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Anesthesia and diabetes


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anesthesia and diabetes

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Anesthesia and diabetes

  1. 1. Anesthesia and diabetes Marwa Ahmad Mahrous Assistant lecturer Department of anesthesia and ICU Sohag university hospitals
  2. 2. Definition Types Diagnosis End-organ dysfunction Complications Anesthetic management
  3. 3. ::DDeeffiinniittiioonn syndrome of abnormal carbohydrate metabolism that is characterized by hyperglycemia
  4. 4. :Classification -type 1(IDDM) insulin-requiring Absolute deficiency of insulin May be autoimmune based Management requires exogenous insulin Patients are prone to ketosis
  5. 5. -type 2 (NIDDM) insulin resistant: Relative deficiency of insulin/peripheral resistance to insulin/excessive hepatic glucose release Generally seen in obese adults Patients produce adequate amounts of insulin to prevent ketosis but are at risk for hyperosmolar state Initially managed with diet control, weight loss, and oral hypoglycemic agents
  6. 6. -gestetional -secondary:Pancreatic disease (decreased insulin production) -Drug induced -Secondary to endocrinopathies such as Cushing’s disease, acromegaly, pheochromocytoma
  7. 7. :Diagnosis According to American Diabetes Association: 1. Fasting (8hr) plasma glucose value 126 mg/dl 2. Symptoms of D.M :polydipsia, polyuria and unexplained weight loss. 3. Random blood glucose value 200mg/dl 4. 2hr post oral glucose challenge value 200mg/dl 5. Haemoglobin A1c ≥6.5%
  8. 8. End-organ dysfunction  Cardiovascular: 1- diabetic patients are at increased risk for hypertension, coronary artery disease,congestive heart failure, diastolic dysfunction, cereberovascular, renovascular and peripheral vascular disease. 2-these patient may have clinically silent myocardial ischemia or infarction. 3- DM considered one of the risk factors when determining preoperative cardiac testing 4-ẞ-adrenergic blockers
  9. 9.  Renal: -avoid nephrotoxic drugs, maintain normovolumia, control of hyperglycemia and/or hypertension and preservation of renal blood flow
  10. 10.  Neuropathy: Peripheral and automonic -autonomic neuropathy may blunt the compensatory cardiovascular response to hypotension so predisposing to haemodynamic liability. May cause gastroparesis so presdisposing to pulmonary aspiration
  11. 11. Autonomic NNeeuurrooppaatthhyy • Orthostatic hypotension • Resting tachycardia • Gastroparesis(vomiting,diarrhea) • Impotence • Cardiac dysrhythmias • Asymptomatic hypoglycemia • Sudden death syndrome
  12. 12.  Non enzymatic glycosylation of proteins and abnormal cross linking of collagen : -leading to decreased joint mobility -if affecting tempromandubilar joint and/or cervical spine will cause difficult airway Stiff joint syndrome  Obesity
  13. 13. Stiff Joint Syndrome -Long-standing type I diabetics are at risk for tthhiiss ssyynnddrroommee, wwhhiicchh iiss MMaanniiffeesstteedd bbyy:: jjooiinntt rriiggiiddiittyy ((mmoosstt ssiiggnniiffiiccaannttllyy aaffffeeccttiinngg jjooiinnttss iinnvvoollvviinngg tthhee aaiirrwwaayy ssuucchh aass tthhee tteemmppoorroommaannddiibbuullaarr, aattllaannttoooocccciippiittaall, aanndd cceerrvviiccaall ssppiinnee jjooiinnttss)), sshhoorrtt ssttaattuurree, aanndd ttiigghhtt, wwaaxxyy sskkiinn. --CChhrroonniicc hhyyppeerrggllyycceemmiiaa rreessuullttiinngg iinn nnoonneennzzyymmaattiicc ggllyyccoossyyllaattiioonn ooff pprrootteeiinnss aanndd AAbbnnoorrmmaall ccrroossss--lliinnkkiinngg ooff ccoollllaaggeenn iinn jjooiinnttss aanndd ootthheerr ttiissssuueess iiss ccuurrrreennttllyy tthhoouugghhtt ttoo bbee tthhee iinniittiiaattoorr ooff tthhee ssttiiffff jjooiinntt ssyynnddrroommee. --LLiimmiitteedd nneecckk mmoobbiilliittyy mmaayy rreessuulltt iinn aa ddiiffffiiccuulltt iinnttuubbaattiioonn aanndd sshhoouulldd bbee iiddeennttiiffiieedd bbeeffoorree aaiirrwwaayy mmaanniippuullaattiioonn.
