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Post Anesthesia Care Complications Including Maternal Care

David Tilton, RN, BSN

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Before the advent of effective anesthesia people rarely requested elective surgery. This is reflected in the 1821 to 1846 annual reports of the Massachusetts General Hospital, which recorded only about one such case each month. In fact, surgery of any type was much less common before anesthesia, and it was usually regarded as a last and desperate resort. The 1897 reminiscence of one elderly Boston physician about the days before anesthesia portrays the intensity of invasive procedures by recalling "yells and screams, most horrible in my memory now, after an interval of so many years" (Southern Nevada Professional Legal Nurse Consultants, 2005).

Oliver Wendell Holmes, Sr., is credited with introducing the term anesthesia into the English language in 1846, a mere four weeks after the first demonstration of ether. In October of that year, at Massachusetts General Hospital in Boston, William T. G. Morton demonstrated the use of ether as a means of rendering a patient unconscious and free from surgical pain. A letter from Holmes to Morton, dated November 21, 1846, reads:

The state should, I think, be called "anaesthesia" (from the Greek word anaesthesia, "lack of sensation"). This signifies insensibility. The adjective will be "anaesthetic." Thus we might say the state of anaesthesia, or the anaesthetic state. (Facts About Anesthesia, 2003)

Holmes was naming the state we now call general anesthesia (the "ae" letter combination having become obsolete). This state is clinically defined by degrees of effect in four criteria:

• Amnesia (loss of recall for the event)
• Analgesia (insensibility to pain)
• Hypnosis (unconsciousness)
• Muscle relaxation

The effects produced by classic or general anesthesia are present in varying extents throughout the entire body. Conduction or regional anesthesia typically involves injecting a local anesthetic agent close to a nerve or nerves for the purpose of limiting nervous conduction to (or from) a specific area of the body without inducing overall loss of consciousness. When small amounts of an anesthetic medication are given to sedate or relax the person for a minor procedure or during regional anesthesia, it is typically referred to as monitored anesthesia.

Complications associated with the use of anesthetic agents were recognized almost immediately after the agents were introduced; however, no consistent standard of monitored care had been established prior to World War II. Increased interest in the evident—as well as the potential—benefits of these agents during the postwar era prompted a surge in new medications and techniques. It also prompted the establishment of post anesthetic observation areas (recovery rooms) in several leading hospitals.

Prior to the establishment of specialized areas, the standard of care in most hospitals was a direct return of postsurgical patients to large open wards, where the best they could be offered was a bed close to the nurse's station, by the doorway. In the classic 1942 textbook Clinical Anesthesia, physician John Lundy advised students that patients should be returned to their rooms with mouth airways in place, and that the floor nurse should "return the airway to the operating room for use by other surgical candidates after the patient recovered" (Lundy, 1942).

As methods and means of collecting data were refined, data on post anesthetic mortality provided clear indications that patients should be located in specially equipped areas immediately after surgery, and that the presence of specially trained personnel were essential during their recovery from the anesthetic agent. As early as the 1960s the establishment of appropriate practices had clearly demonstrated their worth in terms of lives saved.

CURRENT PRACTICE

Current standards of care for the patient in post anesthesia (PAC) calls for anesthesiologists, nurses, and surgeons to work together as a team. Together they observe for the presence of medical, surgical, or anesthesia-related problems, with the goal of providing immediate attention and rapid treatment, thereby minimizing the effects of complications.

Planning for post anesthesia care should begin during the preoperative period, when anesthetic and pain management techniques are discussed with the patient and family. Postoperative care involves several phases, including transferring the patient directly to traditional or phase I recovery (PAC), to accelerated or phase II recovery, or directly to intensive-care units (ICUs) according to the area of specialty (eg, neurosurgical, cardiothoracic, pediatric, neonatal).

Traditional post anesthesia recovery areas function to support postoperative patients during the difficult transition from being anesthetized to being awake. These units (called recovery rooms, PACs, or PACUs) have developed in the direction of short-term critical care areas and frequently serve as functioning ICUs in times of shortage of appropriately monitored beds or when staffing problems occur.

Dedicated special-needs recovery rooms may also be available for patient monitoring following procedures involving high levels of sedation/anesthesia. Frequently they are found in areas of the hospital convenient for that specialty. Common examples of these dedicated areas include endoscopy laboratories, lithotripsy suites, and radiology areas. Typically these specialty service areas provide patients with an accelerated recovery level of care rather than traditional PAC services.

Dramatic increases in the number of outpatient/ambulatory procedures, combined with drastically shortened postoperative stays, have created challenging trends in post anesthesia recovery. Pressing needs for timely discharge to home after a brief stay in a "same day" unit actually increases the need for vigilance by staff so that imminent complications may be recognized and treated before the patient leaves the care of experienced staff. Ambulatory, accelerated, phase II, or outpatient recovery units are all names of care units that focus on specific groups in need of post anesthesia services.

On the other end of the spectrum, intensive-care patients arrive following surgery from emergency room admission or critical care units. Individuals who are expected to need a high level of care following anesthesia may be brought to a phase I PAC for initial monitoring before transfer to a specialty unit for continued observation, or they may be sent directly postprocedure to specialized recovery beds within the specialty units.

Whatever the anticipated risk level of a patient undergoing anesthesia, a global standard of care has been established by the American Society of Anesthesiologists in order to provide guidelines for safe, consistent, post anesthetic care.

ASA STANDARDS FOR POST ANESTHESIA CARE

[These standards were approved by the American Society of Anesthesiologists (ASA) House of Delegates on October 12, 1988, and last amended on October 27, 2004. Excerpted from Standards of the American Society of Anesthesiologists. The American Society of Anesthesiologists. A copy of the full text can be obtained from ASA, 520 N. Northwest Highway, Park Ridge, Illinois 60068–2573.]

The ASA standards apply to postanesthesia care in all locations. These standards may be exceeded based on the judgment of the responsible anesthesiologist. They are intended to encourage quality patient care, but cannot guarantee any specific patient outcome. They are subject to revision from time to time as warranted by the evolution of technology and practice. Under extenuating circumstances, the responsible anesthesiologist may waive the requirements marked with an asterisk (*); it is recommended that when this is done, it should be so stated (including the reasons) in a note in the patient's medical record.

Standard I

All patients who have received general anesthesia, regional anesthesia, or monitored anesthesia care shall receive appropriate post anesthesia management.

1. A postanesthesia care unit (PACU) or an area which provides equivalent postanesthesia care (eg, a surgical intensive care unit, or SICU) shall be available to receive patients after anesthesia care. All patients who receive anesthesia care shall be admitted to the PACU or its equivalent except by specific order of the anesthesiologist responsible for the patient's care.
2. The medical aspects of care in the PACU (or equivalent area) shall be governed by policies and procedures that have been reviewed and approved by the department of anesthesiology.
3. The design, equipment and staffing of the PACU shall meet requirements of the facility's accrediting and licensing bodies.

Standard II

A patient transported to the PACU shall be accompanied by a member of the anesthesia care team who is knowledgeable about the patient's condition. The patient shall be continually evaluated and treated during transport with monitoring and support appropriate to the patient's condition.

Standard III

Upon arrival in the PACU, the patient shall be re-evaluated and a verbal report provided to the responsible PACU nurse by the member of the anesthesia care team who accompanies the patient.

1. The patient's status on arrival in the PACU shall be documented.
2. Information concerning the preoperative condition and the surgical/anesthetic course shall be transmitted to the PACU nurse.
3. The member of the anesthesia care team shall remain in the PACU until the PACU nurse accepts responsibility for the nursing care of the patient.

Standard IV

The patient's condition shall be evaluated continually in the PACU.

1. The patient shall be observed and monitored by methods appropriate to the patient's medical condition. Particular attention should be given to monitoring oxygenation, ventilation, circulation, level of consciousness and temperature. During recovery from all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed in the initial phase of recovery. (This is not intended for application during the recovery of the obstetrical patient in whom regional anesthesia was used for labor and vaginal delivery.)
2. An accurate written report of the PACU period shall be maintained. Use of an appropriate PACU scoring system is encouraged for each patient on admission, at appropriate intervals prior to discharge and at the time of discharge.
3. General medical supervision and coordination of patient care in the PACU should be the responsibility of an anesthesiologist.
4. There shall be a policy to assure the availability in the facility of a physician capable of managing complications and providing cardiopulmonary resuscitation for patients in the PACU.

Standard V

A physician is responsible for the discharge of the patient from the post anesthesia care unit.

1. When discharge criteria are used, they must be approved by the department of anesthesiology and the medical staff. They may vary depending upon whether the patient is discharged to a hospital room, to the intensive care unit, to a short stay unit or home.
2. In the absence of the physician responsible for the discharge, the PACU nurse shall determine that the patient meets the discharge criteria. The name of the physician accepting responsibility for discharge shall be noted on the record.

SCORING SYSTEMS

Systemized methods of patient scoring help to provide an objective measurement for care. Scoring systems aid in determining when an ambulatory surgery patient is ready to go home, or that an extended stay for observation is warranted. A brief discussion of some helpful scoring systems follows.

Simplified Scoring System

The Simplified Scoring System is a straightforward system that lives up to its name by being relatively easy to use. Its scoring is on a scale of 0 through 6, with 6 representing complete recovery (Table 1). It is used as a quick method to assess objectively the progression from surgical anesthesia to recovery. The time intervals set for recording scores are recommended for admission to PACU at 5-, 15-, and 30-minute intervals, and upon discharge (Recovery, 2005.)

TABLE 1

SIMPLIFIED SCORING SYSTEM FOR POSTOPERATIVE RECOVERY

Parameter	Finding	Points
Consciousness	Awake	2
	Arouses and responds to stimuli	1
	Not responding to stimuli	0
Airway	Coughs on command or is crying	2
	Maintains a good airway and is breathing easily	1
	Airway requires maintenance	0
Movement	Moves limbs purposefully	2
	Nonpurposeful movements	1
	Not moving	0
Interpretation Minimum score 0 Maximum score 6 0 indicates still fully anesthetized 6 indicates fully recovered

Using the Simplified System, a total of 0 indicates still fully anesthetized and a total of 6 indicates that the patient is fully recovered.

