Diabetes mellitus and glucocorticoid therapy

Women with diabetes mellitus and women taking oral steroids are common in gynecologic practice. The most common surgical risks for patients with diabetes are cardiovascular problems and wound disruption. The risk of postoperative infection is increased, the culprit usually being gram-negative organisms. In order for the surgeon to reduce these complications, one must have tighter control of blood glucose levels. One must use caution in the rapid correction of high blood sugar levels because this may lead to significant hypokalemia and risk of arrhythmias.

Elective surgery is postponed in women whose blood glucose level is higher than 200 mg/dL to allow for better control of diabetes. Preoperatively, patients with diabetes should be evaluated for electrolytes and acid-base deficits.

Women who are glucocorticoid-deficient or who are taking steroids for other inflammatory conditions, when unstressed, usually have no perioperative problems. However, the additional stress of surgery can elicit acute adrenal crisis (addisonian crisis) with hyperglycemia and insulin resistance. This can occur even with minor stresses such as upper respiratory infections. Blood glucose measurements should be taken during surgery for close monitoring of the patient. Perioperatively, the patient is treated for hypovolemia, hyperkalemia, and hyponatremia as necessary.

Adrenal responses of healthy patients during the perioperative period reveal 5 general tendencies. The first is that acute adrenal insufficiency rarely occurs but can be life-threatening. The second is that women taking steroids long-term, on occasion, have become hypotensive perioperatively. This event is so rare that it is difficult to implicate glucocorticoid or mineralocorticoid deficiency as the cause. The third is that few patients who have suppressed adrenal function have cardiovascular problems if they do not receive supplemental steroids perioperatively. The fourth is that perioperative stress relates to the degree of trauma and the depth of anesthesia. Deep general or regional anesthesia causes the normal intraoperative glucocorticoid surge to be postponed to the postoperative period. The final tendency is that minimal risk is associated with giving these patients high-dose steroid coverage perioperatively.

Two questions must be answered. Which patients definitely need supplementation? If in doubt, how can a patient's need for supplementation with glucocorticoids be determined? Because the risk is low, providing supplementation for any patient who has taken steroids within a year is reasonable. In patients who have used topical steroids, the normal adrenal response may be suppressed for as long as 9 months to 1 year.

Usually, laboratory data determining pituitary-adrenal adequacy are not available prior to surgery. Rather than delay surgery, assuming that any patient who has taken steroids at any time during the preceding year has suppressed pituitary-adrenal functioning and requires perioperative supplementation is reasonable.

The adrenal glands normally secrete 116-185 mg of cortisol daily. Under maximum stress, they may secrete 200-500 mg/d. Good correlation exists between severity and duration of the operation and the response of the adrenal gland. Major surgery includes procedures such as hysterectomy, and minor surgery includes procedures such as bilateral tubal fulguration. Although the amount of supplementation required is not known, a good rule of thumb is to not supplement with a dose lower than what the patient has already been receiving.

One acceptable method of replacement for major surgery is to administer the maximum amount of glucocorticoid that the body manufactures in response to a maximal stress (ie, approximately 200 mg/d of hydrocortisone phosphate/70-kg body weight intravenously). For minor surgical procedures, hydrocortisone phosphate is given intravenously at 100 mg/70-kg body weight/d. Unless infection or some other perioperative complication develops, decrease this dose by approximately 25% per day until oral intake is resumed. Then, begin usual oral maintenance dose of glucocorticoids.

Hyperthyroidism

Hyperthyroidism usually is caused by the multinodular diffuse enlargement associated with Graves disease, but it occurs in pregnancy, thyroiditis, thyroid adenoma, choriocarcinoma, or with pituitary adenomas that secrete thyroid-stimulating hormone (TSH). Complaints usually observed include weight loss, diarrhea, warm moist skin, weakness of large muscle groups, menstrual abnormalities, nervousness, jitteriness, intolerance to heat, tachycardia, cardiac arrhythmias, mitral valve prolapse, and heart failure.

When thyroid function is abnormal, the cardiovascular system usually is affected. The most concerning of these symptoms are tachycardia, irregular heart rhythm, atrial fibrillation, heart failure, and, occasionally, papillary muscle dysfunction. Diarrhea does occur and can cause dehydration, which must be corrected preoperatively.

The prudent surgeon probably should operate on a woman with clinical hyperthyroidism only in a life-or-death situation. Otherwise, she should be made euthyroid prior to any surgical procedure. Antithyroid drugs are administered long-term and are continued on the morning of surgery.

If emergency surgery becomes necessary before the euthyroid state is achieved or if hyperthyroidism gets out of control during surgery, IV administration of esmolol and/or propranolol is titrated to restore normal heart rate. Intravascular fluid volume and electrolyte balance is maintained. However, administering propranolol or esmolol may not prevent thyroid storm.

Thyroid storm

Thyroid storm is a clinical diagnosis of a life-threatening illness in a patient whose hyperthyroidism has been severely exacerbated by illness or operation. Patients experiencing thyroid storm have hyperpyrexia, tachycardia, and alterations in consciousness. The symptoms may appear similar to malignant hyperthermia, pheochromocytoma, or neuroleptic malignant syndrome. Therapy consists of administering antithyroid drugs, blocking the release of hormone with iodine, attending to hydration, and correcting the precipitating cause.

Hypothyroidism

Hypothyroidism is a common disease in women. It occurs in as many as 5% of women. It usually is subclinical, with serum thyroid hormones in the normal range and only serum TSH being elevated. Therefore, it may have little or no perioperative significance.

In women with overt hypothyroidism, however, relative lack of thyroid hormone results in slow mental functioning, slow movement, dry skin, periorbital edema, intolerance to cold, depression of the ventilatory responses to hypoxia and hypercarbia, impaired clearance of free water (with or without hyponatremia), slow gastric emptying, and bradycardia. In extreme cases, cardiomegaly, heart failure, and pericardial pleural effusions manifest as fatigue, dyspnea, and orthopnea.

A rising TSH level is the most sensitive laboratory indicator of a failing thyroid. Preoperative management of hypothyroidism consists of restoring normal thyroid status. One gives the normal dose of triiodothyronine (T₃) or thyroxine (T₄) on a long-term basis and orally the morning of surgery.

Syndrome of inappropriate secretion of antidiuretic hormone

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is secondary to dysregulation of the cells secreting antidiuretic hormone (ADH) and occurs when ADH secretion is sustained despite hyponatremia.

This metabolic abnormality is extremely rare in gynecological surgical patients. However, in some patients with cancer, it occurs 1-2% of the time. Although it is most commonly observed in women with small-cell carcinoma of the lung, it also is observed in women with gynecologic and bladder cancers. The management of this disorder may be difficult.

SIADH occurs in a state of euvolemic hyponatremia. The hyponatremia is caused by over-secretion of ADH. Because free water cannot be excreted normally, persistent ADH secretion causes water retention, hyponatremia, and progressive expansion of intracellular and extracellular fluid. This expansion of extracellular fluid stimulates natriuresis, with a resultant isotonic loss of extracellular fluid, bringing the extracellular compartment back to baseline.

Among the known causes of this syndrome are the use of some anesthetic agents, positive-pressure ventilation, surgical stress, CNS neoplasms, meningitis, brain abscesses, and intracranial hemorrhage. Some drugs also are known to cause the syndrome. These drugs include vincristine, vinblastine, cyclophosphamide, phenothiazines, vasopressin, chlorpropamide, carbamazepine, oxytocin, tricyclic antidepressants, narcotics, and monoamine oxidase inhibitors (MAOIs). Both the surgeon and anesthesiologist should not forget that stress, pain, or nausea can cause SIADH.

Symptoms include anorexia, nausea, vomiting, mild-to-moderate mental status changes or lethargy, and rapid-onset seizures and coma. Presentation includes hyponatremia (<136 mmol/L), volume expansion without edema, natriuresis, hypouricemia, normal or reduced serum creatinine level, normal thyroid and adrenal function, normal blood pressure, no postural hypotension, and no evidence of peripheral edema. The hyponatremia of SIADH occurs in the setting of plasma volume expansion, which is considered the hallmark of SIADH.

Laboratory evaluation should include serum sodium levels and urine and plasma osmolality determinations. The diagnosis of SIADH is made when hyponatremia coexists with serum hypoosmolality (<280 mOsm/kg water) and a urine osmolality of more than 100 mOsm/kg water.

