CASE PRESENTATION

ANESTHESIOLOGY DEPT

LEARNING OBJECTIVES

6. How would you prepare this patient for

1. What is the prevalence of diabetes anesthesia and surgery?
mellitus (DM) in the general 7. What is the effect of anesthesia and
population? surgery on insulin and glucose
2. What are the factors in the etiology of metabolism?
the disease? 8. What anesthetic techniques would
3. How do you classify DM? you employ?
4. What are the complications of DM? 9. What are the common postoperative
5. How would you evaluate and prepare complications you expect in a diabetic
the patient preoperatively? patient?
10. How would you control diabetes in this
patient postoperatively?

1. What is the prevalence of diabetes mellitus (DM) in the general population?

• The worldwide prevalence of DM has risen dramatically over the past two decades, from an
estimated 30 million cases in 1985 to 415 million in 2017. Based on current trends, the IDF
projects that 642 million individuals will have diabetes by the year 2040 (see http://www.idf.org/).
• The prevalence of type 2 DM is rising much more rapidly, presumably because of increasing
obesity, reduced activity levels as countries become more industrialized, and the aging of the
population. The incidence of type 1 diabetes has been increasing at a rate of 3–5% per year
worldwide. The cause for this increase is not well understood, but type 1 DM is increasingly
being diagnosed at younger ages. In 2015, the prevalence of diabetes in individuals aged 20–
79 ranged from 7.2–11.4%.
• Globally, it is estimated that as many of 50% of individuals with diabetes may be undiagnosed
• Currently, Scandinavia has the highest incidence of type 1 DM; the lowest incidence is in the
Pacific Rim where it is twenty- to thirty fold lower.
• The prevalence of type 2 DM and its harbinger, IGT, is highest in certain Pacific islands and the
Middle East and intermediate in countries such as India and the United States.
• Diabetes is a major cause of mortality. In recent years, diabetes has been listed as the seventh
leading cause of death in the United States, but several studies indicate that diabetes-related
 deaths are likely underreported. Data from the IDF suggests that diabetes was responsible for
almost 5 million deaths worldwide, accounting for 14.5% of global all-cause mortality in adults
aged 20–79 years of age
•
2. What are the factors in the etiology of the disease?

Risk Factors for Type 1 Diabetes Mellitus

Family history of diabetes
Diseases of the pancreas
Infection or illness

Risk Factors for Type 2 Diabetes Mellitus

Family history of diabetes
Overweight or obese (BMI ≥25 kg/m2)
Physical inactivity
Race/ethnicity (e.g., African American, Latino, Native American, Asian
American, Pacific Islander)
Previously identified with IFG, IGT, or an hemoglobin A1c of 5.7–6.4%
History of GDM
Hypertension (blood pressure ≥140/90 mmHg)
HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250
mg/dL (2.82 mmol/L)
Polycystic ovary syndrome or acanthosis nigricans
History of cardiovascular disease

3. HOW DO YOU CLASSIFY DM?

· DM is classified on the basis of the pathogenic process leading to hyperglycemia.
· There are two broad categories of DM, designated as either type 1 or type 2 DM.
· However, there is increasing recognition of other forms of diabetes in which the molecular
pathogenesis is better understood and may be associated with a single gene defect.
o These alternative forms may share features of type 1 and/or type 2 DM.
· Both type 1 and type 2 diabetes are preceded by a period of progressive worsening of glucose
homeostasis, followed by the development of hyperglycemia that exceeds the threshold for
clinical diagnosis.

· Type 1 DM
o Develops as a result of autoimmunity against the insulin-producing beta cells, resulting in
complete or near-total insulin deficiency.
 o Type 1 DM is the result of interactions of genetic, environmental, and immunologic factors
that ultimately lead to immune-mediated destruction of the pancreatic beta cells and
insulin deficiency.
o Most, but not all, individuals with type 1 DM have evidence of islet-directed autoimmunity.
However, some individuals who have the clinical phenotype of type 1 DM lack
immunologic markers indicative of an autoimmune process involving the beta cells and
the genetic markers of type 1 DM.
o Type 1 DM can develop at any age, but most commonly develops before the age of 30.

