The hallmark of COPD is the evidence of a productive cough and a progressive decrease in the patient’s exercise tolerance. Three major diseases are part of COPD: asthma, emphysema, and chronic bronchitis.² All are characterized by airway obstruction. These diseases may have medically reversible components, such as bronchospasm, or they may have irreversible components, such as alveolar septal destruction. Some of the reversible components of asthma, such as retained secretions, bronchospasms, and infections, can be corrected with the interaction of the physician, nurse, physical therapist, and respiratory therapist. The treatment of asthma can include oxygen therapy, bronchodilators, chest physiotherapy, and proper hydration.

Chronic bronchitis is associated with chronic cigarette smoking. The nurse can contribute greatly to the patient’s future health with strong influences to refrain from smoking.³ Other therapy for the reversible components can include the use of bronchodilators, chest physiotherapy, and oxygen.

The patient with emphysema usually has airway destruction that is irreversible. As the alveolar septa are destroyed, insufficient alveolar ventilation ensues and eventually leads to hypercarbia. As the disease progresses, carbon dioxide cannot be expelled from the lungs and is retained there. The patient usually increases minute ventilation to try to compensate for the hypercarbia. Respiratory acidosis develops slowly as the various acid-base buffer systems try to neutralize the accumulated acid. In this compensated state, the patient usually has a near-normal pH, high plasma bicarbonate, low chloride concentration, and high total carbon dioxide levels. The PaCO₂ usually is low because some inspired oxygen is unable to cross into the blood from the lungs because of the decreased respiratory diffusion membrane surface area in the lungs. Pulmonary hypertension usually appears as the disease progresses. Cor pulmonale may develop, and because of the pulmonary venous engorgement, the right heart may begin to fail. The patient with emphysema who has irreversible destruction can be treated with chest physiotherapy, bronchodilators, and steroids.

Cigarette smoking as A precursor to the development of COPD

Cigarette smoking has been well established as one of the major precursors to chronic bronchitis and emphysema—two of the three disease components of COPD. Cigarette smoking affects the manner in which a patient recovers from an anesthetic.⁴^,⁵ The perianesthesia nurse should be aware of the diverse reactions that smoking can have on the patient who is emerging from an inhalation anesthetic. Studies on the relationship between smoking and its effects on anesthesia indicate an increase in the risk factor in the patient who smokes. Although the incidence rate of smoking is decreasing slowly, it continues to rise in the teenage population.

Respiratory effects of smoking

A growing body of convincing scientific literature suggests that almost all pulmonary disease is related in some way to the inhalation of infectious or irritant particulate material. Cigarette smoke in its gaseous phase contains nitrogen, oxygen, carbon dioxide, carbon monoxide, hydrogen, argon, methane, hydrogen cyanide, ammonia, nitrogen dioxide, and acetone. In the particulate phase, cigarette smoke contains nicotine, tar, acids, alcohol, phenols, and hydrocarbons. The bottom line is that cigarette smoke contains oxidants, and the oxidants can damage cells and the extracellular matrix components of the lung, leading to significant damage to the tissue in the lungs. Smokers who inhale nicotine from a cigarette into the lungs actually receive 25% to 30% of the nicotine contained in the cigarette. Thirty percent is destroyed with combustion, and 40% is lost in the side stream. Therefore, if a person inhales the smoke from a cigarette that contains 2.5 mg of nicotine, 1 mg of nicotine is actually absorbed by the lungs. In addition, filters are known to make little difference in this absorption. Contrary to some opinions, the smoking of cigars and pipes also presents a risk for pulmonary disease.⁶ Carbon monoxide combines with the hemoglobin molecule at the same point as oxygen does. It has an affinity for this receptor point that is 210-fold greater than that of oxygen⁷; therefore the oxygen-carrying capacity of hemoglobin is reduced, and the end result is that less oxygen is relinquished to the tissues by the hemoglobin. When carbon monoxide combines with hemoglobin, a compound called carboxyhemoglobin is formed. The amount of carboxyhemoglobin in the blood is especially important in the patient who has a diseased myocardium, because myocardial oxygenation is limited by the flow of the blood through the coronary arteries. During stress, such as in surgery and anesthesia, the amount of carboxyhemoglobin saturation could lead to severe myocardial hypoxia in patients who smoke heavily and have coronary artery disease because the diseased coronary arteries cannot increase the flow significantly. The only means of prevention of hypoxia is an increase in the extraction of oxygen from the hemoglobin. Small amounts of carboxyhemoglobin can hinder the uncoupling of the oxygen and thus result in yet more oxygen retention at any given tension. This effect clearly is greater when the oxygen tension is further reduced by local ischemia and any additional vasoconstriction associated with smoking.

Smoking is an important causative factor in chronic pulmonary disease, especially the obstructive type.⁸ The characteristic pulmonary function alterations in smokers usually include a reduction in vital capacity, an increase in residual volume to total lung capacity, an uneven distribution of inspired gas, a decrease in dynamic compliance, and an increase in nonelastic resistance. Most critically, chronic cigarette smoking ultimately causes the forced expiratory volume in the first second (FEV₁) to be less that 80% of normal, a critical sign of COPD.

