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Septic Shock 2010   Dengzide2
 

Septic Shock 2010 Dengzide2

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  • There are over 1 million cases of shock that present to the ED each year. Presentation may be cryptic or obvious. The definition and treatment of shock continue to evolve because of new understanding and technologies. The golden hour represents early intervention.
  • From 1979 through 1987, gram neg bacteria were the predominant organisms causing sepsis. From 1988 onwards, gram pos bacteria have become the predominant organisms. In 2001, gram (+) bacteria accounted for 52% of cases with gram (-) accounting for 38%, polymicrobial infections 5%, anaerobes 1%, and fungi 5%. ** In 1/3 of cases, no organisms are recovered.
  • The pathophysiology of sepsis depends on a complex interaction and cooperation between a whole host of cells, including neutrophils, macrophages and structural cells such as endothelial cells, epithelial cells, and dendritic cells. This slide illustrates the response to pathogens, involving “cross-talk” among many immune cells, including macrophages, dendritic cells and CD4 T cells. Macrophages and dendritic cells are activated by the ingestion of bacteria and by stimulation through cytokines secreted by CD4 T cells. These cells secrete a variety of cytokines, chemokines and lipid mediators which can attract further immune cells into the battlefield. The concept has emerged that although initially sepsis may be characterized by increases in inflammatory mediators, as the sepsis persists, there is a shift toward an anti-inflammatory immunosuppressive state. Alternatively, CD4 T cells that have an anti-inflammatory profile (type 2 helper T cells) secrete IL-10, which suppresses macrophage activation. The factors that determine whether CD4 T cells have Th1 (inflammatory) or Th2 (anti-inflammatory) responses are unknown but appear to be influenced by the type of pathogen, size of the bacterial inoculum and the site of infection. Casualties in this battle are the host cells: endothelial cells, epithelial cells in organs such as the lung, kidney and gut and parenchymal cells such as cardiac myocytes. It also has become clear that during sepsis, T cells become anergic or lose their ability to proliferate or secrete cytokines in response to specific antigens. This sepsis-induced anergy seems to be triggered by apoptotic or programmed cell death. Basically, the cells commit “suicide” by the activation of proteases that disassemble the cell. In the case of lymphocytes, a potential mechanism of apoptosis may be stress-induced endogenous release of glucocorticoids.
  • Sepsis is a common condition. In the US, the incidence of sepsis per 100,000 exceeds AIDS, breast cancer, and first myocardial infarctions. Concerted public awareness campaigns have emphasized the importance of coronary heart disease, AIDS, and breast cancer. Yet, as shown on this slide, the mortality of severe sepsis exceeds AIDS, breast cancer and is only slightly less that that of patients dying suddenly of an acute myocardial infarction. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Incidence, cost and outcomes of severe sepsis in the United States. Crit Care Med 2001; American Heart Association. 2001 Heart and Stroke Statistical Update . Dallas, Tex: American Heart Association, 2000. American Cancer Society. Cancer Statistics . Online edition, accessed 3/29/01.
  • Severe sepsis shows a small peak in incidence in the very young (<1 year). The incidence then remains low until midlife when it begins to climb. As shown on this slide, both sepsis and severe sepsis are most problematic after the age of 50 years. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Incidence, cost and outcomes of severe sepsis in the United States. Crit Care Med 2001; In Press.
  • This is an example of moderate pulmonary PBI with a relatively small area of localized pulmonary infiltrates and only slight evidence that the right side was affected. Responders to the scene should be aware that many ballistic vests actually facilitate transmission of the blast wave into an internal stress wave. However, the vest will save the wearer’s life more often than not. This picture shows penetration of fragments around the contour of a vest. Despite (possibly) sustaining a greater degree of pulmonary PBI, the casualty survived because none of the fragments penetrated his mediastinum or thoracic vessels.
