ANAESTHETIC MANAGEMENT OF DIABETES MELLITUS AND GESTATIONAL DIABETES

1. ANAESTHETIC MANAGEMENT OF DIABETES MELLITUS AND GESTATIONAL DIABETES

2. Anaesthetic management of diabetes includes • Preoperative evaluation • Intraoperative management • Postoperative management

3. Preoperative evaluation • The preoperative evaluation should focus on assessing organ damage and control of blood sugar. • It should focus on cardiovascular , renal, neurologic, and musculoskeletal systems. • It includes history and physical examination and should asses for symptoms and signs of acute hyperglycaemia and should screen for chronic complications.

4. History • Symptoms of hyperglycaemia like polyuria, polydypsia, polyphagia, loss of weight, fatigue, weakness, frequent superficial infections like vaginitis and fungal infections, slow healing of skin lesions after minor trauma , non healing ulcers. • Central nervous system : headache, blurring of vision, numbness , tingling sensation in limbs , documentation of sensory and motor neuropathy ( glove and stocking paraesthesia)

5. Cardiovascular system : history of palpitations, chest pain , associated hypertension. • Respiratory system : history of recurrent pulmonary infections • Renal system : puffiness of face, generalised edema, repeated attacks of burning micturition.

6. Gastrointestinal system : history of nausea, vomiting, early satiety, bloating, epigastric pain, diarrhoea , constipation . • Autonomic neuropathy : bladder and bowel disturbances, absence of sweating, nausea , vomiting, early satiety, bloating, tingling and numbness of extremities.

7. Past history of tuberculosis as a complication of diabetes , history of ischemic heart disease, lower respiratory tract infections, transient ischemic attacks, cerebrovascular accidents. • History of frequent boils , abscess. History of frequent change of refractory errors of eyes. • History of previous surgeries. • History of hypoglycaemic attacks , its frequency , awareness and severity.

8. Personal history : bowel and bladder disturbances, history of smoking and alcoholism. • Family history : of diabetes mellitus . • Drug history: if the patient is taking insulin or oral hypoglycaemic drugs, antihypertensives. Previous history of intake of corticosteroids, thiazides.

9. PHYSICAL EXAMINATION • Height and weight of the patient to calculate the body mass index. • Peripheral pulses should be palpated. • Blood pressure is recorded in the lying down and standing position. • Oral cavity is examined for any caries teeth or fungal infections. • Skin is examined for abscess, fungal infections. • Feet are examined for trophic ulcers, superficial fungal infections, nail diseases, foot deformities like hammer or claw toes and charcot joint.

10. Airway assessment : look for stiff joint syndrome due to diffuse glycosylation of collagen tissues of cervical spine, atlantoaxial, temperomandibular, metacarpophalangeal and interphalangeal joints with limited mobility leading to difficult laryngoscopy and intubation. • Prayer sign : unable to approximate fingers and palms while pressing their hands together. It is positive when there is a gap between the palms.

11. DIABETIC AUTONOMIC NEUROPATHY • Autonomic dysfunction develops in individuals with long standing type 1 or type 2 diabetes mellitus involving the cholinergic , noradrenergic and peptidergic systems. • It can be subclinical or clinical. Subclinical can occur within a year or two after diagnosis, while clinical does not develop for many years and depends on the duration of diabetes and degree of metabolic control.

12. Common manifestations are : cardiovascular: postural hypotension , resting tachycardia, absence of sinus arrythmia, abnormal vasalva response, sudden cardiac death, decreased lv diastolic filling. • Gastrointestinal : oesophageal dysmotility, dysphagia, gastroparesis, nocturnal and post prandial diarrhoea, constipation, anal incontinenece.

13. Genitourinary : vesicopathy, incontinence, impotence, retrograde ejaculation, • Secretomotor : gustatory sweating, nocturnal sweats without hypoglycaemia, anhidrosis of lower extremities. • Vasomotor : dependent pedal edema • Pupillary : decreased pupil size, resistance to mydriatics. • Reduced countergulatory hormone release leading to an inability to sense hypoglycaemia.

14. Clinical examination includes assessment of muscle power, sensations of pinprick, joint position, touch, temperature, vibration sensation. • Tests to assess autonomic neuropathy : • Resting tachycardia : eliminating anxiety, if heart rate is more than 100 at basal conditions , it suggests resting tachycardia.