Chronic bronchitis is the disease most often associated with smoking and is seen often by the perianesthesia nurse. Hypertrophy of bronchial mucous glands with production of excessive mucus is the hallmark of this disease. A vicious cycle develops as this failure to remove the mucus leads to retention of pathogenic organisms and irritants. The resulting distorted alveolar septa and the increased pressure on the alveoli from chronic bronchitis can lead to emphysema.

Cigarette smoke can cause a progression from hyperplasia to metaplasia to neoplasia in the lungs. Eaton-Lambert syndrome is sometimes associated with bronchial carcinoma and is often called the myasthenic syndrome because its symptoms resemble those of myasthenia gravis (MG). This syndrome in some way affects neuromuscular transmission, and patients have the classic symptoms of muscle weakness. These patients are especially sensitive to the skeletal neuromuscular blocking agents used in clinical anesthesia. If the anesthetist is unaware of this syndrome and administers the normal dose of skeletal muscle relaxants, the patient will probably be unable to breathe spontaneously on emergence from anesthesia, even when pharmacologic reversal of the muscle relaxant is attempted. In this situation, postoperative mechanical ventilation is necessary.

Cardiovascular effects of smoking

The correlation between vascular disease and smoking is strong. Smoking can influence thrombosis, and because thrombi and platelets contribute to the development of arteriosclerosis, smoking can contribute to arteriosclerosis and its complications.

Inhalation of nicotine produces a release of catecholamines, activates the carotid and aortic chemoreceptor bodies, and directly stimulates the muscles of the vessel walls. As a result, the immediate effects of smoking even a small number of cigarettes can be fairly marked, with production of increases in heart rate, peripheral resistance, cardiac workload, and blood pressure. Each of these actions causes a greater myocardial oxygen demand. Furthermore, because the smoker’s hemoglobin can provide less oxygen to the myocardium, smoking can cause cardiac arrhythmias, either through myocardial anoxia or epinephrine release.

Surgical considerations

The incidence rate of pulmonary complications in patients who have undergone abdominal or thoracic surgery is high. Changes occur in the pulmonary status of the patient who undergoes anesthesia and surgery. In the postoperative phase, these changes are characterized by gradual or abrupt alveolar collapse. The patient with COPD, when subjected to surgery, then represents an even higher risk for postoperative complications. These patients must be given meticulous preoperative care so that they are in the best possible health when they enter surgery. This preoperative medical treatment usually includes hydration, nutrition, chest physiotherapy, bronchodilators, and prophylactic antibiotics if an infection is present. Serial pulmonary function tests and arterial blood gas determinations are used to monitor the progression of the preoperative treatment.⁷

When the patient’s pulmonary function reaches a peak before surgery (i.e., when the pulmonary function test and arterial blood gas test results no longer show continued improvement), surgery is considered because the patient has reached optimal pulmonary status.

Care of the COPD patient

Perianesthesia care focuses on prevention of complications. The modified stir-up regimen should include frequent cascade coughing, sustained maximal inspirations (SMIs), and repositioning of the patient (see Chapters 12 and 28). An appropriately implemented modified stir-up regimen is of great importance, especially in patients who are recovering from upper abdominal or thoracic operations. Surgery at these sites can cause decreased ventilatory effort and a complete absence of sighs by the patient. Given that the patient already has compromised respiratory function, the possibility of retained secretions and atelectasis is magnified. As a result, these patients represent a significant challenge to the perianesthesia nurse (Box 48-1).

BOX 48-1 Risk Reduction Strategies to Decrease the Incidence of Postoperative Complications in Patients with COPD

Preoperative

• Encourage cessation of smoking for at least 8 weeks.

• Treat evidence of expiratory airflow obstruction (e.g., bronchodilator therapy).

• Treat respiratory infection with appropriate antibiotics.

• Initiate patient education regarding lung volume expansion maneuvers.

Intraoperative

• Use minimally invasive surgical (laparoscopic) techniques when possible.

• Consider using regional anesthesia.

• Avoid the use of long-acting neuromuscular blocking drugs.

• Avoid surgical procedures longer than 3 hours.

Postoperative

• Continue tracheal intubation and mechanical ventilation (likely after abdominal or intrathoracic surgery and a preoperative PaCO₂ > 50 mm Hg and FEV₁/FVC < 0.5; maintain PaO₂ at 60 to 100 mm Hg and PaCO₂ in a range that maintains the pH at 7.35 to 7.45).

• Institute lung-volume expansion maneuvers (voluntary deep breathing, incentive spirometry, continuous positive airway pressure).

• Use chest physiotherapy.

• Maximize analgesia (neuraxial opioids, intercostals nerve blocks, patient-controlled analgesia).

FEV₁, Forced expiratory volume in the first second; FVC, forced vital capacity.

From Stoelting RK, Dierdoff SF: Handbook for anesthesia and co-existing disease, ed 2, New York, 2002, Churchill Livingstone; Data from Smetana GW: Preoperative pulmonary evalution, N Engl J Med 340:93−944, 1999.