Modified Aldrete Scoring System

Another scoring system that lists objective, observable criteria is based on the Apgar score and was developed by J. Antonio Aldrete. It is extensively used because it can be applied immediately and repeatedly as a convenient means to evaluate progress in recovery from anesthesia. A patient score of 9 in the operating room or PACU enables a satisfactory move to a lesser level of care (Barone, Pablo & Barone, 2004.)

Modified Aldrete Score (Postanesthesia Recovery Score)

Consciousness
2 = Fully awake
1 = Responds to name
0 = No response

Activity on command
2 = Moves all extremities
1 = Moves two extremities
0 = No movement

Respiration
2 = Free deep breathing
1 = Dyspneic, hyperventilating, obstructed breathing
0 = Apneic

Circulation
2 = Blood pressure within 20% of pre-op level
1 = Blood pressure within 50%–20% of pre-op level
0 = Blood pressure 50%, or less, of pre-op level

Oxygen saturation
2 = SpO₂ >92% on room air
1 = Supplemental O₂ required to maintain SpO₂ >92%
0 = SpO 2 <92% with O₂ supplementation

Total Score
10 = Score = 9 needed to leave PACU

Notre Dame Post Anesthetic Scoring System

The Post Anesthetic Scoring System of Notre Dame Hospital combines aspects of the Modified Aldrete System with an additional scoring system for the evaluation of postoperative pain, emesis, and other factors indicative of post anesthesia complications (Table 2). Patients are scored in each area at the time of admission and at regular intervals during their stay in the PACU.

This system has the additional benefit of allowing patients to be scored on the second, fifth, and fifteenth days following surgery and their progress mapped. This ability to follow a patient's progression over a longer course is a mixed blessing, as the drive to shorter procedure stays and observation periods makes a portion of this system unusable except in extreme instances.

TABLE 2

NOTRE DAME POST ANESTHETIC SCORING SYSTEM

Organ system	Finding	Points
Circulatory	Blood pressure stable; pulse always <100 (all blood pressure readings are systolic)	0
	Blood pressure change less than 30%; pulse 100–120	1
	Vasopressors or digitalis therapy	2
	Blood pressure <100 despite treatment	3
	Decompensated	4
	Severe shock	5
Respiratory	Rate under 15; breath holding more than 25 sec	0
	Rate 15–20; productive cough	1
	Rate over 20; rales or temperature up to 100°F	2
	Temperature over 100°F, partial atelectasis	3
	Major atelectasis	4
	Pneumonia	5
CNS	Amnesic, satisfied	0
	Confused or recalls induction	1
	Dissatisfied with anesthesia for any reason	2
	Extrapyramidal signs	3
	Major neurologic complications	4
	Coma	5
Gastrointestinal	Nothing	0
	No more than 3 episodes of nausea	1
	Nausea, vomited once only	2
	Vomiting	3
	Ileus	4
	Evisceration or perforation	5
Renal (24-hr volumes)	Voids over 800 mL	0
	Over 800 mL per catheter	1
	Voids 500–800 mL	2
	500–800 mL per catheter	3
	Under 500 mL	4
	Anuria	5

The post anesthesia score for each organ system is designed to be evaluated separately: the lower the score in each organ system, the better. Drawbacks to this system are its inherent complexity and—most important—that unless great care is taken to use the data achieved, reassessments several days after surgery have little meaning in all but the most serious cases (Recovery, 2005).

PREOPERATIVE EVALUATION

The American Society of Anesthesiologists (ASA) has developed a classification system that is used to identify patients preoperatively by degree of risk for complications. Individuals identified as ASA III and above, neonates, premature infants, emergency surgical procedures, abdominal procedures, and operations that require general anesthesia lasting for several hours are all candidates for extended observation in a skilled post anesthesia care setting.

American Society of Anesthesiologists Physical Status
Classification System

ASA I

• Patient's health: excellent, with no systemic disease
• Limitations on activity: none
• Danger of death: none
• Excluded: persons at extremes of age (very young, very old)

ASA II

• Patient's health: disease of one body system
• Status of underlying disease: well controlled
• Limitations on activity: none
• Danger of death: none

ASA III

• Patient's health: disease of more than one body system or one major system
• Status of underlying disease: controlled
• Limitations on activity: present but not incapacitated
• Danger of death: no immediate danger

ASA IV

• Patient's health: poor, with at least one severe disease
• Status of underlying disease: poorly controlled or end-stage
• Limitations on activity: incapacitated
• Danger of death: possible

ASA V

• Patient's health: very poor, moribund
• Limitations on activity: incapacitated
• Danger of death: imminent

Note: The letter "E" added after any ASA scoring (eg, ASA III-E) indicates that the procedure was done on an emergency basis (Risk of Complications, 2005).

The ASA system is a commonly used predictor for complications and is often used for advance scheduling of bed space in an intensive care setting. The irony of any prediction system is that an ASA III or IV patient might breeze through the recovery process after anesthesia and surgery, while a "healthy" ASA I individual might experience severe complications. This reinforces the need for vigilant observation for all patients undergoing anesthesia.

ADMISSION TO THE PACU

No discussion concerning post anesthesia complications would be complete without a brief mention of the expectations of care on arrival at the PACU. Three actions are essential to decreasing the postoperative complication rate. These are:

• Management of the patient's airway with provision of oxygen
• The measurement and recording of vital signs by the nurse with communication of this data to the anesthesiologist
• A report by the anesthesiologist to the PAC nurse assuming care

This report should include, but not necessarily be limited to, the following:

• Patient identification (name, age, sex, language or comprehension limits such as hard of hearing/blindness)
• Diagnosis, brief medical history, surgical procedure, surgeon
• Review of preanesthetic assessment including allergies, medical history, and daily medications
• Anesthetic course, technique, agents used, complications, and anticipated need for pain medications
• Intraoperative fluid balance and laboratory data
• Anticipated problems
• Postanesthetic orders (eg, oxygen administration, fluid administration, anti-emetic and analgesic treatment)

On accepting the patient, the nurse is expected to evaluate and document the patient's status both at the time of admission and at regular intervals until the time of discharge from the unit. Commonly a scoring system such as one of those previously discussed is used. Systems such as the Modified Aldrete tend to be most widely used, yet, due to limitations with cardiac dysrhythmias, oliguria, or severe nausea and vomiting, even the Modified Aldrete should never take the place of sound judgment.

Routine postoperative monitoring includes pulse oximetry, respiration pattern and rate, cardiac rate and rhythm, level of consciousness, blood pressure and temperature. Timing of vital-sign monitoring depends on the condition of the patient but is commonly set at once every 15 minutes for the first hour then each half-hour thereafter.

POST ANESTHETIC COMPLICATIONS

To identify and evaluate the frequency of complications occurring in a post anesthesia care setting, in 1992 the Yale University School of Medicine reported on a massive study of 18,473 consecutive patients entering a PACU at one university teaching hospital. They used a standardized collection form to determine the incidence of intraoperative and PACU complications. Results of this classic study showed that the overall complication rate among patients was 26.7% (Hines, 1992).

In the Yale study, the post anesthesia component of the combined complication rate was 23.7% and the intraoperative complication was rate 5.1% (a small percentage of patients fell firmly into both categories). Of the complications recorded by this study, nausea and vomiting had the highest frequency, respiratory problems, especially the need for upper-airway support, was second, and hypotension serious enough to require treatment was the third most common complication.

A study similar to the original Yale classic was published in June 2005. This larger study, composed of all postoperative patients passing through the PACU at the Vancouver General Hospital, looked at postoperative complications (POC) from April 2001 through March 2004. Interestingly, the authors concluded that "Despite pharmacological and medical aptitude advances in the past ten years, our incidences of POC, such as postoperative nausea and vomiting, hypotension, and dysrhythmias, remain similar to estimates from [the Yale study] in 1992" (Mayson, Beestra & Choi, 2005.)

Complications from the 37,071 patients in the Vancouver General study broke down into the following general groupings: respiratory complications (15.2%); cardiovascular complications (12.3%); postoperative nausea and vomiting (PONV, 9.4%); and excessive pain (7.2%).

A more specific breakdown of respiratory complications showed: the complication of inability to extubate in a timely manner after surgery (5.8%), oxygen desaturation (2.1%), and hypoventilation (2%).

Among the most common cardiovascular complications were hypotension (4.5%), hypertension (4.3%), and dysrhythmias (2.8%).

The incidence of PONV was highest after gynecologic procedures (15.5%), followed by spine surgery (12.96%), reconstructive orthopedics (11.9%), and general surgical procedures (10.9%).

Incidence of excessive pain was highest after spine surgery (12.3%), thoracic procedures (10.36%), gynecologic procedures (9.6%), and general surgical procedures (8.9%).

A common finding of these studies was that complications seen in the PACU could be either postsurgical (ie, resulting from changes brought about by the procedure) or related to the experience of undergoing anesthesia. In either instance, it is accepted practice that an anesthesiologist manages the care of patients during their stay in a recovery setting. However, depending on the nature of the complication, any number of specialists may become involved in that person's immediate care.

Physicians and support staff in the PACU must take the time to become familiar with postoperative problems and their management. The most common complications found in the post anesthesia setting can be categorized as nausea/vomiting, respiratory, cardiovascular, fluid/electrolyte, acute pain, temperature regulation, endocrine, and medications. Case scenarios are presented along with the following discussion of each problem area. Finally, we take a separate look at maternal complications.

Nausea and Vomiting (PONV)

Postoperative nausea and vomiting (PONV) complicates the lives of both patients and healthcare providers. It is frequent enough and of sufficient seriousness that it is considered by many to be the most common reason for delay in discharge as well as for unanticipated admission overnight after ambulatory surgery.

Occurrences of nausea and vomiting tie up both human and material resources and cause misery to the patient and anxiety to loved ones. When severe enough, PONV may result in lengthened recovery time and even require admission to the hospital, both of which may trigger further complications and increase financial burdens.

Nausea is the uncomfortable sensation of an impending episode of vomiting. It is often associated with prodromal symptoms such as increased salivation, frequent swallowing, pallor, and tachycardia. Vomiting is a complicated process, mediated by a central "vomiting center" that resides in the brainstem in the region of the tractus solitarius. The vomiting center (also called the parvicellular reticular formation, or emetic center) receives inputs from the pharynx, gastrointestinal tract, mediastinum, cranial nerves, the higher cortical centers (eg, the visual, gustatory, olfactory, and vestibular centers), and the chemoreceptor trigger zone (CTZ).

