Type I/juvenile/insulin dependent
Type II/maturity onset/non-insulin dependent
Gestational
Stress related
Age
Children, young adults
Adults
Pregnant women
Usually adults
Etiology
Immune mediated/idiopathic
Resistance/deficiency to insulin
Hormones/lack of insulin
Stress of surgery/hospitalization causing insulin lack/resistance, hormonea related
Insulin therapy
Required
May be required/oral hypoglycemics
May be required
May be required
Ketoacidosis
Yes
Hyperosmolar nonketotic coma
No
No
Body weight
Normal to thin
Overweight to obese
Overweight to Obese
Normal to obese
Clinical Effects of Hyperglycemia
Chronic uncontrolled blood glucose levels can lead to effects in virtually every organ system leading to increased morbidity and mortality in diabetic patients (Fig. 34.1). Preoperative evaluation of a diabetic patient should focus on the following factors.
Fig. 34.1
Complications of diabetes mellitus
Hyperglycemia leading to ketoacidosis/nonketotic hyperosmolar coma
Interference with wound healing (decreased granulation tissue formation, fibroblast proliferation and collagen synthesis, and capillary proliferation)
Increased incidence of wound infection (decrease in phagocytosis and chemotaxis of the polymorphonuclear cells)
Thrombus formation (platelet aggregation due to increase in the production of thromboxane and inhibition of plasminogen activator)
Cardiac effects (silent myocardial infarction, hypertension, coronary artery disease, congestive cardiac failure, diastolic dysfunction)
Neurological effects including stroke and peripheral neuropathy (glucose presence increases anaerobic metabolism leading to increased lactic acid levels, and intracellular acidosis aims to keep glucose levels normal during surgery for head injury/stroke patients)
Prone to lung infections (pneumonia)
Retinopathy, cataract formation
Peripheral vascular disease
Renal insufficiency
Autonomic imbalance
A thorough history and physical examination (including functional status), laboratory testing, chest radiograph (cardiomegaly), and an electrocardiogram (silent myocardial infarction) are essential in evaluation of diabetic patients. Noninvasive and invasive cardiac testing may be necessary in high-risk patients. Blood sugar control in the previous 3–4 weeks can be assessed by measuring hemoglobin A1C level (normal 4–6 %). Medications taken by patients should be inquired. In addition, patients may be taking either insulin or oral hypoglycemic agents. Patients with DM may have restricted movements at the temporomandibular (TMJ) and atlanto-occipital joints, thereby potentially making laryngoscopy difficult. The presence of obesity may further aid to problems in airway management.
Patients should be instructed to continue their antihyperglycemic regimen until the evening prior to their surgery, and perhaps skip the AM dose or receive half their morning insulin dose on the day of surgery (see chapter on preoperative evaluation), to prevent hypoglycemia (insulin time chart, Table 34.2). Patients on insulin pump (baseline insulin infusion of short-acting insulin) may be continued on their basal regimen. It is important to remember that patients on metformin may be more prone to developing lactic acidosis. Therefore, metformin may be stopped 24 h before surgery and restarted postoperatively. Blood glucose level (finger stick) should be checked prior to taking a diabetic patient to the operating room. Also, surgery in DM patients should be scheduled as early in the morning, as possible.
Table 34.2
Insulin time chart
Insulin | Preparation | Onset of action | Peak effect | Duration |
---|---|---|---|---|
Rapid acting | Lispro (Humalog) | <15 min | 1 h | 3–5 h |
Aspart (Novolog) | ||||
Glulisine (Apidra) | ||||
Short acting | Regular (Humulin L, Novolin R) | 30–60 min | 2–3 h | 3–6 h |
Intermediate acting | NPH (Humulin N, Novolin N) | 1–2 h | 4–9 h | 14–20 h |
Long acting | Glargine (Lantus) | 1 h | 6–16 h | 24 h |
Detemir (Levemir) | ||||
Inhaled powder | Human insulin (Exubera) | <30 min | 1–2 h | 6–8 h |
Autonomic Imbalance
Autonomic neuropathy occurs in 20–40 % of patients with diabetes mellitus. Patients lack compensatory mechanisms to deal with hemodynamic fluctuations and hypoxia and are prone to sudden cardiac death, arrhythmias, and myocardial infarction. Signs and symptoms of autonomic imbalance include lack of pulse rate variability with respiration, resting tachycardia, orthostatic hypotension, lack of sweating, gastroparesis, impotence, and bladder dysfunction. Orthostatic hypotension may be demonstrated by a positive tilt test (decrease in blood pressure approximately 30 mmHg when moving from a supine to an upright position). Bradycardia may be unresponsive to atropine or ephedrine and may require administration of epinephrine.
