Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion. There may also be symptoms associated with certain infections, such as coughing with pneumonia, or painful urination with kidney infection. In very young people, elderly, and people with weakened immune systems, there may be no symptoms of certain infections and the body temperature may be low or normal, not high. Severe sepsis is a sepsis that causes poor organ function or inadequate blood flow. Inadequate blood flow can be demonstrated by low blood pressure, high blood lactate, or low urine output. Septic shock is low blood pressure because sepsis does not improve after adequate intravenous fluids are given.
Sepsis is caused by an infection-induced immune response. Most commonly, the infection is bacterial, but may also come from fungi, viruses, or parasites. Common locations for primary infections include the lungs, brain, urinary tract, skin, and abdominal organs. Risk factors include young or old age, weak immune system from conditions such as cancer or diabetes, major trauma, or burns. The older diagnostic method is based on meeting at least two systemic inflammatory response syndromes (SIRS) due to suspected infection. By 2016, SIRS is replaced by qSOFA which is two of three things: increased respiratory rate, consciousness change, and low blood pressure. Blood cultures are recommended better before antibiotics begin, however, blood infections are not necessary for diagnosis. Medical imaging should be used to look for possible infection sites. Other potential causes of similar signs and symptoms include anaphylaxis, adrenal insufficiency, low blood volume, heart failure, and pulmonary embolism, among others.
Sepsis is usually treated with intravenous fluids and antibiotics. Usually, antibiotics are given as soon as possible. Often, ongoing care is done in the intensive care unit. If fluid replacement is not sufficient to maintain blood pressure, drugs that increase blood pressure can be used. Mechanical ventilation and dialysis may be needed to support lung and kidney function. To guide treatment, central venous catheters and arterial catheters can be placed for access to the bloodstream. Other measures such as cardiac output and superior vena cava oxygen saturation can be used. Persons with sepsis require precautionary measures for deep venous thrombosis, stress ulcers and pressure ulcers, unless other conditions prevent such intervention. Some may benefit from tight control of blood sugar levels with insulin. The use of controversial corticosteroids. Activated drotrecogin alpha, originally marketed for severe sepsis, has not been found to be helpful, and withdrawn from sales in 2011.
The severity of the disease partly determines the outcome. The risk of death from sepsis as high as 30%, from heavy sepsis as high as 50%, and from septic shock as high as 80%. The number of cases worldwide is unknown because there is little data from developing countries. Estimates show sepsis affects millions of people annually. In developed countries about 0.2 to 3 people per 1000 are affected by sepsis every year, generating about one million cases per year in the United States. The rate of the disease has increased. Sepsis is more common in men than in women. Medical conditions have been described since the time of Hippocrates. The terms " septicemia " and " blood poisoning " refer to their microorganisms or toxins in the blood and are no longer commonly used.
Video Sepsis
Signs and symptoms
In addition to the symptoms associated with provoking causes, sepsis is often associated with fever, low body temperature, rapid breathing, increased heart rate, confusion, and edema. Early signs are rapid heartbeat, decreased urination, and high blood sugar. The signs of established sepsis include confusion, metabolic acidosis (which may be accompanied by faster breathing and cause respiratory alkalosis), low blood pressure due to decreased systemic vascular resistance, higher cardiac output, and blood coagulation dysfunction (where clotting may causing organ failure).
A drop in blood pressure seen in sepsis can cause shock. This can cause dizziness. Severe bruising or bleeding may occur.
Maps Sepsis
Cause
The main sources of infection that cause sepsis are the lungs, stomach, and urinary tract. Usually, 50% of all cases of sepsis begin as an infection in the lungs. No definitive source is found in one-third to one-half of cases.
The infections that cause sepsis are usually bacteria, but may be fungi or viruses. Gram-positive bacteria were the leading cause of sepsis before the introduction of antibiotics in the 1950s. After the introduction of antibiotics, gram-negative bacteria became the dominant cause of sepsis from the 1960s to the 1980s. After the 1980s, gram-positive bacteria, most commonly staphylococci, were thought to account for more than 50% of cases of sepsis. Other commonly involved bacteria include Streptococcus pyogenes , Escherichia coli , Pseudomonas aeruginosa , and Klebsiella species. Fungal sepsis accounts for about 5% of severe sepsis and septic shock cases; the most common cause of fungal sepsis is infection by Candida yeast species, nosocomial infections are often obtained in the hospital.
Diagnosis
Early diagnosis is needed to manage sepsis well, because rapid therapy initiation is the key to reducing deaths due to severe sepsis. Some hospitals use warnings generated from electronic health records to bring attention to potential cases as early as possible.