The CTZ is located within the brainstem, in the area postrema. Because the CTZ is not protected by the blood-brain barrier, it is exposed to bloodborne substances (eg, "toxins") and relays this information to the vomiting center. The activity of the CTZ is modified by a variety of receptors, including dopaminergic, histaminic, muscarinic, and serotonergic.

The vomiting center receives varied input and initiates the vomiting sequence by sending chemical messages that initiate the act of vomiting. Because the vomiting center receives input from different types of receptors, there is no single drug that can block all of the pathways and thus serve as a universally effective anti-emetic agent. Antagonism of any of the receptors contributes to the alleviation of nausea.

Blocking multiple avenues constitutes the basis of action for many of the available anti-emetic medications. Some agents tend to have a more prominent action at one or even two receptors, and it is thought that combining drugs that affect different receptors may promote a greater anti-emetic action than the use of single agents (Ting, 2004).

Risk factors associated with increased incidence of PONV include long duration of anesthesia, the use of inhalation anesthetics, intraoperative use of opioids, the use of reversal agents, and even the undergoing of specific elective procedures that include gynecologic, laparoscopic, middle-ear, orchiopexy, termination-of-pregnancy, and strabismus surgery.

Other pre-existing factors that increase the chances of PONV are being of female gender, pre menstrual period, diabetes, pregnancy and, interestingly enough, being a nonsmoker. Postoperative risk factors that have been identified include the presence of pain, hypotension, hypoxemia, hypoglycemia, gastric bleeding, increased intracranial pressure, inadequate hydration, use of narcotics, the presence of anxiety, and too early oral intake (Candiotti et al., 2005.)

Identifying high-risk groups and careful selection of the most appropriate anesthetic technique is the best way to deal with postoperative nausea and vomiting. Patients with a history of PONV or those at high risk should be treated both prophylactically and intraoperatively. Adequate hydration is essential, and narcotics should be used sparingly. Regional pain-block techniques have been found to be helpful for postoperative pain relief, allowing opiates to be minimized.

Analgesic adjuncts such as the NSAID ketorolac (Toradol) are also useful. However, nitrous oxide, etomidate, ketamine, and neostigmine should be avoided if possible because they are associated with an increased incidence of postoperative nausea. Hypotension, pain, and anxiety must be aggressively controlled.

In high-risk PONV patients, anti-emetic medications should be given early and the patients kept recumbent as much as their condition allows. Oral fluids should be withheld for several hours postoperatively. Other classes of drugs, such as butyrophenones, phenothiazines, or dopaminergic agents may be required in severe cases of PONV.

Aggressive and early treatment of the conditions contributing to nausea in the PACU often averts an extended admission. Patient education includes acknowledging that, although steps can and will be taken to minimize postoperative nausea and vomiting, it is not possible to guarantee the absence of this disturbing complication.

ANTI-EMETIC MEDICATIONS

Medications are an essential tool in the treatment of severe nausea. While the use of prophylactic anti-emetics has been shown to decrease the incidence and severity of postoperative nausea and vomiting, they do not eliminate the problem. Although many drugs are available, only those in common use are mentioned here.

Butyrophenones

Droperidol (Inapsine) has until recently been the most commonly used pharmaceutical intervention in the prevention and treatment of existing nausea and vomiting for surgical patients. Despite a December 2001 Food and Drug Administration (FDA) "black box" warning concerning the potential for cardiac abnormalities amongst certain high-risk populations (eg, patients with a history of cardiac, liver, or kidney disease), droperidol remains a commonly used anti-emetic, though it is no longer considered to be the reigning champion due to heightened monitoring requirements. The FDA recommends that patients receiving droperidol should receive cardiac monitoring before, to establish a baseline, and for 2 to 3 hours after receiving this medication—a recommendation that adds to the patient's cost in both materials and manpower (Wickham, 2004).

Droperidol itself is closely related to the phenothiazines and functions as a dopamine receptor antagonist. It is thought that antagonism of dopaminergic receptors in the CTZ accounts for its potent anti-emetic activity. Metabolism of droperidol occurs in the liver and its elimination half-life is just over 100 minutes. However, anecdotal reports consistently place the clinical effect of droperidol with lengths greater than the drug's half-life (Ting, 2004).

Droperidol has other undesired direct effects as well. One significant secondary effect in droperidol use is that it may trigger extrapyramidal symptoms in approximately 1% of patients with Parkinson's disease (Table 3). In addition, though it has no effect on cerebral metabolic rate or oxygen consumption, droperidol is known to cause a decrease in cerebral blood flow. Droperidol also tends to augment the action of opioids because of its sedative action, which can be a mixed blessing (Parkinson's Disease Clinic, 2005.)

TABLE 3

PONV TREATMENT IN PARKINSON'S DISEASE

Avoid the following medications: Chlorpromazine (Thorazine) Droperidol (Inapsine) Metoclopromide (Reglan, Maxeran) Prochlorperazine (Compazine, Stemetil) Trimethobenzamide (Tigan)	Medications that may be used: Dolasetron (Ansemet) Granisetron (Kytril) Ondansetron (Zofran) Domperidone* (Motilium, available in Canada only)
Source: Parkinson's Disease Clinic, 2005.

Benzamides

Metoclopramide (Reglan) is a gastric motility stimulant that has the additional benefit of increasing lower-esophageal sphincter tone. Doses of 1 mg/kg to 2 mg/kg have been found to decrease the extreme nausea associated with chemotherapy. Large doses may sedate the patient or cause extrapyramidal reactions in vulnerable patients. Hiccups, facial flushing, and headaches may also accompany use (Wickham, 2004).

For surgical outpatients, smaller doses (0.1 to 0.2 mg/kg) have been shown to be effective. Metoclopramide has a short half-life of 2 to 4 hours. Its close chemical relative trimethobenzamide (Tigan) is not as effective as metoclopramide, yet may be useful because of its availability in a suppository form.

Anticholinergics

Scopolamine ("transderm scop") is an anticholinergic agent that has been found to reduce emesis associated with motion sickness. There has been some use of transdermal scopolamine patches the night before surgery. Scopolamine crosses the blood-brain barrier. The drug's adverse effects include dry mouth, dizziness, amblyopia, mydriasis, headache, and sedation. Reports of visual disturbances and hallucinations by some patients have caused it to fall into disfavor.

Phenothiazines

The anti-emetic activity of phenothiazines lies in their ability to antagonize both H1 receptors and dopamine receptors. Two drugs in this class, prochlorperazine (Compazine) and promethazine (Phenergan), are commonly used to treat nausea and vomiting. These agents can be given by either intravenous (IV) or intramuscular (IM) route. The clinical effect of promethazine lasts 4 to 6 hours.

Side effects of phenothiazines include sedation, dizziness, dry mouth, mild increases in heart rate, and orthostatic hypotension. Extrapyramidal reactions are also associated with phenothiazine anti-emetics. Intramuscular administration avoids the venous irritation and thrombophlebitis common with IV injection of promethazine.

Serotonin Antagonists

The serotonin antagonists—dolasetron (Anzemet), granisetron (Kytril),and now ondansetron (Zofran)—were already in use at the time of the FDA warning concerning droperidol. As a class, they were considered by most to be as effective as droperidol, yet their higher price mandated that they be almost exclusively second-line agents. As droperidol slid from its position at number one, however, these agents in turn ascended to the status of first-line agents (and PONV became more costly to address).

The serotonin antagonists bring a certain efficacy to the battle against nausea. The additional benefit of avoiding the extrapyramidal side effects and sedation seen with other agents are a definite plus. They also show a surprisingly minimal side effect profile (rare headache and dizziness, rare and clinically insignificant increase in liver enzymes) (Ting, 2004).

A good example of this class is ondansetron (Zofran). This agent is a selective serotonin antagonist that affects one of serotonin's three specific receptor sites, in this instance the 5-hydroxytryptamine type 3 (5-HT3) receptor, which is found in the limbic system, the cerebral cortex, and the chemoreceptor trigger zone.

Ondansetron appears relatively free of CNS side effects, mainly because it does not stimulate histaminic, cholinergic, adrenergic, or dopaminergic receptors. What it does stimulate is gastric emptying, better than metoclopramide, and there are few if any interactions between ondansetron and other drugs.

Oncologists have found it useful for controlling emesis associated with cancer chemotherapy and radiation therapy. Ondansetron may be used for treatment of PONV as well as for prophylaxis against it, and has recently been released in an orally dissolving tablet formulation that may prove a valuable addition to the IM/IV forms in which the serotonin antagonists are commonly available.

Respiratory Complications

Respiratory complications are among the most frequently seen difficulties in post anesthesia care. The most common of these problems often correlate directly to specific causative effects. Hypoventilation, for example, is commonly a direct result of the effects of the anesthetic agent and technique chosen. Hyperventilation tends to be a result of pain, or, less often, of increased intracranial pressure and pathology.

Bronchospasm can be a result of pre-existing disease conditions or the presence of triggering secretions. Pulmonary edema is associated with fluid overload or cardiac shock. The complication of pulmonary embolism is generally directly associated with venous thrombosis, or, less frequently, fat emboli.

The complication of aspiration (the inhalation of any foreign material into the lungs) may occur more frequently than was once thought. Although predisposing factors may be highly individualized, the traditional view holds that aspiration correlates closely with the presence of vomiting and high gastric content volumes. The presence of gastric volumes in excess of 25 mL in conjunction with a pH of the aspirate <2.5% have been shown to increase the risk, yet some researchers believe that as many as half of those patients fasting before surgery could be considered a higher risk by these criteria.

Should aspiration occur and symptoms develop, supportive techniques may include endotracheal intubation, lung washing to remove and dilute materials, and mechanical support ventilation. The use of steroids, with or without antibiotic therapy, has not been found to improve outcomes in the absence of infection. If aspiration has been suspected in the ambulatory patient, yet the patient remains asymptomatic for two hours (without hypoxemia on room air, and with a normal chest radiograph), it is thought that the patient may safely be discharged (Asai, 2004).

Observable factors that increase the likelihood for postoperative ventilatory support include pre-existing lung disease, obesity, advanced age, a smoking history, low preoperative arterial oxygenation, thoracic and upper abdominal surgery, recent large narcotic administration, and a large intraoperative blood loss with excessive crystalloid replacement.

