糖尿病患者麻醉

1、糖尿病患者手術麻醉,,病例概況,女性，62歲，腹痛3日，擬診上消化道穿孔行剖腹探查術身高158cm，體重85kg，神志淡漠，T39.5高血壓病史16年，口服伊諾普利、尼群地平控制血壓，平素140/80，入院95/55糖尿病病史8年，口服二甲雙胍，血糖控制在6-8mmol/L，入院時血糖26.3，尿酮體+++高血脂，他汀類控制，效果佳ECG竇性心動過速（135bpm），ST-T改變,糖尿?。―M）診斷和分型,The spectr

2、um from normal glucose tolerance to diabetes in type 1 DM, type 2 DM, other specific types of diabetes, and gestational DM is shown from left to right. In most types of DM, the individual traverses from normal glucose to

3、lerance to impaired glucose tolerance to overt diabetes. Arrows indicate that changes in glucose tolerance may be bi-directional in some types of diabetes. For example, individuals with type 2 DM may return to the impair

4、ed glucose tolerance category with weight loss; in gestational DM diabetes may revert to impaired glucose tolerance or even normal glucose tolerance after delivery. The fasting plasma glucose (FPG) and 2-h plasma glucose

5、 (PG), after a glucose challenge for the different categories of glucose tolerance, are shown at the lower part of the figure. These values do not apply to the diagnosis of gestational DM. Some types of DM may or may not

6、 require insulin for survival, hence the dotted line.,分型主要根據(jù)病因，而非根據(jù)發(fā)病年齡和治療方法。1型病因是胰島β細胞衰竭和胰島素缺乏；2型病因包括胰島素缺乏、胰島素抵抗和糖異生增加,糖尿?。―M）流行病學,糖尿病（DM）流行病學,DM發(fā)病率大幅增高老齡化、肥胖、不運動慢性炎癥，導致葡萄糖耐量異常的治療，遺傳背景,糖尿?。―M）流行病學,糖尿病影響圍手術期的并發(fā)癥和死亡率27

7、79名DM患者行CABG手術，與正常人群相比，DM患者ICU和住院時間延長正性肌力藥、輸血、透析↑腎衰、中風、縱隔炎、傷口感染↑30日死亡率2.6%︰1.6%5年累積生存率84.4%︰91.3%,糖尿病（DM）流行病學,許多2型DM直至手術時才發(fā)現(xiàn)DM7310名，CABG,何時發(fā)現(xiàn)并開始治療DM非常重要,DM相關并發(fā)癥 強直性關節(jié)綜合征,多見于青少年起病的DM患者關節(jié)僵硬，身材矮小，皮膚呈蠟樣緊張膠原組織糖基

8、化是可能原因開始于第5指掌指關節(jié)和近指關節(jié)，可以侵犯包括頸椎和胸椎在內的大關節(jié)對于肥胖患者糖尿病是其困難插管的預測因子,DM相關并發(fā)癥 心血管疾病,DM患者圍手術期心血管并發(fā)癥和死亡率增高2-3倍心血管病變占DM患者死亡原因的80%高血壓、冠狀動脈疾病、周圍動脈疾病、收縮性或舒張性心功能異常、心衰大多數(shù)＞65歲的DM患者存在有/無癥狀冠狀動脈疾病，更多發(fā)生無癥狀心肌缺血，有自主神經(jīng)病變者應提高警惕D

9、M性心肌病使心室舒張受限，左室充盈壓增高，導致心衰,DM相關并發(fā)癥 心血管疾病,DM患者高血壓發(fā)生率高于非DM患者，且隨DM時間延長而增加，與DM腎病的進展緊密相關。2型DM患者血壓控制可能比長期的血糖控制更重要，推薦的血壓＜130/80。ACEI或β-blocker可降低DM大血管病變相關的死亡率。,DM相關并發(fā)癥 微血管病變,糖尿病視網(wǎng)膜病變,DM相關并發(fā)癥

10、 微血管病變,糖尿病視網(wǎng)膜病變,Diabetic retinopathy results in scattered hemorrhages, yellow exudates, and neovascularization. This patient has neovascular vessels proliferating from the optic disc, requiring urgent pan retinal laser