  • 16 16
  • Airway/oxygenation: Mask/intubation Hemodynamic stabilization: Fluid: not unusual for a patient to require 4 to 6 L; stabilization of mentation, BP, respirations, HR, skin perfusion, U.O. > 30 cc/hr Inotropic support: If no response to 3 to 4 L of fluid, start dopamine. If no response with DA at 20 ug/Kg/min, then start NE to keep MAP 60 mm Hg Empiric antimicrobial therapy: Whenever possible, blood, urine, CSF should be sent for gram stain and culture before antibiotics are instituted. Antibiotics should be broad spectrum to cover all potential pathogens. Neonates: Ampicillin + Cefotaxime. Infants: Ampicillin + Cefotaxime or Ceftriaxone Children (> 3 Mos): Cefotaxime or Ceftriaxone. Adults: 3 rd generation Cephlasporin or Antipseudomonal beta lactamase-susceptible PCN +/_AG. If high suspicion of GPC, add Vancomycin or Naf. If GNR, add clinda or flagyl. Bicarbonate: HCO3 for pH < 7.2. Treatment of DIC: 1. Eliminate the underlying disorder or source of infection, 2. Replace components as needed, 3. Arrest intra-vascular clotting process. Steroids: only in patients with suspected or documented adrenal insufficiency.,
  • MANAGEMENT There are two goals in the treatment of hemorrhagic shock: control of hemorrhage and maintenance of oxygen delivery. The definitive therapy of hemorrhage is control of the source of bleeding; this often requires operative intervention. Thus, for most patients with hemodynamic instability secondary to hemorrhage, prompt surgical consultation and intervention are mandatory. Prehospital Treatment There have been many debates in recent years over the extent to which patients should be resuscitated prior to operative intervention, both in the prehospital setting and the ED. The concept of field stabilization of trauma victims has been discredited for those with hemorrhagic shock. The prehospital interventions that improve survival include attention to the airway, ventilation, immobilization, and rapid transport; not fluid resuscitation. Standard prehospital interventions directed at restoring blood pressure, such as application of a pneumatic antishock garment (PASG) and infusion of intravenous fluids, have not been shown to improve survival.
  • 24

Septic Shock 2010   Dengzide2 Septic Shock 2010 Dengzide2 Presentation Transcript

  • Septic Shock 中山大学附属第三医院 邓子德 [email_address]
  • What is Shock ?
    • Shock is any condition in which the circulatory system is unable to provide adequate circulation to the vital body organs such as the brain,heart and lungs. As a result of a decrease in the blood pressure.
    • Shock is usually accompanied by renal failure, as a normal compensatory mechanism, because the blood flow to the kidney is decreased to keep enough blood for the vital organs.
  • What is Septic shock ?
    • Septic shock is a serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis , though the microbe may be systemic or localized to a particular site.
    • It can cause multiple organ dysfunction syndrome (formerly known as multiple organ failure ) and death .
    • The mortality rate from septic shock is approximately 50%.
  •  
  • INTRODUCTION
    • Estimated at 300,000- 500,000 patients/year
    • Clinical syndrome that can be caused by any class of microorganism
    • Sepsis
      • Half develop shock with a mortality rate of 45%
      • 13 th leading cause of death in the U.S.
  • Classification of Shock
    • Shock is classified according to the causes to three classes:
      • Hypovolemic shock
      • Distributive shock
      • Cardiogenic shock
  • Causes of Shock
    • Hypovolemic shock is caused by low blood volume.
      • Normal blood volume is 5 L and by losing 1-2 L it can lead to shock.
      • The Decrease in blood volume is caused by:
        • External blood loss: ex. Hemorrhage
        • Internal blood loss: ex. Ruptured spleen caused by blunt trauma.
        • Severe dehydration as a result of:
          • Vomiting
          • Diarrhea
          • This is a typical condition in cholera.
        • Burns
  • Causes of Shock
    • Hypovolemic shock is caused by low blood volume.
      • Normal blood volume is 5 L and by losing 1-2 L it can lead to shock.
      • The Decrease in blood volume is caused by:
        • External blood loss: ex. Hemorrhage
        • Internal blood loss: ex. Ruptured spleen caused by blunt trauma.
        • Severe dehydration as a result of:
          • Vomiting
          • Diarrhea
          • This is a typical condition in cholera.