· Type 2 DM
o Is a heterogeneous group of disorders characterized by:
 variable degrees of insulin resistance
 impaired insulin secretion
 And increased hepatic glucose production.
o Distinct genetic and metabolic defects in insulin action and/or secretion give rise to the
common phenotype of hyperglycemia in type 2 DM
o Type 2 DM more typically develops with increasing age
 However, it is now being diagnosed more frequently in children and young
adults, particularly in obese adolescents.

· OTHER TYPES OF DM
o Other etiologies of DM include specific genetic defects in insulin secretion or action,
metabolic abnormalities that impair insulin secretion, mitochondrial abnormalities, and a
host of conditions that impair glucose tolerance .
o Maturity-onset diabetes of the young (MODY) and monogenic diabetes
 subtypes of DM characterized by autosomal dominant inheritance, early onset
of hyperglycemia (usually <25 years; sometimes in neonatal period), and
impaired insulin secretion
 Mutations in the insulin receptor cause a group of rare disorders characterized
by severe insulin resistance.
o DM may also develop as a result of cystic fibrosis or chronic pancreatitis, in which the
islets become damaged from a primary pathologic process originating in the pancreatic
exocrine tissue.
 Hormones that antagonize insulin action can lead to DM.
 Thus, DM is often a feature of endocrinopathies such as acromegaly and
Cushing’s disease.
 Viral infections have been implicated in pancreatic islet destruction but are an
extremely rare cause of DM.
 A form of acute onset of type 1 diabetes, termed fulminant diabetes, has been
noted in Japan and may be related to viral infection of the islets.
 · GESTATIONAL DM
o Glucose intolerance developing during the second or third trimester of pregnancy is
classified as gestational diabetes mellitus (GDM).
o Insulin resistance is related to the metabolic changes of pregnancy, during which the
increased insulin demands may lead to IGT or diabetes.
o The American Diabetes Association (ADA) recommends that diabetes diagnosed within
the first trimester be classified as preexisting pregestational diabetes rather than GDM.
o Most women with GDM revert to normal glucose tolerance postpartum but have a
substantial risk (35–60%) of developing DM in the next 10–20 years.
o Children born to a mother with GDM also have an increased risk of developing metabolic
syndrome and type 2 DM later in life.

4. WHAT ARE THE COMPLICATIONS OF DM

· MICORVASCULAR
o Eye Disease
 Retinopathy (nonproliferative/proliferative)
 Macular Edema
o Neuropathy
 Sensory and motor (mono and polyneuropathy)
 Autonomic
o Nephropathy
 Albuminuria
 Declining Renal Function
· MACROVASCULAR
o Coronary Heart Disease
o Peripheral Arterial Disease
o Cerebrovascular Disease
· OTHER
o Gastrointestinal (gastroparesis, diarrhea)
o Genitourinary (uropathy/sexual dysfunction)
o Dermatologic
o Infectious
o Cataracts
o Glaucoma
o Cheiroarthropathya
o Periodontal disease
o Hearing loss
· Other comorbid conditions associated with diabetes (relationship to hyperglycemia is
uncertain)
o Depression
o Obstructive sleep apnea
o Fatty liver disease
 o Hip fracture
o Osteoporosis (in type 1 diabetes)
o Cognitive impairment or dementia
• Low testosterone in men.

5. How would you evaluate and prepare the patient preoperatively?

Pre-operative Assessment

· This is the most important step in the management of the diabetic patient
· Involves a thorough history and physical examination
· Review prior anaesthetic records to determine whether there were any difficulties with intubation or
anaesthetics

Lab investigations

• blood glucose
· • BUN -
• ketones
• HbA1c (to assess how well controlled diabetes is)
• K+
• proteinuria
• creatinine

A. HISTORY AND PHYSICAL EXAMINATION

Clinical history should clarify:

· The type of diabetes (DM1, DM2, gestational DM or other types)

· Glycemic control
· Diagnostic time (predictor of chronic complications),
· Drug therapy (oral, noninsulin injectable antidiabetic drugs or insulin)
· Dose and dosing time of medications
· Occurrence and frequency of hypoglycemia should be questioned
· Patient's ability to measure his blood sugar and understand the principles of diabetes therapy should
be evaluated
· If on antidiabetic drugs, it is imperative to know the details of the regimen and about medication
adherence.