  14. 14. -A positive “prayer” sign (inability to approximate their fingers and palms while pressing their hands together with the fingers extended) and palm printing have been reported to identify patients with stiff joint syndrome. -Changes in airway anatomy will create difficulty for intubation in approximately one third of patients with longterm type I diabetes undergoing laryngoscopy.
  15. 15. Complications • Acute Either : -hyperglycemia : DKA NKHS -hypoglycemia • Chronic -vascular -neurological
  16. 16. Chronic effects of Hyperglycaemia 11.. MMiiccrroovvaassccuullaarr PPrroolliiffeerraattiivvee rreettiinnooppaatthhyy DDiiaabbeettiicc nneepphhrrooppaatthhyy ((cclloossee aassssoocciiaattiioonn wwiitthh hhyyppeerrtteennssiioonn,, wwhhiicchh iiss ffoouunndd iinn 3300--6600%% ooff ddiiaabbeettiiccss)) 22.. MMaaccrroovvaassccuullaarr 11.. AAtthheerroosscclleerroossiiss 22.. CCoorroonnaarryy hheeaarrtt ddiisseeaassee ((bbeewwaarree ssiilleenntt iisscchhaaeemmiiaa,, ccaarrddiioommyyooppaatthhyy)) 33.. CCeerreebbrroovvaassccuullaarr ddiisseeaassee 44.. PPeerriipphheerraall vvaassccuullaarr ddiisseeaassee 33.. NNeeuurrooppaatthhiicc 11.. PPeerriipphheerraall ::MMoottoorr ((MMoonnoonneeuurrooppaatthhiieess,, pprreessssuurree ppaallssiieess)) SSeennssoorryy ppoollyynneeuurrooppaatthhyy 22..AAuuttoonnoommiicc  DDiiaarrrrhheeaa  UUrriinnaarryy iinnccoonnttiinneennccee  PPoossttuurraall hhyyppootteennssiioonn  CCaarrddiiaacc ddeenneerrvvaattiioonn  IImmppaaiirreedd vveennttiillaattoorryy ccoonnttrrooll –– rriisskk ooff rreesspp aarrrreesstt wwiitthh aannaaeesstthheessiiaa  GGaassttrrooppaarreessiiss 44.. ““SSttiiffff jjooiinntt ssyynnddrroommee”” ((aaiirrwwaayy)) 5.. IInnccrreeaasseedd iinncciiddeennccee ooff iinnffeeccttiioonnss
  17. 17. Acute effects ooff hhyyppeerrggllyyccaaeemmiiaa  Dehydration and electrolyte disturbances (due to osmotic diuresis)  Acidaemia (accumulation of lactic + ketoacids)  Fatigue, weight loss and muscle wasting (lipolysis and proteolysis in absolute insulin deficiency)  Poor wound healing and impaired wound strength  Diabetic ketoacidotic coma (Type I diabetics due to absolute insulin deficiency)  Hyperosmolar Non-ketotic coma (Type II diabetics)
  18. 18. Diabetic ketoacidosis -Mainly in type 1 IDDM -Decreased insulin activity allows the catabolism of free fatty acids into ketone bodies (acetoacetate and β-hydroxybutyrate), some of which are weak acids . Accumulation of these organic acids results in DKA and an anion-gap metabolic acidosis.
  19. 19. :DKA characterized by • hyperglycemia • dehydration • hyperosmolarity • high anion-gap metabolic acidosis
  20. 20. -precipitating causes for DKA as infection , surgical stress, trauma and /or lack of insulin. -Clinical manifestations of DKA include tachypnea (respiratory compensation for the metabolic acidosis), abdominal pain, nausea and vomiting, and changes in sensorium.
  21. 21. Treatment of DKA  Identifying and treating the precipitating factors  Fluid resuscitation  Glycometabolic control  Electrolyte replacement
  22. 22. The goal for decreasing blood glucose in Ketoacidosis should be 75–100 mg/dL/h or 10%/h. Therapy generally begins with an intravenous insulin infusion at 0.1 units/kg/h. Several liters of 0.9% saline (1–2 L the first hour, followed by 200–500 mL/h) may be required to correct dehydration in adult patients.