        • Burns
  • Causes of Shock
    • 2. Distributive shock is caused by excess vasodilatation (ex. Anaphylactic shock and septicemia)
    • Vasodilatation Arteriole resistance increase blood exchange from the vessels to the peripheral tissues decrease blood return to the heart BP shock
  • Causes of Shock
    • Cardiogenic shock ( heart does not pump enough blood) is caused by:
      • A) Myocardial infarction weak cardiac
      • muscle contraction Ischemia
      • B) Arrhythmia ( such as ventricular fibrillation, which will stop the heart pump and that will decrease BP
        • Note: Supraventricular (Atria) fibrillation will not cause shock because 75% of the blood transfer from the atrium to the ventricles by passive transport.
    Lead to As a result of
  • Causes of Shock
    • C) Valve problems, ex. Valvular stenosis which is narrowing of the valves, or leakage of blood through the valves ( Regurgitation).
    • D) Problems in the A-V shunt.
  • DEFINITIONS
    • SEPTIC SHOCK
      • Sepsis-induced with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to
        • Lactic Acidosis
        • Oliguria
        • Acute alteration in mental status
  • DEFINITIONS
    • SEPTIC SHOCK
      • … Perfusion embarrassment secondary to dilated vascular bed in response to bacteria and their products circulating in the blood…
      • Inadequate Tissue Perfusion!
  • DEFINITIONS
    • Infection
    • Bacteremia
    • SIRS
      • Systemic Inflammatory Response Syndrome
    • MODS
      • Multiple Organ Dysfunction Syndrome
    • Sepsis
    • Severe Sepsis
    • Sepsis-induced Hypotension
  • Infection
    • An infection is the detrimental colonization of a host organism by a foreign species .
    • In an infection, the infecting organism seeks to utilize the host's resources to multiply, usually at the expense of the host.
  • Bacteremia
    • Bacteremia (also Bacteraemia ) is the presence of bacteria in the blood .
    • The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly with blood cultures ) is always abnormal.
    • Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis ), during surgery (especially when involving mucous membranes such as the gastrointestinal tract ), or due to catheters and other foreign bodies entering the arteries or veins (including intravenous drug abuse ).
  •  
  • SIRS
    • 全身炎症反应综合征( SIRS )
    •    是指机体对不同原因的严重损伤所产生的系统性炎症反应,并至少具有以下临床表现中的 2 项:
    •     1 、 体温 大于 38℃ 或小于 36℃ ;
    •     2 、 心率 大于 90 次 / 分钟;
    •     3 、 呼吸 急促,频率大于 20 次 / 分钟或过度通气、 PaCO 2 小于 32mmHg ;
    •     4 、血 白细胞 计数大于 1.2 万或小于4千,或未成熟(杆状核)中性粒细胞比例大于 10% 。
  • Sepsis is a serious medical condition that is characterized by a whole-body inflammatory state (SIRS) and the presence of a known or suspected infection .
  •  
  •  
  • 与脓毒血症相关的几个概念
    • 脓毒血症( Sepsis ) 是指感染所引起的 SIRS 。
    • 严重感染( Severe sepsis ) 伴有器官功能障碍、组织灌注不良或低血压的 Sepsis 。
    • 感染性休克( Septic shock ) 为 Severe sepsis 的一个亚型,是指虽然进行了充分的液体复苏治疗,但仍然存在持续的低血压和组织灌注下降。
  •  
  • MODS
    • 多器官功能障碍综合征( MODS )
      • Multiple Organ Dysfunction Syndrome
    • 指严重 创伤、休克和感染 等过程中 , 短时间 内 同时或相继 出现了 两个或两个以上 的系统、器官功能损害和障碍。
  •  
  • Severe Sepsis: Primary Source
    • Pulmonary: 50%
    • Abdomen/Pelvis: ~25%
    • Primary bacteremia: ~15%
    • Urosepsis: 10%
    • Skin: 5%
    • Vascular: 5%
    • Other: ~15%
    Martin GS, et al. NEJM 2003;348:1546
  • Microbiology of Sepsis Martin GS, et al. NEJM 2003;348:1546
  • Sepsis Battlefield: Cells and Mediators Hotchkiss RS, Karl IE, NEJM 2003;348:138
  • Severe Sepsis: Comparative Incidence and Mortality Angus DC, et al. Crit Care Med 2001; American Cancer Society Incidence Cases/100,000 Mortality Deaths/Year
  • Mortality of Severe Sepsis by Age in the United States Angus DC, et al. Crit Care Med 2001 .