When the patient is completely reactive from anesthesia, the use of the incentive spirometer may be helpful in reducing the incidence of atelectasis. Consequently, the perianesthesia nurse who is responsible for supportive measures should assist and encourage the patient in using the SMI with or without the incentive spirometer. On the basis of subjective research findings, if the perianesthesia nurse explains the rationale of the SMI maneuver and properly instructs the patient in the use of the technique before surgery, the patient is more likely to correctly use the SMI maneuver after surgery with or without coaching. The performance of the SMI maneuver, with or without mechanical devices, should be monitored by the nurse to ensure proper production of a sustained inspiration with a 3-second inspiratory hold. The perianesthesia nurse should also encourage and monitor the patient’s performance of the cascade cough to facilitate early secretion clearance.

Patients with COPD have some component of reactive airways disease. Consequently, the airway becomes compliant and can become compressed during a forced expiratory maneuver. This dynamic compression of the airways is a function of the equal pressure point theory, as discussed in Chapter 12. To reduce the amount of dynamic compression of the airway during exhalation, the patient should be encouraged to use pursed-lip breathing. Breathing through pursed lips during exhalation can be the same as adding 5 to 10 cm H₂O of positive end-expiratory pressure. Increasing the pressure inside the airway during exhalation reduces the amount of dynamic compression of the airways and decreases the amount of air trapping that commonly occurs in patients with COPD.

Audible wheezing will require the use of a fast-acting bronchodilator such as albuterol. Arterial blood gases may be ordered, and capnography may be used to monitor end-tidal CO₂.⁹

The cardiac status should be monitored meticulously because of the frequent involvement of the heart in the pathologic disorders of these patients. Kidney function should also be monitored because it may be altered, especially in patients with fluid retention and edema of the extremities.

The patient with severe COPD who has marked hypercarbia can present difficulties in the PACU. Patients who have severe emphysema usually fit into this category. Ventilatory effort in these patients is stimulated by the hypoxic drive, in which lack of oxygen stimulates ventilation. Hypoxia indirectly stimulates the respiratory center by means of chemoreceptors in the carotid bodies located at the bifurcation of the carotid artery. When the patient receives 100% oxygen to breathe in the PACU, oxygen tensions rise in the inspired gas; the carotid and aortic chemoreceptors cease to function; and the patient quickly becomes apneic. The patient’s respiratory status should be assessed carefully and the physician consulted before 100% oxygen is administered. Mist therapy after surgery aids in liquefying the secretions and helps in the all-important maintenance of a patent tracheobronchial tree. If excessive bronchial drainage is not removed, it provides a convenient avenue for bacteria and might also obstruct the airways, thus leading to insufficient alveolar ventilation and hypoxia.

The patient with COPD should be under constant surveillance for signs of cardiopulmonary decompensation, including shallow rapid gasping respirations, severe dyspnea, substernal retraction, and disorientation. Blood pressure may be elevated or low, but the patient usually has tachycardia, fever, and muscle rigidity. Cyanosis may be present.

Patients who are cigarette smokers have significant postanesthesia risks.⁶ Cigarette smokers who have smoked for a long period of time and have an FEV₁ less than 80% usually have an increased risk of pulmonary complications in comparison with nonsmokers. Patients who smoke more than two packs of cigarettes per day are especially prone to perianesthetic complications. In addition, patients who have had a long history of smoking (>20 pack years) and are presently in a nonsmoking situation still can have pulmonary complications. Many of these complications develop when cigarette smokers have a preexisting chronic respiratory disease, usually bronchitis. The major postoperative complications associated with smoking are infection, atelectasis, pleural effusion, pulmonary infarction, and bronchitis.

Complications associated with chronic cigarette smoking revolve around the inability of the patient to clear secretions. The goal of nursing care in the PACU centers on clearing the tracheobronchial tree, which necessitates frequent suctioning, cascade coughing, and the SMI maneuver. If rales and rhonchi are heard on auscultation, percussion and postural drainage should be initiated.

Because cardiovascular disease is associated with a long history of cigarette smoking, the patient should have continuous electrocardiographic monitoring. Arrhythmias, such as premature ventricular contractions, should be addressed because they may be the first signs of decreased myocardial oxygenation in the cigarette smoker.

Respiratory depressant drugs, such as opioids, should be given in low doses, or they should be avoided completely if the COPD is severe. Repositioning of the patient and splinting of the incision site, in addition to reducing the anxiety usually seen in these patients, reduces the need for opioids. Some form of regional analgesia may be beneficial for these patients.⁸

Myasthenia gravis

The patient with MG deserves special consideration in the PACU because of the respiratory dysfunction and possible pharmacologic ramifications of the disease. The incidence rate of MG has been estimated to be between 1 in 7500 and 1 in 10,000.¹ MG occurs twice as often in females than in males and at earlier ages, and it occurs most often between the ages of 30 and 40 years.⁷ The main symptoms are weakness in one or more of the muscle groups, fatigability on effort, and at least some partial restoration of muscle function after rest.⁷

