Diabetes: Diagnosis, Types, and Complications

Pancreatic Surgery

• Diabetes is marked by hyperglycemia and glycosuria, resulting from either insufficient insulin or a lack of response to insulin.
• Diagnosis involves elevated fasting plasma glucose (over 126 mg/dL) or a glycated hemoglobin (HgbA1c) of 6.5% or higher.
• Values for blood glucose are 12-15% lower than plasma glucose measurements
• Long-term diabetes complications include retinopathy, kidney disease, hypertension, coronary and peripheral vascular issues, and neuropathies.
• Patients with diabetes, especially those hyperglycemic, are more infection-prone.
• Type 1 diabetes is insulin-dependent, while type 2 is insulin-resistant.
• Three acute, life-threatening diabetes complications: diabetic ketoacidosis (DKA), hyperosmolar nonketotic coma, and hypoglycemia.
• DKA results from decreased insulin activity, leading to fatty acid catabolism into ketone bodies, causing anion-gap metabolic acidosis.
• DKA is differentiated from lactic acidosis by elevated plasma lactate (>6 mmol/L) and absent urine/plasma ketones in lactic acidosis.
• Alcoholic ketoacidosis, similar to DKA, can occur in nondiabetic individuals after heavy drinking, blood glucose may be normal or slightly elevated.
• Infection often triggers DKA in well-managed type 1 diabetics and can be the initial DKA presentation.
• DKA symptoms include tachypnea, abdominal pain, nausea, vomiting, and altered sensorium.
• DKA treatment involves correcting hypovolemia, hyperglycemia, and potassium deficit through isotonic fluid infusion with potassium and insulin.
• Blood glucose reduction in ketoacidosis should target 100 mg/dL/h or 10%/h or less, starting with intravenous insulin at 0.1 units/kg/h, adjust if needed.
• Glucose movement intracellularly also shifts potassium, which can cause critical hypokalemia, potassium and glucose levels require monitoring.
• Dehydration correction in adults requires liters of 0.9% saline, initially at 1–2 L/hour, then 200–500 mL/hour.
• When blood glucose falls to 250 mg/dL, add D5W infusion to the insulin to prevent hypoglycemia and maintain glucose for intracellular metabolism.
• Severe acidosis (pH <7.1) rarely needs bicarbonate, it typically resolves with volume expansion and plasma glucose normalization.
• Hyperosmolar nonketotic coma differs from ketoacidosis due to sufficient insulin preventing ketone formation.
• Hyperglycemia-induced diuresis leads to dehydration, kidney failure, lactic acidosis, and disseminated intravascular coagulation occurs.
• Hyperosmolality (over 360 mOsm/L) dehydrates neurons, causing altered mental status and seizures.
• Fluid resuscitation with normal saline, small insulin doses, and potassium supplementation are needed.
• Hypoglycemia, if untreated, can progress from mental changes to convulsions and coma.
• Epinephrine release causes diaphoresis, tachycardia, and nervousness.
• Most hypoglycemia warning signs are masked by general anesthesia, and hypoglycemia constitutes plasma glucose below 50 mg/dL.
• Hypoglycemia treatment in anesthetized or critically ill patients requires IV 50% glucose; awake persons can take oral glucose or sucrose.
• Elevated hemoglobin A1c indicates poor glucose control, increasing hyperglycemia risk and complications post-surgery.
• Undiagnosed, many type 2 diabetics are unaware of their condition.
• Diabetics have a higher incidence of ST-segment and T-wave abnormalities.
• Hypertensive diabetics have over 50% chance of coexisting diabetic autonomic neuropathy.
• Autonomic dysfunction limits responses to intravascular changes, predisposing to instability (e.g., hypotension after induction) and sudden cardiac death.
• Autonomic dysfunction contributes to delayed gastric emptying (diabetic gastroparesis) with cardiac signs possible with normal GI tract.
• Premedication with nonparticulate antacid and metoclopramide is often used in obese diabetics with cardiac autonomic dysfunction.
• Diabetic neuropathy can lead to silent myocardial ischemia and kidney dysfunction, initially proteinuria, then elevated creatinine over 30 years.
• Chronic hyperglycemia causes glycosylation of proteins, limiting joint mobility, neck mobility should be assessed to prepare for possibly difficult intubation.
• Intraoperative glucose control aims to avoid hypoglycemia, maintaining blood glucose under 180 mg/dL.
• Strict control (<150 mg/dL) during surgery or critical illness worsens outcomes compared to "looser" control.
• Above 180 mg/dL and hyperglycemia leads to risks, with neurological impact after cardiac events. Good blood glucose control (<180 mg/dL) during bypass matters.
• Control benefits pregnant diabetics' fetal outcomes, brain glucose dependence means hypoglycemia must be avoided and aseptic technique matters.
• Some management regimens involve administering half the usual morning intermediate-acting dose and checking levels after IV access to lower hypoglycemia
• 15 units of NPH subcutaneously would be given if 30 taken normally, with 5% dextrose solution and intramuscular insulin absorption may be unpredictable.
• One regular insulin unit lowers adult plasma glucose usually by 25–30 mg/dL.
• A better method is to give regular insulin as a continuous infusion at 0.1 unit/kg/h in normal saline, adjusted during glucose fluctuations.
• A dedicated line prevents rate changes from fluids and drugs. Hypoglycemia can be treated with dextrose if glucose falls below 100 mg/dL for catabolic patients. Unit per hour = (Plasma Glucose mg/dL)/150
• Blood glucose target is under 180 mg/dL, above 85 mg/dL and potassium needs to be added to fluids given insulin causes a intracellular.
• Oral hypoglycemics continue until the surgery day unless sulfonylureas and metformin are used due to long half-lives, restart.
• SGLT2 inhibitor hypoglycemics raise risk of ketoacidosis, these are discontinued in advance of surgery with adequate glucose control.
• Many patients need insulin during and after the surgery, stress elevates inflammatory mediators that stress glucose by increasing insulin requirements.
• Brief surgeries don't need exogenous insulin for Type 2's and hyperglycemia appears in non-diabetics.
• NPH is an increased risk of adverse reaction and should not be given or tested.