Within the first three hours of sepsis suspicion, diagnostic studies should include white blood cell counts, serum lactate measurements, and appropriate cultures before starting antibiotics, so far do not delay their use for more than 45 minutes. To identify the causative organism (s), at least two sets of blood cultures using bottles with media for aerobic and anaerobic organisms should be obtained, with at least one drawn through the skin and one drawn through each vascular access device (such as IV catheter) in place over 48 hours. Bacteria present in the blood is only about 30% of cases. Another possible detection method is the polymerase chain reaction. If other sources of infection are suspected, the culture of these sources, such as urine, cerebrospinal fluid, wounds, or respiratory secretions, should also be obtained, as long as it does not delay the use of antibiotics.
Within six hours, if blood pressure remained low despite initial fluid resuscitation of 30 ml/kg, or if the initial lactate> 4 mmol/l (36 mg/dl), central venous pressure and central venous oxygen saturation should be measured. The lactate should be measured again if the initial lactate increases. The evidence for the point of lactate measurement over the usual measurement method, however, is poor.
Within twelve hours, it is important to diagnose or exclude any source of infection requiring emerging source control, such as soft necrotizing soft tissue infection, infections that cause inflammation of the abdominal cavity, bile duct infection, or intestinal infarction. Punched internal organs (free air on abdominal x-rays or CT scans), abnormal chest x-rays consistent with pneumonia (with focal blurring), or petechiae, purpura, or fulminant purpura may be evidence of infection.
Definition
Previously, SIRS criteria have been used to determine sepsis. If the SIRS criterion is negative, it is highly unlikely that the person has sepsis; if positive, there is only a moderate chance that the person is having sepsis. According to SIRS, there are different levels of sepsis: sepsis, severe sepsis, and septic shock. The definition of SIRS is shown below:
- SIRS is the presence of two or more of the following: abnormal body temperature, heart rate, respiratory rate, or blood gas, and the number of white blood cells.
- Sepsis is defined as SIRS in response to the infection process.
- severe sepsis is defined as sepsis with organ dysfunction caused by sepsis or tissue hypoperfusion (manifests as hypotension, increased lactate, or decreased urine output).
- Septic shock is severe sepsis plus persistent low blood pressure, despite intravenous fluid administration.
By 2016, a new consensus is reached to replace screening by systemic inflammatory response syndrome (SIRS) with qSOFA. However, the American College of Chest Physicians (CHEST) voiced concerns that qSOFA and SOFA criteria could lead to delays in the diagnosis of serious infections, leading to delayed treatment. Although the SIRS criteria can be overly sensitive and not specific enough to identify sepsis, SOFA also has its own limitations and is not intended to replace the SIRS definition. qSOFA has also been found to be less sensitive although very specific for the risk of death with SIRS may be better for screening.
End-organ dysfunction
Examples of end-organ dysfunction include the following:
- Lung: acute respiratory distress syndrome (ARDS) (PaO 2 /VIO 2 & lt; 300)
- Brain: symptoms of encephalopathy include agitation, confusion, coma; Causes may include ischemia, bleeding, clot formation in small blood vessels, microabses, multifocal leukoencephalopathy necrotizing
- Liver: synthetic protein function disorder manifests acute as a progressive disorder of blood clotting due to inability to synthesize clotting factors and impaired metabolic function causing bilirubin metabolism disturbed, resulting in unconjugated serum bilirubin levels increased
- Kidney: low urine output or no urine output, electrolyte abnormality, or excess volume
- Heart: systolic and diastolic heart failure, probably because of chemical signals that suppress myocyte function, cellular damage, manifest as troponin leakage (though not always ischemic in nature)
A more specific definition of end organ dysfunction exists for SIRS in pediatrics.