Hypoxemia (the condition of having a below-normal oxygen content in arterial blood) can be detected easily and rapidly in the post anesthesia setting by the routine use of pulse oximetry. It can be confirmed in a more definitive manner with arterial blood gas measurements (PaO₂, less than 60 mm Hg on 2-L flow O₂).

The primary mechanism of postoperative hypoxemia that results in the need for induced ventilation is a decreased functional capacity. This can be caused by pain, abdominal distention, impaired diaphragmatic function, and inability to tolerate the supine position.

Early recognition of this condition can facilitate therapeutic intervention before a life-threatening situation develops. Some features of hypoxia (another term for hypoxemia) may overlap with those of hypercapnia (excess of carbon dioxide in the blood). The early clinical signs of hypoxemia are tachycardia, tachypnea, agitation, and altered mental status, whereas hypotension, bradycardia, obtundation, and cardiac arrest are late signs.

Reactive airway disease (asthma) deserves its own mention because it is a potent cause of bronchospasm postoperatively. The term asthma is being replaced with what many consider a more accurate term—reactive airway disease (RAD). Those with RAD (5% and growing in the United States) have bronchial passages that are more sensitive to irritation than normal. This hypersensitivity leads to inflammation in the tiny airways deep in the lungs. The inflammation in turn causes excess mucus production and tightening of airway muscles that wind around the bronchial tubes like laces.

Swelling, mucus, and muscle tightening interact to cause narrowing of the airways. Wheezing (whistling and labored breathing) usually results, but a dry cough is sometimes the only sign. Tightening of the airway passages in the immediate post anesthesia environment can be handled with placement of a laryngeal mask airway combined with positive-pressure ventilation. This intervention can maintain adequate oxygenation while avoiding the additional physical insult of a second intubation.

Patients with obstructive sleep apnea syndrome (OSAS), or snorers, are at increased risk of reduced oxygen saturation in arterial blood. Sedatives, anesthetics, and lying in the supine position can impair upper-airway muscle activity, jeopardize airway patency, and decrease functional residual capacity, predisposing these patients to desaturation. The use of the combined approach of a sitting position and nasal continuous positive airway pressure (NCPAP), started before surgery and continued postoperatively, has been found to be helpful in handling patients with OSAS.

Bronchospasm (the spasmodic contraction of smooth muscles of the bronchi) is usually associated with asthma, chronic obstructive pulmonary disease (COPD), or smoking. Another uncommon cause of bronchospasm is an allergic reaction to drugs, blood products, or latex. Treatment for life-threatening spasm in the post anesthesia care unit often includes a nebulized selective beta-2 agonist (terbutaline or albuterol), the use of intravenous theophylline (5–6 mg/kg infused as 0.2 mg/kg/hr), along with the concurrent use of inhaled bronchodilators.

Pulmonary embolism, the sudden lodging of a blood clot (or, less commonly, fat or amniotic fluids) in a pulmonary artery with subsequent obstruction of the blood supply, is a very unusual occurrence. Most often a diagnosis is made by exclusion, eliminating other causes first. It should be suspected, however, in the presence of unexpected cardiorespiratory collapse. Precipitating factors include obesity, hypercoagulability, oral contraceptive use, varicose veins, old age, prolonged immobility, fractures of pelvis, hip, or leg, as well as the presence of malignancy.

Symptoms include shock, dyspnea with tachypnea, hyperventilation, and hypoxemia. Preventive measures in high-risk patients include the use of elastic stockings, intermittent pneumatic leggings, and low-dose heparin to inhibit clot formation. Treatment of pulmonary embolism is supportive, with the expectation that the thrombi will lyse within a matter of days to several weeks (Merck, 2005).

Hoarseness and sore throat occur in about one-third of intubated patients, although it does not usually cause respiratory problems (unless the airway was already compromised in some manner). Spontaneous resolution occurs within two weeks in almost all who experience this complication. Prophylactic measures include an experienced intubator and use of bland lubricant.

Medication combined with unconsciousness can lead to potentially dangerous events that can compromise patient respiration in the PACU. These events tend to occur by three major mechanisms:

• Airway obstruction
• Respiratory insufficiency caused by certain medications
• Chemical pneumonia

When a patient is unconscious, slackened nasal or oropharyngeal tissues, muscle rigidity in the neck, or upper-respiratory secretions can obstruct the airway. The risk can be lessened by turning the patient on the side with head flat or slightly lowered.

Check breathing using your stethoscope. Listen for breath sounds—don't rely on chest motion only. Observe and palpate the chest to make sure that both sides expand equally; if they don't, one lung may be obstructed. Check for straining of the accessory breathing muscles, tachycardia, and hypoxia; these are signs that obstruction is interfering with effective breathing. Cyanosis may occur unless the obstruction is relieved.

To relieve obstruction, extend the patient's neck and thrust the jaw forward in a chin lift/jaw thrust maneuver, as when initiating cardiopulmonary resuscitation. This clears the tongue, nasal, and oropharyngeal tissues from the airway. If signs of obstruction persist, secretions may need to be suctioned. Some patients may require the insertion of an oral or nasal airway, or assisted ventilation by mask or bag.

Respiratory insufficiency may occur because inhalation anesthetics and narcotics depress respiratory drive. Intraoperative muscle relaxants compound the problem by weakening the respiratory muscles. The use of supplemental oxygen is a standard practice following any anesthetic until the patient is fully awake. Remember that the patient's need for oxygen increases with shivering, which is a common response to anesthesia and the cooling effects of prolonged surgery.

If during the immediate postoperative period the patient falls asleep and begins to breathe shallowly, it may be due to insufficient oxygen. Arouse the patient and encourage slow, deep breathing. This will often be sufficient while medication is exiting the system.

To assess for respiratory insufficiency, listen for breath sounds and check the rate, depth, and ease of breathing. Anesthesiologists typically ask to be called if respirations fall below 10 per minute or if oximetry measurements show hemoglobin saturation below 90%.

In the case of severe respiratory depression, the patient may be given a narcotic reversal agent such as naloxone (Narcan), or the patient may be placed on mechanical ventilation until medications have been metabolized to the extent that respiratory drive and effort will support effective breathing.

Narcotics and inhalation anesthetics suppress cough and gag reflexes, leaving the still-unconscious patient at a high risk for aspiration of gastric secretions and possible secondary chemical pneumonia. One of the most common preventive measures is to keep the unconscious patient in a side-lying position with the head lowered to decrease the risk of aspiration.

In order to check for aspiration, auscultate all areas of the lungs for wheezing and rales every 10 to 15 minutes and notify the anesthetist if you hear suspicious lung sounds. Other observable symptoms include restlessness, dyspnea, cyanosis, tachypnea, tachycardia, cough, and eventually, fever. The sooner the patient receives treatment, (which may include antibiotics, oxygen, bronchodilators, or steroids) the better the chances of avoiding a life-threatening hospital-acquired pneumonia.

No matter what the complication, the use of a structured assessment plan within the PACU is essential for early recognition and treatment of respiratory complications. Utilize assessment scales for auscultation and pulse oximetry. Constant and consistent observation of the post anesthetic patient is an important habit to develop. This will ensure prompt and appropriate intervention.

Cardiovascular Complications

Cardiovascular instability is often observed in the PACU. The types of procedures that warrant the use of anesthetics, as well as the anesthetic medications themselves, introduce an insult to the bodily system. Physiologically, the human body responds to trauma, even purposeful trauma meant to aid the individual, with shifts and reallocations of blood and bodily fluids. At times these shifts can be dramatic and life-threatening. The routine and systematic postoperative monitoring of blood pressure, pulse, and electrocardiogram tracings (ECG) helps to warn of impending problems.

Staff should be alert for the presence of four keys cardiovascular events in the PACU. These include the following:

• Hypertension
• Hypotension
• Tachycardia
• Bradycardia

Identifying these key events allows clinicians to problem-solve and isolate the causes underlying what is being observed in the PACU (eg, myocardial infarction, internalized hemorrhage, cerebrovascular infarction, emboli).

Acute hypertension can be defined as a blood pressure 20% greater then the patient's preoperative baseline pressures. In post anesthesia care, this increase can be induced by pain, urinary retention, hypothermia, nausea, hypoxia, hypercarbia, myocardial ischemia, or the impairment of blood flow to any major system. Any abnormality in intracranial blood flow will especially affect blood pressure.

Postoperative hypertension is often found in conjunction with arteriosclerotic disease. Arteriosclerosis is thought to promote an exaggerated response to stimuli that may generate vasoconstriction. Some procedures, including abdominal aneurysm repair, carotid endarterectomy, and intracranial surgery, have been associated with a higher incidence of hypertension. Hypertension and cerebral hyperperfusion are often seen in the immediate postoperative period after craniotomy (Mandel, 2002).

Treatment for acute hypertension mandates adequate and early pain relief, bladder catheterization (if indicated), and the use of fast-acting medications with the intent of breaking the vasoconstrictive cycle. It is particularly important to break this cycle when there are signs of end organ damage, such as severe headache, persistent chest pain, or hematuria. Some of the widely used agents for acute treatment of emergent hypertension include the following (Merck, 2005):

• Diazoxide
• Sodium nitroprusside
• Nitroglycerin
• Labetalol
• Nifedipine

Diazoxide is a nondiuretic thiazide, and may be administered by rapid IV injections of 50 to 100 mg (1 to 1.5 mg/kg, less than or equal to 100 mg/dose) given every 5 to 10 minutes until the blood pressure reaches the optimal level. Adverse effects include nausea, vomiting, hyperglycemia, hyperuricemia, tachycardia, and, occasionally, hypotension (generally without shock).

Sodium nitroprusside 0.25 to 10 mcg/kg/min (for ≤ 10 min at the highest dose to minimize the risk of cyanide toxicity) is given by continuous IV infusion and can promptly reduce blood pressure in a hypertensive crisis, but its evanescent effect and potency require almost continuous monitoring of blood pressure in an ICU. Unlike diazoxide, it produces venous and arteriolar dilatation and therefore reduces preload and afterload, making it especially useful for managing hypertensive patients with heart failure. Adverse effects include nausea, vomiting, agitation, muscular twitching, and cutis anserina (goose flesh) if blood pressure is reduced too rapidly. Acute psychosis from thiocyanate intoxication can result from prolonged therapy, especially in patients with renal failure.