Therapy includes treating the underlying disease, restricting fluids to no more than 500-800 mL/d, and minimizing free water intake. Postoperative SIADH and its concomitant hyponatremia may be treated with isotonic or hypertonic (3%) sodium chloride solution combined with a loop diuretic. Torsemide or furosemide usually is added. This method of therapy targets increasing the serum sodium by 1 mmol/L/h or less, to a maximum increase of 10-12 mmol/d.

In patients with chronic hyponatremia and minimal symptomatology, the surgeon should correct the sodium more slowly, at approximately 0.5 mmol/h, to avoid central pontine myelinolysis (a demyelinating lesion of the pons, with destruction of myelin sheaths but sparing of the axis cylinders and nerve cells), which can result from aggressive sodium replacement and result in permanent neurological impairment or death.

Central pontine myelinolysis is a rare entity but has been reported to be more common in young women. Arieff has described this disease in a large number of healthy young women in whom symptomatic hyponatremia developed after elective surgery and who subsequently died or suffered permanent brain damage. Women are not necessarily at any greater risk of developing postoperative hyponatremia than men, but women have a 25-fold increased risk of death or permanent neurologic damage as a result of the hyponatremia. The manifestations include flaccid quadriplegia or paraplegia, dysphagia, dysarthria, facial weakness, and coma.

It is imperative that the surgeon and anesthesia team pay attention to hyponatremia in young women. The physician should correct the sodium concentration at a rate of 0.5 mmol/L/h until the serum sodium concentration reaches 120-125 mmol/L.

Importantly however, remember that young women with acute symptomatic hyponatremia are at risk for severe neurologic sequelae, respiratory arrest, and death. These patients should be treated with hypertonic saline to raise the serum sodium concentration to 125 mmol/L at a rate of 1-2 mmol/L/h. At this serum sodium level, the patient should be asymptomatic and the serum sodium then can be returned to normal gradually over several days, along with water restriction.

Gastrointestinal

Assessing the patient’s nutritional status and symptoms related to bowel function preoperatively is important. GI symptoms require evaluation because of their relationship to the pelvis, either by direct extension of pelvic disease or by extension of a generalized process. If these symptoms are chronic, one must perform a radiographic evaluation.

Patients with nausea, vomiting, and diarrhea require an electrolyte assessment. Patients with a depleted intravascular volume need more aggressive preoperative fluid administration. Attention to fluid administration is important before surgery because dehydration can lead to hypotension and tachycardia at the time of anesthesia induction. Bowel preparation prior to surgery is a common preoperative routine. Emptying the bowel enhances surgical exposure, reduces the chances of bowel injury and contamination, and hastens bowel recovery in the postoperative period.

Urinary

Benign patients who are undergoing gynecological surgery usually do not present with symptoms referable to the bladder and kidneys. Symptoms that do occur are commonly due to pressure on the uterus or obstruction of function (usually ureter). A routine urinalysis is indicated in symptomatic patients.

A baseline IVP rarely is necessary for routine gynecologic procedures. An IVP may be useful in conditions such as ovarian remnant disease, intraligamentous myomas, and severe endometriosis, in which the IVP may provide information about the anatomy of the urinary tract, the presence of anatomic distortion, the presence of anomalies of the tract, or the possibility of long-term urinary tract diseases.

Patients under general anesthesia have a decrease in renal blood flow and a similar reduction in glomerular filtration rate. Thus, anesthesia personnel notice decreased urine output during surgery.

The authors recommend routine cystoscopy to note patency of the ureters bilaterally after all major gynecologic cases.

Psychologic considerations

Surgical procedures on the female genital tract stimulate all kinds of feelings regarding femininity. Although women are concerned about a successful outcome, they also express worries about physical rehabilitation, cosmetic results, impairment in sexual functioning, and a general return to well-being. The surgeon must address these issues in a realistic and positive way. The patient should be allowed an open candid discussion with her surgeon to allow her to have the most comprehensive understanding of the proposed procedure and postoperative course possible.

Antimicrobial prophylaxis

A wound infection develops as a result of a complex interaction between the bacteria inoculated into the wound during surgery and the local and systemic resistance of the host to infection. The size of the bacterial inoculum is correlated directly with the risk of a postoperative wound infection. Factors such as prolonged preoperative hospital stay and the excessive use of antibiotics increase the risk of colonization with hospital-acquired pathogens. Alterations in the resistance of the host to infection may occur systemically or locally (ie, within the wound).

Nutritional support and control of distant infection reduce the risk of wound infection. Achievement of optimal local resistance to infection is predominantly a surgical task. Various factors, such as the presence of blood, foreign bodies, ischemia, or necrotic tissue at the operative site, may impair local host defenses and increase the risk of infection. Meticulous surgical technique helps avoid many of these contributing factors. The primary benefit of antibiotics is a reduction of the inoculum of viable bacteria in the wound.

Principles of antibiotic administration

Timing: Adequate concentrations of the drug must be present in the tissues at the onset and throughout the procedure. The latter problem is particularly significant when antibiotics with a short serum half-life are used, the operative procedure is prolonged, or both.

Route of administration: IV administration of antibiotics is the optimal method to ensure adequate levels are present in tissues during most operative procedures. The exception to this principle is in bowel preparation. Preoperative oral administration of antibiotics is effective in preventing wound infections. Antibiotics administered orally prevent infection by reducing the high colonic bacterial inoculum rather than by achieving high concentrations in the wound.

Duration: A single dose of antibiotics immediately prior to surgery is sufficient for most procedures. If the procedure is going to last longer than 3 hours, consideration should be given to repeating the dose

Choice of antibiotic regimen: The regimen chosen depends on the pathogens usually associated with wound infection in a given operation, the serum half-life of the antibiotic, the antimicrobial susceptibility patterns in the local hospital, and the cost of the medication. Postoperative wound sepsis is the most common nosocomial infection in patients undergoing surgery. Wound sepsis is an important cause of illness resulting in a prolonged hospital stay, an increase in the cost of medical care, and an inconvenience to patients and their families. The most important principle is that the antibiotic selected should be effective against the pathogens most frequently responsible for wound infection after the particular operation. The recommended regimen for women undergoing vaginal hysterectomy, abdominal hysterectomy, or radical hysterectomy is a single IV dose of cefazolin (1 g) or cefotetan (1 g) at induction of anesthesia. Indications for antibiotic prophylaxis include the following:

• Vaginal hysterectomy

   

• Abdominal hysterectomy

   

• Radical hysterectomy

   

• Urogynecologic and reconstructive pelvic surgery

   

• Dilatation and evacuation

   

• Low-risk of infection but significant consequences if infection occurs

   

• Clean-contaminated procedures

   

• Select clean procedures.

Antibiotics administered intravenously immediately before surgery ensure adequate levels in tissues throughout the surgical procedure. Therapy should last less than 24 hours and usually should consist of a single dose. The antibiotic regimen is chosen based on expected pathogens at the surgical site and local susceptibility patterns of these microorganisms. Appropriate use of antibiotics reduces wound infection rates and decreases morbidity and cost.

DEEP VEIN THROMBOSIS/PULMONARY EMBOLISM PROPHYLAXIS; OTHER DRUG CONSIDERATIONS

In the United States, venous thromboembolism remains a leading cause of death and morbidity among hospitalized patients. Overall, approximately 60,000 deaths per year are attributed to venous thromboembolism. Most patients who die from pulmonary embolism do so within 30 minutes of the event, reinforcing the need for rapid and accurate diagnosis. The prevalence of venous thromboembolism after surgery varies and depends on multiple risk factors. Most embolisms occur within 7 days postoperatively in gynecologic surgical patients; however, patients continue to be at risk for the first 3 weeks after discharge.

The rate of postoperative venous thromboembolism ranges from 7-29% in general gynecologic surgery. The rate can be as high as 45% in patients with malignant disease. Pulmonary embolism occurs in 0.1-5% of patients depending on the level of risk. Unfortunately, pulmonary embolism occurs without clinical evidence of deep vein thrombosis (DVT) in 50-80% of patients and is fatal in approximately 10-20%. Preoperative patients should be classified according to levels of risk of thrombosis to determine the benefits and risks of pharmacologic and physical methods of preventing venous thromboembolism.