- Cardiovascular dysfunction (after fluid resuscitation with at least 40Ã, ml/kg crystalloid)
- hypotension with blood pressure & lt; The 5th percentile for age or systolic blood pressure & lt; 2 standard deviations below normal for age, or
- needs vasopressor, or
- the following two criteria:
- unexplained metabolic acidosis with base deficit & gt; 5 mEq/l
- lactic acidosis: lactate serum 2 times the upper limit of normal
- oliguria (urine output & lt; 0.5 ml/kg/h )
- prolonged capillary refill & gt; 5 seconds
- core for the peripheral temperature difference & gt; 3 Ã, Â ° C
- Respiratory dysfunction (in the absence of cyanotic heart disease or known chronic lung disease)
- the ratio of the arterial oxygen partial pressure to the oxygen fraction in the inspired gas (PaO 2 /FiO 2 ) & lt; 300 (definition of acute lung injury), or
- partial-pressure arterial carbon dioxide (PaCO 2 ) & gt; 65 torr (20 mmHg) above the base PaCO 2 (evidence of hypercapnic respiratory failure), or
- the additional oxygen requirement is greater than FiO 2 0.5 to maintain oxygen saturation> = 92%
- Neurological dysfunction
- Glasgow Coma Score (GCS) <= 11, or
- alter mental status with GCS decrease of 3 or more points to someone with developmental delay/intellectual disability
- Hematologic dysfunction
- platelet count & lt; 80.000/mm 3 or 50% down from the maximum in chronic thrombocytopenic, or
- international normalization ratio (INR) & gt; 2
- Disseminated intravascular coagulation
- Kidney dysfunction
- serum creatinine> = 2 times the upper limit of normal for age or a 2-fold increase in early creatinine in people with chronic kidney disease
- Liver dysfunction (applicable only for infant & gt; 1 month)
- total serum bilirubin> = 4 mg/dl, or
- alanine aminotransferase (ALT)> = 2 times the upper limit of normal
The definition of consensus, however, continues to grow, with the latest expanding list of signs and symptoms of sepsis to reflect a clinical bedside experience.
Biomarkers
A review of 2013 concluded moderate quality evidence exists to support the use of procalcinonin levels as a method for distinguishing sepsis from non-infectious SIRS causes. The same review found the test sensitivity to be 77% and the specificity to 79%. The authors suggest that procalcinonin may serve as a useful diagnostic marker for sepsis, but warns that its level alone can not definitively make the diagnosis. A systematic review in 2012 found that the type-active plasminogen receptor urokinase (SuPAR) is a non-specific, nonspecific inflammatory marker and does not accurately diagnose sepsis. This same review concludes, however, that SuPAR has a prognostic value, as higher levels of SuPAR are associated with increased mortality in those with sepsis.
Differential diagnosis
Differential diagnosis for wide sepsis and should examine (to exclude) noninfectious conditions that may cause systemic signs of SIRS: alcohol termination, acute pancreatitis, burns, pulmonary embolism, thyrotoxicosis, anaphylaxis, adrenal insufficiency, and neurogenic shock. Hyperinflammatory syndromes such as hemophagocytic lymphohistiocytosis (HLH) may have similar symptoms and should also be included in the differential diagnosis.
Neonatal sepsis
In general clinical use, neonatal sepsis refers to bacterial bloodstream infection in the first month of life, such as meningitis, pneumonia, pyelonephritis, or gastroenteritis, but neonatal sepsis may also be caused by fungal, viral, or parasitic infections. Criteria with regard to hemodynamic compromise or respiratory failure are useless because they are late in attendance for intervention.
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Pathophysiology
Sepsis is caused by a combination of factors associated with certain attacker pathogens and the host's immune system status. The early phase of sepsis characterized by excessive inflammation (sometimes resulting in cytokine storms) may be followed by periods of prolonged decline in immune system function. Any of these phases can be fatal. On the other hand, systemic inflammatory response syndrome (SIRS) occurs in people without the presence of infection, for example, in those with burns, polytrauma, or the initial state of pancreatitis and chemical pneumonitis. However, sepsis also causes a similar response to SIRS.
Microbial Factors
Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune evasion, and disease formation in the host. Sepsis caused by gram negative bacteria is thought to be largely due to host responses to lipid lipopolysaccharide components, also called endotoxins. Sepsis caused by gram-positive bacteria can occur as a result of the immunological response to the cell wall of lipoteikoid acid. Exotoxins of bacteria that act as superantigens can also cause sepsis. Superantigens simultaneously bind to major histocompatibility complexes and T-cell receptors in the absence of antigen presentation. This forced receptor interaction induces the production of pro-inflammatory (cytokine) chemical signals by T-cells.
There are a number of microbial factors that can cause a typical septic inflammatory cascade. The offending pathogen is recognized by the molecular pattern associated with the pathogen (PAMP). Examples of PAMP include lipopolysaccharide and flagellin in gram-negative bacteria, muramyl dipeptide in peptidoglycan from gram-positive cell wall, and CpG bacterial DNA. This PAMP is recognized by pattern recognition receptors (PRRs) of the innate immune system, which may be membrane-bound or cytosolic. There are four families of PRRs: toll-like receptors, C-type lectin receptors, NOD-like receptors, and RIG-I-like receptors. Always, the PAMP and PRR associations will cause a series of intracellular signal cascades. Consequently, transcription factors such as nuclear factor-kappa B and protein-1 activator, will regulate the expression of pro-inflammatory and anti-inflammatory cytokines.