11、photocoagulation.,DM相關并發(fā)癥 微血管病變,糖尿病視網(wǎng)膜病變視網(wǎng)膜循環(huán)是腦循環(huán)的預測因子術前存在視網(wǎng)膜微血管病變嚴重提示手術后腦功能障礙和死亡率風險增加,DM相關并發(fā)癥 微血管病變,糖尿病腎病,Time course of development of diabetic nephropathy. The relationship of time from ons

12、et of diabetes, the glomerular filtration rate (GFR), and the serum creatinine are shown. (Adapted from RA DeFranzo, in Therapy for Diabetes Mellitus and Related Disorders, 3d ed. American Diabetes Association, Alexandri

13、a, VA, 1998.),DM相關并發(fā)癥 神經(jīng)病變,周圍神經(jīng)痛 靜息痛、夜間痛、下肢多見感覺異常自主神經(jīng)包括膽堿能、去甲腎上腺素能、肽能（如胰多肽、P物質等）心血管系統(tǒng)：靜息性心動過速，體位性低血壓，甚至猝死胃輕癱、膀胱排空異常上肢多汗，下肢無汗（下肢皮膚干裂，潰瘍風險增加）激素釋放的反調控機制減弱，導致不能感知低血糖,DM急性并發(fā)癥

14、 酮癥酸中毒,DM急性并發(fā)癥 酮癥酸中毒,Confirm diagnosis (plasma glucose, positive serum ketones, metabolic acidosis).Admit to hospital; intensive-care setting may be necessary for frequent monitoring or if pH 3.3 m

15、mol/L.Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG).Measure capillary glucose every 1–2

16、h; measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h.Replace K+: 10 meq/

17、h when plasma K+ < 5.5 meq/L, ECG normal, urine flow and normal creatinine documented; administer 40–80 meq/h when plasma K+ < 3.5 meq/L or if bicarbonate is given.Continue above until patient is stable, glucose g

18、oal is 150–250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin i

19、nfusion and subcutaneous insulin injection.,治療,DM急性并發(fā)癥 高血糖性高滲性昏迷,多見于成年2型糖尿病多尿、體重下降、進食減少數(shù)周精神錯亂、嗜睡或昏迷嚴重的脫水、高滲、低血壓和心動過速無DKA特有的惡心、嘔吐、腹痛及Kussmaul呼吸多由嚴重的合并癥誘發(fā)，如心梗、腦梗、膿毒癥、肺炎或其他嚴重感染,臨床特點,DM急性并發(fā)癥 高血糖性高滲性昏迷,DM的治療,

20、DM的治療,aAs recommended by the ADA; Goals should be developed for each patient. Goals may be different for certain patient populations. bA1C is primary goal. cWhile the ADA recommends an A1C < 7.0% in general, in the

21、 individual patient it recommends an ". . . A1C as close to normal (<6.0%) as possible without significant hypoglycemia. . . ." Normal range for A1C—4.0–6.0 (DCCT-based assay). dOne-two hours after beginnin

22、g of a meal. eIn patients with reduced GFR and macroalbuminuria, the goal is <125/75. fIn decreasing order of priority. gFor women, some suggest a goal that is 0.25 mmol/L (10 mg/dL) higher. Source: Adapted from A

23、merican Diabetes Association, 2007.,DM的治療,胰島素分泌刺激劑如磺脲類，通過作用于?細胞的ATP敏感性鉀通道促進胰島素釋放雙胍類如二甲雙胍，抑制肝糖異生并增加外周組織糖利用，但可導致乳酸酸中毒?糖苷酶抑制劑如米格列醇，延緩葡萄糖吸收而降低餐后高血糖噻唑烷二酮類如匹格列酮，與脂肪細胞細胞核內受體結合來降低胰島素抵抗,本例患者如何評估,女性，62歲，腹痛3日，擬診上消化道穿孔行剖腹探查術身高15

24、8cm，體重85kg，神志淡漠，T39.5高血壓病史16年，口服伊諾普利、尼群地平控制血壓，平素140/80，入院95/55糖尿病病史8年，口服二甲雙胍，血糖控制在6-8mmol/L，入院時血糖26.3，尿酮體+++高血脂，他汀類控制，效果佳ECG竇性心動過速（135bpm），ST-T改變,術前評估,是否確診？是否可爭取時間內科治療？膈下游離氣體、急腹癥腹痛3日，未禁食，估計腹腔感染嚴重,爭取時間，盡快完善術前準備，同時盡早