MG is the prototype autoimmune disease because its pathophysiology involves the postsynaptic acetylcholine (ACh) receptors at the myoneural junction. The causative factor is an immune-mediated destruction or blockage that leads to an inactivation of the postsynaptic ACh receptors. Interestingly enough, the presynaptic ACh receptors continue to be normal. More specifically, patients with MG have developed antibodies to muscle acetylcholine receptors. The antibody does not bind exactly on the site that binds the ACh, but it does bind close to it. The ACh receptors are steadily destroyed, with a resulting reduction in the binding of acetylcholine at the postsynaptic myoneural junction. The patient with MG sometimes has a lesion in the myocardium that is a spotty focal necrosis accompanied by an inflammatory reaction. An alteration in the S-T segment and T wave is sometimes seen in these patients.

Ptosis of the eyelid is the most common sign of the disease. Ptosis is usually accompanied by diplopia, blurred vision, or nystagmus. Ocular signs and symptoms often are worsened by bright light. The patient may also have myasthenic facies, which is caused by weakness of the facial muscles and can progress to dysphagia and difficulties in speech.

Respiration is often affected in the patient with myasthenia. Dyspnea can be either inspiratory if the diaphragm is involved or expiratory if the intercostal and abdominal muscles are affected. The patient may also have emotional disturbances caused by anxiety and depression.

Diagnosis of MG is made on the clinical symptoms and the characteristic electromyographic results. The clinical symptoms can be assessed with the neostigmine test or the edrophonium test, both of which involve anticholinesterases that increase the strength of the myasthenic muscle. Should these tests show that MG may be present, serum levels of anti-AChR antibodies can be drawn. These antibodies are usually present in 85% to 90% of patients with myasthenia.

Treatment for this disease consists of various pharmacologic interventions designed to enhance neuromuscular transmission and slow the progression of the disease. Therefore the treatment may include cholinesterase inhibitors, corticosteroids, specific immunosuppressants, plasmapheresis, intravenous immunoglobulin, and thymectomy.¹

Anticholinesterase drugs, which slow down the enzymatic destruction of acetylcholine at the neuromuscular junction, are commonly used. Oral pyridostigmine is the anticholinesterase of choice. Patients with MG seem to favor pyridostigmine over other anticholinesterases because its length of action is 3 to 4 hours when administered orally. Steroids and other immunosuppressive agents may be used in some patients to reduce antibody production responsible for the disease. Plasmapheresis, a plasma exchange, arrests severe refractive MG by reducing the concentration of circulating antibodies. Like the use of intravenous immunoglobulin, plasmapheresis is a short-term treatment.

Thymectomy seems to be an appropriate therapeutic mode because the thymus gland appears to be intimately involved in the disease process. Approximately 75% of the patients with myasthenia who do not have thymoma have improvement after thymectomy. Alternatively, approximately 20% of the patients with MG with thymoma show improvement in the disease process after thymectomy.

Because thymectomy has been used as a therapeutic intervention in the treatment of MG, the perianesthesia nurse will probably render nursing care to many patients with MG. Because of the location of the incision, the myasthenic patient does not usually receive any intraoperative skeletal muscle relaxants. Patients with myasthenia can have an exacerbation of symptoms in the PACU; therefore critical monitoring of the patient’s ventilatory status should be the primary focus of the perianesthesia nursing care. Patients with MG who are recovering from any type of surgical procedure and who have been administered any form of anesthesia (general, inhalation, or regional) can have exacerbated symptoms and myasthenic crisis develop in the PACU. Consequently, respiratory support should always be available for these patients.

Care of the patient with myasthenia gravis

If a muscle relaxant is given during surgery, the patient has the neuromuscular blockade reversed. After reversal in the operating room, the patient must have a complete sustained return of skeletal muscle strength before extubation. If the patient does not meet the criteria for extubation, the endotracheal tube remains in place and the patient is taken to the PACU for ventilatory support. In patients with MG, the skeletal muscle strength may appear to be appropriate immediately after surgery, but may deteriorate a few hours thereafter.⁷

The patient with MG can have various difficulties because of an impaired respiratory system, possible poor nutrition, susceptibility to infection, altered psychiatric status, and possible altered response to drugs used during anesthesia. The patient should be placed in a quiet area, where no direct light shines in the eyes. The patient’s respiratory effort and exchange should be monitored continuously. Oxygen should be administered with humidification, and secretions should be removed with frequent suctioning and postural drainage. Oxygen saturation levels for these patients should be maintained at more than 96%. Any change in respiratory status should be reported to the physician immediately.

Because cardiac mechanisms may be responsible for some sudden deaths in this patient population, cardiac monitoring should be instituted for every patient with myasthenia in the PACU. Monitoring of the fluids administered to patients with MG is also important. Hypovolemia and hypervolemia must be avoided because of their deleterious effects on the already compromised heart and lungs.

The patient should be kept as pain free as possible to facilitate good respiratory exchange. Morphine and other opioids are often potentiated by anticholinesterases; therefore the initial opioid dose should be reduced to half the normal dose and then increased if necessary. If the patient is receiving continuous mechanical ventilation, the normal amount of medication can be given without compromising the patient’s respiratory status.