Host factors
After detecting the microbial antigen, the host systemic immune system is activated. Immune cells not only recognize PAMP, but also molecular patterns of damage (DAMP) from damaged tissue. Uncontrolled immune responses are then activated because the leukocytes are not recruited to certain infectious sites, but they are recruited throughout the body. Then, the state of immunosuppression occurs when proinflammatory T helper cell 1 (TH1) shifts to TH2, mediated by interleukin 10, known as "compensatory anti-inflammatory response syndrome". Apoptosis (cell death) of lymphocytes further exacerbates immunosuppression. Furthermore, multiple organ failure occurs because the tissue can not use oxygen efficiently because of inhibition of cytochrome c oxidase.
Inflammatory responses cause multiple organ dysfunction syndromes through various mechanisms as described below. Increased permeability of the lung vessels leads to leaking of fluid to the alveoli, leading to pulmonary edema and acute respiratory distress syndrome (ARDS). Impaired utilization of oxygen in the liver disrupts the transport of bile salts, causing jaundice (yellowish discoloration of the skin). In the kidneys, insufficient oxygenation results in tubular epithelial tubular injury (from cells lining the renal tubules), and thereby causing acute kidney injury (AKI). Meanwhile, in the human heart, impaired calcium transport, and low production of adenosine triphosphate (ATP), may cause myocardial depression, reduce cardiac contractility and lead to heart failure. In the digestive tract, increased permeability of the mucosa changes the microflora, causing mucosal bleeding and paralytic ileus. In the central nervous system, direct damage to brain cells and neurotransmission disorders causes a change in mental status. Cytokines such as tumor necrosis factor, interleukin 1, and interleukin 6 may activate the procoagulant factor in cells lining the blood vessels, causing endothelial damage. The damaged endothelial surface inhibits anticoagulant properties and increases antifibrinolysis, which can lead to intravascular clotting, blood clot formation in small blood vessels, and multiple organ failure.
The low blood pressure seen in those with sepsis is the result of many processes, including the excessive production of chemicals that dilate blood vessels such as nitric oxide, lack of chemicals that constrict blood vessels such as vasopressin, and activation of the ATP-sensitive potassium channel.. In those with severe sepsis and septic shock, this sequence of events leads to a type of circulatory shock known as distributive shock.
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Management
Early recognition and focused management can improve outcomes in sepsis. Current professional recommendations include a number of actions ("bundles") to be followed as soon as possible after diagnosis. In the first three hours a person with sepsis should have received antibiotics and, intravenous fluids if there is evidence of either low blood pressure or other evidence for inadequate blood supply to the organs (as evidenced by elevated levels of lactate); blood cultures should also be obtained in this period of time. After six hours, blood pressure should be adequate, close monitoring of blood pressure and blood supply to organs should be done, and lactate should be measured again if initially, it is removed. The related package, "Sepsis Six", is being used extensively in the UK; this requires the administration of antibiotics within an hour of recognition, blood cultures, lactate and hemoglobin determination, monitoring of urine output, high flow oxygen, and intravenous fluids.
Regardless of the administration of fluids and antibiotics on a timely basis, sepsis management also involves surgical drainage from the collection of infected fluids and proper support for organ dysfunction. These may include hemodialysis in renal failure, mechanical ventilation in pulmonary dysfunction, blood product transfusion, and drug and fluid therapy for circulatory failure. Ensure adequate nutrition - preferably with enteral feeding, but if necessary, with parenteral nutrition - important during prolonged illness. Medications to prevent deep venous thrombosis and gastric ulcers may also be used.
Antibiotics
Two sets of blood cultures (aerobic and anaerobic) should be taken without delaying antibiotic initiation. Cultures from other sites such as respiratory secretions, urine, wounds, cerebrospinal fluid, and catheter insertion sites (in-situ over 48 hours) may be taken if infection from these sites is suspected. In severe sepsis and septic shock, broad-spectrum antibiotics (usually two, wide-acting antibiotics-wide, or broad-spectrum carbapenem combined with fluoroquinolones, macrolides, or aminoglycosides) are recommended. However, a combination of antibiotics is not recommended for the treatment of sepsis but without shock and immunocompromised people unless this combination is used to extend anti-bacterial activity. The choice of antibiotics is very important in determining the person's survival. Some recommend they be given within an hour to make a diagnosis, stating that for each hour of delay in antibiotic administration, there is a 6% increase in mortality. The others found no benefit with the initial administration.