Classification of risk levels for deep venous thromboembolism among gynecologic surgery patients

• Low risk (<3% risk) - Younger than 40 years and surgery lasting less than 30 minutes

   

• Moderate risk (10-40% risk) - Older than 40 years and surgery of any duration; no other clinical risk factors

   

• High risk (40-70% risk [1-5% risk of pulmonary embolism]) - Older than 40 years plus risk factors, as follows:

   

  • Prior DVT or pulmonary embolism

     

  • Varicose veins

     

  • Infection

     

  • Malignancy

     

  • Estrogen therapy

     

  • Obesity

     

  • Prolonged surgery

     

  • Deficiencies of protein C, protein S, or antithrombin III (AT-III)

     

  • Factor V Leiden mutation

     

  • Prothrombin gene mutation G20210A

Effects of oral contraceptives on prevention of deep vein thrombosis

No studies confirm the clinical benefit of stopping oral contraceptives preoperatively. The hypercoagulable changes induced by oral contraceptives do not return to normal levels for 4-6 weeks after discontinuation of therapy. The risk of postoperative thromboembolism has been reported to be 0.96% for those who use oral contraceptives and 0.5% for those who do not. The risk of stopping oral contraceptives 4-6 weeks before major surgery must be balanced against the risks of pregnancy.

No randomized clinical trials have evaluated the discontinuation of hormone replacement therapy (HRT) before major gynecologic surgery to prevent DVT or pulmonary embolism. Three studies have been quoted by the American College of Obstetricians and Gynecologists. These studies are retrospective case-control studies evaluating the risk of hospital admission for DVT in patients receiving HRT.

Current users of HRT in these studies had an increased risk of venous thromboembolism (odds ratio 2.1-3.6) when compared with matched HRT nonusers. Past use did not affect this risk. However, the absolute risk for both users and nonusers of HRT was noted to be low.

Until randomized clinical trials have evaluated the benefit of stopping HRT, one will have to continue to balance the extremely low risk of DVT against the multiple positive benefits of HRT.

Risk screening for deep vein thrombosis prevention

Because of its high prevalence in whites, patients with a history of DVT may be tested for the factor V Leiden mutation. Patients with a strong family history of thrombosis whose test findings are negative for the factor V Leiden mutation may benefit from testing for the prothrombin gene mutation G20210A, MTHFR gene, and deficiencies in the natural inhibitors, including protein C, protein S, and AT-III.

Patients with a history of thrombosis, recurrent fetal loss, early or severe preeclampsia, severe unexplained intrauterine growth restriction, or unexplained thrombocytopenia may be tested for antiphospholipid antibodies. Fasting plasma homocystine levels may be assessed, especially in women of childbearing age who have had venous or arterial thrombosis, because elevated levels can be treated with vitamins (folic acid, vitamin B-2, vitamin B-6). Perioperative prophylactic heparin has been shown to decrease the incidence of DVT from approximately 30% to less than 10%, without any significant complications.

General recommendations for prophylaxis against deep vein thrombosis

Prophylaxis for low-risk patients: Encourage patients to move their legs frequently while in bed. Provide a footboard for those patients not likely to achieve early ambulation (ie, evening of surgery or next morning). Elastic stockings may be used to compress the legs and divert blood from superficial to deep venous veins, improving flow and reducing stasis.

Prophylaxis for moderate-risk patients: Recommendations are the same as for low-risk patients, plus heparin 5000 U every 8 hours by subcutaneous injection. Initial dose must be given at least 2 hours prior to surgery. Low molecular weight heparin (LMWH) (dalteparin 2500 U qd or enoxaparin 40 mg qd) and/or sequential pneumatic compression stockings are employed prior to anesthetic induction. Compression is initiated prior to muscular relaxation.

Prophylaxis for high-risk patients: Recommendations are the same as for low-risk patients, plus heparin 5000 U subcutaneously every 8 hours, continued until the patient is ambulatory (ie, 1-2 d prior to discharge). LMWH (dalteparin 5000 U qd or enoxaparin 40 mg qd beginning the night before surgery) and/or sequential pneumatic compression stockings are placed prior to anesthetic induction. Compression is initiated prior to muscular relaxation.

Findings on the coagulation profile should be normal before initiating the prophylactic heparin regimens above. Platelet count and aPTT should be monitored every 2-3 days while the patient is on heparin treatment, because thrombocytopenia and full anticoagulation can be observed in patients undergoing these treatments.

If LMWH is used in low doses as a once-a-day regimen, at least 12 hours should elapse after administration and before offering central neural blockade. No regional anesthesia should be employed within 12 hours of an injection of LMWH, and LMWH should be withheld for at least 2 hours after removal of an epidural catheter. The use of graduated compression stockings reduces stasis and is the simplest of the prophylactic approaches. Graduated compression stockings offer the advantages of being inexpensive, easy to use, and free of adverse effects if properly fitted. Graduated compression stockings reduce the prevalence of DVT (especially calf) in low-risk patients. Patients with malignancies and other high-risk conditions have not been evaluated in sufficient numbers to reach conclusions about the use of graduated compression stockings in these settings.

If used at induction of anesthesia and continued until patients are fully ambulatory, pneumatic compression appears to be effective in reducing DVT in medium-risk and high-risk patients. Pneumatic compression may be useful in reducing leg DVT in high-risk patients with malignant disease. The efficacy of pneumatic compression in preventing pulmonary embolism is unknown.

Low-dose unfractionated heparin has been shown to be effective as prophylaxis for DVT and pulmonary embolism in moderate-risk patients without underlying malignancy or other clinical risk factors. Low-dose heparin has been shown to decrease DVT by nearly 70% and pulmonary embolism by 40-50%. Unfractionated heparin, 5000 U administered 2 hours preoperatively and every 8 hours postoperatively, is effective prophylaxis for DVT in patients undergoing gynecologic surgery. LMWH has been used in numerous trials for prophylaxis in abdominal surgery, with at least the same efficacy as unfractionated heparin in preventing DVT.

Some data suggest that patients have a lower bleeding risk with LMWH compared to unfractionated heparin. Once-daily administration and a lower rate of heparin-induced thrombocytopenia are additional advantages of LMWH over unfractionated heparin. In the United States, dalteparin and enoxaparin are considerably more expensive alternatives to standard heparin and have not been shown to be significantly more efficacious or associated with fewer bleeding risks when compared to low-dose unfractionated heparin in moderate-risk patients.

Alternatives for thrombosis prophylaxis for moderate-risk patients undergoing gynecologic surgery include (1) pneumatic compression placed intraoperatively and continued until the patient is fully ambulatory, (2) unfractionated heparin (5000 U) administered 2 hours before surgery and continued postoperatively every 8 hours until discharge, and (3) LMWH (dalteparin 2500 U or enoxaparin 40 mg) administered 12 hours before surgery and once per day postoperatively until discharge.

Alternatives for prophylaxis for high-risk patients undergoing gynecologic surgery, especially for malignancy, include (1) pneumatic compression placed intraoperatively and continued until the patient is fully ambulatory, (2) unfractionated heparin (5000 U) administered 8 hours before surgery and continued postoperatively until discharge, (3) dalteparin (5000 U) administered 12 hours before surgery and then once per day thereafter, and (4) enoxaparin (40 mg) administered 12 hours before surgery and then once per day thereafter.

Uncontrollable bleeding is an unwanted adverse effect of unfractionated heparin. However, the effects of heparin can be rapidly reversed by an infusion of protamine sulfate. Protamine is administered intravenously over 10 minutes at a dose of 1 mg/100 U circulating heparin. The maximum dose is 250 mg. If heparin is given as an IV infusion, the protamine dose should be calculated to neutralize half of the hourly heparin dose

LMWH preparations contain smaller fractions of heterogenous native heparin. LMWH inactivates factor Xa to a greater extent than it does thrombin. Therefore, the aPTT and thrombin time are affected minimally by typical therapeutic doses. The long half-life of LMWH permits twice-daily dosing. Because LMWH has a more predictable anticoagulation response and is associated with a lower incidence of bleeding compared to standard heparin, laboratory monitoring is not required.

Other considerations

Patients on medications for acute and chronic medical conditions

An increasing number of patients present to their surgeon’s office taking medications used to treat multiple diseases. The average hospitalized patient receives more than 10 drugs. Many of these drugs have adverse effects that might make surgery more risky or patient management more difficult. One should always obtain a drug history, including vitamins, herbs, and alternative medicines.

