Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, a critical reduction of tissue perfusion occurs. It may involve the acute failure of many organ systems, including the lungs, kidneys and liver, come. Common causes in immunocompetent patients depict various types of gram-positive and gram-negative bacteria. In immunocompromised patients unusual bacterial and Fungusspezies can be a cause. The signs include fever, hypotension, oliguria and impaired consciousness. The diagnosis is mainly clinically related to culture smears that show the infection. Early detection and treatment are crucial. Treatment includes aggressive hydration, administration of antibiotics, surgical excision of infected or necrotic tissue and drainage of pus and supportive measures.

Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, a critical reduction of tissue perfusion occurs. It may involve the acute failure of many organ systems, including the lungs, kidneys and liver, come. Common causes in immunocompetent patients depict various types of gram-positive and gram-negative bacteria. In immunocompromised patients unusual bacterial and Fungusspezies can be a cause. The signs include fever, hypotension, oliguria and impaired consciousness. The diagnosis is mainly clinically related to culture smears that show the infection. Early detection and treatment are crucial. Treatment includes aggressive hydration, administration of antibiotics, surgical excision of infected or necrotic tissue and drainage of pus and supportive measures.

(Shock). Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, a critical reduction of tissue perfusion occurs. It may involve the acute failure of many organ systems, including the lungs, kidneys and liver, come. Common causes in immunocompetent patients depict various types of gram-positive and gram-negative bacteria. In immunocompromised patients unusual bacterial and Fungusspezies can be a cause. The signs include fever, hypotension, oliguria and impaired consciousness. The diagnosis is mainly clinically related to culture smears that show the infection. Early detection and treatment are crucial. Treatment includes aggressive hydration, administration of antibiotics, surgical excision of infected or necrotic tissue and drainage of pus and supportive measures. Sepsis represents a spectrum of diseases associated with mortality risk, varying from moderately (eg., 10%) to significantly (z. B. 40%), depending on various pathogens and host factors, together with the relevance of the detection and provision of a suitable treatment. EinSeptischer shock is part of a sepsis associated with a significantly increased mortality due to serious disorders of the blood circulation and / or of cell metabolism. Septic shock includes persistent hypotension (defined as the need for vasopressor to mean arterial pressure ? maintain 65 mm Hg and a serum lactate level> 18 mg / dl [2 mmol / l] despite adequate fluid resuscitation [1]). The concept of systemic inflammatory response syndrome (SIRS), defined by certain abnormalities of vital signs and laboratory results, has long been used to identify an early sepsis. However, the SIRS criteria are lacking sensitivity and specificity for increased mortality risk, which is the most important consideration for the use of such a conceptual model. The lack of specificity may be because the SIRS response often is adaptive rather than pathological. Note 1. Singer M, Deutschman CS, Seymour CW, et al: The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA 315: 801-810, 2016. In most cases, etiology septic shock of hospital germs (gram-negative bacteria or gram-positive cocci) is triggered. Often immunocompromised or chronically ill with debilitating ailments are affected. Rarely, Candida or other fungi found as causative agent. Postoperative infection (sunken or superficial) should in patients who have recently had surgery, be considered as the cause of septic shock considered. An unusual special form of the shock caused by staphylococcus or streptococcal toxins. In these cases, one speaks of the toxic shock syndrome. Septic shock occurs most often in newborns (neonatal sepsis) and in elderly people and pregnant women. Predisposing factors may be diabetes mellitus cirrhosis leukopenia (mainly associated with cancer or treatment with cytostatic drugs) Invasive devices (including endotracheal tubes, vascular or urinary catheters, drains and other foreign matter) before treatment with antibiotics or corticosteroids Preferred entry sites of infection are lungs, urinary system dissipating, the gallbladder and gastrointestinal tract. Pathophysiology The pathogenesis of septic shock is currently not fully understood. An inflammatory stimulus (eg. As a bacterial toxin) triggers the production of proinflammatory mediators. These include tumor necrosis factor and IL-1. These cytokines cause neutrophil-endothelial cell adhesion, activate