WordNet

strike with horror or terror; "The news of the bombing shocked her"
(pathology) bodily collapse or near collapse caused by inadequate oxygen delivery to the cells; characterized by reduced cardiac output and rapid heartbeat and circulatory insufficiency and pallor; "loss of blood is an important cause of shock"
subject to electrical shocks
the violent interaction of individuals or groups entering into combat; "the armies met in the shock of battle" (同)impact
an unpleasant or disappointing surprise; "it came as a shock to learn that he was injured" (同)blow
an instance of agitation of the earths crust; "the first shock of the earthquake came shortly after noon while workers were at lunch" (同)seismic disturbance
a bushy thick mass (especially hair); "he had an unruly shock of black hair"
a pile of sheaves of grain set on end in a field to dry; stalks of Indian corn set up in a field; "corn is bound in small sheaves and several sheaves are set up together in shocks"; "whole fields of wheat in shock"
surprise greatly; knock someones socks off; "I was floored when I heard that I was promoted" (同)floor, ball over, blow out of the water, take aback
strike with disgust or revulsion; "The scandalous behavior of this married woman shocked her friends" (同)offend, scandalize, scandalise, appal, appall, outrage
collect or gather into shocks; "shock grain"
collide violently
of or relating to or caused by putrefaction; "the septic action occurs at the bottom of the septic tank"
containing or resulting from disease-causing organisms; "a septic sore throat"; "a septic environment"; "septic sewage" (同)infected

PrepTutorEJDIC

〈C〉(衝突・爆発などの)『衝撃』,(地震の)震動,電撃 / 〈C〉〈U〉(精神的)『打撃』,ショック / 〈U〉ショック症 / 《しばしば受動態で》〈人〉‘を'『ぎょっとさせる』,ひどく驚かせる / (治療のため)〈人・動物〉‘に'電気ショクを与える
(乾燥させるために立てかけた)穀類の刈り束 / 〈穀類〉‘を'刈り束にする
(髪の毛の)もじゃもじゃの固まり《+『of』+『名』》
腐敗性の / 敗血症[性]の
びっくりさせる,ぞっとする / 全くひどい(very bad),不愉快な(offensive)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/01/09 17:25:51」(JST)

wiki en

Septic shock is a medical condition as a result of severe infection and sepsis, though the microbe may be systemic or localized to a particular site.^[1] It can cause multiple organ dysfunction syndrome (formerly known as multiple organ failure) and death.^[1] Its most common victims are children, immunocompromised individuals, and the elderly, as their immune systems cannot deal with the infection as effectively as those of healthy adults. Frequently, patients suffering from septic shock are cared for in intensive care units. The mortality rate from septic shock is approximately 25–50%.^[1]

Definition[edit]

In humans, septic shock has a specific definition requiring several conditions to be met for diagnosis:

First, SIRS (systemic inflammatory response syndrome) must be diagnosed by finding at least any two of the following:

Tachypnea (high respiratory rate) > 20 breaths per minute, or on blood gas, a PCO2 less than 32 mmHg signifying hyperventilation.

White blood cell count either significantly low, < 4000 cells/mm³ or elevated > 12000 cells/mm³.

Heart rate > 90 beats per minute

Temperature: Fever > 38.0 °C (100.4 °F) or hypothermia < 36.0 °C (96.8 °F)

Second, there must be sepsis and not an alternative form cause of SIRS. Sepsis requires evidence of infection, which may include positive blood culture, signs of pneumonia on chest x-ray, or other radiologic or laboratory evidence of infection.
Third, signs of end-organ dysfunction are required such as renal failure, liver dysfunction, changes in mental status, or elevated serum lactate.
Finally, septic shock is diagnosed if there is refractory hypotension (low blood pressure that does not respond to treatment). This signifies that intravenous fluid administration alone is insufficient to maintain a patient's blood pressure from becoming hypotensive.

