Anesthesia and diabetes

Marwa Ahmad Mahrous

Assistant lecturer

Department of anesthesia and ICU

Sohag university hospitals

DefinitionTypes DiagnosisEnd-organ dysfunctionComplicationsAnesthetic management

DefinitionDefinition::

syndrome of abnormal carbohydratemetabolism that is characterized by hyperglycemia

Classification:

-type 1(IDDM) insulin-requiringAbsolute deficiency of insulin

May be autoimmune based

Management requires exogenous insulin

Patients are prone to ketosis

-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

-gestetional

-secondary:Pancreatic disease (decreased insulin production)

-Drug induced

-Secondary to endocrinopathies such as

Cushing’s disease, acromegaly, pheochromocytoma

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%

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

Renal:

-avoid nephrotoxic drugs, maintain normovolumia, control of hyperglycemia and/or hypertension and preservation of renal blood flow

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

Autonomic NeuropathyAutonomic Neuropathy

• Orthostatic hypotension• Resting tachycardia• Gastroparesis(vomiting,diarrhea)• Impotence• Cardiac dysrhythmias• Asymptomatic hypoglycemia• Sudden death syndrome

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

Stiff Joint Syndrome-Long-standing type I diabetics are at risk for this syndrome, which is -Long-standing type I diabetics are at risk for this syndrome, which is Manifested by: joint rigidity (most significantly affecting joints involvingManifested by: joint rigidity (most significantly affecting joints involving the airway such as the temporomandibular, atlantooccipital, and cervicalthe airway such as the temporomandibular, atlantooccipital, and cervical spine joints), short stature, and tight, waxy skin.spine joints), short stature, and tight, waxy skin.

-Chronic hyperglycemia resulting in nonenzymatic glycosylation of proteins-Chronic hyperglycemia resulting in nonenzymatic glycosylation of proteins and Abnormal cross-linking of collagen in joints and other tissues isand Abnormal cross-linking of collagen in joints and other tissues is currently thought to be the initiator of the stiff joint syndrome. currently thought to be the initiator of the stiff joint syndrome.

-Limited neck mobility may result in a difficult intubation and should be -Limited neck mobility may result in a difficult intubation and should be identified before airway manipulation. identified before airway manipulation.

-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.

Complications

• Acute Either : -hyperglycemia : DKA NKHS -hypoglycemia• Chronic -vascular -neurological

Chronic effects of Hyperglycaemia1.1. MicrovascularMicrovascular

Proliferative retinopathy Diabetic nephropathy (close association with Proliferative retinopathy Diabetic nephropathy (close association with hypertension, which is found in 30-60% of diabetics)hypertension, which is found in 30-60% of diabetics)

2.2. MacrovascularMacrovascular1.1. AtherosclerosisAtherosclerosis2.2. Coronary heart disease (beware silent ischaemia, cardiomyopathy)Coronary heart disease (beware silent ischaemia, cardiomyopathy)3.3. Cerebrovascular diseaseCerebrovascular disease4.4. Peripheral vascular diseasePeripheral vascular disease

3.3. NeuropathicNeuropathic1.1. Peripheral :Motor (Mononeuropathies, pressure palsies)Peripheral :Motor (Mononeuropathies, pressure palsies) Sensory polyneuropathySensory polyneuropathy2.2.Autonomic Autonomic

DiarrheaDiarrhea Urinary incontinenceUrinary incontinence Postural hypotensionPostural hypotension Cardiac denervationCardiac denervation Impaired ventilatory control – risk of resp arrest with anaesthesiaImpaired ventilatory control – risk of resp arrest with anaesthesia GastroparesisGastroparesis

4.4. ““Stiff joint syndrome” (airway)Stiff joint syndrome” (airway)5.5. Increased incidence of infectionsIncreased incidence of infections

Acute effects of hyperglycaemiaAcute effects of hyperglycaemia 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)

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.

DKA characterized by:• hyperglycemia• dehydration• hyperosmolarity• high anion-gap metabolic acidosis

-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.

Treatment of DKA

Identifying and treating the precipitating factors Fluid resuscitation Glycometabolic control Electrolyte replacement

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.

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.

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.

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.

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.

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.

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

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.

Treatment Diabetic patients are incompletely able to counter hypoglycemia despite secreting glucagon or epinephrine (counterregulatory failure).Treatment Consists of :-Dextrose adminstration-Correcting the precipitating causesThe treatment of hypoglycemia in anesthetized or critically ill patients Intravenous administration of 50% glucose (each milliliterof 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.

Anesthetic management

Anesthetic management should include:-preoperative

-intraoperative

-postoperative

-Perioperative hyperglycemia

-Perioperative hypoglycemia

Peri-operative goal

maintaining blood glucose values below

180 mg/dl during the perioperative

period while reducing blood glucose

variability and avoiding hypoglycemia.

HowHow??• Provide adequate insulin to the patient to Provide adequate insulin to the patient to

counteract the catabolic processes that develop counteract the catabolic processes that develop in response to surgeryin response to surgery

• Glucose needs to be provided to meet the Glucose needs to be provided to meet the increased metabolic needs, caused by surgical increased metabolic needs, caused by surgical stress, as well as basal metabolic requirementsstress, as well as basal metabolic requirements

• A simple regimen that is immune to errorA simple regimen that is immune to error

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

What are the factors affecting the perioperative What are the factors affecting the perioperative anesthetic management of DManesthetic management of DM??

Type of DMType of DM MedicationMedication End-organ changes End-organ changes Nature of surgery Nature of surgery Urgency of surgeryUrgency of surgery Level of glycemic control Level of glycemic control

-preoperative management-Preoperative evaluation should include a thorough history and physicalexam . -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 thepreceding 1–3 months.

-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.

-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.