Hepatic/Biliary Surgery

• Hepatic blood flow is 25-30% of heart output from blood and portal vein with 30% blood and 50-70% liver requirements.
• Normal arterial flow has demand or hepatic arterial flow is dependent on metabolic demand. All Coagulation all coagulation factors except 8 and von Willebrand factors are made by liver
• Vitamin K is needed for pro and anti thrombolitic factor
• P450 can have high drugs intake
• Bile makes helps in emulsifying bile and lipids.
• Vitamin K deficiencies can occur within days.
• transaminse measurement and liver test is the most telling.
• liver disease can be put into 2: parenchymal disorder; obstructive disorders.
• Total Bilirubin has to be lest than 1.5mg/dl can reflect balances with the liver.
• albumin has to be 3.5 to 5.5 g/Dl anything less indicates a live problem. PT ranges from 11 to 14 is needed to asses V, V11,X and the short half life of factor

Coagulation and Hemostasis

• Coagulation is a balance of the prof and anti coaugulants in ones body and the Inr only deals with pro caugulant
• Hemostasis is composed of 3 different parts; primary,secondary, and tertiary.
• The primary portion contains platelet and van Willebrand disease which can cause mucocutaneous bleeding and can be treated by DDAVP
• Surface receptors must be met, some are thrombin, ADP, Fibrinogen.
• Meds to combat platelet and asprin can block this and decrease throm boxidine 3
• secondary homeostasis deals with coagulation and fibrin helps things stick together
• factors are released by tissue or collagen.
• Thrombin activates thromins and activates clort and acts as the facotr X

Fluid Management

• The normal adult water averages to 2500 ml of water.
• loss averages to 2500 and urine
• Plasma is to be 280 and 290