Types[edit]

A subclass of distributive shock, septic shock refers specifically to decreased tissue perfusion resulting in ischemia and organ dysfunction. Cytokines released in a large scale inflammatory response results in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and hypotension. Hypotension reduces tissue perfusion pressure causing tissue hypoxia. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur.

Causes[edit]

When bacteria or viruses are present in the bloodstream, the condition is known as bacteremia or viremia. Sepsis is a constellation of symptoms secondary to infection that manifest as disruptions in heart rate, respiratory rate, temperature and WBC. If sepsis worsens to the point of end-organ dysfunction (renal failure, liver dysfunction, altered mental status, or heart damage), then the condition is called severe sepsis. Once severe sepsis worsens to the point where blood pressure can no longer be maintained with intravenous fluids alone, then the criteria have been met for septic shock. The precipitating infections which may lead to septic shock if severe enough include appendicitis, pneumonia, bacteremia, diverticulitis, pyelonephritis, meningitis, pancreatitis, and necrotizing fasciitis.

Pathophysiology[edit]

Most cases of septic shock are caused by endotoxin-producing Gram positive bacteria followed by Gram-negative bacteria (Dellinger et al, 2012 Surviving Sepsis Campaign). Endotoxins are bacterial membrane lipopolysaccharides (LPS) consisting of a toxic fatty acid (lipid A) core common to all Gram-negative bacteria, and a complex polysaccharide coat (including O antigen) unique for each species. Analogous molecules in the walls of Gram-positive bacteria and fungi can also elicit septic shock. Free LPS attaches to a circulating LPS-binding protein, and the complex then binds to a specific receptor (CD14) on monocytes, macrophages, and neutrophils. Engagement of CD14 (even at doses as minute as 10 pg/mL) results in intracellular signaling via an associated "Toll-like receptor" protein 4 (TLR-4), resulting in profound activation of mononuclear cells and production of potent effector cytokines such as IL-1 and TNF-α. These cytokines act on endothelial cells and have a variety of effects including reduced synthesis of anticoagulation factors such as tissue factor pathway inhibitor and thrombomodulin. The effects of the cytokines may be amplified by TLR-4 engagement on endothelial cells. TLR-mediated activation helps to trigger the innate immune system to efficiently eradicate invading microbes. At high levels of LPS, the syndrome of septic shock supervenes; the same cytokine and secondary mediators, now at high levels, result in systemic vasodilation (hypotension), diminished myocardial contractility, widespread endothelial injury and activation, causing systemic leukocyte adhesion and diffuse alveolar capillary damage in the lung activation of the coagulation system, culminating in disseminated intravascular coagulation (DIC). The hypoperfusion resulting from the combined effects of widespread vasodilation, myocardial pump failure, and DIC causes multiorgan system failure that affects the liver, kidneys, and central nervous system, among others. Unless the underlying infection (and LPS overload) is rapidly brought under control, the patient usually dies.

Treatment[edit]

Treatment primarily consists of the following.

Volume resuscitation^[2]
Early antibiotic administration^[2]
Early goal directed therapy^[2]
Rapid source identification and control.
Support of major organ dysfunction.
Sequestration of lipopolysaccarides

Among the choices for vasopressors, norepinephrine is superior to dopamine in septic shock.^[3] Both however are still listed as first line in guidelines.^[3]

Antimediator agents may be of some limited use in severe clinical situations however are controversial:^[4]

Low dose steroids (hydrocortisone) for 5 – 7 days led to improved outcomes.^[5]^[6]
Recombinant activated protein C (drotrecogin alpha) in a 2011 Cochrane review was found not to decrease mortality and thus was not recommended for use.^[7] Other reviews however comment that it may be effective in those with very severe disease.^[4] The first and only activated protein C drug, drotrecogin alfa (Xigris), was voluntarily withdrawn in October 2011 after it failed to show a benefit in patients with septic shock, including the more severe disease subgroups.