In general, unnecessary drugs should be discontinued for at least 3, preferably 5, half-lives of the drugs. For essential or beneficial drugs, the optimal dose should be determined and maximized.

Monoamine oxidase inhibitors

Patients presenting for surgery may be under treatment for a variety of affective disorders, including depression. One class of antidepressant medications, MAOIs, presents the surgeon with a treatment dilemma. Should MAOIs be routinely discontinued preoperatively? If so, how long before surgery should withdrawal of the medication be undertaken?

Monoamine oxidase (MAO) is the principal intraneuronal enzyme responsible for deamination of amine neurotransmitters, such as dopamine, norepinephrine, epinephrine, and serotonin. Therapy with MAOIs causes accumulation of neurotransmitters in presynaptic terminals in neuronal tissue. They also cause accumulation of a false neurotransmitter, octopamine, in presynaptic sympathetic nerve terminals, which is a far less potent vasoconstrictor than other neurotransmitters released from nerve terminals. Thus, patients on MAOIs may exhibit exaggerated orthostatic hypotension in response to stimuli that normally only cause a small decline in blood pressure.

The inhibition of MAO often is irreversible, and the effects of MAOIs depend on regeneration of this enzyme. Enzyme regeneration can take as long as 2 weeks after discontinuance of MAOIs.

Traditionally, recommendations have been to discontinue MAOIs 2-3 weeks prior to elective surgery, although no controlled studies support this recommendation. However, currently, several clinical reports indicate that continuing MAOIs in the perioperative period is safe, but the reports include only small numbers of patients. Current recommendations by many authors suggest that MAOIs should not be discontinued prior to surgery.

General anesthesia may be preferable to regional techniques if hypotension cannot be controlled. Meperidine and other narcotics should be avoided in patients who are taking MAOIs because case reports document the occurrence of hyperpyrexic coma following administration of most narcotics

Anticoagulants

The use of anticoagulants poses additional problems in the management of routine and complicated gynecological cases. A frequent concern is the risk of perioperative or postoperative hemorrhage. Perioperative management of patients being treated with anticoagulants requires weighing the risks of increased surgical bleeding from residual anticoagulation versus potential thrombotic or embolic events from stopping the anticoagulant. An effective and safe plan for preoperative weaning from anticoagulant therapy and confirming the return of normal anticoagulation function must be determined prior to surgery. This decision is based, at least in part, on the type of operation and the indications for anticoagulation.

Heparin

Heparin is effective in reducing the risk of thrombosis; however, full anticoagulation can lead to increased bleeding and the risk for hematoma. The incidence of heparin-induced thrombocytopenia varies between 5% and 28% of patients receiving heparin. This occurs after 4-5 days of heparin administration. The diagnosis of heparin-induced thrombocytopenia is based on a platelet count of less than 50% of the pretreatment level or a drop of the platelet count to less than 100,000/mm³.

The aPTT is a classic measurement used to monitor heparin therapy. The aPTT measures the time for clot formation when plasma is added to a thromboplastin activator. This is based on the in vitro activity of the intrinsic coagulation factors VIII, IX, XI, and XIII, but the aPTT also will be abnormal when severe deficiencies of fibrinogen are present.

Warfarin

Warfarin is rapidly absorbed from the gastrointestinal tract, with peak plasma concentrations being reached 1-4 hours after ingestion. The anticoagulant effect of warfarin becomes visible only after a significant decrease occurs in the concentration of normal vitamin K-dependent clotting factors. After terminating therapy, the anticoagulating effect of warfarin disappears progressively over a matter of days but is rapidly reversible by the administration of vitamin K (long-term effect), fresh frozen plasma, or prothrombin complex concentrate (short-term effect).

Presently, PT is the most widely used test to measure a patient's response to warfarin therapy. To standardize the reporting of PT results, in 1983, the International Committee on Thrombosis and Hemostasis and the International Committee for Standardization in Hematology recommended the use of the International Normalized Ratio (INR), which is matched against the international reference preparation (a batch of thromboplastin reagent that is set aside as the World Health Organization standard). All commercially prepared thromboplastin reagents are calibrated against the international reference preparation.

The PT, which normally is 11-14 seconds, measures the activity of fibrinogen; prothrombin; and factors V, VII, and X. Prolongation of the PT of greater than 3-4 seconds from the control is considered significant. This usually corresponds to an INR of greater than 1.5. Only 20-30% of normal factor activity is required for normal coagulation, thus, prolongation of the INR usually reflects liver disease unless vitamin K deficiency is present. Failure of the INR to correct following administration of vitamin K implies severe liver disease.

To minimize the risk of developing perioperative thromboembolism and surgical bleeding, the following recommendations are for the perioperative management of patients taking warfarin. If the INR is between 2 and 3, four scheduled doses of warfarin should be withheld to allow the INR to fall to 1.5 or less before surgery. Warfarin should be withheld for a longer period if the INR normally is maintained above 3 or if achieving a lower INR (<1.3) is necessary for the surgical procedure. The INR should be measured the day before surgery. If the INR is greater than 1.8, administering a small dose of vitamin K (1-2 mg) subcutaneously usually reduces the INR to less than 1.5 by the next morning. Mechanical methods of preoperative and postoperative prophylaxis against thromboembolism should be instituted for the period during which the INR is less than 2.

Patients undergoing emergency surgery who are receiving warfarin or those undergoing emergency surgery who are at high risk for venous thromboembolism may benefit by a rapid reversal of warfarin with the institution of heparin. Reversal of warfarin therapy may be accomplished rapidly with administration of a large dose (10 mg) of parenteral vitamin K (effective in 3-6 h) or immediately with fresh frozen plasma.

Aspirin

Aspirin and other NSAIDs inhibit platelet cyclooxygenase and prevent the synthesis of thromboxane A2. Thromboxane A2 is not only a potent vasoconstrictor, but it also facilitates platelet aggregation and release of factors that amplify coagulation.

Platelet count and bleeding times are the most frequently used tests that reflect platelet function. Typically, platelet counts less than 100,000/mm³ prolong bleeding time. Bleeding time has been suggested as the most reliable predictor of normal bleeding in patients receiving antiplatelet drugs; however, the bleeding time for patients taking aspirin has not been proven to be a reliable indicator of platelet function nor predictor of surgical blood loss. Bleeding time quickly normalizes after aspirin ingestion, but it may take up to a week before platelet function completely normalizes.

Other NSAIDs, such as naproxen and ibuprofen, produce a shorter-term defect that normalizes within 3 days after discontinuation. Thus, platelet function is considered to be decreased for 1 week in patients taking aspirin and for 3 days in patients taking other NSAIDs.

In patients in whom heparinization is necessary perioperatively, a 2-fold increased rate of postoperative bleeding exists. In spite of this increased risk, the reduction in serious morbidity from venous thromboembolism may warrant treatment.

Elective surgery generally should be avoided in the first month after an acute episode of venous thromboembolism. If this is not possible, IV heparin should be given both before and after the procedure while the patient is not anticoagulated with warfarin and the INR is below 2. The aPTT should be kept in the therapeutic range. One should stop IV heparin 6 hours before surgery. This provides sufficient time for heparin to be cleared, to minimize the risk of bleeding. Heparin therapy should not be restarted until 12 hours after most major surgeries and should be delayed even longer if any evidence of active bleeding is present or if the risk of any bleeding is life threatening. The first aPTT is checked approximately 12 hours after restarting therapy, to allow time for a stable anticoagulant response.

Concerns with regional anesthesia and anticoagulation

To lessen the possibility of complications for patients on long-term oral anticoagulation medications, the anticoagulant therapy must be stopped and the INR must be measured prior to initiation of neuraxial block. Soon after discontinuation of warfarin therapy, factor VII levels rapidly normalize (within 24 h), but normalization of coagulation and INR does not occur until factors II and X improve. An INR of 1.5 or less is considered safe enough to perform major regional blocks.

Summary of anticoagulant concerns

Testing of PT and aPTT should be performed prior to surgery on patients on long-term anticoagulation therapy in order to ensure that the anticoagulant effect of warfarin and heparin, respectively, is at a safe level for surgery. Measuring bleeding time is not necessary before surgery in patients taking aspirin, unless they give a history of bleeding problems. Patients on long-term anticoagulation therapy with warfarin may stop warfarin several days before surgery and restart as soon as possible after surgery without excess risk of postoperative venous thromboembolism. Patients receiving anticoagulation for less than 1 month after an acute thromboembolic event should be brought in the day before surgery for heparinization and warfarin reversal and should receive re-anticoagulation with heparin after surgery because of they have a high risk of developing postoperative venous thromboembolism.