Preoperative evaluation includes assessment of metabolic control and any diabetes-associated

complications

• Thorough systemic review with attention to the following detail:

A. Autonomic neurophathy

• Present in up to 40% of type 1 diabetics

• Features include:
• gastroparesis
• gustatory sweating
• nocturnal diarrhoea.
• postural hypotension
• Assess heart rate variability with deep breath
• Normal > 15 bpm
• Neuropathy is likely if < 10 bpm
• blood pressure assessment with emphasis on the search for orthostatic hypotension, a potential sign of
autonomic neuropathy.

B. CARDIOVASCULAR SYSTEM

o Diabetes is an independent risk factor for perioperative cardiac morbidity, diabetes

requiring insulin treatment is a high risk factor in the RCRI
o Diabetics are more prone to;
• ischemic heart disease (eg MI)
• hypertension
• peripheral vascular disease
• cerebrovascular disease
• cardiomyopathy
 Other risk factors for atherosclerosis should be investigated (smoking, hypertension,
dyslipidemia, family history, sedentary lifestyle),

C .RESPIRATORY SYSTEM

 Diabetics are more prone to respiratory infections and might also have abnormal
spirometry

D. GASTROINTESTINAL TRACT

 Gastroparesis is characterized by a delay in gastric emptying without any gastric outlet

obstruction.
 Increased gastric contents increase the risk of aspiration

E. AIRWAY

• Glycosylation of collagen in the cervical and temporo-mandibular joints can cause difficulty in intubation
• Stiff joint syndrome adds significant risk during airway management.
On PE, the patient presents with an inability to move close the palm surfaces of the interphalangeal joints while
pressing one hand against the other—positive "prayer signs

• Airway evaluation should include the size of the thyroid gland, as patients with DM1 have an association
of about 15% with other autoimmune diseases, such as Hashimoto's thyroiditis and Graves' disease

F. RENAL

- Diabetes is one of the common causes of ESRF

- Watch out for features of uremia

B. GLYCEMIC CONTROL

• Postpone elective surgery if possible if glycemic control is poor (HbA1c ≥ 9%).

• For major surgery, if serum glucose is >270 mg/dl preoperatively, surgery should be delayed while rapid
control is achieved with IV insulin.
• If serum glucose is >400 mg/dl , the surgery should pe postponed and metabolic state restabilized.
• BGL should be kept between 5 – 10mmol/l (90-180mg/dl) during the perioperative period .
• For critically ill patients who require admission to the intensive care unit post-operatively, a “tighter” BGL
target (e.g 4.4-6.1 mmol/L) may not convey any greater benefit.
• Hypoglycemia must be avoided.
• All patients with diabetes treated with insulin should be managed in the same way, irrespective of
whether they have type 1 or type 2 diabetes mellitus.

C. Perioperative Glucose Management

• Plan with the surgeon to schedule the surgery as the first case of the day to prevent prolonged fasting.
• Oral hypoglycemic agents are held on the day of surgery to avoid reactive hypoglycemia until oral intake
is restarted.
• Insulin therapy should balance adequate glucose control with the avoidance of hypoglycemia. Insulin is
usually continued through the evening before surgery.
• Schedule the patient to arrive in the early morning and check blood glucose on arrival.
• If patients develop symptoms or measurable hypoglycemia, theyshould be counseled to take a glucose
tablet or clear juice.
• Type 1 diabetics should be continued on basal insulin administration even during preoperative fasting to
prevent ketoacidosis.
• Administer half the usual morning dose of intermediate- or long-acting insulin after arrival to the surgery
center, where a maintenance IV can be started. Hold the usual dose of rapid- or short-acting insulin.
• Use the patient’s own sliding scale to administer short-acting insulin subcutaneously prior to the
scheduled surgery and during short operation
• Patients on insulin pumps may be managed by continuing the pump for short operations or changing
over to an intravenous insulin infusion for longer or major operations.

Goals
 · Establishment of certain glycemic target levels, <180 mg/dL in critical patients and < 140 mg/dL in
stable patients.
· Avoidance of severe hyperglycemia or hypoglycemia.
· Prevention of ketoacidosis.
· Maintenance of physiological electrolyte and fluid balance.
· Reduction of overall patient morbidity and mortality
· Well controlled diabetes prior to elective surgery.
· To Avoid insulin deficiency and anticipate increased insulin requirements.