Several factors determine the most appropriate choice for an initial antibiotic regimen. These factors include local patterns of bacterial susceptibility to antibiotics, whether the infection is considered a hospital or acquired infection, and which organ systems are suspected of being infected. Antibiotic regimens should be reassessed daily and narrowed if appropriate. The duration of treatment is usually 7-10 days with the type of antibiotic used is directed by cultural results. If the culture results are negative, antibiotics should be decreased according to a person's clinical response or discontinued altogether if the infection is not present to reduce the likelihood that the person is infected with some drug resistance organisms. In the case of high-risk persons infected with drug resistance organisms such as Pseudomonas aeruginosa , Acinetobacter baumannii , the addition of antibiotics specific to gram negative organisms is recommended. For Methicillin-resistant Staphylococcus aureus (MRSA), vancomycin or teicoplanin is recommended. For Legionella infection, the addition of macrolide or fluoroquinolone is selected. If fungal infection is suspected, echinocandin, such as caspofungin or micafungin, is selected for people with severe sepsis, followed by triazole (fluconazole and itraconazole) for less sick people. Long-term antibiotic administration is not recommended in people who have SIRS without the origin of infection such as acute pancreatitis and burns unless sepsis is suspected.
The daily dose of aminoglycosides is sufficient to achieve peak plasma concentrations for clinical response without renal toxicity. Meanwhile, for antibiotics with low volume distribution (vancomycin, teicoplanin, colistin), a charge dose is required to achieve an adequate therapeutic level to fight infection. A frequent infusion of beta-lactam antibiotics without exceeding the total daily dose will help to keep antibiotic levels above the minimum inhibitory concentration (MIC), thus providing a better clinical response. Providing continuous beta-lactam antibiotics may be better than giving them intermittently. Access to therapeutic drug monitoring is important to ensure adequate levels of drug therapy while at the same time preventing the drug from reaching toxic levels.
Intravenous fluid
The Sepsis Defensive Campaign has recommended 30 ml/kg of fluid to be administered to adults in the first 3 hours followed by fluid titration according to blood pressure, urine output, respiratory rate, and oxygen saturation with target mean arterial pressure (MAP) of 65 mmHg. In children, the initial amount of 20ml/kg is reasonable because of shock. In cases of severe sepsis and septic shock where the central venous catheter is used to measure blood pressure dynamically, fluids should be administered until the central venous pressure (CVP) reaches 8-12mmHg. Once this goal is met, the central venous oxygen saturation (ScvO2), ie, the oxygen saturation of the venous blood as it returns to the heart as measured in the vena cava, is optimized. If ScvO2 is less than 70%, blood may be given to achieve 10 g/dL hemoglobin and then inotropic is added until ScvO2 is optimized. In those with acute respiratory distress syndrome (ARDS) and sufficient blood tissue fluid, more fluids should be administered with caution.
Crystalloid is recommended as the preferred fluid for resuscitation. Albumin can be used if large amounts of crystalloid are required for resuscitation. The crystalloid and albumin solutions are better than other liquids (such as hydroxyethyl starch) in terms of the risk of death. Starch also carries an increased risk of acute kidney injury, and the need for blood transfusion. Various colloidal solutions (such as modified gelatin) do not bring advantages beyond crystalloids. Albumin also appears to be useless compared to crystalloids.
Blood products
The Defensive Sepsis campaign recommends red blood cell transfusion package for hemoglobin levels below 70 g/L if no myocardial ischemia, hypoxemia, or acute hemorrhage are present. In a 2014 trial, blood transfusions to keep hemoglobin targets above 70 or 90 g/L made no difference to survival rates; meanwhile, those with lower transfusion thresholds receive fewer total transfusions. Erythropoietin is not recommended in the treatment of anemia with septic shock because it can lead to blood clots. Frozen fresh plasma transfusions typically do not correct the underlying clotting abnormalities prior to the planned surgical procedure. However, platelet transfusion is recommended for the following platelet counts (10 ÃÆ'â € Å" 10 9 /L) without risk of bleeding, or (20 ÃÆ'â € "10 9 /L) with a high risk of bleeding, or (50 ÃÆ'â € "10 9 /L) with active bleeding, before planned surgery or invasive procedures. Immunoglobulin IV is not recommended because its beneficial effects are uncertain. The monoclonal and polyclonal preparations of intravenous immunoglobulin (IVIG) do not decrease mortality rates in newborns and adults with sepsis. The evidence for the use of IgM-enriched polyclonal preparations from IVIG is inconsistent. On the other hand, the use of antithrombin to treat disseminated intravascular coagulation is also useless. Meanwhile, blood purification techniques (such as hemoperfusion, plasma filtration, and plasma filtration filtration) to remove inflammatory mediators and bacterial toxins from the blood also show no survival benefit for septic shock.
Vasopressor
If a person has enough fluid resuscitation but the mean arterial pressure is not greater than 65 mmHg, a vasopressor is recommended. Norepinephrine (noradrenaline) is recommended as a starting option.