15. Heart rate response during deep breathing : patient sits quietly and breathes deeply at about 6 breaths pre min for one min. An ECG is recorded throughout. The maximum and minimum R-R interval during each breath cycle is measured with a ruler and converted into beats/ min, the result is expressed as the mean difference between maximum and minimum heart rate for 6 measured cycles in beats/ min. If the difference is >15 normal, 11-15 borderline , <10 abnormal.

16. Immediate heart rate response to change in posture: the patient lies quietly on the couch while the ECG is recorded continuously. The patient is asked to stand up unaided and the point at which the patient stand up is marked on the ECG. The shortest R-R interval at around 15 th beat and longest R-R interval at around 30th beat after standing is measured. If ratio is > 1.04 normal, 1.01-1.03 borderline, < 1.10 abnormal.

17. Valsalva manoeuvre : consists of forced expiration against a standardized resistance for a specified period of time. The patient blows forcefully into the mouth piece attached to mercury manometer to maintain 40 mmhg positive pressure for 15 seconds. Then he releases the pressure rapidly and breathes quietly for one minute. A continous ECG is recorded throughout the procedure. Valsalva ratio is expressed as the ratio of largest R-R interval after the procedure ( reflecting bradycardia following release ) to the shortest R-R interval during the procedure ( tachycardia ) . Ratio >1.20 normal, 1.11-1.19 borderline < 1.10 abnormal.

18. Blood pressure response to standing : B.P is measured while patient is lying down quietly and while he stands up, the postural fall of B.P is taken as the difference between SBP lying and in standing. If the fall > 30 mmhg abnormal, 11-29 borderline < 10 is normal. • Blood pressure response to sustained hand grip: handgrip is maintained at 30 % of the maximum voluntary contraction which is determined by dynameter , for as long as 5 min. B.P is measured 3 times before and at one minute intervals during the hand grip.

19. The result is expressed as the difference between the highest DBP during the hand grip and the mean of the 3 DBP readings taken before the hand grip. A rise > 16 mmhg normal , 11-15 borderline, < 10 abnormal.

20. Anaesthetic importance of autonomic neuropathy : • There are increased chances of aspiration on induction. • Pressor response to tracheal intubation may be exaggerated. • Heart rate response to atropine is blunted. • Profound hypotension is seen under neuraxial blockade. • Increased risk of perioperative cardiac disease.

21. Short QT interval associated with neuropathy may result in serious cardiac arrythmias. • More susceptible to depressant effects of anaesthetic drugs and unexpected cardiac or respiratory arrest is more common. • Abnormal blood pressure fall with induction and highest requirement for intraoperative pressor agents to maintain stable hemodynamics.

22. NEUROPATHIES • It can be symmetric distal polyneuropathy, or asymmetric neuropathy. • Symmetric neuropathies are due to metabolic abnormalities of neurons of schwann cells, whereas the asymmetric neuropathies are due to vascular occlusion and ischemia.

23. Symmetric distal polyneuropathy is divided into 2 types: • A relatively asymptomatic form which is diffuse , distal, occuring in lower extremities with a stocking type of distribution. There is numbness, pins and needles sensation often worse at night. This is progressive and irreversible. • A painful form presenting with burning or dull aching , lancinating pain, worse at night and partially relieved by movement.

24. Early physical findings in both forms are loss of vibration sense and deep tendon reflexes, especially ankle jerk. With progression there will be involvement of joint sensation, touch, pain , temperature, later leading to weakness and wasting of muscles. • Asymmetric neuropathy : diabetic mononeuropathies of the cranial nerves involves 3rd, 6th , 4th cranial nerves. • Mononeuropathies of peripheral nerves manifests as carpal syndrome, foot drop, wrist drop.

25. EFFECTS OF SURGERY ON DIABETES • Surgery whether performed electively or in an emergency causes catabolic stress and secretion of counter regulatory hormones like catecholamines, cortisol, glucagon, growth hormone in both normal and diabetic patients which results in insulin resistance and increased gluconeogenesis, glycogenolysis, lipolysis, proteolysis. • There is also increased sympathetic activity leading to inhibition of insulin secretion.

26. In a non diabetic person these metabolic effects leads to secondary increase in secretion of insulin which has a restraining and controlling influence. • In a diabetic person there is either a absolute deficiency or insulin secretion is delayed or impaired , so that in untreated or poorly controlled diabetes the uptake of metabolic substrate is decreased , catabolism is increased and ultimately metabolic decompensation in the form of diabetic ketoacidosis develops.

