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25Postoperative Counseling and ManagementFever, Respiratory, Cardiovascular, Thromboembolic,

Urinary Tract, Gastrointestinal, Wound, and Operative SiteComplications; Neurologic Injury; Psychological Sequelae

Vern L. Katz

The goal of postoperative care is the restoration of a woman’snormal physiologic and psychological health. The postoperativeperiod encompasses the time from the end of the procedure inthe operating room until the woman has resumed her normalroutine and lifestyle. Classically, this continuum may be dividedinto three overlapping phases based on the woman’s functionalstatus. The role and concerns of the gynecologist gradually evolve as the woman moves from one phase to another. The firstphase, perioperative stabilization, draws the surgeon’s attentionto the resumption of normal physiologic functions, particularly respiratory, cardiovascular, and neurologic. The older thewoman, the more comorbidities she has and, the more complex the procedure, the longer this period lasts. This period encom-passes recovery from anesthesia and the stabilization of homeo-stasis, with resumption of oral intake. Usually, the time period is24 to 48 hours. The second phase, postoperative recovery, usu-ally lasts 1 to 4 days. This phase may occur in the hospital and athome. During this period, patients will resume regular diet,ambulation, and move from parenteral to oral medications fortreatment of pain. Most traditional postoperative complicationsbecome apparent in this time. The last phase is termed the return to normalcy , which lasts 1 to 6 weeks. Care during this timeoccurs primarily in the outpatient setting. During this phase,the woman gradually increases strength and transitions from a sick role back to full and normal activity.

As the woman moves through these phases, physically andpsychologically, her needs will change and the interaction withstaff and her physician also change. She will gradually leavethe patient role and resume a nondependent role. The commu-nication among physicians, patients, and family varies over thecourse of recovery. For example, in the immediate postoperativeperiod, the primary psychological task of dealing with pain andnausea is the immediate concern. Later, however, the return of dignity and dealing with changes in body image will dominatea woman’s attention. It is common for the main questions onthe first postoperative day to be “When can I get these tubesout?” and “When can I shower?” Information or bad news aboutsurgical findings must be tailored and given honestly but appro-priately for the woman’s physical and psychological status. In thefirst phase of recovery, discussion regarding surgical results isusually concrete and simple as the woman drifts in and out of

an awake state. Later, in the postoperative recovery, details cabe discussed. As the woman enters the third phase of returninto normalcy, the implications, perspectives, and treatmentsbecome much more of an issue and are reviewed in detail.

Postoperative complications may occur at any time; howeveearly recognition and management will often preclude largeproblems from developing. Thus, attention to postoperative de-tails cannot be overemphasized. Often, the woman and her family judge the competence of the gynecologist by the compassiodisplayed and attention to detail during this postoperative pe-riod. Complications increase the duration of the postoperativestay in the hospital. In a study of women readmitted for postoperative complications, approximately 40% had been dischargedearlier than the mean length of stay for the corresponding operative procedure. Because many procedures are now laparoscopipatients will usually leave less than or close to 24 hours after sugery. When complications begin to develop, the woman is ahome. Particularly close attention to a postoperative woman’or family’s questions is necessary to detect problems before thereach severe levels. The office receptionist or triage nurse muhave special training and sensitivity to this very important issu

General caveats of postoperative management emphasize attention to the particular needs of each woman. Flexibility andindividual considerations should take precedence over standarorders, but guidelines can help the physician develop his or heown preferences. Individualization is especially important in thpostoperative care of geriatric women. Special nursing attentionand minimal doses of narcotics help prevent confusion and disorientation. Ongoing verbal communications with the nursingstaff help eliminate misunderstandings that might result in lessthan ideal postoperative care.

Surgical stress invokes several physiologic responses meantthe body’s defenses. Many of these responses may be more prolematic than the actual surgery. For example, some women wilrespond to the insulin resistance of surgical trauma with severhyperglycemia, which is detrimental to healing. Peri- and postoperative management strategies are aimed at minimizing opreventing these adverse effects, such as prevention of thromboembolism, or beta blockade in older patients to prevent cardiacomplications (Fig. 25-1). The clinician must be aware of thephysiologic stressors.


