48 Care of the patient with chronic disorders
Plasmapheresis: Removal of plasma from previously withdrawn blood via centrifugation, reconstitution of the cellular elements in an isotonic solution, and reinfusion of this solution into the donor or another person who needs red blood cells rather than whole blood.
Patients in the perioperative phase of their hospitalization usually require a significant degree of advanced practice nursing care. If the patient’s health can be enhanced before surgery, the patient’s ability to have a positive perioperative experience will increase. Patients suffering from a chronic disorder are at greater risk of developing postoperative complications.
In this chapter, selected chronic disorders will be presented to enhance the use of appropriate and informed perianesthesia care. For example, patients with chronic obstructive pulmonary disease (COPD) can have significant preoperative respiratory dysfunction, of which some improvement can be accomplished with intense and knowledgeable nursing care. COPD is a serious condition that starts to develop up to 30 years before significant symptoms; it affects more than 25 million Americans and is responsible for about 80,000 deaths per year.1 These patients have significant risks for anesthesia and surgery. The COPD disease process can be generalized to many pulmonary dysfunctions, as are the other chronic disorders described in this chapter. Therefore patients suffering from some of the other chronic disorders described in this chapter present a significant challenge to the perianesthesia nurse. In an effort to reduce the incidence of postoperative complications in patients suffering from chronic disorders, a complete understanding of the pathophysiology of the disease process will facilitate the appropriate evidence-based nursing interventions will lead to a positive outcome for the perianesthesia patient.
Chronic obstructive pulmonary disease (COPD) describes bronchial obstructive respiratory diseases. It is characterized by dyspnea with or without cough and sputum. The two major clinical manifestations of COPD are airway obstruction and airway destruction. The magnitude of the various disease entities that the term COPD includes is great; therefore individual elaboration on the diseases is difficult because each deserves separate attention. This chapter briefly describes the overall characteristics of COPD and general care required in the postanesthesia care unit (PACU). Variations between patients with COPD exist. The perianesthesia nurse must consult with the physician about the specific nursing care to be administered to the patient with COPD. For discussion of specific COPD diseases, see the bibliography at the end of this chapter.
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 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.
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.
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.
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.
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).
• 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).
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.
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
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.
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.