PREOP FASTING

• Atleast 6 hours for solid foods.

• Patients with gastroparesis, 12 hours may be needed. Such patients are given H receptor 2

blocker (Ranitidine) and prokinetics (metoclopramide).

• When fasting exceeds 8-10 hours then insulin- glucose infusion has to be started to prevent catabolism.

6. How would you prepare this patient for anesthesia and surgery?

Intraoperatively:
Goal:
• Ensure Metabolic Homeostasis and anticipate problems arising from preexisting complications
• Enhancing healthcare team outcomes

Anesthetic Plan depend intimately on the end-organ complications:

• Invasive Monitoring
• Awake Intubation
• Fluid Management and Drug Choices
• Aspiration

Measurement of Blood glucose level

• Monitored every 4 to 6 hours while the patient is NPO
• Additional measurements is determined by:
o duration and magnitude of surgery
* Hyperglycemia (over 180 mg/dl), in surgeries of shorter duration (<less than 4 hours)
with expected hemodynamic stability and minimal fluid shift, can be managed with 2-
hourly subcutaneous correctional insulin (preferably rapid-acting insulin) and BG checks.
* In surgeries that may involve hemodynamic fluctuations, massive fluid shifts, or last
longer than 4 hours duration, BG greater than 180 mg/dl should be managed with
intravenous insulin infusion, and BG monitored every 1 to 2 hours.
o brittleness of the diabetes
• Hourly measurements are reasonable in high-risk patients
• The standard glucose dosage for an adult patient is 5 to 10 g/hr (100 to 200 mL of 5% dextrose
solution hourly).
 • Intraoperative administration of glucose should be guided by the patient’s glucose level with the
goal of preventing hypoglycemia or hyperglycemia.
• Routine administration of additional glucose-containing IV fluids is not recommended.
• It is best to separately record dextrose administration and fluids given.

Monitoring of the patient with significant metabolic impairment

• Hourly determinations of blood glucose
• Arterial pH
• Electrolytes
• Fluid balance
• Positioning on the operating table

Glycemic Control
Factors that influence the glucose levels in the perioperative period:
o Endogenous insulin secretions
o Exogenous insulin administration
o Insulin resistance
o Endogenous glucose production
o Exogenous glucose administration
o Overall glucose consumption

Modulators of perioperative hyperglycemia

Glycemic Goal:
• Intensive insulin therapy (IIT)
o as a means of normalizing elevated glucose levels
o a target glucose range of 80 to 110 mg/dL
o standard care implied a target glucose range of 180 to 200 mg/dL\
*The IIT groups also demonstrated high incidences of hypoglycemia

• NICE-SUGAR
o compared the effect of intensive glycemic control (target 81 to 108 mg/dL, mean blood
glucose attained 115 mg/dL) to standard glycemic control (target 144 to 180 mg/dL,
mean blood glucose attained 144 mg/dL).
*Severe hypoglycemia was also more common in the intensively treated group

Enhancing Healthcare Team Outcomes

• Interprofessional communication and care coordination amongst physicians
• Play a vital role in the optimal management of diabetes in the perioperative period.
• Adequate communication helps minimize adverse events, improves clinical outcomes, and
patient satisfaction.

REFERENCE:
https://www.ncbi.nlm.nih.gov/books/NBK540965/
Barash, P. G. (2017). Clinical anesthesia (8th ed.). Philadelphia, PA: Wolters Kluwer Health/Lippincott
Williams & Wilkins.

7. What is the effect of Anesthesia and Surgery on Insulin and Glucose metabolism?
A. Anti-Insulin Effects
•Anesthesia and surgery cause a stereotypical metabolic stress response that could overwhelm
homeostatic mechanisms in patients with pre-existing abnormalities of glucose metabolism.
•The invariant features of the metabolic stress response include release of the catabolic hormones
• epinephrine,
• norepinephrine,
• cortisol,
• glucagons, and
• growth hormone
and inhibition of insulin secretion and action.
•Surgical stress
• increase serum glucose concentrations secondary to the release of cortisol and
catecholamines
• deleterious effect on pancreatic β-cell function
• Plasma insulin levels fall, and
 • insulin secretory responses to glucose become impaired during surgery
•The important anabolic actions of insulin that may be reversed or attenuated during the stress of
surgery include:
• stimulation of glucose uptake and glycogen storage,
• stimulation of amino acid uptake and protein synthesis by skeletal muscle,
• stimulation of fatty acid synthesis in the liver and storage in adipocytes, and
• renal sodium reabsorption and intravascular volume preservation.