PO STOPERATIVE CARE

The care of the gynecologic surgical patient requires an accurate understanding of the pathophysiologic changes that occur perioperatively. During this period, the body attempts to maintain systemic homeostasis despite multiple iatrogenically induced alterations. Given the proper environment and appropriate interventions, the body eventually should correct for these derangements.

The surgeon's goal during the postoperative period is 2-fold. The first goal is to provide appropriate support that allows for the maintenance of homeostasis and the prevention of potential complications. The second goal is to recognize unfavorable trends in the course of recovery and respond expeditiously to prevent further compromise. With diligent care, the surgical patient eventually should return to her preoperative level of function.

SUPPORTIVE POSTOPERATIVE CARE

Vital signs

Much information can be obtained by close monitoring of vital signs, including blood pressure, pulse, and respiratory rate. More importantly, the trend and changes of these measurements more accurately reflect the patient's ongoing condition. In the immediate postoperative period, the recovery room staff usually obtains frequent measurements. Selected parameters are more important during various stages of the recovery period. Initially, respiratory rate and blood pressure are of greater significance during recovery from anesthesia because these factors reflect hemodynamic stability and the level of anesthetic reversal. Later, after adequate analgesia and pulmonary function has been obtained, pulse rate correlates better with intravascular volume status. After discharge from the recovery room, vitals should be monitored every 4 hours until stable and then every 8 hours depending on the patient's progress.

Postoperative activity

Early ambulation is extremely important after surgery. In addition to improving diaphragmatic excursion with its subsequent decrease in pulmonary atelectasis, early ambulation also prevents the development of DVT.

To further decrease the incidence of pulmonary ventilating defects and improve mobilization of mucous secretions, patients are encouraged to cough and breathe deeply. To assist with this respiratory exercise, an incentive spirometer is used at least every hour while the patient is awake.

Nutrition

A low-residue diet 6 hours after major gynecologic surgery for benign indications is not associated with increased postoperative gastrointestinal complaints, including ileus. Healthy recovery from surgery may include transient loss of appetite and mild nausea. This usually is secondary to anesthetic agents and other perioperative medications. Symptoms can be treated easily with antiemetics such as promethazine at 25 mg intramuscularly every 4 hours as needed. After a major transperitoneal procedure, adynamic ileus may be responsible for continued nausea, abdominal distention, and absence of flatus. The return of small bowel function occurs within 6 hours of surgery and is highlighted by the return of bowel sounds.

Gastric emptying and pyloric sphincter function require 2-3 days and coincide with decreased nausea and decreased nasogastric (NG) tube output. Finally, the return of colonic peristalsis that occurs in 3-5 days is signaled by the passage of flatus.

Management of patients with gastrointestinal dysmotility

The patient should take nothing by mouth for 48 hours or until nausea resolves. An NG tube is inserted if the patient is severely symptomatic with continued vomiting and distention. When NG output decreases and nausea resolves, the tube can be removed. The patient may then advance to a clear liquid diet. Progression to a regular diet should be withheld until full return of gastrointestinal motility. If prolonged dysfunction is noted or anticipated, early nutritional support is recommended (eg, enteral feeding either via a nasal feeding tube, surgically placed feeding jejunostomy). Hyperalimentation via a central venous catheter is used if the enteral route cannot be used to maintain adequate nitrogen balance.

Fluid and electrolyte management

Postoperative fluid management is dependent on current deficits, maintenance requirements, and abnormal losses. The status of the patient's current conditions should be determined first. The patient's fluid status or deficits can be determined by preoperative vomiting, bowel distention, oral intake, intraoperative hemorrhage, extravascular fluid accumulation (third space), and previous fluid replacement.

A physical examination, vital signs, recent weight change, and a record of fluid balance also can help determine the status of the intravascular volume and total body water. If uncertainty exists regarding the patient's actual fluid status, invasive monitoring using a Swan-Ganz catheter can be used to measure central venous pressure (CVP) or left ventricular filling pressure (ie, preload).

The daily maintenance requirement for water in the healthy individual with normal renal function is approximately 1 L. In the surgical patient with a higher insensible loss and less than optimal renal concentrating ability, a daily maintenance requirement from 35-40 mL/kg/d is necessary. Electrolyte replacement after uncomplicated surgery rarely requires more than sodium chloride and potassium supplementation, both at 1 mEq/kg/d. This requirement is met easily by giving dextrose 5% in normal saline (D5NS) with 20 mEq KCl/L at the volume predicted above for daily fluid needs.

In consideration of the volume, electrolytes, and glucose requirements, one generally begins with D5NS with 20 mEq KCl/L at 100-125 mL/h. Additional fluid requirements for low blood pressure, inadequate urine output, or decreased CVP/left ventricular filling volume can be supplemented with isotonic sodium chloride solution. Urine output is important because it is a direct reflection of tissue perfusion. The patient who voids less than 17 mL of urine per hour is, by definition, oliguric. For most patients, a urine flow of less than 30 mL per hour should demand clinical attention.

Oliguria can be prerenal, renal, or postrenal. To determine the cause of the low output, a variety of laboratory data, clinical measurements, and physical findings should be gathered to assist in the diagnosis. Heart rate, orthostatic changes, and daily weights are easily measurable and usually correlate with the intravascular volume status. More accurately, CVP or a Swan-Ganz catheter measuring pulmonary capillary wedge pressure (PCWP) can be used in diagnostically difficult situations. Laboratory data, including serum sodium, BUN-to-creatinine ratio, fractional excretion of sodium, and serum osmolality, are suggestive but often nondiagnostic in the acute situation. Physical examination noting jugular venous distention, mucous membrane turgor, pulmonary rales, S₃ heart sounds, or pitting edema adds valuable data to the clinical evaluation.

Once a working diagnosis is made, therapy should be provided. The patient's response is followed and her condition reevaluated, thus confirming the accuracy of the initial diagnosis. When corrected, potential complications, such as volume overload or acute tubular necrosis, can be avoided.

Postoperative oliguria most commonly has a prerenal etiology. Intravascular volume is decreased most commonly due to operative blood loss and third-space sequestration of extracellular fluid. Cardiogenic failure may be present. Treatment consists of an initial bolus of isotonic solution at 300-500 mL, repeated, but not to exceed 1 L. Failure to respond may require invasive monitoring with a Swan-Ganz catheter. Cardiogenic failure requires diuretics and/or inotropic agents, depending on PCWP and cardiac output (CO).

A postrenal etiology may be found with ureteral obstruction (ie, bilateral to produce anuria). Diagnosis is made with the assistance of renal ultrasound. If the ultrasound is inconclusive, ureteral catheters are diagnostic and therapeutic. A renal etiology should be suspected when prerenal and postrenal causes are excluded.

The most common pathology in the immediate postoperative period is acute tubular necrosis. More specifically, this results from (1) ischemia due to hypoperfusion or (2) nephrotoxicity secondary to aminoglycoside or radiocontrast dye use. Laboratory data should include serum sodium, BUN-to-creatinine ratio, fractional excretion of sodium, serum osmolality, and microscopic examination of the urine. In treatment, close attention must be paid to fluid balance and electrolyte abnormalities. Fluid diuresis is initiated with an IV diuretic such as furosemide. Dosages are doubled until an adequate response (ie, approximately 100 mL/h) is achieved or a maximal dose of furosemide 600 mg/d is reached. If good urinary output cannot be achieved, maintenance fluid replacement should be adjusted to include only insensible losses and ongoing losses from the previous 24 hours. If conservative management fails to maintain homeostasis, hemodialysis should be employed.

Pain control

Preemptive treatment of perioperative pain

The traditional approach to postoperative analgesia is to begin therapy when surgery is completed and pain is experienced. Preemptive analgesia is defined as "antinociceptive treatment that prevents the establishment of altered central processing, which amplifies postoperative pain." Intense noxious stimulation (surgical incision) can sensitize the CNS to subsequent input. Such stimulation may lead to changes in the dorsal horn of the spinal cord that later are perceived as postoperative pain. This may be perceived as even more "painful" than it would otherwise have been.