The PACU nurse should monitor for a myasthenic crisis, which is a severe exacerbation of the symptoms associated with MG. It can occur when an anticholinesterase is underdosed and does not reduce the amount of muscle weakness sufficiently. Alternatively, a cholinergic crisis can occur when too much anticholinesterase is administered, resulting in a surplus of acetylcholine at the myoneural junction and causing a depolarizing type block that leads to skeletal muscle weakness, which could be severe. For all the previous reasons, during PACU care of the patient with MG in the immediate postoperative phase, airway equipment must be kept at the patient’s bedside. Along with the skeletal muscle weakness, muscarinic side effects occur, such as abdominal cramping, miosis, bradycardia, salivation, and diarrhea. See Chapters 10, 11, and 23, which provide the reader an in-depth discussion of the myoneural junction and nicotinic and muscarinic effects.

The emotional status of the patient with myasthenia is of considerable importance. As few clinicians as possible should be responsible for this patient throughout the emergent phase, because the patient is likely to be distrustful of anyone he or she does not know. Communication is important, and the patient should be informed about any nursing procedure to be performed. If the patient with myasthenia has a tracheostomy, paper and pencil should be used to facilitate communication between nurse and patient.

Diabetes mellitus

Diabetes mellitus (DM) affects approximately 29 million people in the United States and is the seventh leading cause of death. It is also believed that DM as a comorbidity is underreported.¹⁰ However, it is what transpires between the diagnosis and death that determines the level of health, the health care needed, and the number of surgical interventions of the patient with DM.

Diabetes is a chronic, progressive disease characterized by the body’s inability to metabolize carbohydrates, fats, and proteins leading to hyperglycemia.¹¹ The degree of hyperglycemia and the incidence of acute or long-term diabetes complications depend on the type of diabetes and the level of DM control over the lifetime of the person with diabetes.

The two forms of diabetes are insulin dependent and non–insulin dependent. Insulin-dependent diabetes, now called type 1, was formerly called juvenile onset diabetes. Type 1 diabetes may be genetic in predisposition, but the majority of those diagnosed with type 1 DM have no first-degree relatives with DM.¹¹ It is characterized by complete dependence on exogenous insulin therapy. Type 1 DM is caused by a vigorous autoimmune destruction of the beta cells in the islets of Langerhans in the pancreas. The onset of DM is usually before the age of 40 years; however, it can develop at any age. By the time of diagnosis, approximately 80% to 90% of the beta cells have been destroyed. Approximately 10% of the people with DM have type 1.¹¹ Treatment centers on meal planning, exercise, and insulin administration (Table 48-1).

Table 48-1 Insulin Formulations Used in the Treatment of Diabetes

The other main form of DM is non-insulin dependent diabetes, or type 2 diabetes. Formerly called adult onset diabetes, type 2 affects approximately 90% of people with DM. This type of DM is characterized by impaired insulin secretion or peripheral resistance to one’s own insulin, resulting in a degree of endogenous insulin production, but not at a level sufficient to produce normal carbohydrate homeostasis. Most people with type 2 DM are older than 40 years and have a family history of diabetes, and 85% are obese.¹¹ As the U.S. population ages, becomes more obese, and is less active, a continued rise in the number of persons with DM is to be expected. Treatment focuses on meal planning, exercise, and weight loss with the possible inclusion of oral hypoglycemics, injectable noninsulin products, and treatment with insulin (Table 48-2).

Table 48-2 Oral Medication or Non-Insulin Injectable Medications for Persons with Diabetes

CHEMICAL CLASS	AGENTS	ACTION
Biguanides	Metformin	Decreases endogenous hepatic glucose production and increases peripheral glucose uptake
Sulfonylureas	Glipizide, glyburide, glimepiride	Increases the secretion of insulin from B cells
Meglitinides	Repaglinide, nateglinide	Increases the secretion of insulin from B cells
Thiazolidinediones	Pioglitazone, rosiglitazone	Improves insulin action in the periphery and the liver
α-Gglycosidase inhibitors	Acarbose, miglitol	Inhibits intestinal α-glucosidase, delaying glucose absorption
GLP-1 receptor agonist	Exenatide (injectable)	Stimulates insulin secretion and facilitates homeostasis follow food ingestion
Amylinomimetic	Pramlintide (injectable)	Regulates glucose concentration after a meal, increases satiety, slows gastric emptying, suppresses glucagon secretion

Adapted from Fain J: Management of clients with diabetes mellitus. In Black J, Hawks J, editors: Medical surgical nursing; clinical management for positive outcomes, ed 8, St. Louis, Saunders.

