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![What is Septic shock
• Septic shock is a subset of sepsis with significantly increased mortality
due to severe abnormalities of circulation and/or cellular metabolism.
• persistent hypotension
• (defined as the need for vasopressors to maintain mean arterial pressure ≥ 65
mm Hg,
• serum lactate level > 18 mg/dL [2 mmol/L] despite adequate volume
resuscitation](https://image.slidesharecdn.com/sepsis-210320053025/85/Sepsis-3-320.jpg)
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Sepsis
- 1.
- 2. What is sepsis* •Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection *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
- 3. What is Septicshock • Septic shock is a subset of sepsis with significantly increased mortality due to severe abnormalities of circulation and/or cellular metabolism. • persistent hypotension • (defined as the need for vasopressors to maintain mean arterial pressure ≥ 65 mm Hg, • serum lactate level > 18 mg/dL [2 mmol/L] despite adequate volume resuscitation
- 4. Etiology • Bacteria • Fungi •Toxins • Post operative infections
- 5. Predisposing factors • Diabetesmellitus • Cirrhosis • Leukopenia (especially that associated with cancer or treatment with cytotoxic drugs) • Invasive devices (including endotracheal tubes, vascular or urinary catheters, drainage tubes, and other foreign materials) • Prior treatment with antibiotics or corticosteroids • Common causative sites of infection include the lungs and the urinary, biliary, and gastrointestinal tracts.
- 6.
- 7. Symptoms and Signs •Early signs • Late Signs • Signs of specific organ involved
- 8. Diagnosis • Clinical manifestations •Blood pressure (BP), heart rate, and oxygen monitoring • Complete blood count (CBC) with differential, electrolyte panel and creatinine, lactate • Invasive central venous pressure (CVP), PaO2, and central venous oxygen saturation (ScvO2) readings • Cultures of blood, urine, and other potential sites of infection, including wounds in surgical patients
- 9. Search of asource of sepsis • urinalysis and urine culture (particularly in patients who have indwelling catheters), • blood cultures and cultures of other suspect body fluids. • ultrasonography, CT, or MRI • Blood levels of C-reactive protein and procalcitonin
- 10. Hypoperfusion caused bysepsis may result in ECG findings
- 11. SIRS • Patients with≥ 2 of the following criteria meet criteria for SIRS and should have further clinical and laboratory investigation: • Temperature > 38° C (100.4° F) or < 36° C 96.8° F • Heart rate > 90 beats per minute • Respiratory rate > 20 breaths per minute or PaCO2 < 32 mm Hg • White blood cell count > 12,000/mcL (12 X 109/L), < 4,000/mcL (4 X 109/L or > 10% immature (band) forms
- 12. qSOFA • Patients with≥ 2 of the following qSOFA criteria should have further clinical and laboratory investigation • Respiratory rate ≥ 22 breaths per minute • Altered mentation • Systolic blood pressure ≤ 100 mm Hg
- 13. Sequential Organ FailureAssessment Score
- 14. What investigations tobe sent • Same as in SOFA scoring • Lactic acid • Central venous oxygen saturation • WBC count
- 15. Arterial Blood Gases •Respiratory Alkalosis • Metabolic Acidosis
- 16. Multi Organ Failure •Hypoxemic respiratory failure • ARDS • Kidney • Liver • Relative Adrenal insufficiency
- 17.
- 18. Hemodynamic monitoring • CVPdoesn’t guide fluid resuscitation in septic shock. • Bedside echocardiography • Invasive hemodynamic monitoring • CVP • Cardiac output • PVR
- 19. Rapid Ultrasound forShock and Hypotension (RUSH) Examination
- 20. Pump • Contractility • Pericardialeffusion • Right ventricular dilatation
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- 22.
- 23. Prognosis • SOFA andChange in SOFA score • Decreasing, increasing • MEDS Score
- 24. MEDS score (Mortalityin ER Sepsis) • Terminal illness with possible death in 1 month (6 points) • Hypoxia or tachypnea (3 points) • Shock from sepsis (3 points) • Platelet count below 150,000 (3 points) • Granulocytic bands >5% of WBC (3 points) • Patient older than 65 years old (3 points) • Lower respiratory infection (2 points) • Patient is from a nursing home (2 points) • Mental status is altered (2 points)
- 25. Treatment • Perfusion restoredwith IV fluids and sometimes vasopressors • Oxygen support • Broad-spectrum antibiotics • Source control • Sometimes other supportive measures (eg, corticosteroids, insulin)
- 26. Patients with septicshock should be treated in an ICU The following should be monitored hourly • CVP, PAOP, or ScvO2 • Pulse oximetry • ABGs • Blood glucose, lactate, and electrolyte levels • Renal function • Urine Output
- 27. Perfusion restoration • Initially1 litre of crystilloids • 30ml/kg (basic target is restoration of effective circulatory volume) • vasopressors
- 28.