•The anti-catabolic effects of insulin include:

• inhibition of hepatic glycogen breakdown,
• inhibition of gluconeogenesis,
• inhibition of lipolysis,
• inhibition of fatty acid oxidation and ketone body formation, and
• inhibition of proteolysis and amino acid oxidation.
Thus, inhibition of insulin secretion and action shifts the perioperative milieu toward hypercatabolism
through a variety of mechanisms.

B. Direct Catabolic Effects of Stress Hormones

The neuroendocrine response to the stress of general anesthesia and surgery leads to activation of
potent counterregulatory hormones:
• norepinephrine is augmented mostly during surgery and epinephrine postoperatively
• stimulate gluconeogenesis and glycogenolysis
• inhibit glucose utilization by peripheral tissues
• inhibit insulin secretion
• Activation of phosphoproteins by cAMP-dependent protein kinases - stimulatory effects of
catecholamines on liver and muscle glycogen breakdown
• phosphorylation of glycogen synthase - decreased glycogen synthesis

These effects predispose to severe hyperglycemia, which is further exacerbated :

- stimulatory effect of epinephrine and norepinephrine on glucagon secretion
- catabolic effects of catecholamines include stimulation of lipolysis and ketogenesis
- Epinephrine increases adipocyte cAMP levels, leading to phosphorylation and activation of
hormone-sensitive lipase. The activated hormone sensitive lipase promotes lipolysis and
release of free fatty acids into the circulation.
- Glucagon, whose levels are augmented by catecholamines, exerts catabolic effects similar
to those of the catecholamines: stimulation of hepatic glucose production and ketogenesis
and inhibition of insulin action in peripheral tissues.

• Hypoinsulinemia, insulin resistance, and excessive catabolism from the action of counterregulatory
hormones is a serious threat to glucose homeostasis in all patients with diabetes, particularly those
whose preoperative metabolic control is less than perfect.
• The logical conclusion is that insulin therapy will be needed perioperatively in the majority of
patients with diabetes undergoing surgery.

REFERENCE:

1. 1) HARRISON’S PRINCIPLE OF INTERNAL MEDICINE 20’TH EDITION

2. 2) Barash, P. G. (2017). Clinical anesthesia (8th ed.). Philadelphia, PA: Wolters Kluwer
Health/Lippincott Williams & Wilkins.
3. 3) Management of Diabetes Mellitus in Surgical Patients Samuel Dagogo-Jack, K. George
M.M. Alberti Diabetes Spectrum Jan 2002, 15 (1) 44-48; DOI: 10.2337/diaspect.15.1.44
8. What anesthetic techniques would you employ?

From: Journal of American College Surgeon

Procedure of Choice:

TOTAL ABDOMINAL HYSTERECTOMY WITH BILATERAL SALPHINGO-OOPHORECTOMY

(TAHBSO)

Choice of Anesthesia:

GA (ETT) with or without epidural for postop pain relief, or neuraxial anesthesia (epidural)

ANESTHESIA for Diabetic Patient

Preoperative:

· Check type, duration and severity of diabetes

· Check current therapy for type and dose
· Check morning blood sugar and HbA1c assay, creatinine level and electrolytes
· Check for presence of coronary artery disease, HTN, cerebrovascular disease and
peripheral vascular disease. Check EKG.
· Consider Na bicitrate and Metoclopramide in patients with GERD and Gastroparesis
· Severe peripheral neuropathy may preclude use of RA
· Long-acting sulfonylurea drugs such as Chlorpropamide should be stopped and
substituted by short-acting agents. Metformin stopped if concern for intraop
metabolic acidosis. Type-2 diabetic patients with marked hyperglycemia on oral
treatment should be switched to insulin before operation

Emergency Surgery:

· Stabilize metabolic control / volume status as much as possible

· Maximize glucose, electrolyte, acid-base status – insulin and glucose infusion
· Saline infusion if volume is depleted
· K+ infusion if renal function is normal and serum K+ is normal or low
· Bicarbonate infusion only in patient with severe acidosis

Intraoperative management:

· Monitoring blood sugar

American Diabetes Association Recommendations for Target Inpatient Blood Glucose

Concentration

Patient Population Blood Glucose Rationale

Target
General Fasting: 90- Better outcomes, decrease infection rates
medical/surgical 126mg/dL

Random: <180
mg/dL

Cardiac Surgery <150 mg/dL Decrease morality, decrease risk of sternal wound
infections

Critically Ill 80-110 mg/dL Decrease mortality, morbidity (SICU); decrease

morbidity; decrease length of stay (MICU)

Acute Neurologic <110 mg/dL Increase mortality if admission blood glucose

disorders >110mg/ dL

· Patients on NPH or PZI:

- increase risk for anaphylactic protamine reactions
- insulin requirements in diabetics vary during surgery

Protocol for Perioperative Insulin Infusion

Mix 50 U regular insulin in 500mL NS (1.0 U/h = 10 mL/h)

Initiate infusion at 0.5 – 1.0 U/h

Check blood glucose level q1-2h and adjust infusion rate as needed

Insulin infusion (U/h) = blood glucose (md/dL)/150

Blood glucose Infusion

concentration

<80mg/dL Turn Insulin infusion off for 30 min; give 25 mL of 50% glucose;
recheck level in 30 min

80-120 mg/dL Decrease insulin infusion rate by 0.3 U/h

120-180 mg/dL No change in Insulin infusion rate

 180-220 mg/dL Increase Insulin infusion rate by 0.3 U/h

>220 mg/dL Increase Insulin infusion rate by 0.5 U/h

Postop:

· Treat N/V in pts with gastroparesis with metoclopramide as pts have increased risk of infection, MI,
hyper/hypoglycemia, CV and renal dysfunction

GENERAL ANESTHESIA

Classification:

Inhalation Gas: Nitrous Oxide

Volatile Liquid: Halothane, Enflurane, Isoflurane, Desflurane, Sevoflurane

Intravenous:

- Inducing Agent: Thiopentone Sodium, Methohexitone, Sod Propofol, Etomidate

- Slower Acting Drugs: Benzodiazepam, Diazepam, Lorazepam, Midazolam
BENEFITS OF INHALATIONAL ANESTHETICS:

Nonflamable; reusable; hypnotic; overall low degree of respiratory depression vs. Intravenous agents,
potent bronchodilators

SIDE EFFECTS OF VOLATILE ANESTHETICS

- Hypotension secondary to vasodilation and myocardial depression

- Potentiates neuromuscular blockade
- During spontaneous ventilation: ↓ RR and ↓ TV, hypercarbia, ↓ ventilatory response to hypoxemia
- Inhibitor of hypoxic pulmonary vasoconstriction (HPV)
- May trigger malignant hyperthermia (MH)
EPIDURAL ANESTHESIA

• This is a medicine that blocks pain.

• Epidural is a combination of sympathetic, sensory, or motor blockade depending on the dose,
concentration, or volume of local anesthetic administered.
• It can be used for labor and delivery.
• An epidural catheter allows the versatility to extend the duration of anesthesia beyond the
original dose by the administration of additional local anesthetic.
• Epidural catheters may be left in place for postoperative analgesia.

Mechanism of Action

• Administered at a physiologic distance when compared to spinal anesthesia.

• The spinal nerve roots and dorsal root ganglia are the important sites of action.
• Several barriers to the spread of local anesthetic to the intended site of action results in the
requirement of larger volumes of local anesthetic when compared to spinal anesthesia.
• The speed of neural blockade depends on the size, surface area, and degree of myelination of
the nerve fibers exposed to the local anesthetic.
EPIDURAL ANESTHESIA INDICATIONS

• Cesarean section
• Procedures of the uterus, perineum
• Hernia repairs
• Genitourinary procedures
• Lower extremity orthopedic procedures
• Excellent choice for elderly or those who may not tolerate a general anesthetic

RISKS AND POSSIBLE COMPLICATIONS

• A sudden drop in blood pressure, which may cause the baby's heart rate to drop temporarily.
• Severe headache after birth.
• Soreness of the back for several days.
• Dizziness, seizures, breathing problems, allergic reaction to the anesthetic, nerve damage, or
paralysis (all very rare).