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This chapter discusses major issues of management during the period from the end of surgery until the return to normalphysiologic and psychological function. Problems and complica-tions arise over the whole spectrum of the postoperative timeframe and are interrelated. Thus, the clinician must be awareat all times of a woman’s changing status during recovery. Forsimplicity, this chapter is organized around organ systems andtheir potential complications. However, few problems arise ina single organ system.

POSTOPERATIVE FEVER

The exact definition of postoperative febrile morbidity variesgreatly among authors. Diurnal fluctuations are characteristicof the normal daily body temperature patterns of humans. Mostdefinitions use a temperature greater than 38 C 24 hours aftersurgery as the indicator of febrile morbidity. It is not unusual forgynecologic patients to have a mild temperature elevation during the first 72 hours of the postoperative period, especially during the late afternoon or evening. Up to 75% of patients develop a temperature greater than 37 C, which is usually not associatedwith an infectious process. In a study of 686 women withhysterectomy for benign indications, Peipert and colleaguesdocumented a febrile morbidity rate of 14%.

Fever is the most common diagnostic problem in the postop-erative patient. Common causes of a fever include atelectasis,pneumonia, urinary tract infection (UTI), nonseptic phlebitis,wound infection, and operative site infection. Two intraopera-tive factors that dramatically increase the risk of postoperativefever are an operative time longer than 2 hours and the necessity for intraoperative transfusion. In Peipert and associates’ study,increased intraoperative blood loss was associated with a 3.5relative risk (RR; 95% confidence interval [CI], 1.8 to 6.8) of developing fever postoperatively.

The physician’s primary goal in examining the postoperativefebrile patient is to determine whether the fever is caused by an

infection. Approximately 20% of postoperative fevers are directlyrelated to infection and 80% are related to noninfectious causes.Some conditions necessitate active intervention, whereas othersare self-limiting. Thus, it is imperative not to treat a postopera-tively febrile patient empirically with broad-spectrum antibiotics.The pathophysiology of postoperative fever is primarily related tothe release of cytokines. The cause of a postoperative fever may bsimple and common, such as atelectasis or dehydration, or un-usual, such as malignant hyperthermia or septicemia. The tempo-ral relationship of the onset of a woman’s febrile response tocommon postoperative complications is depicted in Table 25-1.

WORKUP FOR FEVERThe initial workup for a postoperative fever should emphasizethe most common problems. Medical students memorize thefive Ws in the differential diagnosis: w ind (atelectasis), w ater

Prevention ofintraoperativehypothermia

Afferent neural blockade(infiltration anasthesia,

peripheral nerve blocks,spinal/epiduralanasthesia/analgesia)

Minimally

invasivesurgery

Surgical stress:catabolism, pain, ileus,PONV, immunosuppression,cardiac demands ↑ ,pulmonary function ↓ ,coagulation ↑

Pharmacological intervention• Glucocorticoids (anti-inflammatory)• Analgesics• Antiemetics• blockade• Anabolic agents (growth hormone, insulin)• Nutrition• Preoperative carbohydrate

Figure 25-1 Stresses of surgery and interventionsto counteract adverse responses. (Adapted fromKehlet H, Dahl JB: Anaesthesia, surgery, andchallenges in postoperative recovery. Lancet362:1922, 2003.)

Table 25-1 Onset of Fever for Various Postoperative Complications

Day

Causes 1 2 3 4 5 61 Week orLonger

AtelectasisPneumoniaWound infection

Streptococcalor clostridialOther bacterialOvarian abscessCuff cellulitis

PhlebitisSuperficialDeep

Urinary tract infectionUreteral or bladderinjury

584 Part III GEN ERAL GYNECOL OGY


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(UTI), w ound (infection or hematoma), w alk (superficial ordeep vein phlebitis), and w onder drugs (drug-induced fever).