    • 0%
    • 5%
    • 10%
    • 15%
    • 20%
    • 25%
    • 30%
    • 35%
    • 40%
    • 45%
    • 0
    • 1
    • 5
    • 10
    • 15
    • 20
    • 25
    • 30
    • 35
    • 40
    • 45
    • 50
    • 55
    • 60
    • 65
    • 70
    • 75
    • 80
    • 85
    Age Mortality
    • Without Co-morbidity
    • With Co-morbidity
    • Overall
  • EPIDEMIOLOGY
    • Both gram-negative and gram-positive bacteria account for majority of sepsis cases
    • Microbial blood invasion is not essential
    • Most frequent sites of infection
      • Lungs
      • Abdomen
      • Urinary Tract
  • EPIDEMIOLOGY
    • Fungemia
      • Immunocompromised patients
    • Patient
      • Males > Females
      • Age- Older adults
        • 55-60 years old
        • Predisposing factors of DM/CA
  • EPIDEMIOLOGY
    • Factors that predispose to gram-negative bacteremia
      • Diabetes mellitus / liver cirrhosis / burns
      • chemotherapy / invasive procedures
    • Factors that predispose to gram-positive bacteremia
      • Vascular catheters / IV drug abuse
      • Indwelling mechanical devices / burns
  •  
  •  
  • PATHOPHYSIOLOGY
    • Starts as a focus of infection
    • Results in either blood stream invasion or proliferation of the organism at the infected site
    • Release of large amount of exogenous toxins
      • Exotoxins
      • Endotoxins
      • Other components
  • PATHOPHYSIOLOGY
    • Body’s response is the release of
      • Vasoactive Mediators
        • Nitric Oxide
      • Endogenous mediators
        • Tumor Necrosis factor
        • Platelet Activating Factor (PAF)
        • Myocardial Depressant Substances (MDS)
      • Humoral Defense Mechanisms
        • Complement
        • Kinins
        • Coagulation Factors
  • SIRS/MODS
    • SIRS (> 2 below)
      • T >38 or <36
      • HR > 90 bpm
      • RR > 20 or
      • PCO2 < 32 mm Hg
      • WBC >12 or < 4 or
      • > 10 % bands
    • MODS
      • Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.
  •  
  • CLINICAL FEATURES
    • CONSTITUTIONAL
      • Hyperthermia or hypothermia
      • Tachycardia
      • Tachypnea- Hyperventilation with respiratory alkalosis
      • Wide pulse pressure
      • Mental status changes-
  • CLINICAL FEATURES
  • CLINICAL FEATURES
    • CONSTITUTIONAL
      • Hyperventilation with respiratory alkalosis
      • Most frequent mental status change
        • Obtundation
      • Neurological findings are nonfocal
        • Mild disorientation-coma
  • CLINICAL FEATURES
    • CARDIOVASCULAR
      • Initially warm extremities
      • Markedly diminished cardiac response to volume administration
      • Dehydration
      • Myocardial depression
  • CLINICAL FEATURES
    • PULMONARY
      • Common association with ARDS
      • Lung edema resulting from increased alveolar-capillary permeability
      • Dyspnea & hypoxemia
      • Noncompliant “heavy” lungs
      • Bilateral pulmonary infiltrates
      • Abnormal opacities on CXR
  • CHEST RADIOGRAPH
  • CHEST RADIOGRAPH
  • CLINICAL FEATURES
    • RENAL
      • Acute renal failure(ARF) with azotemia
      • Renal Insufficiency
      • Glomerulonephritis
      • Oliguria
      • Active urinary sediment
        • Red blood cells/Cast/Protein
  • CLINICAL FEATURES
    • HEPATIC
      • Liver dysfunction with elevated LFT’s
      • Jaundice
      • Hepatocellular dysfunction
      • Prolonged or severe hypotension may induce
        • Hepatic Injury
        • Ischemic bowel necrosis
  •  
  • CLINICAL FEATURES
    • HEMATOLOGIC
      • Hemolysis of RBCs
      • Neutrophilia with “left shift”