In addition to reducing acute perioperative pain arising from surgical wounds, preemptive analgesia also possibly may offer prophylaxis against certain pathologic chronic pain states. One routine method of preemptive pain management is to use NSAIDs such as rofecoxib (Vioxx) at 50 mg twice-daily orally the day before surgery and 50 mg orally the day of surgery. In addition, injection of the skin at the incision site with a few milliliters of 1% lidocaine or 0.25% Marcaine prior to incising adds to the analgesic effect. Anecdotally, patients require less narcotic overall for pain control and go home earlier. This effect is even greater for outpatient procedures such as tubal fulguration.

Patient-controlled analgesia

Liberal use of postoperative analgesics is essential for recovery. Adequate pain control allows for early ambulation, improved pulmonary toilet, and decreased overall stress. The most effective regimen for pain control involves small frequent dosing, such as the use of a PCA pump. This system consists of a preprogrammed infusion pump that is controlled by a hand-held button. An IV dose of premeasured narcotic is delivered when the button is depressed, providing a timely bolus of analgesia. Patients on PCA have decreased overall narcotic use and have improved pain control. The addition of an intramuscular or oral NSAID preoperatively provides added analgesia and quicker return to function than narcotics alone. With a healthy progression to recovery, patients usually can be switched to an oral narcotic within 2-4 days. For those who are difficult to wean from IV narcotics, intramuscular injection can be used, thus prolonging the half-life of the effective dose.

Patient-controlled epidural analgesia

Considerable interest has been raised in combining potent analgesic effects of drugs delivered into the epidural space with the advantages of the patient participation associated with the PCA concept. The epidural catheter is placed in standard fashion, a loading dose (opioid, local anesthetic, or both) is given, and the PCA pump is set to define the patient-activated bolus doses and lockout interval between doses. Usually a continuous background epidural infusion rate also is provided. Morphine, fentanyl, and hydromorphone all have been used with success. Drug requirements have been reported to be 4- to 5-fold less than in patients receiving IV PCA hydromorphone. Patients also may have a more rapid return of bowel function and a shorter hospital stay.

Incision care

The management of the incision is based on the normal biology of the healing process, which is conceptually divided into 3 phases.

Initial phase (inflammation): Local chemical mediators are released, causing an influx of leukocytes. Epidermal migration results in epithelialization within 24-48 hours (closure). Endothelial budding and production of granulation begin. Epithelialization and neovascularization of the skin edges occurs by approximately the fifth postoperative day.

Second phase (fibroblast proliferation): Rapid collagen deposition is noted from the fifth postoperative day and reaches its maximal volume by the 17th day. Collagen fibers are disoriented, with suboptimal interfibrillar cross-linking. Tensile strength of the incision steadily increases from the fifth day onward due to the production of this collagen lattice.

Third phase (maturation): Complex cross-linking occurs with replacement of the previous fibers with a thicker, more organized, polarized collagen. Tensile strength continues to increase with this remodeling for as long as 2 years without any additional increase in collagen content.

Incision care is based on understanding these biological principles. With the attainment of epithelial closure, the operative dressing can be removed after 24-48 hours. If wound drainage is noted upon inspection, a sterile dressing must be replaced until the drainage ceases and closure is attained. The timing of suture removal is based on 2 opposing guidelines. Staples or sutures should be left in place until adequate tensile strength is obtained by collagen deposition and maturation. On the other hand, allowing sutures to stay in place for a long period increases scar formation at the sites of skin penetration.

In healthy individuals with an abdominal incision, sutures or staples generally can be removed on the third postoperative day. This allows for maximal cosmetic benefit while providing adequate support for wound stability. The timing of the removal can be adjusted depending on the importance of each opposing factor.

Types of incisions

The surgeon may choose either a vertical or a transverse skin incision when performing gynecologic surgery. The ultimate choice hinges on factors such as presence of prior abdominal scars, desired exposure, expected and/or associated pathology, and risk for wound separation or dehiscence. To some degree, the decision also is based on the surgeon's past experience and on consumer pressures favoring a low transverse incision.

The midline vertical, transverse Maylard, and transverse Pfannenstiel incisions are the 3 most commonly employed types, while the transverse Cherney and paramedian vertical incisions are used on occasion.

In general, vertical incisions allow greater access to the pelvis, result in less blood loss, provide greater feasibility for incisional extension around the umbilicus, and allow easier examination of the upper abdomen.

Transverse incisions are preferred cosmetically, are generally less painful, have been associated with a lower risk of subsequent herniation, and provide approximately equal visualization of the pelvis. Some argue that the incidence of postoperative pulmonary complications is lower when a transverse incision is used, particularly in patients with preexisting pulmonary problems such as obstructive lung disease.

Historically, transverse incisions have been associated with fewer incidences of dehiscence and herniation. However, some recent data refute this dictum, and thus, the controversy remains.

Shock

Shock is a state of inadequate tissue perfusion and is directly proportional to blood pressure. Causes of postoperative hypotension include hypovolemia from decreased intravascular volume, decreased peripheral resistance from sepsis or neurogenic collapse, and cardiogenic failure. The clinical presentation can be very helpful in differentiating these types of shock and may direct subsequent management. Because the central problem is lack of perfusion to vital organs, oliguria and decreased mental status are objective signs of inadequate tissue perfusion. Due to its life-threatening potential, immediate therapy should be initiated before diagnostic evaluation. An IV fluid bolus should be given to those thought to have vascular collapse, and the patient should be placed in the Trendelenburg position (ie, head down and feet up).

When the patient stabilizes and if the cause of the hypotension is still in doubt, invasive monitoring may be required. A central line placed in the superior vena cava can be used to measure the intravascular volume. The CVP normally ranges from 8-12 cm water.

In patients with possible right heart failure, other cardiac dysfunction, sepsis, respiratory failure, or severe preeclampsia, CVP is inadequate to evaluate left heart filling pressure. A Swan-Ganz catheter allows for a more accurate measurement of left ventricular end-diastolic pressure (ie, left atrial pressure). PCWP, normally from 10-18 cm Hg, is a measurement of left heart filling volume, thus correlating with intravascular fluid status.

Hypovolemia

Signs and symptoms of hypovolemia include low CVP or PCWP. Treatment consists of replacement with isotonic sodium chloride solution until normal parameters are reached. Serial blood counts are taken, and a transfusion is initiated for a symptomatic drop in hematocrit. Monitor coagulation parameters if more than 4 U are transfused. Derangements in coagulation components require correction with fresh frozen plasma or platelets. Persistent blood loss requires surgical reexploration or intra-arterial embolization.

Decreased peripheral resistance

Signs and symptoms of decreased peripheral resistance include fever, rigors, leukocytosis, and hypotension with normal intravascular volume. Cardiac output (CO) is high while systemic vascular resistance (SVR) is low. Treatment consists of measurement of CO and SVR, normalization of PCWP with fluid, and initiation of vasopressors. Dopamine is started at 2 mcg/kg/min and is titrated to maintain a mean arterial pressure greater than 60 mm Hg. Eliminate the source of sepsis and maintain appropriate antibiotic coverage, initially with broad-spectrum antibiotics; narrow according to culture results.

Cardiogenic shock

Signs and symptoms consist of a high PCWP and low CO. SVR usually is either high or in the reference range. Myocardial function is obtained by dividing CO by body surface area, yielding the cardiac index (CI). Treatment consists of dobutamine starting at 2 mcg/kg/min for inotropic support initially. Maintain a CI above 3 L/min/m². Identify other treatable causes of cardiogenic dysfunction, such as arrhythmia, hypoxia, acidosis, pericardial tamponade, and massive pulmonary embolism. Continued myocardial decompensation may require an intra-arterial balloon pump and subsequent evaluation for mechanical cardiac support.

Respiratory management

Respiratory care plays an important role in the care of the postoperative patient. Anesthesia, splinting, and immobilization lead to retention of pulmonary secretions and atelectasis. Turning, ambulation, coughing, and use of an incentive spirometer are integral parts of an aggressive pulmonary toilet program. Bronchodilators may be beneficial in patients who smoke or have underlying pulmonary disease.