The Centers for Disease Control and Prevention estimates that 25.8 million persons in the United States have DM, comprising 8.3% of the total population.¹⁰ Of these, 18.8 million have been diagnosed, whereas 7 million remain undiagnosed. As the U.S. youth become more sedentary and obese, the incidence of type 2 DM in children is skyrocketing. In 2010, approximately 215,000 people younger than 20 years old had a diagnosis of type 1 or type 2 DM (Table 48-3).¹⁰

Table 48-3 Diagnosed Persons with Diabetes Aged 20 Years or Older – U.S. 2010

GROUP	NUMBER WITH DIABETES (%)
Age ≥20 years	25.6 million (11.3)
Age ≥65 years	10.9 million (26.9)
Men	13.0 million (11.8)
Women	12.6 million (10.8)
Non-Hispanic whites	15.7 million (10.2)
Non-Hispanic blacks	4.9 million (18.7)

From Centers for Disease Control, U.S. Department of Health and Human Services. National Diabetes Fact Sheet 2011, available at http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed May 5, 2012.

The diagnosis of DM has traditionally been determined by the fasting blood glucose (FBG) level. FBG greater than 126 mg/dL (7.0 mmol/L) indicates DM. An oral glucose tolerance test (OGTT) with a 75-g sugar load may also be used, with a resultant blood glucose (BG) of greater than 200 mg/dL (11.1 mmol/L) indicating DM. The glycosylated hemoglobin (HbA1c), now referred to as the A1C level, is a newer determinant of a diagnosis of DM. The A1C level was used for two decades to determine diabetes control, and in 2010 the American Diabetes Association allowed a laboratory-based standardized A1C to be used for diagnosis.¹² As the red blood cell travels throughout the body on its approximately 6-week life cycle, glucose molecules attach to the hemoglobin molecule in the red blood cell. The A1C test reports a percentage, correlating to the average BG level over the last 2 to 3 months (Table 48-4).

Table 48-4 Criteria for the Diagnosis of Diabetes

Although hyperglycemia is most often cited as the primary problem with diabetes, it is usually the resultant long-term physiologic changes that cause the person with DM to require surgery. It is estimated that people with diabetes have a 50% chance of requiring surgery in their lifetime and that approximately 20% of all surgical patients will have DM.¹³ DM is the leading cause of nontraumatic lower limb amputations, increasing the likelihood of intervention in any surgical setting.

Determination of any long-term diabetes complications should be made in the preoperative period, hopefully weeks before the scheduled surgery (Box 48-2). Input from the primary care physician or diabetes specialist should be sought. Patient information from the medical record can also provide a thorough assessment for the emergent surgical patient with diabetes. Results of a current A1C provide an overview of the glucose control over the last 2 to 3 months; A1C values under 7% help to ensure fewer postoperative infections.¹³ None of these complications are unique to people with diabetes, but the incidence of these complications is higher in those with diabetes. Macrovascular disease reflects an increase in atherosclerosis with deposits of lipids within the inner layer of vessel walls. Increased levels of BG over time cause a thickening of the cell basement membrane and intracellular edema and altered cell function. The resulting thickness causes a greater distance of travel for nutrients and cellular waste decreasing the oxygen and nutrition entering the cell and causing cellular waste buildup.¹¹

Anesthesia and diabetes

Preoperative guidelines for medications depend on the person’s home regimen and should be discussed with the person’s primary care physician and diabetes specialist before the surgical intervention. Varied combinations of medications make it unlikely to find a standardized preoperative plan that works for all patients with type 1 or type 2 DM. If possible, the person with diabetes should be scheduled for an early morning surgery to reduce the time without oral intake.¹¹ Ongoing preoperative monitoring of BG levels helps to prevent acute complications during the perioperative and postoperative periods.

In general, people with DM who take oral medications or non-insulin injectables should be advised to hold those medications the evening before or the day of surgery, primarily for prevention of hypoglycemia. Sulfonylureas can interfere with ischemic myocardial preconditioning and theoretically increase the risk of perioperative myocardial ischemia and infarction.¹⁴ Metformin is withheld to prevent the possibility of lactic acidosis.

Persons with type 1 DM may be advised to reduce the bedtime insulin to prevent hypoglycemia while NPO before surgery; however, some form of maintenance insulin must be continued to prevent hyperglycemia from the lack of basal insulin. Basal insulin is the amount of exogenous insulin per unit of time necessary to prevent hepatic gluconeogenesis and ketogenesis. People with type 1 DM are usually maintained on a basal dose of one or two injections of a long-acting insulin or multiple injections of an intermediate insulin or continuous subcutaneous insulin infusion (i.e., insulin pump with a rapid acting analog).¹⁵ Nutritional insulin is the amount of exogenous insulin necessary to prevent hyperglycemia associated with any type of nutritional supplement, such as discrete meals, total parenteral nutrition, and enteral feedings. Correctional or supplemental insulin is used to correct unexpected hyperglycemia that occurs before or between meals.¹⁵ Nutritional and correctional insulin is usually a rapid-acting insulin or a short-acting insulin may be chosen. Each hospital tends to adopt different procedures for the person with diabetes using an insulin pump. Refer to individual hospital policies for details. In general, the pump may be set to the “suspend” mode for minor or short-duration surgeries. Longer procedures from which the person will have a longer period of sedation necessitate the removal of the pump and implementation of an IV insulin drip. The bagged and labeled pump and equipment should be sent home with the family and that action documented.