27. Effects of hyperglycaemia : acute and chronic hyperglycaemia appear to increase the risk of ischemic myocardial injury by decreasing coronary collateral blood flow and coronary vasodialator reserve , impairing coronary microcirculation and causing endothelial dysfunction. • Acute hyperglycaemia causes dehydration , impaired wound healing , an increased rate of infection worsening cns and spinal cord injury with ischemia and hyperviscosity with thrombogenesis.

28. The possibility of infection and delay in wound healing result from a reduction in neutrophil number and function , impaired chemotaxis , phagocytosis , reduction in capillary volume , decrease in tensile strength , decrease in fibroblast and collagen synthesis and increase in edema.

29. Investigations • Complete blood count :hemoglobin for anemia . Total and differential counts for infections . • Blood glucose levels : fasting and post prandial blood glucose levels for diagnosis. • Glycosylated hemoglobin for monitoring the long term control of blood glucose levels. • Urine routine : specific gravity, rbcs, pus cells, protein, sugar, ketone bodies, casts, culture and sensitivity tests are done.

30. Lipid profile : triglycerides, HDL, LDL, VLDL, serum cholesterol. • Blood urea and serum creatinine. • Electrocardiogram: to diagnose IHD . • Chest xray : pulmonary TB or fungal infections are very common in diabetes. Cardiomegaly from hypertension should be looked for. Straight xray of the abdomen is done to exclude the pancreatic calcification, fibrocalculus pancreatic disease is very common in type 1 DM.

31. Echocardiogram :for ejection fraction, wall motion abnormalities, chamber enlargements. • Thread mill tests : to diagnose subclinical ischemia. • Ophthalmoscopic examination : fundoscopy for diabetic retinopathy. • Barium meal examination of g.i tract and endoscopy are done to study motility of g.i tract. • Nerve conduction tests in peripheral neuropathy.

32. Glycosylated hemoglobin • It is also called as glyco hemogobin or diabetic control index. • It is the standard method of assessing the long term glycaemic control. • It can be used as an assessment of glycemic control in a patient with known diabetes , but is not sensitive to make the a diagnosis of diabetes and is usually normal in patients with impaired glucose tolerance.

33. Glycosylated Hb refers to the glucose derived products of normal adult Hb . Glycation is a post translational , non enzymatic addition of sugar residue to amino acids of protein. • Among the glycated Hbs , most abundant form is HbA1c . It is produced by the condensation of glucose with N terminal valine of each beta chain of HbA. • The rate of synthesis of HbA1c is directly related to the exposure of RBCS to glucose.

34. When the plasma glucose level increases there is an increase in non enzymatic glycation of hemoglobin , this alteration reflects the glycemic history over the previous 2- 3 months since RBCS have an average life span of 120 days. • The non diabetic range of HbA1c is less than 6.05 % and the goal of intensive therapy in a patient with diabetes is to maintain HbA1c at less than 7.5 %

35. Because of the superior specificity and reliability HbA1c assay is performed by high performance liquid chromatography . It has become the standard method for most glycated Hb measurements. • HbA1c approximates following mean plasma glucose values : 6 % -135mg/dl , 7% -170 mg/dl , 8 % - 205 mg/dl. Therefore a rise in the HbA1c by 1% , there is an increase in blood glucose levels by 35 mg/dl.

36. Values of HbA1c are frequently increased in poorly controlled and with diagnosed DM, HbA1c levels may constitute greater than 15%. • With optimal control , the HbA1c moves towards normal. Primary treatment goal in a patient with DM is less than 7%. • Values are increased in iron deficiency anemia, splenectomy, alcohol and lead toxicity. • Decrease is seen in hemolytic anemia, chronic blood loss, pregnancy , chronic renal failure, hemoglobinopathies.

37. The degree of glycation of other proteins such as albumin has been used as an alternative indicator of glycemic control when HbA1c is inaccurate in hemolytic anemia and hemoglobinopathies. • The fructosamine assay using albumin is an example of alternative measurement of glycemic controls reflects the glycemic control over 2-4 weeks.

38. Preoperative instructions for elective procedure • Surgery should be scheduled as the first case for the day early in morning. • Reassurance to minimize the stress . Anxiolytics like diazepam 0.2mg/kg or alprazolam 0.25- 0.5mg is prescribed on the night before surgery. • In the presence of ketosis coming for elective surgery , it should be delayed till correction of acidosis and volume and electrolyte restoration. • Premedication with metaclopramide10mg i.v , or ranitidine 50 mg i.v in the morning to avoid aspiration due to gastroparesis.

