septic shock 2010 dengzide2

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Septic Shock

中山大学附属第三医院邓子德

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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.

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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%.

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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%– 13th leading cause of death in the U.S.

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Classification of Shock

• Shock is classified according to the causes to three classes:– Hypovolemic shock – Distributive shock– Cardiogenic shock

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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 le

ad 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– DiarrheaThis is a typical condition in cholera.

• Burns

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Causes of Shock1. Hypovolemic shock is caused by low blood volum

e. Normal blood volume is 5 L and by losing 1-2 L it can l

ead to shock. The Decrease in blood volume is caused by:

External blood loss: ex. Hemorrhage Internal blood loss: ex. Ruptured spleen caused by blunt traum

a. Severe dehydration as a result of:

Vomiting DiarrheaThis is a typical condition in cholera.

Burns

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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

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Causes of Shock

3. 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

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Causes of ShockC) 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.

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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

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DEFINITIONS SEPTIC SHOCK

… Perfusion embarrassment secondary to dilated vascular bed in response to bacteria and their products circulating in the blood…

Inadequate Tissue Perfusion!

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DEFINITIONS• Infection• Bacteremia• SIRS

– Systemic Inflammatory Response Syndrome

• MODS– Multiple Organ Dysfunction Syndrome

• Sepsis• Severe Sepsis• Sepsis-induced Hypotension

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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.

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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).

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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、 PaCO2 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% 。

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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.

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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。

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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。

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Severe Sepsis: Primary SourceSevere 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

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Microbiology of Sepsis

Martin GS, et al. NEJM 2003;348:1546

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Sepsis Battlefield: Cells and MediatorsSepsis Battlefield: Cells and Mediators

Hotchkiss RS, Karl IE, NEJM 2003;348:138Hotchkiss RS, Karl IE, NEJM 2003;348:138

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Severe Sepsis: Severe Sepsis: Comparative Incidence and MortalityComparative Incidence and Mortality

Angus DC, et al. Crit Care Med 2001; American Cancer Society

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Mortality of Severe Sepsis by Age in the Mortality of Severe Sepsis by Age in the United StatesUnited States

Angus DC, et al. Crit Care Med 2001.

•0%

•5%

•10%

•15%

•20%

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•0 •1 •5 •10 •15 •20 •25 •30 •35 •40 •45 •50 •55 •60 •65 •70 •75 •80 •85

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•Without Co-morbidity

•With Co-morbidity

•Overall

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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

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EPIDEMIOLOGY

• Fungemia– Immunocompromised patients

• Patient– Males > Females– Age- Older adults

• 55-60 years old• Predisposing factors of DM/CA

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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

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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

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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

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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.

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CLINICAL FEATURES

• CONSTITUTIONAL– Hyperthermia or hypothermia– Tachycardia– Tachypnea- Hyperventilation with

respiratory alkalosis– Wide pulse pressure– Mental status changes-

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CLINICAL FEATURES

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CLINICAL FEATURES

• CONSTITUTIONAL– Hyperventilation with respiratory

alkalosis– Most frequent mental status change

• Obtundation

– Neurological findings are nonfocal• Mild disorientation-coma

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CLINICAL FEATURES

• CARDIOVASCULAR– Initially warm extremities

– Markedly diminished cardiac response to volume administration

– Dehydration

– Myocardial depression

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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

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CHEST RADIOGRAPH

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CHEST RADIOGRAPH

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CLINICAL FEATURES

• RENAL– Acute renal failure(ARF) with azotemia

– Renal Insufficiency

– Glomerulonephritis

– Oliguria

– Active urinary sediment• Red blood cells/Cast/Protein

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CLINICAL FEATURES

• HEPATIC– Liver dysfunction with elevated LFT’s– Jaundice– Hepatocellular dysfunction– Prolonged or severe hypotension may

induce• Hepatic Injury• Ischemic bowel necrosis

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CLINICAL FEATURES

• HEMATOLOGIC– Hemolysis of RBCs

– Neutrophilia with “left shift”

– Neutropenia (RARE)

– Thrombocytopenia• Seen with bacteremia

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CLINICAL FEATURES

• HEMATOLOGIC– Disseminated Intravascular

Coagulation (DIC)

– Decreased serum iron levels

– Minor bleeds from painless stomach/duodenal erosions

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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

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CLINICAL FEATURES

• Disseminated Intravascular Coagulation (DIC)– Decompensated results in clinical

bleeding

– Thrombosis

– Prolonged PT/PTT values

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CLINICAL FEATURES

• ENDOCRINE– Hyperglycemia in diabetic patients

– Hypoglycemia- uncommon

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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

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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

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DIAGNOSIS

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RECOGNITION OF SHOCK

• Pulse Rate• Respiratory Rate• Capillary Refill• Pulse Pressure• Skin and core temperature• Mental Status• Urine Output

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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

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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)

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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

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Clinical Presentation Generalized Septic Shock

• Biphasic Presentation–“Warm” shock - early phase

• Hyperdynamic response

– “Cold” shock - late phase• Decompensation

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MANAGEMENT(TREATMENT)

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MANAGEMENT• ABCs• Oxygen• Hemodynamic Stabilization

– Fluid– Inotropic support

• Antibiotics• Drainage/ Surgery• Bicarbonate• Treatment of DICABC 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

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Source ControlSource ControlSource 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 resectionGRADE 1C

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病灶源头控制技术 举例

引流 腹腔内脓肿，脓胸，腐败性关节炎，肾盂肾炎，胆管炎等。

清创 坏死性筋膜炎，感染性胰腺坏死，肠梗死，纵膈炎等。

拔除装置 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。

其他 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。

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。

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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

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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

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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

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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

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Blood TransfusionRBC transfusion if Hb < 7 g/dL

except heart, lung, brain problems

No FFP even PT, PTT abnormalunless bleeding or planned procedure

Platelet< 5000/mm3 transfuse

5000~30,000/mm3 & bleeding risk transfusekeep > 50,000/mm3 for surgery or invasive procedure

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STEROIDSSTEROIDS

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Corticosteroid TherapyCorticosteroid 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

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Rapid ACTH Test Can Identify Septic Rapid ACTH Test Can Identify Septic Patients at High Risk of DeathPatients 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

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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.

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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

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Severe Sepsis:Severe Sepsis:Initial Resuscitation (Initial Resuscitation (11stst 6 hours 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.

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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

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Thank you！中山大学附属第三医院

邓子德dengzide@163.com