  23. 23. When plasma glucose decreases to 250 mg/dL, an infusion of D 5 W should be added to the insulin infusion to decrease the possibility of hypoglycemia and to provide a continuous source of glucose (with the infused insulin) for eventual normalization of intracellular metabolism. Patients may benefit from precise monitoring of urinary output during initial treatment of DKA. Bicarbonate is rarely needed to correct severe acidosis (pH < 7.1) as the acidosis corrects with volume expansion and with normalization of the plasma glucose concentration.
  24. 24. Guidelines for DKA management 1. Routine monitoring, arterial access, central venous line 2. Aggressive crystalloid replacement 1-3 L in the first hour, with 0.9 saline. 3. Intravenous insulin titrated by serial plasma glucose determinations adding dextrose infusion as glucose values 200mg/dl 4. Supplementation of potassium, phosphrus and magnesium as guided by serial plasma determination.
  25. 25. Hyperosmolar nonketotic state -Occur predominantly in type 2 DM -Comparing with DKA ,NKHS patients are typically more dehydrated, hyperosmolar and hyperglycemic. -Ketoacidosis is not a feature of hyperosmolar nonketotic coma possibly because enough insulin is available to prevent ketone body formation.
  26. 26. :NKHS characterized by  Neurologic alterations : may include confusion , coma , seizures and/or focal neurological deficits.  Severe dehydration with significant hypotension leading to lactic acidosis (NKHS patients lack acidemia due to ketone bodies)  Thrombotic events due to hypovolumia, hypotension and hyperviscosity.  Hyperosmolality (frequently exceeding 360 mOsm/L) induces dehydration of neurons, causing changes in mental status and seizures.
  27. 27. NKHS management  Fluid resuscitation is the mainstay of treatment (0.9 saline)  Due to greater hyperglycemia and hyperosmolarity in NKHS, these pateints are at increased risk of developing cerebral edema  so more gradual (>24hr) correction of hyperglycemia and hyperosmolarity is recommended along with frequent neurologic evaluations.
  28. 28. Hypoglycemia  hypoglycemia is present when plasma glucose is less than 50 mg/dL. Hypoglycemia in the diabetic patient is the result of an absolute or relative excess of insulin relative to carbohydrate intake and exercise. Causes of hypoglycemia: -residual effects of long acting drugs -overaggressive antidiabetic treatment -decreased caloric intake
  29. 29. Diagnosis of hypoglycemia  Two major ways to detect hypoglycemia: -altered mental status up to coma and death. -physiologic responses to increased catecholamines But the ability to recognize these manifestions during perioperative period and under anesthesia , is compromized  Detection of hypoglycemia under anesthesia requires high index of suspicion and frequent determination of plasma glucose levels.
  30. 30. Treatment Diabetic patients are incompletely able to counter hypoglycemia despite secreting glucagon or epinephrine (counterregulatory failure). Treatment Consists of : -Dextrose adminstration -Correcting the precipitating causes The treatment of hypoglycemia in anesthetized or critically ill patients Intravenous administration of 50% glucose (each milliliter of 50% glucose will raise the blood glucose of a 70-kg patient by approximately 2 mg/dL). Awake patients can be treated orally with fluids containing glucose or sucrose.
  31. 31. Anesthetic management Anesthetic management should include: -preoperative -intraoperative -postoperative -Perioperative hyperglycemia -Perioperative hypoglycemia
  32. 32. Peri-operative goal maintaining blood glucose values below 180 mg/dl during the perioperative period while reducing blood glucose variability and avoiding hypoglycemia.