      • Neutropenia (RARE)
      • Thrombocytopenia
        • Seen with bacteremia
  • CLINICAL FEATURES
    • HEMATOLOGIC
      • Disseminated Intravascular Coagulation (DIC)
      • Decreased serum iron levels
      • Minor bleeds from painless stomach/duodenal erosions
  • CLINICAL FEATURES
    • Disseminated Intravascular Coagulation
      • Frequent finding in septic shock
      • Gram-negative infections precipitate DIC more readily than do gram-positive
      • Consumption of coagulation factors and platelets
      • Activation of the extrinsic clotting pathway
      • Fibrin deposition in the microcirculation and subsequent multiple-organ failure
  • CLINICAL FEATURES
    • Disseminated Intravascular Coagulation (DIC)
      • Decompensated results in clinical bleeding
      • Thrombosis
      • Prolonged PT/PTT values
  • CLINICAL FEATURES
    • ENDOCRINE
      • Hyperglycemia in diabetic patients
      • Hypoglycemia- uncommon
  • CLINICAL FEATURES
    • ACID-BASE
      • Respiratory alkalosis
      • Hypoxemia due to ventilation perfusion mismatches
      • Metabolic acidosis reflects inadequate tissue perfusion
      • Worsens with the production of more lactic acid from tissue hypoxia
  • CLINICAL FEATURES
    • CUTANEOUS
      • Direct bacterial involvement of the skin/ underlying soft tissue
        • Cellulitis/fasciitis
      • Lesions occurring as a consequence of sepsis/hypotension/DIC
        • Acrocyanosis/necrosis of peripheral tissues
      • Lesions secondary to infective endocarditis
        • Microemboli/immune complex vasculitis
  • DIAGNOSIS
  • RECOGNITION OF SHOCK
    • Pulse Rate
    • Respiratory Rate
    • Capillary Refill
    • Pulse Pressure
    • Skin and core temperature
    • Mental Status
    • Urine Output
  • Diagnosis of Septic Shock
    • Serious Infections
      • Pneumonia / acute pyelonephritis /acute abdomen / meningitis
    • Atypical Presentation
      • Elderly/ immune compromised / very young
      • No fever/ no localized infection source
    • Differential Diagnosis
      • All other nonseptic causes of shock
  • Clinical Presentation Generalized Septic Shock
    • Vital signs
      • Blood pressure : SBP of < 90 mm Hg with evidence of inadequate organ perfusion
      • Pulse : > 100 per minute
      • Respiratory rate: > 20 per minute
      • Temperature: >38 degrees Centigrade or < 36 degrees Centigrade (rectal temperature is most accurate in ED)
  • Clinical Presentation Generalized Septic Shock
    • Hypotension not reversed by rapid volume replacement of at least 1 liter crystalloid
    • Widened pulse pressure
    • Mental status: Obtundation
    • Urine output: < 1cc/kg per hour
    • Hot/flushed skin
    • Respiratory alkalosis/ Metabolic acidosis
  • Clinical Presentation Generalized Septic Shock
    • Biphasic Presentation
      • “ Warm” shock - early phase
        • Hyperdynamic response
      • “ Cold” shock - late phase
        • Decompensation
  • MANAGEMENT (TREATMENT)
  • MANAGEMENT
    • ABCs
    • Oxygen
    • Hemodynamic Stabilization
      • Fluid
      • Inotropic support
    • Antibiotics
    • Drainage/ Surgery
    • Bicarbonate
    • Treatment of DIC
    ABC 的原则: Airway :呼吸道及颈椎的保护 Breathing :维持呼吸和换气。 Circulation :循环及出血控制
  • Source Control
    • Source Control Technique Examples
    • Drainage Intra-abdominal abscess
    • Thoracic empyema
    • Debridement Necrotizing fasciitis
    • Infected pancreatic necrosis
    • Device removal Infected vascular catheter
    • Urinary catheter
    • Definitive control Cholecystectomy
    • Sigmoid resection
    GRADE 1C