the coagulation system and cause micro-thrombosis. Numerous other mediators are released. These include leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2. These substances counteract anti-inflammatory mediators such as IL-4 and IL-10, which in turn result in a negative feedback mechanism. At first, it leads to dilation of arteries and arterioles, and the decrease in peripheral vascular resistance, cardiac output, however, typically increases. This phase is also called “hot shock”. Later, the cardiac output usually decreases the blood pressure drops (with or without an increase in peripheral resistance), and the typical features of shock appear. Even in the phase of increased cardiac output lead vasoactive mediators to bypass the capillary exchange vessels (distributive defect). The low capillary flow as a result of this shunt phenomena diminished along with the Kapillarobstruktion by microembolization the O2 supply and worsens the disposal of CO2 and other waste materials. The decreased perfusion leads to dysfunction and failure of one or more organs. These include kidney, lung, liver, central nervous system and heart. To coagulopathy occurs by intravascular coagulation with consumption of essential clotting factors as well as by excessive reactive fibrinolysis. In most cases there is a combination of both processes. Symptoms and signs The symptoms and discomfort of sepsis can be very subtle and easily with signs of other diseases (eg. As delirium, primary heart failure, pulmonary embolism) are confused, especially in postoperative patients. The sepsis patient typically has a fever, tachycardia, diaphoresis and tachypnea with normal blood pressure. Other signs of the causative infection may also be present. Once sepsis worsens or septic shock develops, confusion and impaired vigilance may be early clinical indications, especially in the elderly and very young patients. It comes to blood pressure. Nevertheless, the skin still feels paradoxically warm. Later, the extremities are cold and pale, with peripheral cyanosis and mottling. By organ failure further clinical manifestations and symptoms are formed according to the affected organ system out (z. B. oliguria, dyspnea). Diagnosis Clinical manifestations monitoring of blood pressure, heart rate and O2 blood count with differential electrolytic image and creatinine, lactate measurement of the invasive central nervous pressure (CVP), PaO 2 and central venous O2 saturation (ScvO2) smears of blood, urine and other potential sites of infection, including wounds in surgical sepsis patients need in patients with a known infection then be assumed when it comes to systemic inflammation or organ dysfunction. It should also be sought in a patient with otherwise unexplained symptoms of systemic inflammation after an infection in the past. Other tests such as urinalysis, urine culture (v. A. In catheterized patients), blood cultures and cultures of other suspect body fluids should be created. In patients with suspected surgical or hidden causes of sepsis ultrasonography, CT or MRI may be necessary depending on the suspected cause. The blood levels of C-reactive protein and procalcitonin are often elevated in severe sepsis and may facilitate the diagnosis. However, these parameters are not specific. Finally, the diagnosis remains a clinical. For other causes of shock (eg. As hypovolemia, myocardial infarction) should be excluded by history, physical examination, electrocardiogram and serum parameters. Even in the absence of myocardial infarction, it may by hypoperfusion, which is triggered by the sepsis, cause ischemia in the EKG as non-specific ST-segment and T-wave changes, T wave inversion or supraventricular and ventricular arrhythmias. It is important to recognize an organ dysfunction as early as possible. There were a number of scoring systems developed, but the SOFA score ( “sequential organ failure assessment score”) and the fast SOFA score (qSOFA) have been validated in terms of the mortality risk and are relatively easy to use. The qSOFA criteria to identify patients who are more clinical and should have laboratory tests (all three criteria must be present): respiratory rate ? 22 / min Changed mindset Systolic blood pressure ? 100 mmHg The SOFA score is a little more robust, but requires laboratory tests (see table: result of the evaluation of sequential organ failure (SOFA)). Result of the evaluation of sequential organ failure (SOFA) Parameter Score: 0 Score: 1 Score: 2 Score 3 Score: 4 Pao2F? IO2 ? 400 mm Hg (53.3 kPa) <400 mm Hg (53.3 kPa) <300 mm Hg (40 kPa) <200 mm Hg (26.7 kPa) to assist breathing <100 mm Hg (13.3 kPa) with respiratory support platelet ? 150 x 103 / ul <150 <100 <50 <20 bilirubin ? 1.2 mg / dL (20 .mu.mol / l) 1.2-1.9 mg / dl (20-32 .mu.mol / l) 2.0- 5.9 mg / dl (33-101 micromol / l) 6.0 to 11.9 mg / dl (102-204 micromol / l)> 12.0 mg / dL (204 mu mol / liter) Cardiovascular MAP ? 