Perioperative management of a patient with Diabetes mellitus

R.Srihari

Topics for discussion

• WHO diagnostic criteria for Diabetes mellitus• Implications of surgery in a diabetic• Investigations• Principles of anesthetic management• Effects of anesthetic drugs on blood sugar• Hyperglycemic emergencies

WHO DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS

• Diabetes:– Fasting plasma glucose >7mmol/l (126mg/dl)– 2 hours plasma glucose > 11.1 mmol/l (200mg/dl)

• Impaired Glucose Tolerance:– Fasting plasma glucose >7mmol/l (126mg/dl)– 2 hours plasma glucose : 7.8-11.1 mmol/l (140-200mg/dl)

• Impaired Fasting Glucose:– Fasting plasma glucose 6.1-6.9(110-125mg/dl)– 2 hours plasma glucose <7.8 mmol/l (<140 mg/dl)

Implications of surgery in a diabetic surgery

• The perioperative problems posed by surgery in the diabetic patient:– Stress response to surgery(magnitude depends on the site

of surgery, tissue injury etc)• Secretion of catecholamines, cortisol and growth hormone

oppose glucose homeostasis as these hormones have anti insulin and hyperglycemic effects

Glycogenolysis and Gluconeogenesis are stimulated and peripheral glucose uptake is decreased causing hyperglycemia and ketosis

– Rise in blood sugar during surgery is related to magnitude and inflammation:• Excessive release of inflammatory cytokines such as

Tumour Necrosis Factor, IL-1 and IL-6 and immobility

Hyperglycemia

– In fasting patients, undergoing elective intra-abdominal procedures

Blood glucose levels typically increases to between 126-180 mg/dl

– During cardiac surgery glucose values rise above 270mg/dl in subjects without Diabetes and above 360mg/dl

– Stress may precipate Diabetic crisis

– Interruption of oral intake, which may be further prolonged after gastrointestinal surgery

lead to starvation

Predispose to ketosis

Preoperative insulin administration is needed to control blood sugar

Patient can be reverted to his/her presurgery diabetes management only after he resumes his normal oral intake

– Altered consciousness in perioperative period may mask the symptoms and signs of hypoglycemia

– Circulatory disturbance associated with anesthesia and surgery may interfere with absorption of subcutaneous insulin So it is ideal to administer iv insulin

– Hyperglycemia is associated with increased risk of complications such as wound infection and poor neurological outcomes in susceptible

• Goals of perioperative diabetic management:

– Avoidance of hypoglycemia– Avoidance of marked hyperglycemia– Maintenance of fluid/electrolyte balance– Prevention of ketoacidosis/hyperosmolar states– Return to stable glycemic control as soon as

possible

• Preoperative Evaluation:– Clinical Evaluation:• Focus on cardiopulmonary risk assessment• CAD more common in patients with Diabetes

– Hypertension– Obesity– Chronic Kidney Disease – Cerebrovascular Accident– Autonomic neuropathy

– Diabetes related:• Determination of the type of diabetes :since type 1

Diabetes mellitus more at risk of DKA

• Long term complications of DM:– Retinopathy – Nephropathy– Neuropathy– Autonomic neuropathy– Coronary Artery Disease– Peripheral Vascular Disease– Hypertension

• Assessment of baseline glycemic control:– Includes frequency of monitoring range of blood glucose levels ;

HbA1c

• Detailed history of Diabetes therapy – Insulin type– Dose– Timing

• Characteristics of surgery – Duration– Region

Investigations• Hemoglobin:– Anemia is present in patients with renal dysfunction – Baseline investigation– To guide blood transfusion intraoperatively

• Total Leucocyte count:– To look for infection

• Urine routine:– To look for microalbuminuria alerts presence of diabetic

nephropathy

• Serum creatinine:– To detect renal dysfunction

• Fasting and Post-prandial blood sugars:– To assess quality of control

• Glycosylated Hb:– HbA1c <7% implies good control of blood sugar

control over the preceding 8-12 weeks

• S.Electrolytes:– To detect abnormalities in patients with vomiting, diarrhoea, poor oral

intake or tube feeding, intestinal obstruction – Also in patients on insulin therapy, ACEI, Diuretics and renal

dysfunction Potassium abnormal

• ECG:– To detect asymptomatic myocardial ischemia

• Echocardiography:– Should be done in patients with long standing diabetes and in patients

with cardiovascular symptoms

• Chest X-Ray:– Tuberculosis is common in diabetics due to impaired

immmunity – Patients with abdominal distension may have

pneumonia secondary to basal atelectasis or aspiration

• Morning of surgery investigations:– Serum electrolytes– Fasting Blood Sugar– Urine Ketones

• Glycemic targets:

Anesthetic Management

• Timing:– Diabetic patients should be placed first on the operating list

• This shortens their preoperative fast and risk of hypoglycemia and ketosis

• Fasting:– Delayed gastric emptying due to diabetic autonomic

neuropathy is found in up to 50% of patients with type 1 Diabetes Mellitus patiens