  33. 33. ??HHooww • PPrroovviiddee aaddeeqquuaattee iinnssuulliinn ttoo tthhee ppaattiieenntt ttoo ccoouunntteerraacctt tthhee ccaattaabboolliicc pprroocceesssseess tthhaatt ddeevveelloopp iinn rreessppoonnssee ttoo ssuurrggeerryy • GGlluuccoossee nneeeeddss ttoo bbee pprroovviiddeedd ttoo mmeeeett tthhee iinnccrreeaasseedd mmeettaabboolliicc nneeeeddss,, ccaauusseedd bbyy ssuurrggiiccaall ssttrreessss,, aass wweellll aass bbaassaall mmeettaabboolliicc rreeqquuiirreemmeennttss • AA ssiimmppllee rreeggiimmeenn tthhaatt iiss iimmmmuunnee ttoo eerrrroorr
  34. 34. Peri-op problems  Stress response to surgery with catabolic hormone secretion  Interruption of food intake, pre- and perhaps post-surgery (also PONV)  Altered consciousness, masking the symptoms of hypoglycaemia  Circulatory disturbance that may alter the uptake of s.c. insulin  The altered physiological state resulting from end organ pathology
  35. 35. What are the factors affecting tthhee ppeerriiooppeerraattiivvee ??aanneesstthheettiicc mmaannaaggeemmeenntt ooff DDMM  TTyyppee ooff DDMM  MMeeddiiccaattiioonn  EEnndd--oorrggaann cchhaannggeess  NNaattuurree ooff ssuurrggeerryy  UUrrggeennccyy ooff ssuurrggeerryy  LLeevveell ooff ggllyycceemmiicc ccoonnttrrooll
  36. 36. preoperative management- -Preoperative evaluation should include a thorough history and physical exam . -Prior anesthetic records should be reviewed to determine whether difficulties with intubation or perioperative diabetic complications were documented previously. -Laboratory investigations should include determination of blood glucose, potassium, blood urea nitrogen (BUN), and creatinine in addition to a urinalysis for glucose, ketones, and protein. -Glycosylated hemoglobin (HbA1c) levels reflect the adequacy of glucose control over the preceding 1–3 months.
  37. 37. -Hemoglobin A 1c Abnormally elevated hemoglobin A 1c concentrations identify patients who have maintained poor control of blood glucose over time. These patients may be at greater risk for perioperative hyperglycemia, perioperative complications, and adverse outcomes. -The perioperative morbidity of diabetic patients is related to their preexisting end-organ damage.
  38. 38. -ECG Myocardial ischemia or old infarction may be evident on an ECG despite a negative history. -chest radiograph cardiac enlargement,pulmonary vascular congestion, or pleural effusion, but is not routinely indicated.
  39. 39. Premedication with a nonparticulate antacid and metoclopramide is often used in an obese diabetic patient with signs of cardiac autonomic dysfunction.
  40. 40. RReeggiimmeenn ddeeppeennddss oonn • Type of diabetes and its usual treatment • Extent of surgery • The amount of surgical stress and the catabolic response to that stress • Beware major surgery and emergency surgery, especially trauma or surgery related to infective processes
  41. 41. TTyyppee II ddiiaabbeetteess Preoperative Insulin Traditional Approach  Give 1/4 to 1/2 the daily dose of intermediate-acting insulin subcutaneously  Add 1/2 unit of intermediate-acting insulin for each unit of insulin prescribed  Start IV glucose 5-10 g/h
  42. 42. Preoperative Insulin Continuous IV Infusion • These patients should all be treated on I.v. insulin infusion before, during and after surgery. • This is true for major surgery, although there are some alternatives in minor surgery • Place 50 U. Regular Insulin in 1000 ml NS • Give 10 ml/h • Measure blood glucose q.h. • Adjust infusion rate to keep glucose level at 120-180 mg/dl • Turn infusion off for 30 min if glucose level falls below 80 mg/dl • Provide sufficient glucose (5-10g/h) and potassium (2-4 mEq/h)
  43. 43. New insulin delivery modes 1. Continuous subcutaneous infusions 2. Continuous intra-peritoneal infusions
  44. 44. Type IIII ddiiaabbeetteess oonn ddiieett aalloonnee  If fasting blood glucose < 7.8 mmol/l or 140.4 mg/dl  Close observation including hourly dextrose measurement (glucometer in theatre)  Conversion to a GIK regime if the glucose rises >8.0 mmol/l or 144 mg/dl
  45. 45. If the patient is taking an oral hypoglycemic agent preoperatively rather than insulin, the drug can be continued until the day of surgery. Sulfonylureas and metformin have long halflives and many clinicians will discontinue them 24–48 h before surgery. They can be started postoperatively when the patient resumes oral intake. Metformin is restarted if renal and hepatic function remain adequate.