COMMONLY USED LOCAL ANESTHETICS

 9. COMMON POSTOPERATIVE COMPLICATIONS EXPECTED IN A DIABETIC PATIENT

Relation among perioperative injury, hyperglycemia, and

outcomes.

Infections account for 66% of postoperative complications

and nearly one quarter of perioperative deaths in patients
with DM.

Postoperative hyperglycemia- in surgical patients, is

associated with an increased risk of infection, renal and
pulmonary complications, and also mortality.

Postoperative myocardial infarction- incidence is

increased in diabetic patients, and the complication rate is
higher

Diabetic patients are at an increased risk of:

• cognitive decline,
• dementia,fractures,
• cancer,
• obstructive sleep apnea, and
• hearing disorders.

END-ORGAN COMPLICATIONS

• Atheroscelerosis

-develops earlier
-more widespread than in nondiabetics

Manifestations:

• coronary artery disease,

• peripheral vascular disease,
• cerebrovascular disease,
• renovascular disease
• Postoperative Myocardial Infarction

• Cardiomyopathy- in the face of angiographically normal arteries

• Diabetic Nephropathy- leading cause of end-stage renal disease

o Albuminuria- precedes steady decline in renal function
 o microalbuminuria -
 Type 1:earliest stage of diabetic nephropathy
 Type 2: marker for development of nephropathy
• Diabetic Neuropathy
o Most common: chronic sensorimotor distal symmetric polyneuropathy
and autonomic neuropathy
• Diabetic stiff joint syndrome
o frequent complication of type 1 DM

HYPEROSMOLAR NONKETOTIC COMA

• Presumably: combination of an impaired thirst response and mild renal insufficiency--

allows the hyperglycemia to develop.
• The marked hyperosmolarity may lead to coma and seizures, with the increased plasma
viscosity producing a tendency to intravascular thrombosis.
• Syndrome characteristic:metabolic disturbance responds quickly to rehydration and small
doses of insulin.

DIABETIC KETOACIDOSIS

• It is defined by the biochemical triad of:

o Ketonemia
o Hyperglycemia
o Acidemia
 increase in the hydrogen ion concentration of the blood, resulting in a decrease
in pH
• What are the warning signs of DKA?
o DKA usually develops slowly. But when vomiting occurs, this life-threatening condition
can develop in a few hours. Early symptoms include the following:
 Thirst or a very dry mouth
 Frequent urination
 High blood glucose (blood sugar) levels
• 250- to 500-mg/dL range
 High levels of ketones in the urine

HYPOGLYCEMIA

• Hypoglycemia or low blood sugar is when your blood sugar levels have fallen low enough that
you need to take action to bring them back to your target range.
• This is usually when your blood sugar is less than 70 mg/dL.
(American Diabetes Assoc., 2021)
• Clinically significant hypoglycemia is defined by Whipple triad:
o Symptoms of neuroglycopenia
  weakness, tiredness, or dizziness; difficulty with concentration; confusion; blurred
vision
o Simultaneous blood glucose concentration below 40 mg/dL
o Relief of symptoms with glucose administration
• Hypoglycemia in hospitalized patients has been defined as
blood glucose below 70 mg/dL (3.9 mmol/L) and
severe hypoglycemia as less than 40 mg/dL (2.2 mmol/L).
(Barash et al., 2017)

References:

• Book:

o Clinical Anesthesia 8th Edition- Barash

o Pocket Anesthesia – Urman and Ehrenfeld

• Website

o https://www.nysora.com/regional-anesthesia-for-specific-surgical
procedures/abdomen/epidural-anesthesia-analgesia/
o https://www.slideshare.net/ArthiRajasankar/epidural-1
o https://slideplayer.com/slide/5960136/
o https://www.slideshare.net/DeepakKumarGupta2/general-anaesthesia-52366531

10. How would you control diabetes in this patient postoperatively?

● In the post-anesthesia care unit (PACU), it is imperative to review the intraoperative hyperglycemia
management and continue close glucose monitoring with either intravenous or subcutaneous
insulin.

A) Ambulatory
■ After recovery in the PACU, ambulatory surgery patients who are stable and tolerating oral
intake can be discharged home on the previous antihyperglycemic regimen.