Undiagnosed gastroparesis may prolonged retention of food in the stomach

Increased risk of regurgitation and aspiration

– Ideally 12 hour fast may be beneficial in diabetic patient without surgery

– Some studies have shown beneficial effects of preoperative oral erythromycin on gastric motility

• Intravenous fluids:– Ringers lactate:

• Lactate undergoes gluconeogenesis in the liver and may complicate blood sugar control when given in large volumes

– Normal saline:• In large doses: Hyperchloremic acidosis

– Hence both fluids need to used judiciously according to individual conditions

– Dextrose solution

• Standard monitoring:– ECG, NIBP, SpO2, EtCO2 MANDATORY– Advanced monitoring may be needed depending on the

comorbidities

• Sugar control:– Permissive Hyperglycemia is unacceptable in current

practice with availabilty of more accurate, rapid and easy to use glucose

Postoperative wound healing and infection is influenced by adequacy of glycemic control

– Glucose supplementation:• Patients receiving long acting insulin are at risk of

hypoglycemia is glucose is not suplemented• Perioperative administration of glucose enhances

postoperative glucose utilization rates

– Insulin supplementation: • Essential in patients with absolute insulin deficiency

and infection to prevent lipolysis and proteolysis with resultant ketosis some of metabolic effects of suppression of insulin secretion are reversed by intraoperative insulin infusion

Anesthesia

• Induction:– Choice of agent for general anesthesia depends on

severity of systemic illnesses

Epidural analgesia may be insituted after due consideration to autonomic neuropathy/ IHD/ Peripheral neuropathy

MUST BE AVOIDED IN PATIENTS WITH SEPSIS

– Epidural analgesia may help to attenuate neurohumoral stress response

+To avoid systemic analgesics like NSAIDS and opioids which may have serious side effects in the diabetics

– A rapid sequence induction should be preferred technique for an anticipated difficult airway

– Careful induction with Etomidate/Fentanyl/Thiopentone should be done

due to exaggerated hypotension due to autonomic neuropathy

Succinyl choline should be avoided in patients with peripheral neuropathy due to risk of increased release of potassium

Atracurium/Mivacurium may be used in case of renal dysfunction

Rocuronium can be for rapid sequence induction

• Maintenance of anesthesia:– Isoflurane or Sevoflurane in air-oxygen mixture– Nitrous oxide can be used but in patients with intestinal

obstruction should be avoided

– Patients with perforated peritonitis should be ventilated postoperatively to increase oxygen delivery

– Bowel distension and dense abdominal closure also makes postoperative ventilation desirable

– Airway pressure; if pressure after surgery with return of airway reflexes can be extubated at the end of surgery

• Effects of anesthetic drugs on blood sugars:– Induction agents:

• Ketamine: Significant hyperglycemia• Etomidate: Block adrenal steroidgenesis dec cortisol

– Inhalational agents:• In vitro studies shown to inhibit insulin response to glucose in

reversible manner

– BZDs: dec ACTH release decreases cortisol when used in high

doses decrease sympathetic response

but stimulate growth hormone secretion

result in decrease in glycemic response to Sx

– High dose opiates, anesthetic technique produces hemodynamic, hormonal and metabolic stability

They effectively block sympathetic nervous system and HPA axis

Probably by direct effect on hypothalamus

HOWEVER, MIDAZOLAM AND FENTANYL MAY CAUSE HYPERGLYCEMIA BY REDUCING GLUCOSE CLEARANCE

– Ganglion blocking agents:• May block sympathetically mediated hepatic

gluconeogenesis with resultant hypoglycemia

– Beta blockers are associated with slower recovery from hyperglycemia

Diabetic Emergencies

• Diabetic ketoacidosis• Hyperosmolar hyperglycemic non-ketotic state

• Introduction:– Diabetic ketoacidosis (DKA) and hyperosmolar

hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) two of the most serious acute complications of diabetes

– DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis.

– Each represents an extreme in the spectrum of hyperglycemia.

• Definitions:– DKA:• Metabolic acidosis is the major finding, while serum

glucose concentration is <800mg/dl. (~300-500mg/dl)

– HHS:• Little or no ketoacid accumulation, but glucose

concentration exceeds 1000mg/dl + plasma osmolarity >380 mOsm/kg and neurological abnormalities - +++

• Pathophysiology:Increased gluconeogenesis + hepatic and renal glucose production

+Impaired glucose utilization in peripheral tissues

Hyperglycemia + Hyperosmolarity

Increased counter regulatory hormones lipolysis

free fatty acid oxidation ketone bodies (Beta hydroxy butyrate, acetone, acetoacetate)

• Precipitating Factors:

– The most common events:• Infection (often pneumonia or urinary tract infection) • Discontinuation of or inadequate insulin therapy. • Compromised water intake due to underlying medical

conditions, particularly in older patients, can promote the development of severe dehydration and HHS

• Other conditions and factors associated with DKA and HHS include:– Acute major illnesses such as myocardial infarction,

cerebrovascular accident, sepsis, or pancreatitis.– New onset type 1 diabetes, in which DKA is a common

presentation.– Drugs that affect carbohydrate metabolism, including

glucocorticoids, higher-dose thiazide diuretics, sympathomimetic agents (eg, dobutamine and terbutaline) and second-generation “atypical” antipsychotic agents

– Cocaine use, which has been associated with recurrent DKA

• CLINICAL PRESENTATION:– Diabetic ketoacidosis (DKA) usually evolves rapidly, over a 24-hour

period.– In contrast, symptoms of hyperosmolar hyperglycemic state (HHS)

develop more insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission.