25、開始內科治療，處理酮癥,術前評估,術前還需哪些檢查？,動脈血氣電解質肝腎功能,K+ 3.2，Na+ 136，Cl- 99，HCO3 9，pH 7.05，CO2 33，肌酐、尿素氮稍升高 ，白蛋白 28,術前評估,術前內科治療水化胰島素糾酸電解質,術中管理,麻醉和手術對葡萄糖代謝的影響七氟烷和異氟烷對葡萄糖耐量的損害程度相同，與手術刺激無關手術可產(chǎn)生應激反應，使機體處于分解代謝狀態(tài)，改變程度與手術大小有關硬膜外麻醉可減少

26、應激反應激素的釋放而對血糖影響小,術中管理,麻醉方法的選擇全麻插管保護氣道椎管內阻滯、神經(jīng)阻滯對機體代謝影響小,術中管理,擇期手術手術當日胰島素的用法反復測量血糖是關鍵未使用胰島素的2型DM患者，術晨不給降糖藥，二甲雙胍術前24h停藥，一般手術無需輸注含糖液體，大手術及術后幾天不能進食者應靜脈給予含糖液，并使用胰島素,術中管理,擇期手術手術當日胰島素的用法使用胰島素的患者接受大于2h的手術，同時輸注葡萄糖和胰島素可能對患者有益

27、。5%的葡萄糖125ml/h或2ml/kg.h，胰島素5U負荷量，維持的速度為最近測得的血糖（mg/dl）/150（嚴重感染或應激大的手術100），或者1U/h重要的是密切監(jiān)測血糖和電解質,術中管理,本例患者如何監(jiān)測？,術中管理,如何處理術中高血糖？血糖超過14mmol/l需靜脈給予胰島素單次劑量胰島素5-10u，成人胰島素一般1u降低血糖0.6mmol/l，或者降低1mmol/l血糖需胰島素1.7u持續(xù)輸注胰島素,術中管理,如

28、何識別和處理術中低血糖？全身麻醉下表現(xiàn)為難以解釋的休克和,Neuroglycopenic symptoms of hypoglycemia are the direct result of central nervous system (CNS) glucose deprivation. They include behavioral changes, confusion, fatigue, seizure, loss of cons

29、ciousness, and, if hypoglycemia is severe and prolonged, death. Neurogenic (or autonomic) symptoms of hypoglycemia are the result of the perception of physiologic changes caused by the CNS-mediated sympathoadrenal discha

30、rge triggered by hypoglycemia. They include adrenergic symptoms (mediated largely by norepinephrine released from sympathetic postganglionic neurons but perhaps also by epinephrine released from the adrenal medullae) suc

31、h as palpitations, tremor, and anxiety. They also include cholinergic symptoms (mediated by acetylcholine released from sympathetic postganglionic neurons) such as sweating, hunger, and paresthesias. Clearly, these are n

32、onspecific symptoms. Their attribution to hypoglycemia requires a corresponding low plasma glucose concentration and their resolution after the glucose level is raised (Whipple's triad).Common signs of hypoglycemia

33、include diaphoresis and pallor. Heart rate and systolic blood pressure are typically raised, but these findings may not be prominent. Neuroglycopenic manifestations are often observable. Transient focal neurologic defici

34、ts occur occasionally. Permanent neurologic deficits are rare.,術中管理,如何識別和處理術中低血糖？全身麻醉下臨床表現(xiàn)被掩蓋，常出現(xiàn)難以解釋的大汗、低血壓、心動過速確診依靠血糖監(jiān)測Oral treatment with glucose tablets or glucose-containing fluids, candy, or food is appropriate

35、if the patient is able and willing to take these. A reasonable initial dose is 20 g of glucose. If the patient is unable or unwilling, because of neuroglycopenia, to take carbohydrates orally, parenteral therapy is neces

36、sary. Intravenous glucose (25 g) should be given and followed by a glucose infusion guided by serial plasma glucose measurements. If intravenous therapy is not practical, subcutaneous or intramuscular glucagon (1.0 mg in

37、 adults) can be used, particularly in patients with T1DM. Because it acts by stimulating glycogenolysis, glucagon is ineffective in glycogen-depleted individuals (e.g., those with alcohol-induced hypoglycemia). It also s

38、timulates insulin secretion and is therefore less useful in T2DM. These treatments raise plasma glucose concentrations only transiently, and patients should therefore be urged to eat as soon as is practical to replete gl