Septic Shock 2010 Dengzide2

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 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 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

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

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 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

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]

Septic Shock 2010 Dengzide2

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