Nitroglycerin, similar to sodium nitroprusside, relaxes the resistance of vessels and the capacitance of veins. Compared with sodium nitroprusside, it has a greater effect on veins than on arterioles. Intravenous infusions of nitroglycerin have been used to manage hypertension during and after coronary bypass, heart failure, acute MI, unstable angina pectoris, and acute pulmonary edema. The most frequent adverse reaction is headache, which occurs in about 2% of patients; tachycardia, nausea, vomiting, apprehension, restlessness, muscular twitching, and palpitations have also been observed.

Labetalol, 20 to 40 mg intravenously every 10 minutes, or as an infusion, is as effective as nitroprusside, diazoxide, or nitroglycerin in managing hypertensive crises. Serious hypotensive episodes have not been observed when labetalol is given by this method, and adverse effects have been minimal. Because of its blocking activity, labetalol should probably not be used for hypertensive emergencies in patients with acute left ventricular failure or in asthmatic patients.

Nifedipine given orally usually reduces blood pressure rapidly. It has been associated with acute cardiovascular and cerebrovascular events (sometimes fatal), and is not recommended for treating hypertensive emergencies or urgencies. It is not indicated for managing hypertension.

HYPOTENSION

Hypotension is a common and feared complication in the post anesthetic period. The common usage of the term refers to an abnormally low systemic blood pressure as compared to preprocedure baseline pressures. Any factor that seriously lowers cardiac output or peripheral vascular resistance (or both) can significantly lower systolic blood pressure. There is a fine line between hypotension and shock.

It is important to recognize that a patient may not be hypotensive, yet could develop shock in a short period of time. Clinical findings like oliguria, altered mental status, peripheral cyanosis, or pallor and cool skin temperature are red flags for impending hypotension/shock. Accompanying clinical findings that sometimes support the diagnosis of shock include tachycardia, tachypnea, and hypothermia (Mandel, 2002).

New-onset hypotension in the PACU is almost always a sign of an unwanted medication interaction, hypovolemia, or blood loss. Other causes can include exposure of body cavities for prolonged periods, the handling of bowel and mesentery, as well as dissections in the retroperitoneal space (eg, in abdominal aortic aneurysm dissections or pancreaticoduodenectomy). The specific treatment of hypovolemic hypotension is to restore adequate circulating intravascular volume. This can be done with one or a combination of whole blood, packed red blood cells, albumin or hetastarch, or a balanced electrolyte solution such as lactated Ringer's solution.

Vasoactive drugs such as phenylephrine may also be used to constrict the intravascular compartment until appropriate amounts of fluids are infused. Repeat hemoglobin and hematocrit determinations are useful for proper gauging of an ideal response to treatment. Under normal conditions, a hematocrit of 28% is considered optimal for both cardiac output and oxygen carrying capacity.

Treatment of hypotension thought to be related to medication effects includes the use of specific reversal agents when indicated, deep breathing in order to "wash out" inhalation agents, the use of supplemental oxygen, and adequate fluid replacement. In the treatment of hypotension, the mainstays of treatment are the achievement of homeostasis, fluid resuscitation, and the use of blood products.

The use of pressor agents (vasopressors) may be needed in some settings, but these agents should not be substitutes for adequate volume resuscitation. Vasopressors are agents that augment both coronary and cerebral blood flow during the low-flow states associated with shock. The following vasopressors are commonly used to treat hypotension in the PACU:

• Dopamine (Intropin)
• Norepinephrine (Levophed)
• Epinephrine (Adrenalin)
• Vasopressin (Pitressin)

Dopamine (Intropin) works by stimulating both adrenergic and dopaminergic receptors. Its hemodynamic effect has been found to be dose dependent. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and mesenteric vasodilatation. Higher doses produce cardiac stimulation and renal vasodilatation.

Dosage in adults is 1–5 μ/kg/min intravenously, not to exceed 50 μ/kg/min intravenously. After initiating therapy it is common to increase the dose by
1–4 μ/kg/min IV every 10 to 30 minutes until the optimal response is obtained. In more than 50% of patients, satisfactory maintenance is achieved with doses less than 20 μ/kg/min intravenously. When using dopamine, it is important to closely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during infusion.

Norepinephrine (Levophed) and epinephrine (Adrenalin) are pressors that are used in protracted hypotension following adequate fluid-volume replacement. They stimulate beta1-adrenergic and alpha-adrenergic receptors, which in turn increase cardiac muscle contractility and heart rate as well as vasoconstriction. The result is increased systemic blood pressure and coronary blood flow increases. In an adult, a dosage rate of 2 μ/kg/min intravenously, titrated to effect (low-normal blood pressure, 80–100 mm Hg systolic) is sufficient to perfuse vital organs.

Vasopressin (Pitressin) has vasopressor and anti-dieretic hormone (ADH) activity. It increases water reabsorption at the distal renal tubular epithelium (ADH effect) and promotes smooth-muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). In adults, dosage rates are 0.1 to 0.5 U/minute intravenously, titrating as needed. Once hemodynamically stable, it is common to continue at the same dose for 12 hours and taper over 24 to 48 hours.

TACHYCARDIA

Tachydysrhythmias in the PACU most often consist of sinus tachycardia (heart rate greater than 100 bpm) or supraventricular tachycardia (SVT). It is important to ascertain the hemodynamic response of the patient to the dysrhythmia. In patients with SVT who are not hemodynamically stable, synchronized cardioversion may be indicated.

Unstable SVT shows manifestations of hypotension, mental status change, and pulmonary edema or myocardial ischemia. If the patient is hemodynamically stable, it is important to determine if the dysrhythmia is a physiologic response to physical or emotional stress and then correct the underlying problem. Common causes for tachycardia seen in the PACU include pain, hypovolemia, anemia, fever, hypoxia, and hypercapnia.

In the PACU, pain is probably the most common cause of tachycardia. Pain may originate from the surgical incision site, but it may also be present due to an over-distended bladder or even a strain resulting from positioning during the procedure. Treatment of the first includes appropriate analgesics and positioning, while the latter necessitates voiding.

During surgical procedures there is potential for massive fluid shifts due to third spacing and evaporation. Third spacing is the movement of bodily fluids from their usual location within vascular spaces into those areas outside of the vascular system, while evaporation is the process by which the body loses fluid into the atmosphere.

Evaporation is greatly increased whenever the protective confines of the skin are breached. The skin is the primary protection for the moist tissues that form the inner portions of our bodies. It is not uncommon for patients to present to the PACU with a relatively depleted intravascular fluid load. Compensatory physiologic tachycardia is a protective mechanism to provide adequate tissue profusion. The appropriate treatment is volume replacement.

Anemia due to surgical blood loss may also produce a compensatory physiologic tachycardia. The underlying cardiac status often determines the approach to tachycardia due to anemia. Does the tachycardia present an increased myocardial oxygen demand in a patient with coronary artery disease that cannot be met without inducing rate related ischemia? The acuity of the anemia must also be addressed. In today's practice of transfusion medicine, it is important to be as conservative as possible in administering blood products because of the increased risk of infectious disease transmission (Mandel, 2002).

Fever is a physiologic response that may accompany a wide variety of illnesses, and it provides a marker of disease activity. In the surgical patient, it may represent as underlying infection and is the response to endogenous or exogenous pyrogens. It may also be caused by overzealous heating of intravenous fluids and inspired gases, and/or overheating of the operating room and heating blanket. The etiology of fever should always be investigated. In the PACU, fever may produce tachycardia that, in the patient with underlying coronary artery disease, can cause ischemia. Treatment options include use of antipyretics, cooling blankets, and ice packs in severe cases.

On a related note, shivering is a mechanism that the body uses to produce heat. Often patients arrive shivering in the PACU. Shivering can result in a significant increase in oxygen consumption, which may be detrimental to the patient with limited cardiac reserve. Treatment includes warming the patient and possibly judicious use of meperidine (Demerol) for the express purpose of decreasing shivering.

Tachycardia is also a physiologic response to hypoxia and may first become apparent when the patient arrives in the PACU. In the immediate postoperative period, hypoxia may represent the residual effects of anesthetic drugs or response to the type of surgery. Hypoxia may be a reflection of alveolar dilution of oxygen secondary to nitrous oxide elimination, the phenomenon of so-called diffusion hypoxia. It may also represent alveolar hypoventilation due to the continued respiratory depressant effects of the potent volatile anesthetics or residual effects of muscle relaxants.

The mechanical effect of upper-abdominal or thoracic surgery on respiratory mechanics is known to decrease ventilatory effort. Right-to-left intrapulmonary shunting of blood due to atelectasis, ventilation-perfusion mismatching due to decreased functional residual capacity, decreased cardiac output, pulmonary embolism, aspiration, pulmonary edema, bronchospasm, and pneumothorax are all potentially correctable causes of hypoxia and possible cardiac dysrhythmias (Mandel, 2002).

Alveolar hypoventilation likewise may lead to hypercarbia that in turn may be a factor in tachycardia and hypertension, both of which may be deleterious to the patient with coronary artery disease. The treatment is to ensure adequate ventilation by determining the cause of the abnormality and correcting it.

BRADYCARDIA

Sinus bradycardia is a heart rate slower then 60 beats per minute (bpm). Normal, however, is simply what applies most often in a majority of persons. Sinus bradycardia is a good example of how misleading normalcy may be. A sinus rate of less then 60 bpm might be perfectly acceptable in a young, athletic patient who arrives in the PACU after a minor surgical procedure; yet this rate might signal more ominous cardiac dysrhythmias in other patients. This underscores the importance of knowing the pre-procedure baseline, or what is normal for this patient. It is imperative to ascertain the cause of a slow dysrhythmia, and when it is pathogenic, to correct it. One asymptomatic heart rate (<60 bpm), for example, may be the result of increased vagal tone, as seen after administration of anticholinergic medications.

This category of medications, anticholinergics, is frequently used to reverse the effects of neuromuscular antagonists often used in general surgical procedures. If the patient is hemodynamically stable, careful observation may be all that is necessary. Other treatment options include re-administration of any anticholinergic medications given earlier.

Often the anticholinergic of choice is a class of medications known as antimuscarinics. These drugs block the activity of acetylcholine at the muscarinic receptors (ie, atropine and scopolamine). Beneficial results of antimuscarinic use during the immediate postoperative recovery period include quickening of the heart rate, relaxation of the smooth muscles (including the airways and gut), and a reduction in the secretion of saliva, digestive juices, and sweat.