Care of the patient with diabetes

Perioperative goals for glycemic control include: the maintenance of fluid and electrolyte balance, prevention of ketoacidosis, avoidance of marked hyperglycemia, and avoidance of hypoglycemia.¹³ If any of these problems occur, immediate treatment is imperative and diligent investigation is required to determine the underlying cause. Surgery induces a stress response mediated by the neuroendocrine system through the release of catecholamines, glucagon, and cortisol. Surgery and possibly anesthesia cause an elevation of sympathetic tone with a release of cortisol and catecholamines. The relative insulin deficiency (type 2) and the absolute insulin deficiency (type 1) limit the body’s ability to compensate for this deficiency, requiring supplemental insulin during the perioperative period. This stress response of hyperglycemia may also occur with surgical patients without DM, demonstrating a need for glucose control for all surgical patients. Multiple studies have shown that control of the perioperative serum glucose level has a positive effect on the outcomes of all patients (Table 48-5).¹⁴

Table 48-5 Acute Complications of Diabetes

Evidence-Based Practice

Smith and colleagues conducted a retrospective study to explore the effect of hyperglycemia in the postanesthesia care unit (PACU) on postoperative complications, length of stay (LOS), and mortality in patients with diabetes undergoing spine, colon, or joint surgery. Results of the study determined that patients with blood glucose (BG) > 200 mg/dL in the PACU had a significantly longer LOS than patients with a maximum BG of 140 to 200 mg/dL. They also found that the rate of total complications significantly increased as the BG levels increased. There was a 70% increase in complications when the PACU BG was > 200 mg/dL.

Implications for practice

To establish consistent best practices in BG management in the PACU, perianesthesia nurses should advocate for consistent and clear parameters for BG for the perianesthesia patient. Prospective, controlled studies on the management of hyperglycemic patients in the PACU are needed and could be conducted by perianesthesia nurses. In the meantime, the PACU nurse should be aware of the latest research indications for care.

Source: Smith DK, et al: A study of perioperative hyperglycemia in patients with diabetes having colon, spine, and joint surgery, J Perianesth Nurs 24:362−369, 2009.

The nature and duration of the surgical procedure affects the glucose levels and the insulin interventions needed. In patients who require minor surgical procedures of short duration or limited general, local, epidural, or spinal anesthesia might need only minimal changes in their diabetes regimen. Procedures of longer than 2 hours under general anesthesia will have greater glucose variations and require more frequent monitoring and treatment.¹⁵ Intravenous regular insulin is used for glucose control during surgery. Doses and frequency may be determined by hospital or surgical center protocols. Subcutaneous insulin is not used because the absorption is affected by the person’s body temperature, circulating blood volumes, and certain anesthetics.¹¹

Postoperative goals for the patient with DM include the universal outcomes of stabilizing vital signs, correcting fluid and electrolyte imbalances, preventing wound infection and promoting wound healing. Prevention of hypoglycemia depends on BG monitoring and physical indicators such as a decrease in blood pressure or an increased heart rate in the still unresponsive patient. Patients with peripheral vascular disease, neuropathy, or both require frequent skin inspection for signs of breakdown, pressure spots, or shearing injuries to the skin.¹¹ However, for the person with diabetes, reestablishing control of their DM is imperative.

What is considered to be the optimal BG levels for the postoperative period has been one of debate for several years. However, statistics demonstrate that infection accounts for 66% of postoperative complications for those with DM. Mortality rates in people in diabetes have been estimated at fivefold greater than for those without DM. Both infection and mortality are thought to be caused by impaired leukocyte function, altered chemotaxis, and phagocytic activity.¹⁴

Furnary and colleagues ¹⁶ and Van den Berghe et al¹⁷ determined that tight glycemic control decreased the incidence of deep sternal wound infections and decreased mortality, respectively. A postoperative BG level between 80 mg/dl (4.4 mmol/L) and 110 mg/dl (6.1 mmol/L) was designated as the standard for cardiac surgical or critical care patients. The basic goal of balancing the BG levels while still preventing hypoglycemia remains paramount in the medical and surgical efforts to decrease mortality and morbidity. Current studies have shown that although tight glycemic control may still be beneficial for the postcardiac surgical patient, others benefit from less stringent goals of between 80 (4.4 mmol/L) and 150 mg/dL (8.3 mmol/L). Other guidelines propose “reasonable” normoglycemia with the majority of BG levels less than 180 to 200 mg/dL (<10 to 11 mmol/L).¹³ The American Diabetes Association Standards of Medical Care has endorsed an FBG level of less than 140 mg/dL (7.8 mmol/L) for general hospitalized patients with random BG readings less than 180 mg/dL (10 mmol/L).¹²^,¹⁸

Diabetes and BG control throughout the perianesthesia period determines the success of the procedure, the adverse or positive outcomes, and the overall health of the person with diabetes. DM remains the leading cause of kidney failure and is a major cause of heart disease and stroke; all of these are risks that may have an impact on the outcome of any surgical case. Minimizing BG variability during the perianesthesia period should be part of any glycemic control strategy.¹⁸ Nursing consideration of the preoperative DM status, the perioperative BG levels, and the postoperative outcomes influence the person with DM for months beyond the surgical intervention portion of their health care.