A technique that has shown success and is currently used in Japan, if not elsewhere, involves sequestering the lipopolysacharides that effectively cause septic shock. The antibiotic toraymyxin coincidentally does this, but is also too toxic to be administered. The Japanese technique binds this toraymixin to an immobile material like polystyrene, and pass the blood over it, but this isn't always practical. Recent peer-reviewed research has found a substance derived from the very same spermine found in semen, to bind to lipopolysaccharids which, so far, seems to be non-toxic as well. Further information may be found here ^[8]^[9]

Epidemiology[edit]

Sepsis has a worldwide incidence of more than 20 million cases a year, with mortality due to septic shock reaching up to 50 percent even in industrialized countries.^[10]

According to the US CDC, septic shock is the 13th leading cause of death in the United States, and the #1 cause of deaths in intensive care units. There has been an increase in the rate of septic shock deaths in recent decades, which is attributed to an increase in invasive medical devices and procedures, increases in immunocompromised patients, and an overall increase in elderly patients. Tertiary care centers (such as hospice care facilities) have 2-4 times the rate of bacteremia than primary care centers, 75% of which are nosocomial infections.

The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. Approximately 70% of septic shock cases were once traceable to Gram staining gram-negative bacilli that produce endotoxins; however, with the emergence of MRSA and the increased use of arterial and venous catheters, Gram-positive cocci are implicated approximately as commonly as bacilli. In rough order of increasing severity, these are bacteremia or fungemic; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death.

35% of septic shock cases derive from urinary tract infections, 15% from the respiratory tract, 15% from skin catheters (such as IVs); over 30% of all cases are idiopathic in origin.

The mortality rate from sepsis is approximately 40% in adults, and 25% in children, and is significantly greater when left untreated for more than 7 days.^[11]

References[edit]

^ ^a ^b ^c Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 102-103 ISBN 978-1-4160-2973-1
^ ^a ^b ^c Levinson, AT; Casserly, BP, Levy, MM (April 2011). "Reducing mortality in severe sepsis and septic shock". Seminars in respiratory and critical care medicine 32 (2): 195–205. doi:10.1055/s-0031-1275532. PMID 21506056. Cite uses deprecated parameters (help)
^ ^a ^b Vasu, TS; Cavallazzi, R, Hirani, A, Kaplan, G, Leiby, B, Marik, PE (Mar 24, 2011). "Norephinephrine or Dopamine for Septic Shock: A Systematic Review of Randomized Clinical Trials". Journal of intensive care medicine 27 (3): 172–8. doi:10.1177/0885066610396312. PMID 21436167. Cite uses deprecated parameters (help)
^ ^a ^b Sandrock, CE; Albertson, TE (February 2010). "Controversies in the treatment of sepsis". Seminars in respiratory and critical care medicine 31 (1): 66–78. doi:10.1055/s-0029-1246290. PMID 20101549. Cite uses deprecated parameters (help)
^ Annane D, Sebille V, Charpentier C, Bollaert PE, Francois B, Korach JM, Capellier G, Cohen Y, Azoulay E, Troche G, Chaumet-Riffaut P, Bellissant E. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002 Aug 21;288(7):862-71. doi:10.1001/jama.288.7.862 PMID 12186604
^ "BestBets: Do low dose steroids improve outcome in septic shock?".
^ Martí-Carvajal, AJ; Solà, I, Lathyris, D, Cardona, AF (Apr 13, 2011). "Human recombinant activated protein C for severe sepsis". In Martí-Carvajal, Arturo J. Cochrane database of systematic reviews (Online) 4 (4): CD004388. doi:10.1002/14651858.CD004388.pub4. PMID 21491390. Cite uses deprecated parameters (help)
^ http://www.ncbi.nlm.nih.gov/pubmed/17583517
^ http://www.ncbi.nlm.nih.gov/pubmed/15755654
^ Researchers make blood poisoning breakthrough
^ Huether, S.E., & McCance, K.L. (2008). Understanding Pathophysiology. 4th Edition.