Bradycardia may also be caused by arterial hypoxemia and impending cardiac arrest, in which case adequate oxygenation is vital. Bradycardia can be a compensatory mechanism used by the body to relieve unrecognized elevated intracranial pressure (ie, the Cushing's reflex). Thus bradycardia seen in response to hypertension may occur to ensure adequate cerebral perfusion pressure. The treatment for bradycardia in this situation is normalization of intracranial pressure. Finally, bradycardia may represent a physiologic response to hypothermia, and careful rewarming of the patient should be undertaken.

When the heart rate slows past a point of productive perfusion, ectopic beats—either atrial or ventricular premature depolarizations—begin to appear. The presence of ectopy alone does not necessarily imply underlying cardiac disease. Ectopic beats may, however, be associated with myocardial pathology and are often associated in the PAC setting with electrolyte imbalances, hypoxia, acid-base abnormalities, and hypertension. They may be side effects from certain medications such as digitalis toxicity, or more rarely may be caused by endocrine disorders such as thyrotoxicosis.

Hypokalemia and hypocalcemia are the more common electrolyte abnormalities associated with ectopic rhythms, and should be suspected and tested for, particularly in patients who experienced excessive diuresis intraoperatively, are alkalotic, or have received numerous blood transfusions. Management includes measurement of electrolytes, correction of acid-base abnormalities, and electrolyte replacement when indicated.

Transvenous pacing should be available for use in the presence of symptomatic bradycardia that is not responsive to electrolyte replacement, supplemental oxygen or conventional pharmacologic treatment.

Fluid and Electrolyte Complications

Complications due to fluid and electrolyte imbalances occur primarily in older or debilitated patients, in hypertensive patients pretreated with diuretics, in diabetic and neurosurgical patients, and in those who have undergone long procedures with large fluid shifts. Hyponatremia, hypocalcemia, and hypermagnesemia may all work to delay a return to full consciousness. Any abnormal findings in these higher-risk patients warrant immediate measurement of electrolytes and prompt correction of abnormalities.

Hyponatremia (often referred to as water intoxication) is most often due to the syndrome of inappropriate antidiuretic hormone (SIADH) release, although free water absorption during such procedures involving large amounts of irrigant such as transurethral resections of the prostate (TURP) can also be a cause. SIADH can be associated with stress, general anesthesia, positive pressure ventilation, the presence of pulmonary carcinoma, or diseases of the pituitary system. Hyponatremia can also occur as a complication after major head injury, when cerebral salt-wasting syndrome may occur. Treatment of hyponatremia includes diuresis with furosemide IV (Lasix) and, in an emergency situation, infusion of hypertonic saline.

Hypocalcemia occurs when total serum calcium levels fall below 4 to 5 mEq/L. Causes include hepatic failure, massive volume replacement, acute pancreatitis, hypoparathyroidism, and endstage renal disease. Acute decrease in ionized calcium is associated with extreme hyperventilation, bicarbonate injection, and the rapid infusion of citrated blood (in this instance, calcium remains present, yet is chelated or bound into an unavailable form). Signs and symptoms include confusion, seizures, hypotension, prolonged QT wave, and muscle spasm (including laryngeal muscle spasm). Treatment requires correction of hyperventilation and replacement with calcium chloride.

Hypermagnesemia (greater than 2.5 mEq/L) tends to occur most commonly in eclamptic patients treated with magnesium sulphate as well as those with endstage renal disease. Symptoms include suppression of deep-tendon reflexes, sedation, and coma. Cardiovascular collapse occurs at levels over 10 to 15 mEq/L. Treatment involves discontinuation of exogenous sources, support of cardiorespiratory function, and intravenous calcium.

Acute Pain Complications

Intense, uncontrollable postoperative pain is a problem that should not occur. A multitude of pain-control medications and techniques, including epidural and intraspinal opioids, intercostal nerve blocks, interpleural analgesia, and PCA (patient-controlled analgesia), can be used to provide a postsurgical experience with no more than slight pain for the majority of patients. These measures can be augmented by the addition of nonpharmacologic interventions for the management of pain that include the application of cold or ice, proper immobilization/positioning, effective pre-education, and re-education regarding the control of pain and relaxation.

The presence of intense postsurgical pain worsens all other postoperative complications. Deep breathing and activity are restricted, which increases the risk of atelectasis, pneumonia, and deep-vein thrombosis. Tachycardia occurs in response to pain. Fluid shifts and physiologic responses are altered by intense pain.

The early use of appropriate analgesia reduces the number and severity of most immediate postoperative problems.

Some serious misconceptions exist concerning the use of analgesic agents in the immediate post anesthesia environment. Misconceptions include:

• Opioid doses need to be kept as small and infrequent as possible in order to avoid "addiction."
• Doses larger than "the standard" will not be effective for improving pain relief and inevitably cause heavy sedation and respiratory depression.
• Nursing and/or medical staff will simply "know" how much to medicate and when pain relief medications are needed.
• Patients requesting more pain relief than "normal" are psychologically abnormal or are becoming "addicted."
• If non-opioid analgesics are ordered in addition to opiates, then these should be utilized in preference or to the exclusion of the opioid medication. (Mandel, 2002)

Types of analgesic agents include nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates. Unlike opiate analgesics that have an effect on the central nervous system, NSAIDs act mostly at peripheral sites, inhibiting the action of prostaglandins via antagonism of the cyclo-oxygenase (COX) enzyme. This is an enzyme required in the synthesis of prostaglandin, a sensitizer of peripheral nociceptors. Older NSAIDs tend to act to block both COX 1 and 2 sites. This means that the use of these NSAIDs may be associated greater possibility of coagulopathies and gastrointestinal problems. Newer agents that block only COX 2 sites have been developed, offering new choices for pain control.

Ketorolac (Toradol) is an NSAID finding frequent postsurgical use. In the PACU it is most frequently given IM. Because it is a peripherally acting analgesic and does not affect opiate receptors, this makes it a powerful adjunct to narcotic analgesia. One intramuscular dose of 30 mg affords pain relief similar to that of 100 mg of meperidine, with a longer duration of action, less drowsiness, and fewer incidences of nausea and vomiting. This drug has anti-inflammatory, antipyretic, and pronounced analgesic activity. In comparison, it is considered to be a more potent analgesic than aspirin, phenylbutazone, naproxen, or indomethacin.

Ketorolac prevents prostaglandin synthesis by inhibiting cyclo-oxygenase, the principal enzyme that catalyses the reaction with arachidonic acid to form prostaglandins. No evidence suggests that it produces withdrawal reactions after long-term use. Although ketorolac increases bleeding time, it is not yet clear in the literature if the clinical consequences are significant. It would be prudent that certain types of patients not receive this drug (eg, craniotomy patients or patients that are clearly at risk of hemorrhage into a confined space).

Questions about safety in postoperative kidney transplant patients have also not been answered. Until more information is available, ketorolac probably should be avoided in these patients due to the risk of acute kidney toxicity. Pregnant patients are at risk when receiving this drug because it may cause abnormal cardiovascular changes in the neonate due to its prostaglandin-inhibiting properties.

The best time for planning postprocedural analgesia is before administering the anesthesia. This allows time for pre-procedure patient instruction and assurance, which will greatly reduce anxiety levels. It also allows for decisions about the use of narcotics during the procedure and plans for placement of postsurgical pain control measures (if indicated) before the anesthetic agents are reversed or allowed to wear off.

When planning analgesic choices, it is important to consider the anticipated level of patient anxiety. This allows, for example, early use of oral medications for ambulatory patients who show no contraindications such as nausea or lack of bowel tones. It is important to remember that pain medication should be given on a regular basis in addition to as-requested, with the patient being allowed the right of refusal. The manner in which each individual responds should be reflected in the type of drug, dosage, frequency, and route of administration.

There are a number of ways to administer drugs for acute postoperative pain relief. Most commonly, drugs are given IV. By this method, opioids have a short distribution phase and titrated doses may be given at 10- to 15-minute intervals until the desired degree of analgesia is reached or indications such as slowed respiration (less than 10 breaths per min) show that other means should be utilized. Morphine sulfate in 1- to 2-mg increments or meperidine (Demerol) in the 10- to 15-mg range are the most common acute IV opioids used in the postoperative setting.

Most opioids can also be given intermittently by the intramuscular route. This route should not be used in hypovolemic, hypotensive patients because cardiac output and muscle perfusion may be impaired, negating the benefit of this route of delivery. Standard dosing for morphine is 0.15 mg/Kg, and for meperidine 1.5 mg/Kg, although these doses tend to be on the conservative side and may not be adequate for good postoperative pain relief.

Commonly used sublingual and oral drugs include buprenorphine (0.2–0.4 mg), ibuprofen (300–400 mg), acetaminophen (650–1000 mg), aspirin (650–1300 mg) or naproxen (250–500 mg). Individual response should allow for change of type of drug, dosage, or frequency or route of administration. Discussion and planning for postoperative pain relief is appropriate during pre-anesthetic assessment.

Postoperative pain control should be started intraoperatively and managed aggressively with rapid and short-acting opiates in the PACU.

Patient-controlled analgesia (PCA) allows the patient to self-administer potent analgesics. Features central to PCA include an adequate loading dose initiated at the time the system is prepared, an incremental dosage scheme, with a lockout interval and time period maximum to prevent excessive dosing. Computer technology permits programming, storage, and retrieval of data. Patient-controlled analgesia may be used in conjunction with oral medications and, less commonly, by the epidural route.

The advantages of PCA are safety, simplicity, and effectiveness. Disadvantages include lack of understanding on the part of the healthcare providers and/or the patient, failure of the device, and IV infiltration. Use of PCA may delay the diagnosis of significant postoperative complications such as myocardial ischemia, especially when the patient uses the PCA to treat pain that is nonsurgical in origin. An advantage of using PCA and loading-dose schemes is that initial utilization of analgesics can be used to predict later pain-control requirements.

The management of postoperative analgesia depends on many factors, especially on the nature of the surgical procedure and the patient's pain threshold. Regional blocks, local anesthetic infiltration into wounds, analgesic suppositories combined with opioids, and preoperative or intraoperative administration of ketorolac can be used to treat or control pain both intraoperatively and in PAC. A multi-mechanism approach to postoperative pain management will increase patient satisfaction, shorten mean time to discharge, and reduce the incidence of postoperative complications, especially nausea and vomiting (PONV).