B) Non-critically Ill
■ Non-critically ill patients who require hospitalization are admitted from PACU to the
surgical/medical ward on subcutaneous (SC) insulin.
■ In the case of poor or no oral intake, basal plus correctional insulin is preferred
■ In a patient with regular oral intake, the insulin regimen should consist of basal, nutritional,
and correctional components.

Insulin Regimen:
 ● Basal insulin- Controls hyperglycemia when a patient is not eating (at night, in between
meals or when fasting) and can be given as long-acting insulin (glargine or detemir) once
or twice daily.
● Nutritional insulin- Also referred to as meal-time or prandial insulin, helps control
hyperglycemia related to carbohydrate intake (meals, enteral, or parenteral nutrition), with
either rapid-acting insulin (lispro, aspart or glulisine) or short-acting insulin (regular).
● Correctional insulin- Is used to counteract hyperglycemia that is above the goal, with either
rapid-acting or short-acting insulin. When correctional insulin is given in addition to
nutritional insulin, then the same formulation is combined into one single dose.

Dosage:
■ The insulin regimen can be dosed based on weight or pre-hospitalization regimen.
■ Patients on home insulin regimen with good glycemic control should have their basal insulin
reduced by 20 to 25% if the oral intake is inadequate.

For weight-based dosing:

● in an average patient, the starting total daily dose (TDD) of insulin is 0.4 to 0.5 U/Kg/day
● in insulin-sensitive patients (type 1 DM, insulin naive) starting dose should be reduced
to 0.2 to 0.3 U/Kg/day
● in insulin-resistant (obese, on high-dose steroids) starting dose should be increased to
0.6 to 0.7 U/Kg/day

■ Once the TDD is determined, half of TDD is administered as basal insulin, and 1/6 of TDD
will be administered as nutritional insulin with each of the three meals.
■ When eating, BG is generally monitored four times a day (before meals and at bedtime),
and correctional insulin administered accordingly.
■ The patient who is receiving nothing by mouth should have BG monitored every 6 hours for
correction with regular insulin or every 4 hours for correction with rapid-acting insulin.

C) Critically Ill
■ Critically ill patients should be managed in a medical or surgical intensive care unit with
continuous insulin infusion (CII) with regular insulin, with BG monitoring every 1 to 2
hours, as dictated by institutional protocol.
■ The transition from CII to long or intermediate-acting SC insulin is done once these patients
are:
● hemodynamically stable with no vasopressor requirement
● have optimal glycemic control with minimal variability
● a steady infusion rate in the past 6 to 8 hours.
■ Due to the extremely short half-life of intravenous insulin and delayed onset of action of
long/intermediate-acting insulin, it is essential to overlap IV and SC insulin by 2 to 3
hours.
 ■ Premature discontinuation of IV insulin creates a hiatus in the basal insulin supply, which
risks rebound hyperglycemia or metabolic decompensation (especially in type 1
diabetes).
■ Subcutaneous basal insulin at the time of transition is dosed based on either
(a) the rate of insulin infusion
(b) weight
(c) home insulin dose
■ In a patient with minimal or no caloric intake, 100% of the calculated TDD is administered
as basal.
■ In contrast, in patients with optimal caloric intake, 50% is given as basal, and 50% as
nutritional insulin.
■ For the weight-based method, TDD is calculated similarly to non-critically ill patients, half of
which is a basal dose and the other half as nutritional insulin.
■ In patients with good glycemic control on home insulin therapy, 70 to 80% of the home
basal insulin dose can be administered at the time of transition.
■ After the transition, similar to non-critically ill patients, hyperglycemia is managed with
correctional insulin every 4 to 6 hours in a fasting patient and four times a day (before to
meals and at bedtime) in a patient who is eating.

Type 1 Diabetes
• Due to minimal to no pancreatic beta-cell function, type 1 diabetics should have a basal-supply
of insulin at all times (even if nothing by mouth), either subcutaneously or intravenously.
• Failure to do so can cause them to decompensate into diabetic ketoacidosis easily.

Type 2 Diabetes
• therapy can be transitioned to the patient’s chronic regimen as the patient resumes oral intake.
• Type 2 diabetics who have had a gastric bypass procedure can have rapid resolution of their
glucose intolerance and will often need their oral agents and insulin reduced or even
discontinued in the postoperative period.
• This effect appears to be due to changes in the incretin hormones such as GIP and GLP-1,
rather than weight loss.