  46. 46. Type II diabetes oonn oorraall hhyyppooggllyyccaaeemmiicc • There are 4 groups of oral hypoglycaemic agents (OHA) • Sulphonylureas Enhanced secretion of insulin in response to glucose and increased sensitivity at its peripheral actions • Biguanides Promote glucose utilization and reduce hepatic glucose production • Thiazolidinediones (Rosiglitazone) Enhance insulin action in the periphery Inhibit hepatic gluconeogenesis Enhances glucose uptake into tissues via GLUT-4 glucose transporter Preserves the β-cells of the pancreas • Modifiers of glucose absorption e.g.. Ά-glucosidase inhibitor acarbose Suppress the breakdown of complex carbohydrates in the gut delaying the rise of blood sugar postprandially
  47. 47. Stop tthhee OOHHAA bbeeffoorree ssuurrggeerryy?? • The long acting sulphonylureas should be stopped 3 days before surgery and converted to shorter acting drugs, or insulin if coming for major surgery • Metformin need not be stopped (recommendation used to be 2 days) Risk of lactic acidosis extremely low • Omit morning OHA dose • If the patient is for minor surgery the OHA is omitted on the day of surgery and they can then be treated without insulin, with close observation and conversion to GIK if the glucose rises above 8.0 mmol/l • If the patient is for major surgery the patient should be established on insulin pre-op, even if well controlled. There is good evidence that continuous I.v insulin infusions are superior to intermittent s.c.boluses and also to I.v. boluses.
  48. 48. Intraoperative management the patient receives a fraction—usually half—of the total morning insulin dose in the form of intermediate-acting insulin. To decrease the risk of hypoglycemia, insulin is administered after intravenous access has been established and the morning blood glucose level is checked.
  49. 49. intraoperative hyperglycemia (>150–180 mg/dL) is treated with intravenous regular Insulin according to a sliding scale. One unit of regular insulin given to an adult usually lowers plasma glucose by 25–30 mg/dL. It must be stressed that these doses are approximations and do not apply to patients in catabolic states (eg, sepsis, hyperthermia).
  50. 50. Regular insulin can be added to normal saline in a concentration of 1 unit/mL and the infusion begun at 0.1 unit/kg/h. As blood glucose fluctuates, the regular insulin infusion can be adjusted up or down as required. The dose required may be approximated by the following formula: A general target for the intraoperative maintenance of blood glucose is less than 180 mg/dL.
  51. 51. When administering an intravenous insulin infusion to surgical patients, adding some (eg, 20 mEq) KCl to each liter of fluid may be useful, as insulin causes an intracellular potassium shift .
  52. 52. MMiinnoorr ssuurrggeerryy  IIff ppaattiieenntt iiss eexxppeecctteedd ttoo rreessuummee oorraall iinnttaakkee qquuiicckkllyy aafftteerr ssuurrggeerryy,, aa rreedduucceedd aapppprrooaacchh mmaayy bbee aacccceeppttaabbllee  TThheessee ppaattiieennttss wwiillll bbee ggiivveenn ½ tthheeiirr iinntteerrmmeeddiiaattee aaccttiinngg iinnssuulliinn,, aanndd aa 55%% ddeexxttrroossee ssoolluuttiioonn aatt 110000--115500 mmll//hhoouurr ttoo pprreevveenntt hhyyppooggllyyccaaeemmiiaa..  IInnttrraa--oopp aanndd rreeccoovveerryy rroooomm bblloooodd ssuuggaarr mmoonniittoorriinngg iiss eesssseennttiiaall..  IItt iiss ssuuggggeesstteedd tthhaatt tthhee bblloooodd ssuuggaarr iiss mmeeaassuurreedd eevveerryy 3300 mmiinnss ttoo hhoouurrllyy..