The proper workup of a postoperative fever, similar to that of any problem in gynecology, involves the three classic stepsof his-tory, physical examination, and laboratory evaluations, with major emphasis placed on the physical examination. The physicalexamination emphasizes the following: examination of the lungsfor atelectasis and pneumonia; the wound and operative site for

infection or hematoma formation; the costovertebral angles fortenderness, which might suggest pyelonephritis; and superficialveins in the arms for superficial phlebitis and deep veins in thelegs for deep vein phlebitis.

The findings of the history and especially the physical exam-ination and considerations of cost containment all influencethe extent of laboratory tests ordered. Ordering a specific listof laboratory tests is unrewarding. The three most commonly ordered laboratory tests are complete blood count, chestroentgenography, and urinalysis. A study by Schwandt andcoworkers has emphasized that chest radiography and urinecultures are best ordered only for specific clinical signs notas reflex orders. Other common tests include culture andGram stains of body fluids, including sputum, urine, and

blood. One study of over 300 women who were febrile follow-ing hysterectomy did not identify a single positive bloodculture. Women with persistent and undiagnosed fevers may need liver function tests or special imaging studies, such aspelvic ultrasound or computed tomography (CT) to detectproblems such as compromised ureters, abscesses, or foreignbodies.

Each major complication will be discussed in detail later inthe chapter. However, several specific generalizations concerning the type and characteristics of fever patterns should be empha-sized. Fever is a common postoperative finding, occurring in ap-proximately 75% of women. Rarely is the cause of the fever a serious infection. Microatelectasis is thought to be the cause of approximately 90% of fevers occurring in the first 48 hours afteroperation. Patients who develop fever as a result of an indwelling catheter, such as plastic intravenous (IV) lines or Foley catheters,are afebrile for several days and then experience an abrupt tem-perature spike. In contrast, wound or pelvic infections, which areusually clinically diagnosed from the fourth to seventh postop-erative days, usually are associated with a low-grade fever that be-gins early in the postoperative period. An empiric trial of IV heparin for 72 hours is often a diagnostic and therapeutic trialfor pelvic thrombophlebitis in refractory cases of postoperativefever of unknown origin.

Importantly, infection in the older woman will not alwayspresent with classic findings. The amount of temperature eleva-tion may not reflect the severity of the infection. Not uncom-monly, the first signs of infection in older adults will bemental status changes. Additionally, the degree of leukocytosis,being blunted or absent, may not reflect infection.

A woman with a drug-induced fever feels better and does notlook as ill as her temperature course indicates. The tachycardia associated with the elevated temperature is usually much lessthan usually anticipated with a similar temperature elevation sec-ondary to inflammation or infection. The presence of eosino-philia suggests a drug-induced fever. However, drug fever israre and is usually a diagnosis of exclusion. Presumptive evidenceof a drug-induced fever is established when the fever disappearsafter discontinuation of the drug.

Superficial thrombophlebitis often produces an enigmatic fever. Often, there is tenderness at the IV site.Thus, it is importantto change any IV lines empirically that have been in place folonger than 48 to 72 hours. This is particularly true for centravenous catheters and epidural catheters, in which an infectionmay not show clinical signs of localized tenderness or erythemThe cause of febrile transfusion reactions is a concern. Howeveusually the reactions are caused by leukocyte or platelet ant

bodies. As long as a major blood type incompatibility is nofound, treatment may be conservative.The basic fever workup should be repeated at intervals unti

the diagnosis is established. The woman should be reexamineand selective laboratory tests reordered. Rare causes of postopeative fever include pulmonary embolism (PE), thyroid stormand malignant neoplasms. These diagnoses usually present withother signs and symptoms as well as temperature elevation. It important to consider that fever is a potentially beneficial physiologic response to the patient. Therefore, unless the woman imarkedly symptomatic secondary to the elevated temperature, iis not necessary to order an antipyretic medication. Cellulardamage only occurs when the core temperature exceed41 C. Active cutaneous cooling does not reduce core tempera

ture and may have undesirable effects, such as increasing thmetabolic rate and activating the autonomic nervous system.

MANAGEMENT OF A FALLING HEMATOCRIT

Bleeding is one of the most feared postoperative complicationsSignificant arterial bleeding in the first 24 hours often necesstates reoperation. This complication is discussed later in thechapter, along with the management of shock and pelvihematomas.