  • 病灶源头控制 迅速消除微生物污染源是生理功能急性恶化的严重脓毒症病人最大程度提高生存率的必要措施。 这些措施必须在充分复苏后实施。 乙状结肠切除术治疗憩室,胆囊切除术治疗坏疽性胆囊炎,截肢治疗梭菌性肌坏死。 其他  受感染的血管导管、尿管、细菌定殖的气管插管、受感染的子宫内避孕装置等。 拔除装置  坏死性筋膜炎,感染性胰腺坏死,肠梗死,纵膈炎等。 清创  腹腔内脓肿,脓胸,腐败性关节炎,肾盂肾炎,胆管炎等。 引流  举例 病灶源头控制技术
  • MANAGEMENT
    • Oxygenation/Ventilation
      • Intubation based on clinical status
      • Maintain oxygen sat levels > 90%
    • IV access with Hemodynamic Stabilization
      • NS/Isotonic crystalloid at 0.5 L Q5-10 min
      • 20ml/kg for Pediatric patients
    • Standard Monitoring
    • Central Venous Pressure Monitoring
      • Monitors fluid resuscitation
  • MANAGEMENT
    • Inotropic Support
      • No response to fluids/ Elevated CVP/ PE
      • Dopamine Infusion 5-20mcg/kg/min
      • Norepinephrine Infusion (mean B/P 60mmHg)
    • Empiric Antibiotic Therapy
      • Antibiotics appropriate for presumed source of sepsis after obtaining blood cultures/ LP
      • Initially cover for all gram + and gram –
      • IV in maximum doses
  • MANAGEMENT
    • Definitive treatment of infection source
      • Find occult infection source
      • I & D of abscesses
      • Remove catheter/device if possible
      • Surgery as indicated
    • Bicarbonate
      • Consider use in severe acidosis
      • pH of < 7.2
  • MANAGEMENT
    • DIC
      • Eliminate the underlying disorder/source of infection
      • Substitute coagulation lost in the clotting process
        • Fresh-frozen plasma and/or platelets
      • Stop the intravascular clotting process
        • Heparin Therapy
        • Antithrombin III
  • Blood Transfusion
    • RBC transfusion if Hb < 7 g/dL
    • except heart, lung, brain problems
    • No FFP even PT, PTT abnormal
    • unless bleeding or planned procedure
    • Platelet
    • < 5000/mm 3  transfuse
    • 5000~30,000/mm 3 & bleeding risk  transfuse
    • keep > 50,000/mm 3 for surgery or invasive procedure
  • STEROIDS
  • Corticosteroid Therapy
    • IV hydrocortisone should be given only to adult septic shock patients after it has been confirmed that their BP is poorly responsive to fluid resuscitation and vasopressor therapy.
    Crit Care Med 2008 SSC Update
  • Rapid ACTH Test Can Identify Septic Patients at High Risk of Death
    • Relative adrenal insufficiency
    • Failure to increase cortisol by > 9 µg/dl
    • at 30- or 60-min following 250 µg ACTH stimulation test
    Annane D, et al. JAMA 2000;283:1038-45
  • Early Goal Directed Therapy (EGDT)
    • This is a program designed for implementation of Early Goal Directed Therapy (EGDT) in management of the septic patient.
    • This program includes information about antibiotics, steps to complete EGDT, adjunct therapies and walks the clinician through EGDT.
  • EVALUATION OF RESPONSE
    • Support ABC’s as previously described
    • General
      • Monitor patients BP, Pulse, Respirations, CNS Status, and Urine Output.
    • Renal Function
      • Adults: 30-50ml/hr
      • Pediatrics: 1 ml/kg/hr
      • Infants: 2 ml/kg/hr
  • Severe Sepsis: Initial Resuscitation ( 1 st 6 hours )
    • Should begin as soon as the syndrome is recognized and should not be delayed pending ICU admission.
    • Elevated serum lactate concentration identifies tissue hypoperfusion in patients at risk who are not hypotensive.
  • SUMMARY
    • Management Goals
      • Identify etiology of shock and begin to intervene early in course before point of irreversible cell damage occurs
      • Optimize ABC’s
      • Follow serial clinical parameters and adjust interventions based on evolution of illness
  • Thank you ! 中山大学附属第三医院 邓子德 [email_address]