In the postoperative patient, acute hypoxia is likely due to a ventilation/perfusion (V/Q) mismatch. This may arise if alveoli are perfused but not ventilated, commonly observed with postoperative atelectasis. If alveoli are ventilated adequately but perfused poorly, as with pulmonary emboli or pulmonary edema, an alveolar dead space is present. Ventilation failure often is due to excessive sedation from anesthetics or narcotics. Treatment of respiratory dysfunction requires oxygen therapy when the PaO₂ falls below 60 mm Hg. Oxygen can be administered by nasal cannula or face mask. A maximum of 4 L can be given by cannula, corresponding to a fraction of inspired oxygen (FIO₂) of 35%. A non-rebreathing face mask is superior to nasal cannula because it can deliver up to 40-60% FIO₂.

Patients who cannot maintain a PO₂ of 60 mm Hg, a PCO₂ less than 50 mm Hg, or a respiratory rate of less than 45 require intubation and mechanical support. FIO₂ should be kept below 50% to decrease the risk of oxygen toxicity from the production of free oxygen radicals. Use of positive end-expiratory pressure (PEEP) can support oxygenation by reducing functional reserve capacity (FRC), thus reducing the requirements of FIO₂. PEEP should not be administered above 10 mm water without close hemodynamic monitoring because of the risk of barotrauma and pneumothorax.

Postoperative fever

Temperature elevation higher than 100°F (38°C) in the surgical patient should alert the surgeon of potential complications. Evaluation and subsequent therapy are dependent on how soon after surgery the fever develops. Postoperative fever may be broken down into the following 3 categories.

First 24-48 hours

Minor: Pyrogens are released from hematogenous seeding of leukocytes or bacteria (eg, manipulation of a pelvic abscess). Pulmonary atelectasis develops from hypoventilation secondary to mechanical splinting from incisional pain. Treatment is symptomatic and consists of antipyretics, an incentive spirometer, and increased ambulation.

Major: Necrotizing wound infection is uncommon. Signs may include crepitus, pain, and edematous discoloration. Treatment consists of aggressive intraoperative debridement and drainage and broad-spectrum antibiotics.

Postoperative days 2-4

UTI, an infected IV line, or pneumonia may be present. The workup should include a thorough physical examination, including IV sites, urinalysis, chest x-ray, and sputum culture. Treatment for UTI or pneumonia consists of appropriate broad-spectrum antibiotics. For infected IV lines, remove the line, apply local heat, and elevate.

Fifth postoperative day and beyond

The differential expands to wound infections, for which the skin must be opened and drained. Broad-spectrum antibiotics are administered and adjusted when culture results are available. Local wound care with adequate drainage is necessary. If no evidence of a wound infection is present, a CT scan is obtained to examine for intra-abdominal or intrapelvic abscess. Abdominal abscess requires surgical or percutaneous drainage. IV antibiotics also may be required.

Postoperative complications

Electrolyte and acid-base abnormalities may be present. Hypernatremia is a relative deficit of water volume compared to sodium concentration. The major causes of hypernatremia include (1) decreased water intake compared to solute intake (ie, concentrated enteral feeding or hypertonic parenteral fluid administration), (2) excessive water loss compared to sodium loss (eg, diabetes insipidus, glycosuria, diuretic use), (3) intrinsic renal disease with decrease renal tubule response to ADH, and (4) endocrine disturbance (eg, Cushing syndrome, hyperaldosteronism).

Symptoms include confusion, seizures, stupor, and coma. Laboratory tests should include urine electrolyte evaluation, which may indicate the cause of increased sodium concentration. Treatment consists of correction of the primary cause and slow replacement with dextrose 5% in water (D5W) or hypotonic fluid.

Hyponatremia is more common than hypernatremia. The major cause of hyponatremia is an actual decrease in extracellular sodium (ie, depletional hyponatremia). Signs and symptoms (ie, clear evidence of decreased extracellular fluid volume) include low plasma volume, poor tissue turgor, and hypotension. Diagnosis is made with urine sodium measurements; findings are normal.

An increase in extracellular water (ie, a dilutional hyponatremia) is most common. Symptoms of edema include significant third-space filling of extracellular fluid, such as in the gastrointestinal tract. Patients with a low serum sodium concentration, on occasion, may have SIADH. SIADH may accompany intracranial lesions, pulmonary disease, malignant disease, and administration of drugs such as diuretics and vinca alkaloids. The treatment is to restrict the patient's intake of water to approximately 1 L/d. However, if the serum sodium falls below 110 mEq/L, the risk of seizures is significant. If symptomatic, patients require careful administration of hypertonic solutions. However, fluid overload and congestive heart failure can result from aggressive hypertonic infusions.

Potassium

In assessing alterations of potassium balance in the postoperative patient, the surgeon must have knowledge of the internal mechanisms for potassium distribution related to serum pH. Patients who are acidotic have an increase in serum concentration of hydrogen ions. This results in an increased movement of these ions into cells. To maintain neutrality, potassium ions are pumped out of cells, thus increasing the potassium concentration in serum.

Conversely, in alkalosis, the serum potassium decreases as the potassium moves into cells. In addition, cellular destruction at the time of surgery can lead to leakage of intracellular potassium into serum, with a subsequent rise in serum potassium.

Hyperkalemia

When the serum K+ exceeds 7 mEq/L, a significant risk of a fatal cardiac arrhythmia develops. Early warning signs can be seen on the ECG, with peaking of T waves followed by prolongation of the PR interval and widening of the QRS complex. Treatment of hyperkalemia consists of stopping K+ administration. If life-threatening, administer NaHCO₃ (causes transient hydrogen and K+ flux). Serum K+ then can be lowered by infusion of glucose and insulin (1 U of insulin for every 5 g of glucose). Administer the ion-exchange resin Kayexalate (enema), which binds K+ into the gastrointestinal tract.

Hypokalemia

When plasma K+ falls below 3.5 mEq/L, the patient is considered hypokalemic. Patients generally do not become symptomatic unless the plasma K+ is less than 3 mEq/L. Fatigue, myalgia, and muscular weakness of the lower extremities are common complaints. More severe hypokalemia might lead to progressive weakness, hypoventilation, and, eventually, complete paralysis. Profound K+ depletion is associated with an increased risk of arrhythmias.

One cause may include diminished intake. Another cause, transcellular shift, ie, movement of K+ into cells, may transiently decrease the plasma K+ without altering total body K+ content. Metabolic alkalosis causes hypokalemia as a result of K+ redistribution and excessive renal K+ loss. A third cause of hypokalemia may be nonrenal K+ loss. Moderate to severe K+ depletion often is associated with vomiting or nasogastric suction and is due primarily to increased renal K+ excretion. Loss of gastric contents results in volume depletion and metabolic alkalosis, both of which promote kaliuresis. Finally, renal K+ loss may result in hypokalemia. Diuretic use is a common cause of K+ depletion.

Treatment consists of avoidance by ingesting potassium maintenance solutions. Hypokalemia is corrected with 20-40 mEq KCl/L of IV fluids. In severe cases (ie, <3 mEq/L), 10 mEq KCl can be administered intravenously 50 mL solution over 1 h).

Acid-base abnormalities

The acid-base status of the patient is best assessed by ABG determinations and serum carbon dioxide levels. Values outside of normal parameters usually can be categorized into specific acid-based abnormalities.

Respiratory acidosis

Causes include hypoventilation in the recovery room secondary to anesthetic/narcotics/paralysis. Diagnosis of acidosis is made when PCO₂ is high. Correction of hypoventilation in such patients leads to correction of the respiratory acidosis.

Respiratory alkalosis

Patients with a high pH and low PCO₂ have respiratory alkalosis, which usually is secondary to hyperventilation. The most common causes of hyperventilation are hypoxia, anxiety, excess mechanical ventilation, shock, and septicemia. It rarely is caused by compensation for metabolic acidosis (unless due to NaHCO₃ administration), shock, or sepsis.

Paresthesia and tetany resembling hypokalemia can be observed with severe respiratory alkalosis. The treatment of respiratory alkalosis is simply correcting the underlying cause.

Metabolic acidosis

Metabolic acidosis is characterized by a low pH and a low bicarbonate and can be observed with lactate acidosis from hypoxia, ketoacidosis from diabetes, and renal acidosis from uremia. An additional cause is loss of alkali from intestinal fistulas. Once again, the treatment of metabolic acidosis is to correct the underlying cause. If the pH is below 7.25, the administration of NaHCO₃ is indicated. For patients on respirators, the respirator can be adjusted to make the patient hyperventilate, which lowers the PCO₂, thus helping correct the acidosis. In severe cases of metabolic acidosis with significant amount of bicarbonate replacement, calcium should be given because the serum calcium will drop with the correction of the acidosis.