Temperature Regulation Complications

Temperature complications in PAC are expressed as either too little or too much. Too little—hypothermia—is a common postoperative problem. Hypothermia may be caused by a number of factors, including low ambient temperatures in procedure areas, the inability to regulate internal temperatures effectively due to the effects of anesthesia, the exposure of internal "wet" membranes to evaporation, and the infusion of cold fluids. Decreased internal temperature may have the following effects:

• Impairment of the immune system
• Increase in the incidence of infection
• Increase in the rate of blood loss, leading to the need for transfusions
• Increase in the incidence of myocardial infarction
• Prolongation of the need for mechanical ventilation
• Decrease in anticipated drug metabolism
• Increase in mortality rates

Practical means to prevent hypothermia include the use of warming measures, both intraoperatively and in the PACU. These measures are simple, effective, and are cost effective for the patient as well as the facility promoting their use. One practical method of initiating warming is to wrap the patient in heat-retaining materials (instead of paper drapes), especially around the head. The next step is to use warm air/forced air devices to aid in heat retention and re-warming. The pre-warming of fluids, especially intravenous and irrigation fluids that will be used in and on the patient are other practical, cost-effective measures for decreasing hypothermia post procedure.

In a few instances intentional, mild intraoperative hypothermia may be induced. This is most commonly done during neurosurgical cases, especially during aneurysm clipping. Ideally, in these cases the temperature should not fall below 95.0° F (35° C). Rewarming is initiated during the closure of the patient's dura, usually with forced hot air, to return the overall body temperature to normal. These patients are typically destined for ICU follow-up to allow for close observation and monitoring without the pressure for prompt discharge. Because the surgery has affected the neural pathways, it is especially important to ensure that normothermia is maintained postoperatively.

Children are particularly prone to heat loss because of their relatively large body surface to total weight ratio. After even short procedures, their internal temperature may be markedly reduced. Maintenance of normothermia is important in children who have undergone tonsillectomy, for example, when the risk of postoperative bleeding is ever present. Remember that premature and small infants are unable to shiver and thereby increase their metabolism to cope with heat loss. They can be kept warm with the use of conduction, radiation, and convection.

Too much temperature is less common, yet no less a problem. Malignant hyperthermia (MH) is a rare yet present danger in PAC. Malignant hyperthermia is caused by a genetic disorder and magnified by stress. It can be triggered by any volatile anesthetic (eg, chloroform, ether, Halothane, Enflurane, Isoflurane, Sevoflurane, Desflurane) as well as by some muscle relaxants (eg, Suxamethonium). Malignant hyperthermia is a life-threatening disorder, however with the use of modern techniques and alert staff, mortality has been greatly reduced.

Malignant hyperthermia is an autosomal-dominant inherited disorder. The incidence of the genetic MH predisposition is 1:10,000 and the clinical incidence is about 1:30,000. This means not every patient with a genetic predisposition to MH will develop an MH crisis even when exposed to known triggering agents. It is important to keep in mind, however, that most individuals with the genetic predisposition for malignant hyperthermia have no knowledge of their risk.

Malignant hyperthermia can arise unexpectedly even with those in the peak of physical health. One example is the story of U.S. volleyball star Judy Bellomo, who in January 1990 died during thyroid surgery as a result of the sudden and unexpected onset of malignant hyperthermia. During what was anticipated to be an uneventful procedure the sudden extreme elevation in her body temperature resulted in multiple organ failure. As is typical in such cases, neither Bellomo nor her physicians had been aware that she was at risk for MH (Greenberg, 1991).

The symptoms of MH include hyperventilation, tachycardia, increasingly high temperatures, marked metabolic acidosis, sweating, and decreased oxygen saturation. Laboratory signs include hyperkalemia, raised creatine kinase and myoglobinuria caused by damage to the cell membranes. Treatment includes immediate cooling, stopping administration of the suspected triggering agent, placing the patient on 100% oxygen, establishment of more intravenous access routes, and aggressive invasive monitoring. Further treatment includes administration of dantrolene and the correction of acid-base abnormalities. Without treatment, an episode of MH can progress to cause kidney damage, internal bleeding, massive muscle destruction, brain swelling, and death due to cardiac arrest and concurrent multiple organ failure.

Since the introduction of the pharmaceutical agent dantrolene in 1979, the number of deaths from MH has been significantly reduced. This product is classed as a direct-acting skeletal muscle relaxant and works by blocking muscle contraction (hypermetabolism). Dantrolene is effective in treating an MH crisis because it inhibits the release of calcium within the muscle cells. Unfortunately, dantrolene is expensive (up to $1,200 per treatment for a 150-pound adult, with price varying according to availability), complicated to use, has a limited shelf life, and is not carried within most hospital pharmacies (Drugbank, 2006).

A person who is at risk for MH and who faces surgery should take the initiative to make sure that an adequate, unexpired supply of the drug will be available in the operating room and that the anesthesiologist knows how to administer it. The anesthesiologist's preoperative evaluation should include a detailed medical and anesthetic history, a family history of anesthetic exposure, any unexpected deaths or muscle disorders in the family, and any occurrence of dark urine (from muscle breakdown) or high fever associated with previous anesthesia. When a family or personal susceptibility to MH is known, anesthetic choices can be carefully thought out prior to procedure and dantrolene can be given both before anesthetic induction and post procedure if warranted.

Treatment of temperature abnormalities in the PAC period must begin before the patient's arrival. Depending on the age of the patient, the operating rooms should be warmed, as should all fluids instilled to body cavities. Anesthetic agents and oxygen should be administered only through humidified warming systems. Monitoring systems must be in place and emergency equipment and medications available at all times. Patient-use warming systems (pads or air blankets) must be available in all operating rooms. Only the part of the body involved in the procedure should be exposed. Cleaning and disinfecting solutions that are applied to the patient's skin should be at body temperature. The top of the patient's head should always be covered.

Endocrine Complications

Endocrine complications in post anesthesia care fall mainly into three categories:

• Diabetic emergencies
• Acute adrenal insufficiency (adrenal or Addisonian crisis)
• Thyroid crisis (thyroid storm)

Adrenal and thyroid complications in the acute postoperative area are rare. Most common by far are endocrine problems related to diabetes.

DIABETES

The stress of surgical procedures (including prior emotional stress, the effects of general anesthesia, and the trauma of the procedure) can markedly increase plasma glucose in diabetic patients and induce diabetic ketoacidosis (DKA) in type I diabetes mellitus patients. In individuals who normally take one or two daily injections of insulin, one-third to one-half the usual morning dose can typically be given in the morning before the procedure and an IV infusion of 5% glucose in either 0.9% sodium chloride solution or water at a rate of 1L (50 g of glucose) over 6 to 8 hours should be considered for use during the procedure.

After the operation, plasma glucose and the plasma reaction for ketones must be checked. Unless a change in dosage is indicated, the preoperative dose of insulin is typically repeated in the PACU and the glucose infusion continued. Plasma glucose and ketones are monitored at 2- to 4-hour intervals, and regular insulin is given every 4 to 6 hours as needed to maintain the plasma glucose level between 100 and 250 mg/dL (5.55 and 13.88 mmol/L). This is continued until the patient can be switched to oral intake and returned to a more typical 1- or 2-dose insulin schedule (Merck, 2005).

Some physicians prefer to withhold subcutaneous insulin on the day of the operation and to add 6 to 10 U of regular insulin to 1 L of 5% glucose in 0.9% sodium chloride solution or water infused initially at 150 mL/h on the morning of the operation based on the plasma glucose level. When this method is used, it is common to continue the infusion through the initial period of recovery, with insulin adjustment based on plasma glucose levels obtained in the recovery room and at 2- to 4-hour intervals thereafter (Merck, 2005).

Insulin is not required for diabetic patients who have maintained a satisfactory plasma glucose level by diet alone or in combination with oral hypoglycemic agents before the operation. Sulfonylureas, when used, should be withheld from 2 to 4 days before the operation, and plasma glucose levels should be measured pre- and postoperatively and every 6 hours while the patient receives IV fluids.

Hyperosmolar, nonketotic coma (>1000 mg/dL glucose) is a rare cause of hyperglycemia caused by a disturbance of the thirst mechanisms that occurs most frequently in older, debilitated patients or in other groups after major trauma (usually head injury). Severe dehydration, coma, and seizures are common with this process. In acute treatment, the response to small doses of insulin (10–20 units) and intravenous rehydration is prompt.

Diabetes insipidus (DI, or emergent diabetes) is caused by the underproduction of antidiuretic hormone and is usually associated with head trauma, hypophysectomy, or a global cerebral hypoxic event. The diagnosis depends on the presence of polyuria (>300 mL/hr), hypernatremia, decreased urine osmolarity, increased plasma osmolarity, decreased urine specific gravity, hypotension, dehydration, and coma. Vasopressin tannate, 5 to 10 units subcutaneously, is considered to be a specific therapy. One-desamino 8-D arginine vasopressin (4–8 mg) (DDVAP) is usually effective by nasal insufflation or intravenous administration. The dose may have to be repeated (Merck, 2005).

Insulin-dependent diabetic children and those with endstage renal disease are very sensitive to small doses of insulin in the perioperative period. The regular insulin dose should be carefully adjusted and the blood sugar measured frequently, especially if general anesthesia is employed and the patient is not able to convey feelings.

Hyperglycemia in diet-controlled diabetics is not usually problematic because the stress response to surgery and anesthesia generally releases catecholamines that reduce sugar levels. It is, however, important to monitor blood-sugar levels in patients undergoing intracranial surgery or in other situations where diabetic patients may have been given steroids, which increase the production of glucose.

ACUTE ADRENAL INSUFFICIENCY

A significant number of patients who otherwise appear healthy in the preoperative period actually have "limited adrenocortical reserve" and are at increased risk for experiencing acute adrenocortical insufficiency when under stress. Surgery, anesthesia, and the post anesthesia time period certainly qualify as stressful. An adrenal crisis is characterized by profound asthenia (weakness), severe pain in the abdomen, lower back, or legs, peripheral vascular collapse, and renal shutdown with azotemia (the presence of nitrogenous bodies, especially urea, in increasing amounts in the blood). Body temperature may be subnormal, although severe hyperthermia due to infection can also occur.