Vital signs should be ordered at frequent intervals during thefirst 24 hours to detect hypovolemia. Most women will have suficient intravascular volume to compensate (during the earlyphases of hemorrhage) through the redistribution of blood flowfrom less vital to more vital organs. Low urine output may be thearliest sign of a decrease in intravascular volume. Thus, following an operation, sizable amounts of unrecognized intraperito-neal or retroperitoneal bleeding are sometimes present withouthe woman having subjective symptoms or appreciable changein her vital signs or urine output. Minimum urine output shouldbe 0.5 mL/kg/hr. Womenof medium and larger size should pro-duce more urine, just as petite patients will produce less. A consistent orthostatic decrease in blood pressure of more than10 mm Hg may indicate a possible decrease of 20% of the bloovolume. Thus, a hematocrit may be helpful at two intervalsduring the postoperative course. I prefer a hematocrit at 24and 72 hours following the operative procedure. A hematocridrawn 24 hours following an operation may not truly reflecpostoperative blood loss.

Thenormalphysiologic response to thestressof theoperationand tissue destruction is a release of increased levels of aldostrone, cortisol, and antidiuretic hormone (ADH). The higherlevels of aldosterone produce an increase in sodium and wateretention, whereas increased levels of ADH promote free wateretention. This has been called the ebb phase of postoperativephysiology. It is common for women to have notable lower extremity edema for the first few postoperative days, because theare often given significant amounts of IV fluids. Depending o

25 Postoperative Counseling and Management


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the type and amount of intraoperative and postoperative IV fluids, the hematocrit on the first postoperative day may be mis-leading and reflect fluid changes rather than intraoperative orpostoperative hemorrhage. The hematocrit from the third post-operative day is a more accurate measurement of postoperativechange. If the woman is doing well, stress hormone levels declineand water retention stops. The woman will begin to experience a brisk diuresis, sometimes termed the flow phase , beginning

around the third postoperative day. Hematocrits should beobtained in a standard fashion to eliminate sampling errors.For example, hematocrit samples drawn from central lines orduring blood gas determinations often give false values becauseof the heparin or saline flush solutions.

After the effects of the operative blood loss are subtractedfrom the preoperative hematocrit, each further reduction in he-matocrit of 3 to 5 points reflects a postoperative hemorrhage of approximately 500 mL. The safe level of postoperative anemia isa controversial issue. Most young healthy women without com-plicating medical illness will tolerate a hematocrit value of 20%to 22% without transfusion. These patients should be observedfor orthostatic changes in their vital signs. Importantly, and instark contrast, women with cardiac and pulmonary disease

and women older than 60 years should be transfused to maintaina hematocrit above 30%. The morbidity and mortality associ-ated with a surgical procedure are directly related to the amountof intraoperative and postoperative blood loss and not thecorresponding level of preoperative anemia.

RESPIRATORY COMPLICATIONS

Alterations of pulmonary function are an expected physiologicchange in women having general anesthesia and operations thatopen the peritoneal cavity. Of importance, respiratory complica-tions directly cause 25% of deaths in women who die during the

first 7 postoperative days. Many respiratory problems are

secondary to inadequate ventilation by women as they try tominimize acute pain from the operative incision.

ATELECTASIS

The term atelectasis is derived from two Greek words that mean“imperfect expansion.” The severity of atelectasis ranges fromlack of expansion of a small group of terminal bronchiolesand alveoli to complete collapse of a lung. In most patients, at-electasis is the failure to maintain patency of the small pulmo-nary airways and alveoli. Atelectasis is the most commoncause of postoperative temperature elevations.Studies have dem-onstrated that there is no association between fever and theamount of atelectasis diagnosed radiologically. The incidenceof atelectasis depends on the number of predisposing risk factorsand the vigor with which the clinical diagnosis is established.