Norepinephrine increases blood pressure through the effects of vasoconstriction, with little effect on stroke volume and heart rate. If a single vasopressor is not enough to raise blood pressure, epinephrine (adrenaline) or vasopressin may be added. However, one of the side effects of adrenaline is to reduce blood flow to the abdominal organs and can lead to increased levels of lactate. Vasopressin may be used in septic shock because studies have shown that there is a relative lack of vasopressin when shock continues for 24 to 48 hours. However, vasopressin reduces blood flow to the heart, fingers, and abdominal organs, resulting in a lack of oxygen supply to these tissues. Dopamine is not usually recommended. Although dopamine is useful for increasing the volume of heart stroke, it causes a more abnormal heart rhythm than norepinephrine and also has an immunosuppressive effect. Dopamine is not shown to have protective properties in the kidneys. Dobutamine may be used if poor cardiac function or insufficient blood flow despite sufficient fluid and blood pressure.
Steroids
The use of steroids in sepsis is controversial. The study did not give a clear picture of whether and when glucocorticoids should be used. The Separate Sepsis Campaign 2016 recommends its use in patients with septic shock if intravenous fluids and vasopressors are able to stabilize one's cardiovascular function. Low-dose hydrocortisone is only used if intravenous fluids and vasopressors are unable to adequately treat septic shock. The 2015 Cochrane review found evidence of low-quality benefits.
During critical illness, the state of adrenal insufficiency and tissue resistance to corticosteroids may occur. This has been called corticosteroid-related insufficiency of critical illness. Treatment with corticosteroids may be most useful in patients with septic shock and early baseline ARDS, whereas their role in others such as those with severe pancreatitis or pneumonia is unclear. However, the proper way to determine corticosteroid insufficiency is still problematic. It should be suspected in those who are less responsive to resuscitation with fluids and vasopressors. Both ACTH stimulation testing and random cortisol levels are recommended to confirm the diagnosis. The method of discontinuation of glucocorticoid drugs is variable, and it is unclear whether the drugs should be reduced gradually or stopped abruptly. However, the 2016 Defensive Sepsis Campaign is recommended for tapered steroids when vasopressors are no longer needed.
Anesthesia
Target volume of 6 mL/kg of predicted body weight (PBW) and plateau pressure less than 30 cm H 2 O is recommended for those who require ventilation due to severe ARDS caused by sepsis. High positive end-expiratory pressure (PEEP) is recommended for moderate to severe ARDS in sepsis because it opens more lung units for oxygen exchange. Recruitment maneuvers may be required for severe ARDS by briefly increasing transpulmonary pressure. It is recommended that the head of the bed be raised if possible to improve the ventilation. However ,? 2 adrenergic receptor agonists are not recommended to treat ARDS as it can reduce survival rates and precipitate abnormal heart rhythms. A spontaneous breathing experiment using continuous positive air pressure (CPAP), T piece, or inspiration pressure augmentation can help in reducing ventilation duration. Minimizing intermittent or continuous sedation is helpful in reducing the duration of mechanical ventilation.
General anesthesia is recommended for people with sepsis requiring surgical procedures to remove infective sources. Usually inhalation and intravenous anesthetics are used. The requirements for anesthesia can be reduced in sepsis. Inhalation anesthetics can reduce the level of proinflammatory cytokines, alter the adhesion and proliferation of leukocytes, induce apoptosis (cell death) of lymphocytes, possibly with toxic effects on mitochondrial function. Although etomidate has minimal effects on the cardiovascular system, it is often not recommended as a cure for intubation in this situation because it can lead to poor adrenal function and an increased risk of death. A small proportion of the available evidence, however, has not found a change in the risk of death with etomidate.
Paralytic agents should be avoided unless ARDS is suspected.
Goal directed therapies
Goal-directed early therapy (EGDT) is an approach to the management of severe sepsis during the initial 6 hours after diagnosis. This is a step-wise approach, with the goal of physiologically optimizing cardiac preload, afterload, and contractility. This includes early antibiotics. EGDT also involves monitoring of hemodynamic parameters and specific interventions to achieve key resuscitation targets that include maintaining central venous pressure between 8-12 mmHg, mean arterial pressure between 65-90 mmHg, central venous oxygen saturation (ScvO 2 ) is greater than 70% and urine output is greater than 0.5 ml/kg/hr. The goal is to optimize oxygen delivery to the network and achieve a balance between systemic delivery and demand for oxygen. The exact decrease in lactate serum may be equivalent to ScvO 2 and more easily obtained.