• The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss. As the degree or duration of hyperglycemia progresses, neurologic symptoms, including lethargy, focal signs, and obtundation, can develop This can progress to coma in later stages. Neurologic symptoms are most common in HHS, Hyperventilation and abdominal pain are primarily limited to patients with DKA.

• Neurologic symptoms — – Neurologic deterioration primarily occurs in patients with an effective

plasma osmolality above 320 to 330 mosmol/kg

– Mental obtundation and coma are more frequent in HHS than DKA because of the usually greater degree of hyperosmolality in HHS

– In addition, some patients with HHS have focal neurologic signs (hemiparesis or hemianopsia) and/or seizures

– Mental obtundation may occur in patients with DKA, who have lesser degrees of hyperosmolality, when severe acidosis exists

– However, stupor or coma in diabetic patients with an effective plasma osmolality lower than 320mosmol/kg demands immediate consideration of other causes of the mental status change.

• Abdominal pain in DKA —– Patients with DKA may present with nausea, vomiting, and abdominal

pain; although more common in children, these symptoms can be seen in adults

– Abdominal pain is unusual in HHS– Abdominal pain was associated with the severity of the metabolic

acidosis but did not correlate with the severity of hyperglycemia or dehydration.

• Possible causes of abdominal pain include – delayed gastric emptying – ileus induced by the metabolic acidosis and associated electrolyte

abnormalities – Other causes for abdominal pain, such as pancreatitis, should be sought

when they occur in the absence of severe metabolic acidosis and when they persist after the resolution of ketoacidosis.

• Physical examination — • Signs of volume depletion are common in both DKA and

HHS and include decreased skin turgor, dry axillae and oral mucosa, low jugular venous pressure, tachycardia, and, if severe, hypotension. • Patients with DKA may have a fruity odor (due to

exhaled acetone; this is similar to the scent of nail polish remover) • deep respirations reflecting the compensatory

hyperventilation (called Kussmaul respirations).

• Diagnostic Evaluation:• Both diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic

state (HHS) are medical emergencies that require prompt recognition and management

– Initial evaluation — The initial evaluation of patients with hyperglycemic crises should include assessment of cardiorespiratory status, volume status, and mental status.

– The initial history and rapid but careful physical examination should focus on:• Airway, breathing, and circulation (ABC) status• Mental status• Possible precipitating events (eg, source of infection, myocardial

infarction)• Volume status

• The initial laboratory evaluation of a patient with suspected DKA or HHS should include determination of:– Serum glucose– Serum electrolytes (with calculation of the anion gap), blood urea

nitrogen (BUN), and plasma creatinine– Complete blood count (CBC) with differential– Urinalysis and urine ketones by dipstick– Plasma osmolality– Serum ketones (if urine ketones are present)– Arterial blood gas if the serum bicarbonate is substantially reduced

or hypoxia is suspected– Electrocardiogram

• Additional testing:– cultures of urine, sputum, and blood, serum lipase and

amylase, and chest radiograph should be performed on a case-by-case basis

– Measurement of glycosylated hemoglobin (A1C) may be useful in determining whether the acute episode is the culmination of an evolutionary process in previously undiagnosed or poorly controlled diabetes or a truly acute episode in an otherwise well-controlled patient

• Management:– Intravenous fluids:

• Start with isotonic fluids at 1 litre/ hour (15-20ml/kg/hr)• When blood glucose falls to 250mg/dl change to 5%

Dextrose in 0.45%/0.9% normal saline at 150-200 ml/hr

– Insulin:• Regular insulin: 0.15 units/kg as Intravenous bolus then infuse

at 0.1units/kg/hour• Adjust infusion so that blood glucose decreases by 50-75 mg/dl• When glucose levels reach 250mg/dl, decrease infusion rate to

0.05-0.1 units/kg/hour Maintain blood glucose at 150-200 mg/dl

• Begin s/c insulin when DKA resolves (pH >7.3)

– Potassium:• If initial serum Potassium < 3.3 mEq/L – hold insulin infusion give 40 mEq/l/hr till K >3.3 mEq/L

• If initial serum potassium 3.3-4.9 give 20-30 mEq Potassium in each litre to keep S.K at 4-5 mEq/L

• If initial Serum Potassium >5 do not give Potassium but check levels every 2 hourly

– Bicarbonate:• Given only when severe metabolic acidosis is present pH<6.9• Bicarb deficit: 0.6 x Wt(Kg) x (24- measured bicarbonate)

– Phosphate:• Supplementation indicated only in severe

hypophosphatemia– Correction by administering 20-30 mEq/l with each litre of

fluid