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 敗血症および全身性炎症反応症候群：定義、疫学、および予後 sepsis and the systemic inflammatory response syndrome definitions epidemiology and prognosis
2. 成人における重症敗血症および敗血症性ショックのマネージメント management of severe sepsis and septic shock in adults
3. 敗血症性ショック：小児における迅速な覚知および初期蘇生 septic shock rapid recognition and initial resuscitation in children
4. Septic shock: Ongoing management after resuscitation in children
5. 小児における全身性炎症反応症候群（SIRS）および敗血症：定義、疫学、臨床症状、
および診断 systemic inflammatory response syndrome sirs and sepsis in children definitions epidemiology clinical manifestations and diagnosis

English Journal

Differential diagnosis and treatments of necrotizing otitis externa: A report of 19 cases.

Chen YA, Chan KC, Chen CK, Wu CM.SourceDepartment of Otolaryngology, Chang-Gung Memorial Hospital, No. 5, Fu-Shing street, Kwei-Shan Hsiang, Tao-Yuan Hsien, Taiwan; Chang Gung University, Linkou, Taiwan.
Auris, nasus, larynx.Auris Nasus Larynx.2011 Dec;38(6):666-70. Epub 2011 Feb 24.
OBJECTIVE: Necrotizing otitis externa is an uncommon but potentially life-threatening infection disease of the external auditory canal and temporal bone. Its presentation and natural course had been largely altered through the years. The aim of this study was to analyze the clinical presentation, ba
PMID 21353408

Encapsulating Peritoneal Sclerosis Complicated by an Intra-abdominal Abscess.

Morishita K, Otomo Y, Aiboshi J, Kaji M.SourceDepartments of Acute Critical Care and Disaster Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
American journal of kidney diseases : the official journal of the National Kidney Foundation.Am J Kidney Dis.2011 Aug;58(2):325-8. Epub 2011 May 20.
We present a case of a 68-year-old woman who developed encapsulating peritoneal sclerosis (EPS) with an intra-abdominal abscess. The patient was referred to our hospital with abdominal pain, nausea, and vomiting. She had end-stage kidney disease secondary to diabetes mellitus that had been treated w
PMID 21601337

Japanese Journal

敗血症性ショックを伴う腎膿瘍を発症した軽度先天性水腎症の1例

荒畑幸絵,北澤克彦,松本弘 [他]
日本小児科学会雑誌 115(1), 102-106, 2011-01
NAID 40018699545

臨床研究・症例報告抗菌薬に加え高用量の免疫グロブリンを併用し後遺症なく救命した肺炎球菌による敗血症性ショックの2カ月児例

秋山類,岡田広,小森功夫 [他]
小児科臨床 64(3), 423-428, 2011-03
NAID 40018268620

Related Pictures

★リンクテーブル★

リンク元	「敗血症」「敗血症性ショック」「感染性ショック」「toxic shock」「敗血性ショック」
関連記事	「shock」「septic」

「敗血症」

Septic shock
	Classification and external resources
ICD-10	A41.9
ICD-9	785.52
DiseasesDB	11960
MedlinePlus	000668
MeSH	D012772

　　[★]

英: sepsis, (昔の概念→)septicemia
関

定義

感染症による全身性炎症反応症候群(SIRS)をセプシス(sepsis, 広義の敗血症？)とする
感染症の病原体は、一般細菌(グラム陽性菌・陰性菌)、真菌、寄生虫、ウイルスなど
皮膚や粘膜の傷とか、種々の臓器にある感染巣から、細菌がリンパ流から血中に入り、全身に播種されて、新たに転移性の感染巣をつくり、重篤な全身症状を引き起こす。