In the initial trial, targeted therapies of the initial goal were found to reduce mortality from 46.5% to 30.5% in those with sepsis, and the Defensive Sepsis Campus has recommended its use. However, three larger randomized controlled trials (ProCESS, ARISE, and ProMISe), did not show a 90-day mortality benefit from initial, directed goal therapy when compared with standard therapy in severe sepsis. It is possible that some parts of EGDT are more important than others. After this trial the use of EGDT is still considered fair.
Newborns
Neonatal sepsis can be difficult to diagnose because newborns may be asymptomatic. If newborns show signs and symptoms that indicate sepsis, antibiotics are immediately initiated and altered to target specific organisms identified with diagnostic tests or discontinued after the cause of infection for symptoms has been ruled out.
More
Treating fevers in people with sepsis does not affect outcomes.
The Cochrane Review 2012 concludes that N-acetylcysteine ​​does not reduce mortality in those with SIRS or sepsis and may even be dangerous.
Recombinant activated C proteins (drotrecogin alpha) were initially introduced for severe sepsis (as identified by high APACHE II scores), in which it was thought to provide survival benefits. However, subsequent research has shown that increased side effects - the risk of bleeding in particular - and not decreasing mortality. It was removed from sales in 2011. Another drug known as erytoran also has not shown any benefits.
In those with high blood sugar levels, insulin to lower it to 7.8-10 mmol/L (140-180 mg/dL) is recommended with a lower level of potentially worsening outcome. Glucose levels taken from capillary blood should be interpreted with caution because such measurements may be inaccurate. If a person has an arterial catheter, arterial blood is recommended for a blood glucose test.
Intermittent or continuous renal replacement therapy may be used if indicated. However, sodium bicarbonate is not recommended for someone with lactic acidosis after hypoperfusion. Low molecular weight heparin (LMWH), unfractionated heparin (UFH), and mechanical prophylaxis with intermittent pneumatic compression tools are recommended for everyone with sepsis at the risk of moderate to high venous thromboembolism. Prevention of stress ulcers with proton-pump inhibitors (PPIs) and H2 antagonists is useful in a person with risk factors for developing upper gastrointestinal bleeding (UGIB) such as mechanical ventilation for more than 48 hours, coagulation disorders, liver disease, and renal replacement. therapy. Achieving full or partial enteral intake (delivery of nutrients through the feeding tube) is chosen as the best approach to provide nutrition for someone who is contraindicated for oral intake or can not tolerate orally within the first seven days of sepsis when compared with intravenous nutrition.. However, omega-3 fatty acids are not recommended as an immune supplement for someone with sepsis or septic shock. Use of prokinetic agents such as metoclopramide, domperidone, and erythromycin is recommended for those who are septic and can not tolerate enteral feeding. However, these agents can trigger an extension of the QT interval and consequently provoke ventricular arrhythmias such as torsades de pointes. Use of prokinetic agents should be reassessed daily and stopped if no longer indicated.
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Prognosis
Approximately 20-35% of people with severe sepsis and 30-70% of people with septic shock die. Lactate is a useful method for determining prognosis with those with levels greater than 4 mmol/L with 40% mortality and those with levels less than 2 mmol/L having a mortality of less than 15%.
There are a number of prognostic stratification systems such as APACHE II and Death in Sepsis Emergency Department. APACHE II factors in a person's age, underlying condition, and various physiological variables to produce an estimated risk of death from severe sepsis. From individual covariates, the severity of the underlying illness greatly affects the risk of death. Septic shock is also a strong predictor of short and long term mortality. Similar case fatality rates for culture-positive and culture-negative sepsis weight. Mortality figures in Darsi Emergency Department (MEDS) are simpler and more useful in emergency settings.
Some people may experience severe long-term cognitive decline after severe sepsis episodes, but the absence of basic neuropsychological data in most people with sepsis makes this incident difficult to measure or study.
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Epidemiology
Sepsis causes millions of global deaths each year and is the most common cause of death in hospitalized people. Incidence of sepsis worldwide is estimated to reach 18 million cases per year. In the United States sepsis affects about 3 out of 1,000 people, and severe sepsis contributes more than 200,000 deaths per year.
Sepsis occurs in 1-2% of all hospitalizations and accounts for 25% of ICU bed utilization. Because it is rarely reported as a major diagnosis (often a complication of cancer or other disease), incidence, mortality, and morbidity rates of sepsis tend to be underestimated. A study by the Research and Quality Health Agency (AHRQ) of selected countries found that there were about 651 fixed hospitals per 100,000 population with a septic diagnosis in 2010. This is the second leading cause of death in non-coronary intensive care units. (ICU) and the tenth most common cause of death (the first is heart disease). Children under 12 months and the elderly have the highest incidence of severe sepsis. Among US patients who had some sepsis hospital admissions in 2010, those who were repatriated to skilled or long-term care facilities after initial hospitalization were more likely to be re-admitted than those who were repatriated to other forms of treatment. A study from 18 United States found that, among Medicare patients in 2011, sepsis was the second most common reason for re-enrollment in 30 days.