Rheumatoid arthritis

Rheumatoid arthritis (RA) is a relatively common disease that affects the connective tissue of the body. The clinical course varies, but it tends to be progressive and lead to characteristic deformities. Many patients become incapacitated over time. The disease affects more women than men, and its incidence rate in temperate climates is approximately 3%. The cause is not completely understood, but the disease is thought to be an autoimmune phenomenon. The outstanding clinical feature of this disease is proliferative inflammation. The patient often appears chronically ill, undernourished, and anemic.¹⁹

These patients often undergo surgery to correct restrictive deformities caused by the disease process (Table 48-6). On arrival in the PACU, they require comprehensive nursing management. Some of the hazards to be aware of in patients with rheumatoid arthritis are listed in Table 48-7.

Table 48-6 Corrective Surgery for Rheumatoid Arthritis

OPERATIVE SITE	COMMON OPERATIVE PROCEDURE
Neck	Atlantoaxial arthrodesis
Shoulder	Synovectomy and partial excision of acromion
Elbow	Synovectomy and radial head excision, resection arthroplasty
Wrist	Synovectomy and excision of distal ulna
Hand	Metacarpal phalangeal arthroplasty and flexor and extensor tenosynovectomy
Hip	Cup or total replacement, arthroplasty
Knee	Synovectomy (often bilateral), arthroplasty
Foot	Resection arthroplasty (often bilateral)

From Nagelhout J, Plaus K: Nurse anesthesia, ed 4, St. Louis, 2010, Saunders.

Table 48-7 Perianesthesia Hazards in Patients with Rheumatoid Arthritis

AREA OF CONCERN	COMPLICATION
Respiratory System
Airway	Hypoplastic mandible restriction, cervical spine motion, atlantoaxial subluxation, laryngeal tissue damage
Ventilation	Rheumatoid nodules in lung, chronic diffuse interstitial fibrosis, costovertebral joint disorder that inhibits ventilation, thoracic vertebrae flexion deformity that inhibits ventilation, tuberculous lung
Cardiovascular System
	Pericardial, myocardial, coronary artery disorders, aortic valve regurgitation, arrhythmias
Hemopoietic, Hepatic, and Renal Systems
	Anemia, leukopenia, bleeding tendency (decreased platelets), renal amyloidosis
Miscellaneous
	Skin fragility; postoperative chest complications, such as atelectasis, hypercarbia, and hypoxia; multiple joint disease

Modified from Bready L, et al: Decision making in anesthesiology, ed 4, St. Louis, 2007, Mosby.

Care of the patient with rheumatoid arthritis

Sickle cell disease

Sickle cell disease is an inherited type of hemolytic anemia. It is a chronic disease marked by exacerbations. The clinical manifestations are based entirely on sickling of the red blood cells and its consequences.

More than 100 abnormal hemoglobins have been described in humans. When these hemoglobins are exposed to low oxygen tensions, this particular form of hemoglobin causes the red blood cell to distort its shape (sickle) and cause infarction and other complications. Normal hemoglobin is labeled hemoglobin A, whereas this sickling hemoglobin is labeled hemoglobin S.⁷

Hemoglobin S is thought to have arisen in Arabia in Neolithic times and from there to have spread eastward and westward; it is found today in parts of India, east and west Africa, the West Indies and among African Americans.

The common sickle cell disorders are sickle cell trait (SA), homozygous sickle cell disease (SS), sickle cell-hemoglobin C disease, and sickle cell-thalassemia. A combination of thalassemia and sickle cell anemia occurs in sickle cell-beta thalassemia.

Sickle cell trait is found in about 8% to 12% of the African-American population ²¹, which is heterozygous for sickling, and represents a combination of sickle hemoglobin (SA) and normal hemoglobin (AA). The red blood cells of such persons contain 20% to 40% hemoglobin S, but are not misshapen in normal living conditions. The person may have sickling with exposure to any conditions that cause hypoxia, such as depressed respiratory function from anesthetics in the PACU.

The most common form of sickle cell disease is the homozygous sickle cell disease. It occurs in 1 in 400 to 500 African Americans. These persons have inherited sickling genes from both parents, and they usually have 80% to 100% hemoglobin S. Sickling is present all the time, and minor reductions in oxygen tension can cause a sickle cell crisis. The onset of symptoms occurs around the age of 2 years; rarely do these persons live past the age of 40 years.²¹

Sickle cell-hemoglobin C disease is caused by the presence of the gene for sickle hemoglobin and the gene for hemoglobin C. The course of the disease is usually milder than that of the homozygous sickle cell disease, although the person has discomfort and occasional sickle cell crises.

Sickle cell thalassemia, which occurs in persons who have traits for sickle cell thalassemia and beta thalassemia, has a less severe course and symptoms in comparison with the other forms of these diseases. The sickle cell crises are not seen as commonly in this disease.