Ketoacidosis
High blood glucose levels can lead to a life-threatening condition called diabetic ketoacidosis. This usually occurs in type I diabetics, but can also occur in type II diabetics. Due to the lack of insulin, there is profound hyperglycemia with blood glucose levels up to 500 mg/dl. There is an increase in anaerobic metabolism leading to an accumulation of ketone bodies (acetoacetate, β-hydroxybutyrate). Infection is the commonest precipitating factor in causing diabetic ketoacidosis.
Signs and Symptoms of Diabetic Ketoacidosis
Anion-gap metabolic acidosis
Nausea and vomiting, thirst (hypovolemia)
Abdominal pain, constant urination (diuretic effect of glucose)
Dyspnea
Agitation, confusion, and ultimately coma
Treatment of Diabetic Ketoacidosis
Intravenous regular insulin, 0.2 units/kg bolus, followed by an infusion of 5–10 units/h or 0.1 units/kg/h.
The blood glucose levels are gradually reduced at a rate of not more than 100 mg/dl/h.
Blood glucose levels are measured every 30 min–1 h (may require an arterial line for repeated blood samples).
Urine output and vital signs are monitored.
When the blood glucose reaches 250 mg/dl, a D5W infusion is started to prevent hypoglycemia from occurring.
Hydration (aggressive)—normal saline 500–1,000 ml/h initially.
Electrolyte replacement, especially potassium as insulin carries glucose and potassium into the cell.
Nonketotic Hyperosmolar Hyperglycemic Coma
This syndrome usually occurs in elderly patients with type II DM. This clinical condition is characterized by:
High blood glucose levels >600 mg/dl.
Hyperglycemic diuresis and dehydration-plasma hyperosmolality >330 mOsm/L.
Reduced brain water may cause seizures, confusion, and coma.
Acute renal failure and lactic acidosis.
There is enough insulin to prevent formation of ketone bodies.
Treatment includes fluid administration, potassium supplementation, and insulin.
Hypoglycemia
Hypoglycemia is the most feared complication in patients with DM. DM patients may not tolerate blood glucose levels lower than 50 mg/dl, as they have chronically elevated blood glucose levels. Hypoglycemia leads to catecholamine secretion causing sweating, tachycardia, and hypertension. Central nervous symptoms may include dizziness, seizures, and coma. Hypoglycemia may be difficult to recognize in anesthetized patients, those taking beta blockers, or in patients with severe autonomic neuropathy. Renal failure prolongs the duration of action of insulin and hypoglycemic agents, making these patients prone to developing hypoglycemia. Treatment includes a high degree of suspicion and prompt administration of 50 ml of 50 % dextrose intravenously.
Intraoperative Blood Glucose Management
Although the lowest blood glucose level prior to surgery in DM patients is under debate, the general consensus is to proceed with surgery with a blood glucose level between 100 and 200 mg/dl. Patients with a blood glucose level greater than 180 mg/dl may be given regular (short-acting) insulin, keeping in mind that 1 unit of regular insulin (subcutaneously/intravenously) will decrease the blood glucose level by about 25–30 mg/dl.
Blood glucose levels should be measured intraoperatively every 45 min–1 h. Mild to moderately elevated blood glucose levels may be managed by small doses of regular insulin. Higher blood glucose levels (>400 mg/dl) are managed by running an insulin infusion, adequate hydration and potassium supplementation. This is because insulin increases the uptake of glucose and potassium into the cells, thereby, leading to hypoglycemia and hypokalemia in the plasma.
Postoperative Care
A blood glucose level should be measured in the recovery room before discharging the patient. Pain, nausea, and vomiting should be treated appropriately. It is important to remember that nausea and vomiting in a patient with DM may be a sign of severe hyperglycemia. Similarly, hypoglycemia should also be watched for and treated aggressively. Patients should be started on an insulin sliding scale or their oral antihyperglycemic regimen once oral intake is begun. Comorbid conditions, such as hypertension, coronary artery disease, and renal failure, should be taken into account in treating DM patients.
Thyroid Disorders
Hyperthyroidism
Overactivity of the thyroid gland causes increased secretion of thyroid hormones resulting in hyperthyroidism. Hyperthyroidism causes increased metabolism in almost every organ of the body (Table 34.3). Thyroid hormone secretion is controlled by the anterior pituitary and the hypothalamus. Figure 34.2 depicts the negative feedback mechanism regulating thyroid hormone secretion.