Of all postoperative respiratory complications, 90% are re-lated to atelectasis. The immediate postoperative period is char-acterized by a decrease in functional residual capacity and lungcompliance (Fig. 25-2). Thus, the work of breathing is in-creased. Microatelectasis is most common when small airway(< 1 mm in diameter) become blocked by secretions. Whensmall airways remain closed by a combination of mucous plugand bronchospasm, the gas distal to the obstruction is absorbed.This process results in atelectasis. These changes occur duringthe first 72 hours following an operation. When atelectasis be-comes progressive and involves a large area of lung tissue, theris an associated decrease in oxygen saturation and a decrease iarterial oxygen pressure (PO2 ). This is associated with a normalto low arterial carbon dioxide pressure (PCO 2 ).

Pulmonary and nonpulmonary factors that favor prematureairway closure and development of atelectasis are listed inBox 25-1. The supine position decreases the functional residualcapacity by approximately 20% compared with the erect posi-tion. Obesity, smoking, age older than 60 years, prolonged

operative time, presence of a nasogastric tube, and coexisting

Inspiratorycapacity

Resting tidalvolume

T o t a l l u n g c a p a c i

t y

Functionalresidualcapacity

V i t a l c a p a c i

t y

Residualvolume

Inspiratory reserve volume

Expiratory reserve volume

Tidal volume atany level of

activity

Figure 25-2 Graphic illustration of lung volumes and capacities. (From Wellman JJ: Respiratory care in the surgical patient. In Lubin MF,Walker HD, Smith RB [eds]: Medical Management of the Surgical Patient. Stoneham, MA, Butterworth, 1982.)



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medical conditions, such as cardiac or lung disease and pulmo-nary infection, all predispose women to atelectasis.

In normal breathing periodic, involuntary deep inspirationshelp expand all areas of the lung. Pain, the supine position, nar-cotics, and abdominal distention contribute to a pattern of mo-notonous shallow breathing without spontaneous deep sighs inthe postoperative period. Because of the pain of an abdominalincision, chest wall breathing dominates over abdominal breath-ing. The resultant decrease in the movement of the diaphragmcontributes to the development of atelectasis. A further decreasein functional residual capacity, a decrease in surfactant, and a depression of mucociliary transport all contribute to ventilation-perfusion ( _V/ _Q) mismatches and reduced _V/ _Q ratios. The endresults are gas trapping, atelectasis, and vascular shunting. Inmost individuals, microatelectasis is patchy and localized to smallareas. However, the severity of atelectasis varies and may involve a complete lung.Distribution ofpulmonaryblood flow is influencedby gravity. A greater proportion of pulmonary blood flows to de-pendent areas of the lungs in the supine patient. This increasedblood flow, combined with the atelectasis in dependent areas, re-sults in an increased impairment of oxygenation, as well as a de-crease in the elimination of carbon dioxide. Obese patients, ingeneral, should be kept slightly upright, not prone, for the first24 hours to improve vital capacity and ventilation, thus decreasing atelectasis.

The endotracheal tube may contribute to the development of atelectasis. Even correctly placed endotracheal tubes are associ-ated with destruction of cilia in the respiratory tract epithelium. Women with nasogastric tubes have a higher incidence of atel-ectasis, more commonly related to a decrease in deep breathing than to aspiration of stomach contents. Atelectasis may presentas the classic triad of fever, tachypnea, and tachycardia develop-ing within the first 72 hours following an operation. On physicalexamination, tubular breathing, decreased breath sounds, andmoist inspiratory rales may be heard. These findings are most

prominent over the bases of the lung. If the condition progressesan increase in productive cough and leukocytosis result. Cheradiographic films may demonstrate a patchy infiltrate withelevations of the diaphragm. There may be a corresponding shiof the trachea and mediastinum when atelectasis involves a largsegment of the lung.

Atelectasis usually resolves spontaneously by the third to fifpostoperative day. Nevertheless, major efforts are made to pre

vent atelectasis, especially in high-risk individuals. The foundations of prevention of atelectasis are the encouragement ouneven ventilation and the production of episodes of prolongedinspiration to increase functional residual capacity. Thus, the pa-tient is encouraged to walk, take deep breaths, cough, turn fromside to side, and remain semierect rather than supine. Early mobilization and ambulation have been documented to be as effective as chest physical therapy in the prevention of pulmonarcomplications. Keeping pain relief to a level at which the womawill be able to cooperate and not have monotonous shallowbreathing is also helpful. The most important aid to preventand treat atelectasis is a simple bedside incentive spirometry dvice. Many women need encouragement by the hospital staff tuse these devices effectively. The primary risk of atelectasis

progression to pneumonia. Randomized clinical trials and systematic reviews have noted that preventivemeasures significantlreduce problematic atelectasis and pneumonia. Thus, thesesimple measures should be ordered for all patients.