39. On the morning of surgery fasting blood sugars, serum electrolytes, urine sugars, urine ketone bodies to be assessed. • Consent has to be taken.

40. Minor surgery : diabetic patient is expected to start near normal oral feeding by the same evening of surgery. • Shift from long acting oral hypoglycemic drugs or insulin to short acting oral hypoglycemic agents or insulin. • Nil per orally for 8 hours preoperatively • On the morning of the surgery –place first on the list • Skip oral hypoglycemic agents or insulin • If FBS < 80mg/dl infuse D5W • >120 mg/dl infuse normal saline. • Resume oral hypoglycemic agents or insulin with the first meal.

41. Major surgery: following the surgery, the patient is expected to be on i.v fluids for 24-48hrs. • All type 1 and type 2 DM who are poorly controlled. • The patients are admitted 2-3 days before surgery. • A thorough preoperative evaluation is done. • Switch over to i.v insulin bolus / infusion. • Correction of metabolic and electrolyte abnormalities. • Close perioperative monitoring. • Blood glucose and potassium is monitored 1 hour preoperatively, and 2 hourly from the start of the infusion, once during the surgery, once in the recovery room area, 2 hours postoperatively.

42. Well controlled type 2 DM do not require insulin for minor surgery. • Poorly controlled type2 DM and all type1 DM having minor surgery and all diabetics having major surgery need insulin. • For major surgery , if the serum glucose is greater than 270mg/dl preoperatively , the surgery should be delayed while rapid control is achieved with intravenous insulin. • If the serum glucose is greater than 400 mg/dl , the surgery is postponed and metabolic state is re stabilised.

43. Change of treatment from oral hypoglycaemic drugs to insulin in case of : • Uncontrolled type 2 DM • During major surgeries • During CABG • Gestational DM • Critically ill patients • Ketoacidosis • Uncontrolled infections.

44. Uncontrolled diabetic patient coming for emergency surgery • Emergency surgery places the diabetics at the risk of developing diabetic ketoacidosis or hyperglycemic hyperosmolar syndrome. • Surgery should be delayed for 4-6 hrs to optimise the metabolic status.

45. Diabetic ketoacidosis develops in type 1 DM and is usually precipitated by infection, trauma, severe stress. • Patients present with hyperglycaemia, hyperosmolarity, dehydration, ketosis, acidosis. • Severe dehydration is secondary to osmotic diuresis, vomiting , hyperventilation, reduced oral intake which can cause significant hypotension, circulatory shock, acute tubular necrosis.

46. Insulin therapy is initiated with a 10 unit intravenous bolus of regular insulin, followed by continuous insulin infusion. • The rate of infusion is determined if one divides last serum glucose by 150 , or 100 if patient is receiving steroids, infection, overweight. • When serum glucose levels reaches 250mg/dl , the intravenous fluid is 5 % dextrose.

47. Fluid therapy : the volume of fluid required for therapy varies with the overall deficit, 2-3 l of 0.9% saline in 1-3 hrs 5-10 ml/kg/hr. subsequently 0.45% saline at 150-300 ml/hr • Potassium replacement: if potassium is >5.5 no potassium is given , 3.5 to 5.5 20 mmol is given , < 3.5 40 mmol is given. • Sodium bicarbonate is most often not required and acidosis gets corrected after starting of insulin infusion. If pH is < 7.1 and hco3 <10 meq /l 1 ml/kg of 8.4% sodium bicarbonate is given.

48. Monitor the vitals , blood glucose, electrolytes every hour for first 24 hrs. • The above treatment is continued until the patient is stable and glucose goal is 150- 250mg/dl and acidosis is resolved. Insulin infusion is decreased to 0.05- 0.1 units/kg/hour.

49. Hyperglycemic hyperosmolar state • This syndrome is characterised by extreme dehydration resulting from a sustained hyperglycaemic diuresis under circumstances in which the patient is unable to drink sufficient water. • The biochemical hallmark is extreme hyperglycemia in the absence of significant ketoacidosis. • Fluid replacement : the average fluid deficit is about 10l . Initially 2-3 l of 0.9% saline is given over 1-2 hrs, subsequently 0.45% saline is used. • Once the plasma glucose is less than 300mg/dl , 5% dextrose saline is used.

50. Regular insulin should be given as a low dose intravenous infusion . The goal is to keep the glucose level around 200mg/dl. • Potassium supplementation is required, lactic acidosis is treated with intravenous sodium bicarbonate. • Infections are treated with antibiotics.