  53. 53. Minor surgery  Keep glucose between 4.4 – 8.0 mmol/l  Both I.v insulin infusions and I.v glucose may be needed to achieve control.  Once the patient has had their first meal post-op they can be given the rest of their insulin dose depending on the measured blood glucose
  54. 54. MMaajjoorr ssuurrggeerryy  Places a much larger catabolic stress on patients  A glucose, Potassium and insulin (GIK) infusion is a simple reliable way of controlling the patient’s blood sugar in the perioperative period  Ideally it should be started in the preoperative period especially in those patients that are not well controlled  It is essential that there are frequent, accurate measurements of the blood sugar made throughout the perioperative period
  55. 55. SSuuggggeesstteedd GGIIKK rreeggiimmeenn  NNoorrmmaall iinnssuulliinn tthhee ddaayy bbeeffoorree ssuurrggeerryy  DDoo aa bblloooodd ssuuggaarr oonn tthhee ddaayy ooff ssuurrggeerryy,, aanndd oonnccee rreessuulltt kknnoowwnn ssttaarrtt iinnffuussiioonn  11.. 11 lliitteerr 1100%% ddeexxttrroossee ++ 4400 mmEEqq//ll KKCCLL aatt 00..11gg ddeexxttrroossee//kkgg//hhrr  22.. IInnssuulliinn iinnffuussiioonn ooff 5500 UU rraappiidd aaccttiinngg iinnssuulliinn iinn 225500 mmll 00..99%% NNaaCCll ppiiggggyybbaacckkeedd ttoo tthhee ddeexxttrroossee aanndd rruunn aatt 11--22 UU//hhrr ddeeppeennddiinngg oonn hhoouurrllyy ((oorr mmoorree)) mmeeaassuurreemmeennttss ooff gglluuccoossee  CCaarree sshhoouulldd bbee ttaakkeenn tthhaatt nneeiitthheerr iinnffuussiioonn iiss aalllloowweedd ttoo ssttoopp wwhhiillee tthhee ootthheerr ccoonnttiinnuueess rruunnnniinngg
  56. 56. Factors Adversely Affecting Diabetic Control Perioperatively  Anxiety  Starvation  Anaesthetic drugs  Infection  Metabolic response to trauma  Diseases underlying need for surgery  Other drugs e.g. steroids
  57. 57. Metabolic Responses to Surgery • Hormonal • Secretion of stress hormones • Cortisol • Catecholamines • Glucagon • Growth Hormone • Cytokines • Relative decrease in insulin secretion • Peripheral insulin resistance • Metabolic • Increased gluconeogenesis and glycogenolysis • Hyperglycaemia • Lipolysis • Protein breakdown
  58. 58. Metabolic Response to Surgery and Diabetes  Hyperglycaemia  Glucagon, cortisol and adrenaline secretion as part of the neuroendocrine response to trauma, combined with iatrogenic insulin deficiency or glucose overadministration may result in hyperglycaemia  Causes osmotic diuresis, making volume status difficult to determine and risking profound dehydration and organ hypoperfusion, and increased risk of UTI  osmotic diuresis, delayed wound healing, exacerbation of brain, spinal cord and renal damage by ischaemia  Results in hyperosmolality with hyperviscocity, thrombogenesis and cerebral oedema  Management  Frequently measure blood glucose and administer insulin
  59. 59. Metabolic Response to Surgery and Diabetes  Ketoacidosis  Any patient who is in a severe catabolic state and has an insulin deficiency (absolute or relative) can decompensate into keto-acidosis  Most common in type 1 patients  Increased risk postoperatively, often precipitated by the stress response, infection, MI, failure to continue insulin therapy.  characterised by hyperglycaemia, hyperosmolarity, dehydration (may lead to shock and hypotension) and excess ketone body production resulting in an anion gap metabolic acidosis.
  60. 60. Monitoring of blood sugar The key to any management regimen is to monitor plasma glucose levels frequently. Patients receiving insulin infusions intraoperatively may need to have their Glucose measured hourly. Those with type 2 diabetes vary in their ability to produce and respond to endogenous insulin, and measurement every 2 or 3 h may be sufficient. Likewise, insulin requirements vary with the extensiveness of the surgical procedure. Bedside glucose meters are capable of determining the glucose concentration in a drop of blood obtained from a finger stick (or withdrawn from a central or arterial line) within a minute. These devices measure the color conversion of a glucose oxidase– impregnated strip. Their accuracy depends, to a large extent,on adherence to the device’s specific testing protocol. Monitoring urine glucose is of value only for detecting glycosuria.
  61. 61. intraoperative management- -No single anesthetic technique is proven to be superior in diabetics. -Blood glucose should be monitored frequently intraoperatively regardless of the anesthetic technique chosen.
  62. 62.  General anesthesia the usual adrenergic and neuroglycopenic symptoms of hypoglycemia are diminished or absent.  Regional anesthesia allow the patient to notify the anesthesiologist of complications such as hypoglycemia or myocardial ischemia, although this is less reliable in patients with significant autonomic neuropathy.  Local anesthesia diabetic nerves seem to be more sensitive to local anesthetics and are more susceptible to local anesthetic-induced nerve injury
  63. 63. : Intraoperative fluids  Non-dextrose-containing fluid should be used to replace blood loss, urine output, and third-space or insensible deficits.  Dextrose is infused only as needed to avoid hypoglycemia and limit protein catabolism.  Finally, normothermia is maintained, and postoperative analgesia is provided to limit excessive stress and resultant antiinsulin effect.