Premedication with a nonparticulate antacid and

metoclopramide is often used in an obese diabetic

patient with signs of cardiac autonomic

dysfunction.

Regimen depends onRegimen depends on

• 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

Type I diabetesType I diabetes

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

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)

New insulin delivery modes

1. Continuous subcutaneous infusions

2. Continuous intra-peritoneal infusions

Type II diabetes on diet aloneType II diabetes on diet alone

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

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 functionremain adequate.

Type II diabetes on oral hypoglycaemicType II diabetes on oral hypoglycaemic• 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 peripheryInhibit hepatic gluconeogenesisEnhances glucose uptake into tissues via GLUT-4 glucose transporterPreserves the β-cells of the pancreas

• Modifiers of glucose absorption e.g.. Ά-glucosidase inhibitor acarboseSuppress the breakdown of complex carbohydrates in the gut delaying the

rise of blood sugar postprandially

Stop the OHA before surgery?Stop the OHA before surgery?• 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.

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.

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).

Regular insulin can be added to normal saline in aconcentration 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 maintenanceof blood glucose is less than 180 mg/dL.

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 .

Minor surgeryMinor surgery

If patient is expected to resume oral intake quickly If patient is expected to resume oral intake quickly after surgery, a reduced approach may be acceptableafter surgery, a reduced approach may be acceptable

These patients will be given ½ their intermediate These patients will be given ½ their intermediate acting insulin, and a 5% dextrose solution at 100-150 acting insulin, and a 5% dextrose solution at 100-150 ml/hour to prevent hypoglycaemia. ml/hour to prevent hypoglycaemia.

Intra-op and recovery room blood sugar monitoring is Intra-op and recovery room blood sugar monitoring is essential.essential.

It is suggested that the blood sugar is measured every It is suggested that the blood sugar is measured every 30 mins to hourly.30 mins to hourly.

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

Major surgeryMajor surgery 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

Suggested GIK regimenSuggested GIK regimen

Normal insulin the day before surgeryNormal insulin the day before surgery Do a blood sugar on the day of surgery, and once result Do a blood sugar on the day of surgery, and once result

known start infusionknown start infusion 1. 1 liter 10% dextrose + 40 mEq/l KCL at 0.1g 1. 1 liter 10% dextrose + 40 mEq/l KCL at 0.1g

dextrose/kg/hrdextrose/kg/hr 2. Insulin infusion of 50 U rapid acting insulin in 250 ml 2. Insulin infusion of 50 U rapid acting insulin in 250 ml

0.9% NaCl piggybacked to the dextrose and run at 1-2 U/hr 0.9% NaCl piggybacked to the dextrose and run at 1-2 U/hr depending on hourly (or more) measurements of glucosedepending on hourly (or more) measurements of glucose

Care should be taken that neither infusion is allowed to stop Care should be taken that neither infusion is allowed to stop while the other continues runningwhile the other continues running

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

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

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

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.

Monitoring of blood sugarThe 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.

-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.

General anesthesiathe 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 anesthesiadiabetic nerves seem to be more sensitive to local anesthetics and are more susceptible to local anesthetic-induced nerve injury

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.

A few anaesthetic considerationsA few anaesthetic considerations First case in the morning to minimize the First case in the morning to minimize the

starvation periodstarvation period No anaesthetic technique is indicated or No anaesthetic technique is indicated or

contraindicated in diabetics, and the stress contraindicated in diabetics, and the stress imposed by the anaesthetic is usually minor imposed by the anaesthetic is usually minor compared to the stress of the surgery.compared to the stress of the surgery.

The challenge is to give the most stable The challenge is to give the most stable anaesthetic possible and limit the anaesthetic possible and limit the hyperglycaemic reaction to surgical stresshyperglycaemic reaction to surgical stress

LA requirements lowerLA requirements lower Risks of nerve injury higherRisks of nerve injury higher Combination of LA with epinephrine may pose Combination of LA with epinephrine may pose

greater risk of ischemic or edematous nerve injury greater risk of ischemic or edematous nerve injury (or both) in diabetic(or both) in diabetic

Document peripheral neuropathy Document peripheral neuropathy keeps the patients and relatives informed keeps the patients and relatives informed avoids medico-legal hassles later on avoids medico-legal hassles later on

Insulin response to hyperglycemia Insulin response to hyperglycemia high thoracic (T1-T6) blockade high thoracic (T1-T6) blockade ? ? inhibited inhibited low blockade, (T9 - T12) low blockade, (T9 - T12) no effect no effect

Regional blocksRegional blocks

Regional anaesthesiaRegional anaesthesia Pro:Pro:

Regional anaesthesia blunts the increases in Regional anaesthesia blunts the increases in coritcol, glucagon, and glucose.coritcol, glucagon, and glucose.

Spinal or epidural may modulate the catecolamine Spinal or epidural may modulate the catecolamine secretion, preventing high glucose and ketosis. This secretion, preventing high glucose and ketosis. This effect could continue in the post operative period, if effect could continue in the post operative period, if the block is continuedthe block is continued

An awake patient is a good monitor to prevent An awake patient is a good monitor to prevent hypoglycaemiahypoglycaemia

A swifter return to normal eatingA swifter return to normal eating

Regional anaesthesiaRegional anaesthesia

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

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

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

PostoperativeClose 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 actioncan last longer than 24 h. Another reason for close monitoring is the progression of stress hyperglycemia in the recovery period.

Perioperative hyperglycemiaPerioperatively, 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 andresults in glycosuria. Glucose-induced osmotic diuresis may lead to dehydrationand an increased risk of urinary tract infection.

Blood glucose levels should be frequently monitored and maintainedat <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.

Perioperative hypoglycemiaIt 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 ofresidual 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.

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.

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.

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.

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