Treatment should be started immediately when a diagnosis of adrenocortical failure has been made. If the patient is acutely ill, confirmation by an ACTH response test should be postponed until the patient has recovered. Hydrocortisone 100 mg as a water-soluble ester (usually succinate or phosphate) is injected intravenously over 30 seconds. This is followed by infusion of 5% dextrose in 0.9% sodium chloride solution containing 100 mg hydrocortisone ester given over 2 hours. Additionally, 0.9% sodium chloride is given until dehydration and hyponatremia have been corrected. Serum K may fall during rehydration, requiring careful replacement. Hydrocortisone therapy is typically given continuously to a total dosage in 24 hours of more than 300 mg. Restoration of blood pressure and general improvement may be expected within one hour after the initial dose of hydrocortisone.

Vasopressor drugs may be needed transiently until the full effect of hydrocortisone is apparent. An intravenous infusion of metaraminol bitartrate, 100 mg in 500 mL of sodium chloride injection, may be given at a rate adjusted to maintain blood pressure. In an acute Addisonian crisis, a delay in instituting corticosteroid therapy may result in the patient's death, particularly if hypoglycemia and hypotension are present. A total dose of 150 mg hydrocortisone is usually given over the second 24-hour period if the patient has improved markedly, and 75 mg is given on the third day. Long-term recovery depends on the treatment of the underlying cause of the insufficiency (eg, infection, trauma, metabolic stress) and adequate supportive hydrocortisone therapy (Merck, 2005).

THYROID STORM

Thyroid storm is a life-threatening emergency requiring prompt and specific treatment. It is rare in children. It is characterized by the abrupt onset of florid symptoms of hyperthyroidism, with some exacerbated symptoms and atypical signs. Signs and symptoms associated with thyroid storm include fever, marked weakness, and extreme restlessness, with wide emotional swings, confusion, psychosis, and even coma. Tachycardia, widened pulse pressure, tremor, abnormal eye movements, atrial fibrillation, increased sweating, hypersensitivity to heat, and palpitations, fatigue, and occasionally diarrhea may also be present.

Many symptoms of acute hyperthyroidism are similar to those of adrenergic excess or adrenal crisis. Older adults, particularly those with toxic nodular goiter, may present atypically with apathetic or masked hyperthyroidism. One of the most frustrating aspects of acute hyperthyroidism is that the patient may present with cardiovascular collapse and shock initially, bypassing clues as to what is actually occurring. Thyroid storm results from untreated or inadequately treated underlying hyperthyroidism and may be precipitated by infection, trauma, a surgical procedure, embolism, diabetic acidosis, or toxemia of pregnancy or labor.

Propranolol is often indicated in the treatment of thyroid storm. It rapidly decreases heart rate, usually within 2 to 3 hours when given orally and within minutes when given intravenously. Propranolol is also indicated for the prompt management of tachycardia found in other forms of hyperthyroidism (including thyroiditis), and especially in older patients with no history of congestive heart failure, since it ordinarily takes several weeks to get relief from the antithyroid drugs. Calcium channel blockers may be useful for controlling tachyarrhythmias in patients in whom other forms of blockers are contraindicated.

The administration of iodine should be initiated in the acute setting. One gram of sodium iodide by intravenous infusion over 24 hours is recommended. Propylthiouracil is also preferred for the treatment of thyroid storm because the typical dosage (800–1200 mg/day) partially blocks the peripheral conversion of T4 to T3. Correction of underlying dehydration and electrolyte imbalances, along with cooling in the presence of hyperthermia, should also be instituted. Once the acute thyroid crisis is over, treatment inevitably consists of reduction of the thyroid gland by iodine isotope therapy or surgery (Merck, 2005).

Medication Complications

When a complication arises in the post anesthesia care unit and no clear causative factor can be determined, think drug interaction. There are numerous drug interactions that can lead to toxicity. Drug interactions can also alter the desired therapeutic end point, or, at the very extreme, be life-threatening.

A mix of at least a dozen different medications are utilized in even an uncomplicated procedure involving anesthesia, and, with the multitude of medications and other pharmacoactive agents available both over the counter and by prescription, it is not surprising that the potential for drug interactions exists. Interactions include drug combinations that require monitoring and dosage adjustments when given together as well as drugs that have increased benefit when administered together. Significant drug-to-drug interference is usually by means of one of the following mechanisms:

• Increased difficulty of absorption
• Interference with distribution
• Problems with metabolism
• Problems with elimination

It is important to identify drug interactions that are clinically meaningful. It is also important to understand the potential loss of efficacy and/or toxicity that may occur when certain drugs are administered together. Every medication possesses both desirable and undesirable effects. When all other obvious causes of a complication fail to explain the outcome, turn to the medication administration sheet for answers. Most pharmacists and nearly all institutional pharmacies have access to computer programs that screen for drug interactions. Many of these software packages assign a level of clinical significance to the potential drug-drug interactions; others detect every possible interaction, a "benefit" that actually complicates matters because it is then difficult to know what is clinically significant.

Maternal Complications

The maternal patient represents a subtle divergence from the norm in the adult female population. Balancing the anesthesia needs for the individual patient is challenging. In maternal/newborn care, the challenge is more than doubled. Remember, a maternal patient may need anesthesia or heavy sedation at a time other than delivery! When anesthesia is given for surgical or special procedures other than birth, special monitoring of mother and child is likely to be required during the immediate post anesthesia period (Norwitz & Park, 2005).

During pregnancy, the cardiovascular system changes to accommodate the increased demands placed on it by child and mother. At term, blood volume has increased by more then 40%. Of that increase, the plasma volume change is greater than that of the red cells, resulting in an anticipated lowering of hemoglobin levels and a tendency toward the complication of dilutional anemia.

Cardiac output adjusts during the second trimester to meet the approximately 20% increase in oxygen consumption as the mother breathes for two, and exceeds a 50% increase from baseline during the time of labor. These changes are reflected in a faster heart rate and increased peripheral vascular resistance with a decrease in the diastolic blood pressure. Uterine displacement leads to a tendency for compression of the inferior vena cava as well as the aorta (especially when the mother is supine), and may result in episodes of maternal hypotension and fetal distress (Norwitz & Park, 2005.)

The increase in blood component plasma volume accompanying pregnancy results in an effective decrease in the viscosity of the maternal blood. Perhaps as a design accommodation to this, the coagulation factors I, VII, X, and XII are found to be at increased levels, especially in the final stages of term (Norwitz & Park, 2005.)

The increase in coagulation factors produces a tendency toward hypercoagulability. This creates a need for increased vigilance in the PACU to prevent and detect coagulation complications such as deep vein thrombosis and emboli.

Blood volume changes also shift the standards of awareness for the complication of hypotension. In the presence of an anticipated increase in heart rate, lowering of hemoglobin, and increase in cardiac output, the definition of hypotension for the maternal patient is a systolic pressure below 100 mm Hg, or 20% lower than pre-anesthetic level (30% in hypertensive patients). Remember that maternal patients are already disposed toward dilutional anemia. Large amounts of fluids must be used with great caution.

Respiratory changes also occur in the maternal patient. Capillary engorgement through the respiratory tract trends toward the point of edema, and increased fragility of the mucous membranes can result in severe hemorrhage from nasogastric or endotracheal tube insertion.

The changes resulting from pregnancy result in an increase of alveolar ventilation of around 70%. This increased ventilation leads toward respiratory alkalosis with a compensatory change in renal excretion of bicarbonate and correction of pH. All of this helps offset another complicating tendency associated with the process of labor and potentiated with the induction of general anesthesia: the possibility of hypercarbia and hypoxia. Oxygen saturation must therefore be closely monitored during the early stages of recovery.

In the 2001–2004 Vancouver General Study, the largest subgroup of patients experiencing PONV were those who had experienced gynecologic procedures. In maternal patients, physiologic changes associated with pregnancy potentate the difficulties associated with vomiting (Mayson, Beestra & Choi, 2005.)

The elevated progesterone levels that accompany pregnancy work to decrease overall gastric mobility and food absorption while, as term approaches, lower esophageal sphincter tension increases. Concurrently, gastric acidity and volume reach new highs due to placental gastrin secretion and uterine pressures on the gastroesophageal space. The result of these changes is a heightened danger of vomiting and aspiration .

The increased risk of aspiration is just one reason regional anesthesia is preferred for the maternal patient. The possible adverse effects of systemic agents on the child is another consideration when reviewing anesthetic options. However, complications can arise with regional anesthetic agents as well. The cardiovascular changes of pregnancy result in an engorgement of the vasculature associated with the epidural space, increasing the potential for puncturing an epidural vein. (On a related note, cardiovascular changes decrease actual epidural space, leading to a lessening of the amount of regional anesthetic needed for effect as compared to nonpregnant patients) (Faure, 2006).

The presence of heightened levels of local anesthetic agents (Procaine-Novocaine, Chloroprocaine-Nesacaine, Tetracaine-Pontocaine, Lidocaine-Xylocaine, Bupivacaine-Marcaine) in the blood can result in central nervous system effects ranging from drowsiness and slurred speech to feeling drunk, ringing in the ears, seizures, and coma. Cardiovascular effects such as irregular heart rhythm, A-V block, ventricular fibrillation, and cardiac collapse may also occur (Faure, 2006.)

CONCLUSION

Complications in the post anesthesia care period are common. Most problems are easily recognized, and prompt intervention can avert serious consequences. A formal assessment tool enables the nurse to take charge of a situation instead of allowing circumstances to dictate procedures. The immediate postoperative period in the post anesthesia care unit is the beginning of periodic evaluation and assessment that continues for 24 hours.

The purpose of this time-increment assessment is to identify problems such as sore throat, hoarseness, nerve paresthesias, explicit recall, postdural puncture headaches, continued PONV, and inflammation over sites of invasive monitors. Respiratory problems requiring re-intubation, cardiovascular instability, acute renal failure, acute pulmonary edema, and altered mental status are postoperative problems that require careful attention to determine what may be contributing to the problems.

For the staff, the use of anesthesia is an everyday occurrence; for the patient who has undergone anesthesia, it is unusual. The postoperative follow-up provides the opportunity for patient education, reassurance, treatment of any adverse events, and the chance to ensure a positive experience for the patient in relation to anesthetic care. The most important measure to prevent the development of complications is good communication among the anesthesiologist, surgeon, consultants, and nursing staff.

Posted March 17, 2006

Expires September 1, 2008

Copyright © 2002, 2006 Wild Iris Medical Education. All rights reserved.