  64. 64. A few anaesthetic ccoonnssiiddeerraattiioonnss  FFiirrsstt ccaassee iinn tthhee mmoorrnniinngg ttoo mmiinniimmiizzee tthhee ssttaarrvvaattiioonn ppeerriioodd  NNoo aannaaeesstthheettiicc tteecchhnniiqquuee iiss iinnddiiccaatteedd oorr ccoonnttrraaiinnddiiccaatteedd iinn ddiiaabbeettiiccss,, aanndd tthhee ssttrreessss iimmppoosseedd bbyy tthhee aannaaeesstthheettiicc iiss uussuuaallllyy mmiinnoorr ccoommppaarreedd ttoo tthhee ssttrreessss ooff tthhee ssuurrggeerryy..  TThhee cchhaalllleennggee iiss ttoo ggiivvee tthhee mmoosstt ssttaabbllee aannaaeesstthheettiicc ppoossssiibbllee aanndd lliimmiitt tthhee hhyyppeerrggllyyccaaeemmiicc rreeaaccttiioonn ttoo ssuurrggiiccaall ssttrreessss
  65. 65. RReeggiioonnaall bblloocckkss  LLAA rreeqquuiirreemmeennttss lloowweerr  RRiisskkss ooff nneerrvvee iinnjjuurryy hhiigghheerr  CCoommbbiinnaattiioonn ooff LLAA wwiitthh eeppiinneepphhrriinnee mmaayy ppoossee ggrreeaatteerr rriisskk ooff iisscchheemmiicc oorr eeddeemmaattoouuss nneerrvvee iinnjjuurryy ((oorr bbootthh)) iinn ddiiaabbeettiicc  DDooccuummeenntt ppeerriipphheerraall nneeuurrooppaatthhyy  kkeeeeppss tthhee ppaattiieennttss aanndd rreellaattiivveess iinnffoorrmmeedd  aavvooiiddss mmeeddiiccoo--lleeggaall hhaasssslleess llaatteerr oonn  IInnssuulliinn rreessppoonnssee ttoo hhyyppeerrggllyycceemmiiaa  hhiigghh tthhoorraacciicc ((TT11--TT66)) bblloocckkaaddee ® ?? iinnhhiibbiitteedd  llooww bblloocckkaaddee,, ((TT99 -- TT1122)) ® nnoo eeffffeecctt
  66. 66. RReeggiioonnaall aannaaeesstthheessiiaa  PPrroo::  RReeggiioonnaall aannaaeesstthheessiiaa bblluunnttss tthhee iinnccrreeaasseess iinn ccoorriittccooll,, gglluuccaaggoonn,, aanndd gglluuccoossee..  SSppiinnaall oorr eeppiidduurraall mmaayy mmoodduullaattee tthhee ccaatteeccoollaammiinnee sseeccrreettiioonn,, pprreevveennttiinngg hhiigghh gglluuccoossee aanndd kkeettoossiiss.. TThhiiss eeffffeecctt ccoouulldd ccoonnttiinnuuee iinn tthhee ppoosstt ooppeerraattiivvee ppeerriioodd,, iiff tthhee bblloocckk iiss ccoonnttiinnuueedd  AAnn aawwaakkee ppaattiieenntt iiss aa ggoooodd mmoonniittoorr ttoo pprreevveenntt hhyyppooggllyyccaaeemmiiaa  AA sswwiifftteerr rreettuurrnn ttoo nnoorrmmaall eeaattiinngg
  67. 67. RReeggiioonnaall aannaaeesstthheessiiaa  Con:  If autonomic neuropathy is present, profound hypotension may occur. This could be disastrous in a patient with cardiac complications  Infections and vascular complications may be increased (epidural abscesses are more common in diabetics)  A diabetic neuropathy presenting post-op may be attributed to the regional blockade
  68. 68. General Anaesthesia  Pro:  High dose opiate technique may be useful to block the entire sympathetic nervous system and the hypothalamic pituitary axis  Better control of blood pressure in patients with autonomic neuropathy
  69. 69. General Anaesthesia  Con  May have difficult airway (“Stiff-joint syndrome”)  Full stomach due to gastroparesis  Controlled ventilation is needed as patients with autonomic neuropathy may have impaired ventilatory control  Aggravated haemodynamic response to intubation  Anaesthesia masks the symptoms of hypoglycaemia
  70. 70. Postoperative Close monitoring of blood glucose must continue postoperatively. There is considerable patient-to patient variation in onset and duration of action of insulin preparations . For example, the onset of action of subcutaneous regular insulin is less than 1 h, but in rare patients its duration of action may continue for 6 h. NPH insulin typically has an onset of action within 2 h, but the action can last longer than 24 h. Another reason for close monitoring is the progression of stress hyperglycemia in the recovery period.