Table 34.3
Clinical manifestations of hyperthyroidism
Neurological | Anxiety, nervousness, fine tremor, fatigue, hyperactivity, irritability, sweating, heat intolerance |
Ophthalmic | Exophthalmos in Grave’s disease, eyelid lag, eyelid retraction |
Cardiac | Palpitations, arrhythmias (tachycardia, atrial fibrillation) |
Miscellaneous | Weight loss with increased appetite, hair loss, loss of libido, diarrhea, osteoporosis, polyuria, polydipsia |
Fig. 34.2
Regulation of thyroid hormone secretion via a negative feedback mechanism. TRH thyroid-releasing hormone, TSH thyroid-stimulating hormone
Causes
The most common cause of hyperthyroidism is Graves’s disease. This is an autoimmune disease with hyperfunctioning of the entire thyroid gland. It is caused by circulating thyroid-stimulating IgG antibodies which stimulate the production of the thyroid hormones. Other causes of hyperthyroidism include presence of hyperactive nodules (hot thyroid nodules), inflammation (thyroiditis), amiodarone (a drug with similar structure to thyroxine), and thyroid carcinoma.
Diagnosis
Measuring levels of thyroid-stimulating hormone (TSH), total and free thyroxine (T4), and total and free triiodothyronine (T3)
Measuring thyroid-stimulating antibodies (Graves’s disease) and antithyroid peroxidase (Hashimoto’s thyroiditis)
Radioactive iodine uptake by the thyroid gland and thyroid scan
A low TSH and high thyroid hormone levels confirm then diagnosis of hyperthyroidism. Primary pituitary failure may also produce a low TSH level (rare)—euthyroid sick syndrome.
Treatment
Temporary—antithyroid hormone synthesis medications—methimazole and propylthiouracil, and beta blockers like propranolol, which control both beta adrenergic symptoms and also block the peripheral conversion of T4 to T3
Permanent—radioactive iodine I-131 thyroid ablation or subtotal/total thyroidectomy (large goiter, compression of the neck structures, thyroid cancer)
Anesthetic Considerations
Patients should be euthyroid before surgery. Non-emergent surgery should be avoided unless the patient is euthyroid. Preoperative thyroid medications, including beta blockers (heart rate less than 85/min), should be continued in the perioperative period. For emergency surgery, the heart rate can be controlled with esmolol (infusion of 100–300 mcg/kg/min). Preoperative evaluation should include a thorough airway evaluation, as patients with goiter may have airway difficulties and tracheal deviation. It may be prudent to avoid addition of epinephrine to local anesthetic solutions for regional anesthesia.
Premedication: midazolam, narcotics (avoid anticholinergics).
Induction: A large goiter may warrant awake intubation with a reinforced endotracheal tube. Thiopental/propofol can be used for induction (avoid ketamine). General endotracheal anesthesia is usually administered for surgery. Alternatively, an LMA can be used which allows visualization of vocal cords via a fiberoptic scope in a spontaneously breathing patient. Hyperthyroid patients are frequently hypovolemic, which may cause hypotension during induction.
Maintenance: Intraoperatively, the heart rate, cardiac function, body temperature, and fluid status should be closely monitored. Esmolol can be used to treat tachycardia, while sympathomimetic drugs (desflurane, ketamine, pancuronium) should be avoided. Patients with hyperthyroidism may have associated myopathy or myasthenia gravis warranting for close muscle relaxation monitoring. Patients with exophthalmos should have their eyes carefully taped to avoid injury. It is important to note that MAC is unchanged in hyperthyroid patients.
Complications of Thyroidectomy
Complications of thyroidectomy are listed in Table 34.4. To minimize RLN injury, one can use specialized endotracheal tubes with external wires to detect EMG activity from electrical stimulation of the RLN. In addition, visualization of vocal cords by a fiberoptic bronchoscope through an LMA can be used by the anesthetist to confirm vocal cord response to electrical stimulation of the RLN by the surgeon.
Table 34.4
Complications of thyroidectomy
Unilateral RLN damage, one cord midline | Hoarseness |
Bilateral RLN damage, midline vocal cords | Total airway obstruction, aphonia—secure airway emergently |
Superior laryngeal nerve damage | Hoarseness, pulmonary aspiration risk |
Hematoma | Airway compromise |
Inadvertent parathyroidectomy | Hypocalcemia, laryngospasm |
Thyroid storm | Life-threatening emergency |
Thyroid storm is a rare but life-threatening exacerbation of hyperthyroidism. It is a hypermetabolic state, which occurs due to sudden and massive release of thyroid hormones into the circulation. It may occur intraoperatively, but usually occurs 6–24 h postoperatively. Precipitating factors include acute illness or infection, trauma, surgery, or radioiodine therapy. Signs and symptoms (may mimic malignant hyperthermia) include anxiety, sweating, tachycardia, hyperthermia, arrhythmias, myocardial ischemia, and congestive cardiac failure. Treatment of thyroid storm is summarized in Table 34.5.
Table 34.5
Treatment of thyroid storm
Hydration |
Supplemental oxygen |
Antipyretics, cooling blankets |
Hydrocortisone—decreases peripheral conversion of T4 to T3 |
Propylthiouracil—blocks thyroid hormone synthesis |
Potassium iodide—blocks release of thyroid hormones |
Propranolol—blocks effects of released thyroid hormones
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