Thromboembolic disease

Thrombosis of veins in the lower extremities or the pelvis is a common complication of gynecological surgery. Patients typically present with a warm leg that is edematous, painful, and tender. Stasis is a major cause of venous clotting. This usually occurs as a result of either venous outflow obstruction or from conditions that render the legs hypotonic. Outflow obstruction may be caused by obesity, a gravid uterus, or congestive heart failure, whereas hypotonic limb occurs during anesthesia or from prolonged bedrest.

A major complication of lower extremity thrombosis is pulmonary embolism. Pulmonary embolism occurs when a proximal thrombus breaks off and travels to the pulmonary artery. These small clots frequently reach the pulmonary circulation and occlude some small vessels, then retract, undergo fibrinolysis, and disappear without any clinical symptoms. Significant obstruction of pulmonary arteries can cause a whole spectrum of clinical problems due to massive obstruction, leading to sudden death due to recurrent occlusion of the pulmonary vasculature that leads to chronic pulmonary hypertension. Pulmonary infarction is, in fact, a rare event that occurs in fewer than 10% of patients with pulmonary emboli.

Signs and symptoms alone are not sufficient for a diagnosis of DVT. Compression ultrasonography combined with venous Doppler studies are the primary tests used today. When the diagnosis is in question, contrast venography is the diagnostic standard.

For the diagnosis of pulmonary embolism, the more expensive, more invasive diagnostic procedure is a radioisotope V/Q lung scan, which detects the V/Q defect. If the diagnosis remains in question, pulmonary angiography is the criterion standard.

A spiral (helical) CT scan is a procedure that is getting more attention today. This procedure is performed by coupling a high-speed rotating CT scanner to a worm gear that drives the patient platform. Instead of discrete tomographic "cuts," a single long spiral of data is obtained, and the computerized reconstruction creates virtual cuts through the data to produce traditional-appearing images.

This method offers several advantages over traditional CT scans. It is very fast, and the spiral technique permits very rapid scanning over a large area, so that the entire lung may be imaged within the time patients can hold their breath. The entire scan can be performed during the first circulation pass of an injected bolus of venous contrast, and vessels can be tracked from cut-to-cut at high spatial resolutions. These "CT-angiograms" have shown great promise in the detection of pulmonary embolism by a relatively noninvasive method. Invasive pulmonary angiography possibly will be completely replaced by spiral CT angiography within the next few years.

Treatment of DVT or pulmonary embolism consists of anticoagulation therapy. Heparin is the drug of choice but only prevents further progression of the existing problem. The heparin loading dose usually is 5,000-10,000 U intravenously initially, followed by a continuous infusion at 18 U/kg/h, with the rate adjusted to maintain an aPTT at 2-times control.

Massive life-threatening pulmonary emboli may require embolectomy via transvenous suction or open pulmonary embolectomy. After adequate control of the acute process, prolonged anticoagulation is attained with warfarin to maintain a PT at 1.3-times control. With continued emboli despite adequate anticoagulation or in patients in whom the use of warfarin is contraindicated, a vena caval (ie, Greenfield) filter is used to trap the venous clots.

Thrombolytic therapy

Systemic thrombolytic therapy with streptokinase, urokinase, or recombinant tissue-plasminogen activator hastens the resolution of thrombi and reduces the morbidity from the postthrombotic syndrome but has not yet been shown to reduce mortality in patients with DVT or pulmonary embolism.

Thrombolytic therapy may be considered in the treatment of patients who are at low risk of bleeding and who have extensive iliofemoral venous thrombosis or acute massive embolism and are hemodynamically unstable. Absolute contraindications to thrombolytic therapy include active bleeding and surgery less than 10 days prior to administration.

Urinary retention

Urinary retention can lead to patient discomfort and a prolonged hospital stay. In the postoperative patient, retention is due to a few etiological factors. Most commonly, retention occurs in patients who have anti-incontinence procedures (Burch or slings) with either overcorrection or inflammation. Similarly, during prolonged gynecological procedures or with significant postoperative pain, bladder capacity may be surpassed. The bladder becomes overdistended, and its ability to contract is minimized. This dysfunction may continue postoperatively despite decompression.

Preventive measures include intraoperative Foley catheter placement. Treatment of patients with overdistension dysfunction requires placement of an indwelling Foley catheter for 24-48 hours, thus allowing recovery of the injured musculature. One also may consider the use of Urecholine to increase bladder tone.

In patients who remain unable to void or have high postvoid residual urine volumes longer than 3-4 days postoperatively, self-clean intermittent catheterization (CIC) has proven to be an effective alternative to an indwelling catheter.

Self-CIC requires a cooperative well-motivated patient or family. The services of a special nurse who instructs the patients and families in the regimen; provides them with written instructions to refresh their memory, outline precautions, and point out danger signals; and provides continuing support for patients is helpful. Most patients are able to quit self-CIC within 1-2 weeks of surgery, when their postvoid residual’s fall below 100 cc. Bacteriuria is common, but overt UTIs are rare, especially in patients who are on antibiotic prophylaxis.

If the gynecologic surgeon understands and pays close attention to the pathophysiologic changes that occur in the perioperative patient, the surgeon is able to provide appropriate support to prevent complications and recognize unfavorable trends in the recovery period. This understanding allows the surgeon to achieve the goal of returning the patient to her preoperative level of function.

• Archer C, Levy AR, McGregor M: Value of routine preoperative chest x-rays: a meta-analysis. Can J Anaesth 1993 Nov; 40(11): 1022-7[Medline].

• Arieff AI, Llach F, Massry SG: Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. Medicine (Baltimore) 1976 Mar; 55(2): 121-9[Medline].

• Eagle KA, Brundage BH, Chaitman BR: Guidelines for perioperative cardiovascular evaluation for noncardiac surgery. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Perioperative Cardiovascular Evaluation for Noncardi. J Am Coll Cardiol 1996 Mar 15; 27(4): 910-48[Medline].

• Goldman L, Caldera DL, Nussbaum SR: Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977 Oct 20; 297(16): 845-50[Medline].

• MacMillan SL, Kammerer-Doak D, Rogers RG: Early feeding and the incidence of gastrointestinal symptoms after major gynecologic surgery. Obstet Gynecol 2000 Oct; 96(4): 604-8[Medline].

• National Institutes of Health: Prevention of venous thrombosis and pulmonary embolism. NIH Consensus Development. JAMA 1986 Aug 8; 256(6): 744-9[Medline].

• Owens WD, Felts JA, Spitznagel EL Jr: ASA physical status classifications: a study of consistency of ratings. Anesthesiology 1978 Oct; 49(4): 239-43[Medline].

• Reeves WB, Bichet DG, Andreoli TE: Posterior Pituitary and Water Metabolism. In: Wilson JB, Foster DW, eds. William's Textbook of Endocrinology. 9th ed. Philadelphia, Pa: WB Saunders; 1998: 377-8.

• Roizen MF: Cost-effective preoperative laboratory testing. JAMA 1994 Jan 26; 271(4): 319-20[Medline].

• Roizen MF: Anesthetic Implications of Concurrent Diseases. In: Miller RD, ed. Miller's Anesthesia. Philadelphia, Pa: Churchill Livingtone; 2000: 903-99.

• Supkis DE, Varon J: Anesthesia for the Cancer Patient: An Overview . Anesthesiol Clin North America 1998; 16: 524-5.

• Surwit EA, Tam TY: Postoperative Managment. In: Sciarra JJ, ed. Gynecology and Obstetrics. Vol 1. Philadelphia, Pa: Harper & Row; 1990: 1-9.

• Velanovich V: The value of routine preoperative laboratory testing in predicting postoperative complications: a multivariate analysis. Surgery 1991 Mar; 109(3 Pt 1): 236-43[Medline].

• Velanovich V: Preoperative screening electrocardiography: predictive value for postoperative cardiac complications. South Med J 1994 Apr; 87(4): 431-4[Medline].

• Walton L: Preoperative Management. In: Sciarra JJ, ed. Gynecology and Obstetrics. Vol 1. Philadelphia, Pa: Harper & Row; 1990: 1-9.