- 29. Antibiotics • After takingcultures • First dose in first hour • Empirical antibiotics • Vancomycin • Gm negative coverage
- 30.
- 31. Other supportive measures •Blood glucose control • Corticosteroids
- 32. Key Points • Sepsisand septic shock are increasingly severe clinical syndromes of life- threatening organ dysfunction caused by a dysregulated response to infection. • An important component is critical reduction in tissue perfusion, which can lead to acute failure of multiple organs, including the lungs, kidneys, and liver. • Early recognition and treatment is the key to improved survival. • Resuscitate with intravenous fluids and sometimes vasopressors titrated to optimize central venous oxygen saturation (ScvO2) and preload, and to lower serum lactate levels. • Control the source of infection by removing catheters, tubes, and infected and/or necrotic tissue and by draining abscesses. • Give empiric broad-spectrum antibiotics directed at most likely organisms and switch quickly to more specific drugs based on culture and sensitivity results.
Editor's Notes
- #5 Most cases of septic shock are caused by hospital-acquired gram-negative bacilli or gram-positive cocci and often occur in immunocompromised patients and patients with chronic and debilitating diseases. Rarely, it is caused by Candida or other fungi. A postoperative infection (deep or superficial) should be suspected as the cause of septic shock in patients who have recently had surgery. A unique, uncommon form of shock caused by staphylococcal and streptococcal toxins is called toxic shock syndrome. Septic shock occurs more often in neonates (see Neonatal Sepsis), the elderly, and pregnant women. Predisposing factors include Diabetes mellitus Cirrhosis Leukopenia (especially that associated with cancer or treatment with cytotoxic drugs) Invasive devices (including endotracheal tubes, vascular or urinary catheters, drainage tubes, and other foreign materials) Prior treatment with antibiotics or corticosteroids Common causative sites of infection include the lungs and the urinary, biliary, and gastrointestinal tracts.
- #7 The pathogenesis of septic shock is not completely understood. An inflammatory stimulus (eg, a bacterial toxin) triggers production of proinflammatory mediators, including tumor necrosis factor (TNF) and interleukin (IL)-1. These cytokines cause neutrophil–endothelial cell adhesion, activate the clotting mechanism, and generate microthrombi. They also release numerous other mediators, including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2. They are opposed by anti-inflammatory mediators, such as IL-4 and IL-10, resulting in a negative feedback mechanism. Initially, arteries and arterioles dilate, decreasing peripheral arterial resistance; cardiac output typically increases. This stage has been referred to as warm shock. Later, cardiac output may decrease, blood pressure falls (with or without an increase in peripheral resistance), and typical features of shock appear. Even in the stage of increased cardiac output, vasoactive mediators cause blood flow to bypass capillary exchange vessels (a distributive defect). Poor capillary flow resulting from this shunting, along with capillary obstruction by microthrombi, decreases delivery of oxygen and impairs removal of carbon dioxide and waste products. Decreased perfusion causes dysfunction and sometimes failure of one or more organs, including the kidneys, lungs, liver, brain, and heart. Coagulopathy may develop because of intravascular coagulation with consumption of major clotting factors, excessive fibrinolysis in reaction thereto, and more often a combination of both.
- #8 Symptoms and signs of sepsis can be subtle and often easily mistaken for manifestations of other disorders (eg, delirium, primary cardiac dysfunction, pulmonary embolism), especially in postoperative patients. With sepsis, patients typically have fever, tachycardia, diaphoresis, and tachypnea; blood pressure remains normal. Other signs of the causative infection may be present. As sepsis worsens or septic shock develops, an early sign, particularly in older people or the very young, may be confusion or decreased alertness. Blood pressure decreases, yet the skin is paradoxically warm. Later, extremities become cool and pale, with peripheral cyanosis and mottling. Organ dysfunction causes additional symptoms and signs specific to the organ involved (eg, oliguria, dyspnea).
- #10 urinalysis and urine culture (particularly in patients who have indwelling catheters), blood cultures, and cultures of other suspect body fluids. In patients with a suspected surgical or occult cause of sepsis, ultrasonography, CT, or MRI may be required, depending on the suspected source. Blood levels of C-reactive protein and procalcitonin are often elevated in severe sepsis and may facilitate diagnosis, but they are not specific. Ultimately, the diagnosis is clinical.
- #11 Other causes of shock (eg, hypovolemia, myocardial infarction [MI]) should be ruled out via history, physical examination, ECG, and serum cardiac markers. Even in the absence of MI, hypoperfusion caused by sepsis may result in ECG findings of cardiac ischemia including nonspecific ST-T wave abnormalities, T-wave inversions, and supraventricular and ventricular arrhythmias.