  71. 71. Perioperative hyperglycemia Perioperatively, there are increased levels of counterregulatory hormones (catecholamines, glucocorticoids, growth hormone, and glucagon) mediating the stress response, resulting in relative insulin resistance and difficulty in controlling blood glucose levels. Hyperglycemia may impair wound healing, inhibit white blood cell (WBC) chemotaxis and function (associated with an increased risk of infection), worsen central nervous system (CNS) and spinal cord injury under ischemic conditions, and result in hyperosmolarity leading to hyperviscosity and thrombogenesis. The presence of hyperglycemia may also portend the development of DKA or a nonketotic hyperosmolar state. Blood glucose >180 mg/dl (10 mmol/L) exceeds the Tmax of the kidney and results in glycosuria. Glucose-induced osmotic diuresis may lead to dehydration and an increased risk of urinary tract infection.
  72. 72. Blood glucose levels should be frequently monitored and maintained at <180 mg/dl (10 mmol/L) with appropriate administration of insulin. One unit of regular insulin generally lowers the blood glucose by Approximately25-30 mg/dl (1.5 mmol/L) in a 70-kg patient. Intravenous shortacting regular insulin (Humulin R) should be used for initial control of blood glucose. The absorption and efficacy of SC insulin may be unpredictable in the perioperative period because of unreliable cutaneous blood flow and should be avoided initially. Finally, it may be reasonable to maintain blood glucose at the upper end of the normal range in postoperative patients to avoid hypoglycemia.
  73. 73. Perioperative hypoglycemia It is commonly defined as a blood glucose <50 mg/dl (2.8mmol/L) in adults and <40 mg/dl (2.2 mmol/L) in children. Hypoglycemia may develop perioperatively as a result of residual effects of preoperativelong-acting oral hypoglycemic agents or perioperative insulin administration and may be exacerbated by perioperative fasting or insufficient glucose infusion. Recognition of perioperative hypoglycemia may be delayed because presenting symptoms may be altered or absent as a result of the effects of drugs such as anesthetics, analgesics, sedatives, and sympatholytic agents. In addition, diabetics with autonomic neuropathy have blunting of the adrenergic response associated with hypoglycemia.
  74. 74. Neuroglycopenic symptoms and symptoms of the adrenergic response to hypoglycemia are the two main manifestations of hypoglycemia. Neuroglycopenic manifestations generally begin with confusion, irritability, fatigue, headache, and somnolence. Prolonged, severe hypoglycemia may cause seizures and even focal neurological deficits,coma, and death.
  75. 75. Hypoglycemia must be considered early in the differential diagnosis of any new neurological symptoms in the postoperative period, because prolonged hypoglycemia results in irreversible neurological deficits. Adrenergic symptoms and signs, including anxiety, restlessness, diaphoresis, tachycardia,hypertension, arrhythmias, and angina are due to catecholamines released in response to hypoglycemia. Patients with symptomatic hypoglycemia generally respond promptlyto IV dextrose unless there has been severe hypoglycemia of sufficient duration to cause permanent neurological damage. After obtaining a sample to determine the blood glucose, initiate therapy in an adult with 50 ml of 50% (25 gm) dextrose (D50). Each milliliter of D50 raises the blood glucose by about 2 mg/dl (0.11 mmol/L) in a 70-kg patient. Additional boluses of D50 or an infusion of 5–10% dextrose may be needed to treat severe hypoglycemia and to prevent recurrent hypoglycemia.
  76. 76. Therapy should not be delayed while awaiting confirmation of hypoglycemia. Glucagon (1–2 mg), diazoxide, and octreotide (50–200 μg) have been used rarely to treat refractory, sulfonylurea-induced cases of hypoglycemia. Blood glucose levels should be monitored frequently during the treatment of hypoglycemia, and the underlying cause of the hypoglycemia should be identified and treated.
  77. 77. Sources of the lecture: • Clinical anesthesiology 2013 • ASA refresher course 2002, 2012 • Perioperative Management of Diabetes Mellitus Amir B. Channa FFARCS, D.A. (Eng) KKUH - Riyadh