全身性炎症反応症候群の診断基準

下記項目のうち2項目以上が当てはまる

1. 体温>38℃ or 体温<36℃
2. 心拍数>90bpm
3. 呼吸数>20回/min or PaCO2<32mmHg
4. (白血球数>12,000/ul or 白血球数<4,000/ul) or ( 幼若好中球>10% )　←　ここでいう幼若好中球とは桿状好中球のことである。

敗血症の周辺疾患概念

1. 全身性炎症反応症候群 systemic inflammatory response syndrome SIRS

発熱や白血球増加などの全身の炎症の徴候によって特徴づけられる病態(SIRSの診断基準に合致する病態)

2. 敗血症 sepsis

SIRSが感染の結果である場合

3. 重症敗血症 severe sepsis

主要臓器障害を伴う敗血症

4. 敗血症性ショック septic shock

輸液投与に不応性の低血圧を伴う重症敗血症

5. 多臓器機能障害症候群 multiorgan dysfunction syndrome MODS

2つ以上の主要臓器の機能異常

6. 多臓器不全 multiorgan failure MOF

2つ以上の主要臓器の不全状態

病態生理

LPS

LPSが血液凝固を促進→血小板、フィブリノゲン、凝固因子消費　→　血栓形成　→　プラスミノゲンを消費して血栓溶解 (FDP産生)　→

→出血傾向　→　皮下出血、歯肉出血、顕微鏡的血尿(出血性敗血症)

原因となる病原体

細菌：グラム陽性球菌(ブドウ球菌、レンサ球菌)、グラム陰性桿菌(大腸菌、緑膿菌、肺炎桿菌、プロテウス)
真菌：Candida albicans

症状

悪寒、戦慄を伴う発熱、頻脈、頻呼吸、全身倦怠感、呼吸困難、意識障害、ショック、乏尿
敗血症による多臓器不全で障害を受けやすい臓器：肺、腎臓、心血管系、中枢神経系

重症敗血症の40%に急性呼吸促迫症候群を合併

検査

血液検査

白血球：12,000/ul以上のことが多い(SIRSの定義)

左方移動、重症例では白血球減少

血小板数：血管内凝固に伴い低下
CRP：基準値以上
凝固系・線溶系：凝固能低下、線溶系亢進

培養

血液培養
カテーテルの先端(留置カテーテルがある場合)

治療 (ICU.644)

酸素投与

敗血症における組織の酸素化

敗血症では細胞の酸素摂取能が損なわれている　→　重症敗血症患者の組織酸素濃度がなぜ健常者よりも高くなる　(ICU.645)
重症敗血症や敗血症性ショックにおいては

敗血症における酸素摂取量(ICU.645)

敗血症における酸素摂取量(VO2)の増加は、好中球の活性化の過程(呼吸バースト)で酸素が消費された結果。

初期蘇生

重症敗血症や敗血症性ショックの患者に対する最初の6時間の管理目標

1.中心静脈庄8-12mmHg
2.平均動脈庄≧65mmHg
3.尿量≧0.5 mL/kg/h
4.SVO2≧70% or SCVO2≧70%

SVO2：混合静脈血酸素飽和度、肺動脈血酸素飽和度

SCVO2：中心静脈血酸素飽和度、上大静脈血酸素飽和度

輸液負荷

循環血液量減少が明らかであるか疑われる場合：

1. 500-1,000mLの晶質液 or 300-500mLの膠質液を30分かけて投与
2. 初期蘇生の目標値に達するまで、または輸液過多寸前になるまで1)を行う。

昇圧薬(ICU.646)

1. 輸液負荷を行っても低血圧が持続する場合、ドパミン or ノルアドレナリンを投与

ドパミン：5-20 ug/kg/min：心拍出量増加：腹腔内蔵機の血流減少

ノルアドレナリン：0.2-1.3 ug/kg/min：心拍出量不変、血管収縮

2. 1. に不応の場合、パソプレシン

パソプレシン：0.01-0.04 U/min：血管収縮薬：心拍出量減少→心不全の既往で慎重

経験的抗菌薬治療(ICU.646)