- #15 CBC, arterial blood gases (ABGs), chest x-ray, serum electrolytes, BUN (blood urea nitrogen), creatinine, PCO2, and liver function are monitored. Serum lactate levels, central venous oxygen saturation (ScvO2), or both can be done to help guide treatment. White blood cell (WBC) count may be decreased (< 4,000/mcL [< 4 × 109/L]) or increased (> 15,000/mcL [> 15 × 109/L]), and polymorphonuclear leukocytes may be as low as 20%. During the course of sepsis, the WBC count may increase or decrease, depending on the severity of sepsis or shock, the patient's immunologic status, and the etiology of the infection. Concurrent corticosteroid use may elevate WBC count and thus mask WBC changes due to trends in the illness.
- #16 Hyperventilation with respiratory alkalosis (low PaCO2 and increased arterial pH) occurs early, in part as compensation for lactic acidemia. Serum bicarbonate is usually low, and serum and blood lactate levels increase. As shock progresses, metabolic acidosis worsens, and blood pH decreases. Early hypoxemic respiratory failure leads to a decreased PaO2:FIO2 ratio and sometimes overt hypoxemia with PaO2< 70 mm Hg.
- #18 Many patients with severe sepsis develop relative adrenal insufficiency (ie, normal or slightly elevated baseline cortisol levels that do not increase significantly in response to further stress or exogenous adrenocorticotropic hormone [ACTH]). Adrenal function may be tested by measuring serum cortisol at 8 AM; a level < 5 mcg/dL (< 138 nmol/L) is inadequate. Alternatively, cortisol can be measured before and after injection of 250 mcg of synthetic ACTH; a rise of < 9 mcg/dL (< 248 nmol/L) is considered insufficient. However, in refractory septic shock, no cortisol testing is required before starting corticosteroid therapy.
- #24 Overall mortality in patients with septic shock is decreasing and now averages 30 to 40% (range 10 to 90%, depending on patient characteristics). Poor outcomes often follow failure to institute early aggressive therapy (eg, within 6 hours of suspected diagnosis). Once severe lactic acidosis with decompensated metabolic acidosis becomes established, especially in conjunction with multiorgan failure, septic shock is likely to be irreversible and fatal. Mortality can be estimated with different scores including the MEDS score. The multiple organ dysfunction score measures dysfunction of 6 organ systems and correlates strongly with risk of mortality. CLINICAL CALCULATOR: MEDS Score: Mortality in ER Sepsis CLINICAL CALCULATOR: Multiple Organ Dysfunction Score (MODS)
- #28 Estimates of successful reperfusion include ScvO2 and lactate clearance (ie, percent change in serum lactate levels). Target ScvO2 is ≥ 70%. Lactate clearance target is 10 to 20%. Risk of pulmonary edema can be controlled by optimizing preload; fluids should be given until CVP reaches 8 mm Hg (10 cm water) or PAOP reaches 12 to 15 mm Hg; however, patients on mechanical ventilation may require higher CVP levels. The quantity of fluid required often far exceeds the normal blood volume and may reach 10 L over 4 to 12 hours. PAOP or echocardiography can identify limitations in left ventricular function and incipient pulmonary edema due to fluid overload. If a patient with septic shock remains hypotensive after CVP or PAOP has been raised to target levels, norepinephrine (highly individualized dosing) or vasopressin (up to 0.03 units/minute) may be given to increase mean BP to at least 65 mm Hg. Epinephrine may be added if a second drug is needed. However, vasoconstriction caused by higher doses of these drugs may cause organ hypoperfusion and acidosis.
- #30 Parenteral antibiotics should be given as soon as possible after specimens of blood, body fluids, and wound sites have been taken for Gram stain and culture. Very prompt empiric therapy, started immediately after suspecting sepsis, is essential and may be lifesaving. Antibiotic selection requires an educated guess based on the suspected source (eg, pneumonia, urinary tract infection), clinical setting, knowledge or suspicion of causative organisms and of sensitivity patterns common to that specific inpatient unit or institution, and previous culture results. Typically, broad-spectrum gram-positive and gram-negative bacterial coverage is used initially; immunocompromised patients should also receive an empiric antifungal drug. There are many possible starting regimens; when available, institutional trends for infecting organisms and their antibiotic susceptibility patterns (antibiograms) should be used to select empiric treatment. In general, common antibiotics for empiric gram-positive coverage include vancomycin and linezolid. Empiric gram-negative coverage has more options and includes broad-spectrum penicillins (eg, piperacillin/tazobactam), 3rd- or 4th-generation cephalosporins, imipenems, and aminoglycosides. Initial broad coverage is narrowed based on culture and sensitivity data.
- #31 The source of infection should be controlled as early as possible. IV and urinary catheters and endotracheal tubes should be removed if possible or changed. Abscesses must be drained, and necrotic and devitalized tissues (eg, gangrenous gallbladder, necrotizing soft-tissue infection) must be surgically excised. If excision is not possible (eg, because of comorbidities or hemodynamic instability), surgical drainage may help. If the source is not controlled, the patient’s condition will continue to deteriorate despite antibiotic therapy.