venous access. [23]

Early goal-directed therapy (EGDT) has not been shown to confer a survival benefit in more recent studies.

[24] All studies comparing EGDT to standard practice have shown an increase in the administration of crystalloid and packed red blood cells in the first six hours and the placement of central lines. Furthermore, survival was influenced most by the maintenance of blood pressure independent of the fluid or vasoactive used and not CVP or MVO2. [25] The Surviving Sepsis Campaign guidelines continue to support EGDT as the standard of practice for managing severe sepsis and septic shock.

The placement of an arterial line becomes essential in the management of vasoactive-refractory shock for close monitoring of blood pressure and tissue oxygenation status via regular blood gasses with crucial attention to lactate levels and pO2.

Patients with sepsis have a high metabolism, and thus prolonged starvation should be avoided. Early nutrition can help protect gut mucosa and prevent the translocation of organisms from the GI tract into systemic circulation.

Go to: Differential Diagnosis
Distributive shock
Hemorrhagic shock
Adrenal crisis
Cardiogenic shock
Toxic shock syndrome
Drug toxicity
Go to: Prognosis
Septic shock is a severe illness, and despite all the advances in medicine, it still carries a high mortality, exceeding 40%. Mortality does depend on many factors, including the type of organism, antibiotic sensitivity, number of organs affected, and patient age. The more elements that match SIRS, the higher the mortality. Data suggest that Tachypnea and altered mental status are excellent predictors of poor outcomes. Finally, prolonged use of inotropes to maintain blood pressure is also associated with adverse effects. Even those who survive are left with significant functional and cognitive deficits.

Go to: Complications
Acute/chronic renal injury DIC
Mesenteric ischemia
Acute liver failure
Myocardial dysfunction
Multiple organ failure
Go to: Enhancing Healthcare Team Outcomes
The management of septic shock is best done with an interprofessional team that includes ICU nurses. The key is early diagnosis and resuscitation to maintain end-organ perfusion. The fluid type for resuscitation has little bearing on outcomes, but the key is maintaining adequate perfusion pressure. Patients with sepsis are prone to many complications, which have high mortality. Thus, close monitoring and prevention of these complications are vital. Primary disorders like diabetes and renal or liver failure must be treated. Drugs that affect the immune system should be discontinued. The dietitian should be consulted as there is good evidence that early enteral nutrition is beneficial. The nurse should ensure DVT and pressure sore prevention. The nurse should also monitor all catheters for infection and remove those unnecessary ones. The pharmacists should follow the culture results and ensure that the patient is on organism-sensitive antibiotics. Clinicians should maintain aseptic techniques during procedures, and hand washing should be practiced. The entire team should communicate with each other to ensure that the patient is receiving optimal care.

The outcomes of septic shock depend on the patient’s age, associated comorbidities, renal function, need for dialysis, the requirement for mechanical ventilation, and response to treatment.

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