Some medical conditions increase a person's susceptibility to infection and develop sepsis. Common risk factors for sepsis include age (especially very young and old); conditions that weaken the immune system such as cancer, diabetes, or the absence of the spleen; and major trauma and burns.
From 1979 to 2000, data from the US National Hospital Expenditure Survey showed that the incidence of sepsis increased by fourfold to 240 cases per 100,000 population with a higher incidence in men when compared with women. Over the same time span, hospital mortality rates were reduced from 28% to 18%. However, according to the national inpatient sample from the United States, the incidence of severe sepsis increased from 200 per 10,000 inhabitants in 2003 to 300 cases in 2007 for populations over the age of 18 years. The incidence rate is very high among infants with an incidence of 500 cases per 100,000 population. Deaths associated with sepsis increase with age from less than 10% in the 3 to 5 year age group to 60% in the sixth decade of life. Increasing the average age of the population, more people with chronic disease, on immunosuppressive drugs, and an increase in the number of invasive procedures performed have led to an increase in sepsis levels.
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History
Terms "?????" (sepsis) was introduced by Hippocrates in the fourth century BC, and that means the process of decomposition or decomposition of organic matter. In the eleventh century, Avicenna used the term "blood decay" for diseases associated with severe purulent processes. Although severe systemic toxicity has been observed, it was only in the 19th century that a particular term - sepsis - was used for this condition.
The term "septicemia", also spelled "septicemia", and "blood poisoning" refers to microorganisms or toxins in the blood and are no longer commonly used. The modern term for this is bacteremia.
At the end of the 19th century it was widely believed that microbes produce substances that can injure mammary mothers and that the dissolved toxins released during infection cause fever and shock commonly occur during severe infections. Pfeiffer coined the term endotoxin in the early 20th century to show the pyogenic principle associated with Vibrio cholerae . It is soon realized that endotoxin is expressed by most and possibly all gram-negative bacteria. The character of enteric endotoxin lipopolysaccharides was described in 1944 by Shear. The molecular character of this material is determined by Luderitz et al. in 1973.
It was found in 1965 that the strain of C3H/HeJ rats was immune to endotoxin-induced shock. The genetic place for this effect is dubbed Lps . These mice were also found to be hypersanibular to infection by gram-negative bacteria. This observation was eventually linked in 1998 by the discovery of toll-like 4-receptor gene (TLR 4). A genetic mapping work, conducted over five years, shows that TLR4 is the only prospective locus within the LPS critical area; this strongly implies that mutations in TLR4 must take into account the phenotype of lipopolysaccharide resistance. Defects in the TLR4 gene that cause endotoxin-resistant phenotypes are found to be caused by mutations in the cytoplasm.
Controversy occurred in the scientific community over the use of a mouse model in sepsis research in 2013, when scientists published an overview of the immune system of mice compared to the human immune system, and showed that at the system level, the two worked very differently; the authors note that since the date of their article more than 150 sepsis clinical trials have been conducted on humans, almost all of them backed up by promising data on mice, and that all failed. The authors call for abandoning the use of mouse models in sepsis research; others rejected it but called for more caution in interpreting the results of rat studies, and more carefully designed preclinical studies. One approach is to rely more on studying biopsy and clinical data from people who have had sepsis, to try to identify biomarkers and drug targets for intervention.
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Society and culture
Economy
Sepsis is the most expensive condition hospitalized in the United States in 2013, with an overall cost of $ 23.6 billion for nearly 1.3 million hospitalizations. The cost for sepsis hospital has more than quadrupled since 1997 with an annual increase of 11.5 percent. With payers, it is the most expensive condition billed to Medicare and the uninsured, the second most expensive being billed to Medicaid, and the fourth most expensive being billed to private insurers.
Education
A major international collaboration entitled "Sepsis Surviving Campaign" was founded in 2002 to educate people about sepsis and improve patient outcomes with sepsis. The campaign has published an evidence-based review of management strategies for severe sepsis, with the aim of publishing a full set of guidelines in subsequent years.
Sepsis Alliance is a charitable organization created to raise awareness of sepsis among the general public and health care professionals.
src: www.bloodjournal.org
Note
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References
src: ii4change.com
External links
- Sepsis in Curlie (based on DMOZ)
- SIRS, Sepsis, and Septic Shock
Source of the article : Wikipedia
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