70 mm Hg MAP <70 mm Hg dopamine <5 mcg / kg / min for ? 1 h or Each dose of dopamine dobutamine 5.1 to 15 mcg / kg / min for ? 1 h or epinephrine ? 0.1 mcg / kg / min for ? 1 h or noradrenaline ? 0.1 mcg / kg / min for ? 1 h dopamine> 15 mcg / kg / min for ? 1 h or epinephrine> 0.1 mcg / kg / min for ? 1 h or noradrenaline> 0.1 mcg / kg / min for ? 1 h Glasgow Coma Scale score * 15 points 13-14 points 10-12 points 6-9 points <6 points creatinine <1.2 mg / dL (110 mu mol / l) 1.2-1.9 mg / dl (110-170 micromol / L) 2.0 to 3.4 mg / dl (171-299 micromol / L) 3.5-4.9 mg / dl (300-400 micromol / l)> 5.0 mg / dL (440 mu mol / l) urine excretion – – – <500 ml / day of <200 ml / day * a higher score indicates a better neurologic function. FrIO2 = fractional inspired O2; kPa = kilopascals; MAP = mean arterial pressure; PaO 2 = arterial oxygen partial pressure. Adapted from Singer M, Deutschman CS, Seymour CW, et al: The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA 315: 801-810, 2016. Clinical Calculator: Glasgow Coma Scale blood count, arterial blood gases, chest x-ray view, serum electrolytes, BUN and creatinine, Pco2 and liver function tests should be investigated. Serum lactate levels, central venous O2 saturation (ScvO2) or both may be determined to guide the treatment. The white blood cell count may be reduced (<4,000 / uL) or elevated (> 15,000 / uL) and granulocytes can be as low as 20%. In the course of sepsis, the white blood cell count may be increased depending on the severity of the sepsis or of shock, of the immunological condition of the patient and etiology of the infection, or decrease. A concomitant administration of corticosteroids may increase the leukocyte count, and in this way the changes in the number of leukocytes, which are due to disease development collapse. Hyperventilation with respiratory alkalosis (low PaCO2 and rise in the price of arterial pH) can be found at an early stage, partly due to the compensatory lactic acidosis. The serum-HCO3 is usually reduced and the lactate values ??in blood and serum are elevated. In the course of further development of the shock action, the metabolic acidosis recessed, and the serum pH decreases. Early hypoxic respiratory failure resulting in reduced PaO2: FIO2 ratio and sometimes recognizable hypoxemia with PaO 2 <70 mmHg. Diffuse infiltration because of the Acute Respiratory Distress Syndrome (ARDS) can be detected on the chest x-ray. Urea and creatinine usually rise progressively as a sign of renal failure. Bilirubin and transaminases may be increased. A liver failure is rather uncommon in patients with normal liver function output. Many patients with severe sepsis develop adrenal insufficiency (normal or slightly elevated basal levels of cortisone, but in response to further stress or exogenous ACTH not rise). The adrenal function can be examined by determining the Kortisolwertes at 8:00 AM. A mirror <5 mg / dl is striking. An increase to <9 g / dl indicates a failure. Alternatively, before the levels of cortisol and are determined by injection of 250 ug of synthetic ACTH. However, the refractory septic shock no determination of cortisol levels is needed before treatment with corticosteroids is started. Hemodynamic measurements by means of central venous pulmonary artery catheter (Monitoring and analysis of intensive care patients: Procedure) can be used helpful in uncertainty concerning the form of the shock. Similarly, in cases that (l z. B.> 4-5 0.9% NaCl solution within 6-8 h) making an extended volume replacement necessary. An echocardiogram at the bedside in the ICU is a practical and non-invasive alternative method for hemodynamic monitoring. In septic shock cardiac output is increased and the peripheral vascular resistance is reduced, whereas in other types of shock the heart minute volume is usually reduced and the peripheral resistance is increased. Neither the central venous pressure (CVP) nor the pulmonary artery occlusion pressure (PAOP) is significantly altered in septic shock. This is in contrast to hypovolemic, obstructive or cardiogenic shock. Emergency sonography for investigating shock and hypotension (RUSH) video created by Hospital Procedures Consultants, www.hospitalprocedures.org. var model = {videoId: ‘3904436198001’, playerId ‘H1xmEWTatg_default’, imageUrl ‘http://f1.media.brightcove.com/8/3850378299001/3850378299001_4412182323001_vs-55c8ffd2e4b02826db66107f-672293880001.jpg?pubId=3850378299001&videoId=3904436198001′ title: ’emergency ultrasound for examination of shock and hypotension (RUSH)’, description: ‘ u003Ca id = “v38395641 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eNotfallsonographie in shock and hypotension (RUSH) includes echocardiographic methods and can be used to determine the type of shock u003c / p u003e u003c / div u003e. ‘credits’ video created by Hospital Procedures Consultants

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