重症敗血症や敗血症性ショックと診断したら1時間以内に抗菌薬を静脈内投与する
抗菌薬投与前に少なくとも2セットの血液検体を採取　→　血液培養＆感受性検査のため
イミペネム/メロペネムの単剤
MRSAのリスクリスク有り：イミペネム/メロペネム + バンコマイシン/リネゾリド

コルチコステロイド(ICU.646)

昇庄薬を必要とするすべての敗血症性ショック患者に推奨
ヒドロコルチゾン：200-300mg用を2-3回に分割して静脈内投与もしくは経口投与、7日間継続
副腎不全の改善

「敗血症性ショック」

　　[★]

英: septic shock
同: 敗血症ショック、感染性ショック、細菌性ショック、エキソトキシンショック(厳密には定義が違う？)
関: ショック、敗血症

概念

微生物の感染によって起こる。グラム陰性菌(endotoxic shock)で起こるが、グラム陽性菌・真菌でも起こりうる。(BPT.102)
必ずしも全身性の菌血症は必須ではない。局所の生物の血管外感染にたいする宿主の炎症反応で十分おこりうる。(BPT.102)
敗血症ショックの70%がグラム陰性菌由来のエンドトキシンによる(endotoxic shock)

特徴

warm shock：LPSによるショックでは末梢血管の血管透過性が亢進し、末梢血管抵抗が低下するが、体液が組織に移行して体が温かく感じられる。
血管末梢抵抗の低下により、代償的に高心拍出量状態となるり、ついには低心拍出量状態、多臓器不全となる。末期では体温は下がる。

病態生理 BPT.103

1. LPSが血中に放出される
2. 循環血液中のLPS-binding proteinと結合する
3. 2.の複合体は単球、マクロファージ、好中球上に発現しているCD14に結合する
4. CD14と共役しているTLR-4が細胞内にシグナルを伝達する。
5. TLR-4からのシグナルにより、IL-1, TNF等のサイトカインを放出
6. IL-1, TNFは血管内皮細胞に作用して抗凝固因子(TFPI、thrombomodulin)の産生を低下させる。　←　この作用は血管内皮上のTLR-4-CD14にLPSが結合することで増強される。

低用量のLPS

1. 単球、マクロファージ、好中球を活性化。補体系の直接の活性化。
2. LPSに反応してTNFを産生した単球性の食細胞はこんどはIL-1を産生する
3. 血管内皮はTNFとIL-1に反応してIL-6, IL-8を産生し、接着分子を発現する。

高用量のLPS

1. サイトカインにより産生されたエフェクター(NO、血小板活性化因子(PAF))が増加
2. 多量のTNFとIL-1によって発熱、急性相反応物(APR)の産生、好中球の増多
3. 血管内皮細胞は前凝固状態になる

高用量のLPSによってもたらされる帰結

(1) 全身性の血管拡張(低血圧)
(2) 心筋収縮力の減弱
(3) びまん性の血管内皮障害と活性化、これにより白血球の血管内皮の接着が促進され、肺における肺胞のびまん性血管内皮損傷がおこる。
(4) 凝固系の亢進がDICを引き起こす。

症状

warm shock: 初期は発熱を伴う。発汗、呼吸促迫、頚静脈平坦、脈圧増大(高心拍出量状態を反映。低血圧の代償)、頻脈(発熱による)、心拍数増加、末梢血管抵抗低下、意識低下、尿量減少。
cold shock: 末期には体温は低下する。
呼吸性アルカローシス：乳酸蓄積とサイトカイン増加で頻呼吸となるため(CBT QB vol2 p.554)

新生児

低体温、無呼吸発作、出血斑

治療・管理

対症療法

初期におけるショックに対する治療　→　輸液負荷、昇圧薬、

輸液負荷

Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296-327.