In summary, basilar atelectasis is the most common postop-erative pulmonary problem experienced by gynecologic patientIf atelectasis does not clear, the woman should be treated witchest physical therapy, intermittent positive pressure breathingaerosol therapy, or intermittent continuous positive airway pressure by mask. Rarely, bronchoscopy may be indicated to removlarge mucus plugs.

PNEUMONIA

Postoperative pneumonia is commonly associated with atelectasis because bacterial infections often begin in collapsed areas the lungs. Predisposing factors to the development of pneumonia include chronic pulmonary disease, heavy cigarette smokingalcohol abuse, obesity, advanced age, nasogastric tubes, long operative procedures, gram-negative bacterial infections, postoperative peritonitis, and debilitating illnesses.

The symptoms and signs of pneumonia are fever, cough, dyspnea, tachypnea, andpurulent sputum.When pain occurs, it may be felt in the back or chest. The classic physical finding of pneumonia is coarse ralesover theinfectedarea.The patient usually haa higher temperature and more systemic toxicity than a womanwith atelectasis. Leukocytosis is pronounced in most patientsalthough it may be delayed or attenuated in older women. Chesroentgenogramsoftendemonstratediffusepatchy infiltratesof thelung. Radiographicdiagnoses are approximately 60% accuratefobacterial or viral pneumonia in women with laboratory-provenpneumonia. Gram staining of the sputum helps differentiate be-tween bacterial colonizationand infection. In cases of pneumonia,thesmearcontains a large number of inflammatory cellswith bothintracellular and extracellular bacteria.

The management of pneumonia is similar to the manage-ment of atelectasis, with the addition of parenteral antibioticsThe initial choice of parenteral antibiotics is usually based othe Gram stain and subsequently on sputum cultures. Most lung

Box 25-1 Nonpulmonary and Pulmonary Factors FavoringPremature Airway Closure and Atelectasis

Nonpulmonary FactorsSupine positionObesityIncreased abdominal girth (ileus, pneumoperitoneum)Breathing at low lung volumes

Bindings around the chest and abdomenIncisional painSedative narcotic drugsProlonged effect of paralyzing drugsImmobilityExcessively high concentrations of oxygen for prolongedperiods

Pulmonary FactorsInterstitial edemaLoss of surfactant with air space instabilityAirway obstruction

Inflammatory with swelling of bronchial and interbronchialtissueConstriction of bronchial smooth muscleRetained secretions

From Wellman JJ: Respiratory care in the surgical patient. In Lubin MF, Walker HK,Smith RB (eds): Medical Management of the Surgical Patient. Stoneham, MA,Butterworth, 1982.



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infections result when the contents of the mouth (mucus andbacteria that have a physiologic pH) are inhaled and subse-quently produce bacterial pneumonia.

One in 3000 procedures may be complicated by pneumonitisproduced by the aspiration of gastric fluid (sterile and highly acidic). The aspiration produces a severe chemical pneumonitis. Aspiration and its complications are a cause of approximately 30% of anesthetic mortalities. Women at high risk for aspiration

pneumonia include older women, obese women, and those witha hiatal hernia or emergency surgery associated with a full stom-ach. The morbidity from aspiration is secondary to particulatematter entering into the lungs and the caustic nature of gastricacid. The combination of these insults leads to a destructive in-flammatory response. When aspiration is significant and severe,adult respiratory distress syndrome often develops. Secondary infection usually complicates aspiration pneumonitis, andbroad-spectrum antibiotics should be given when this diagnosisis entertained. Preventive measures include early removal of na-sogastric suction, antacid ingestion, and H2 blockers in the peri-operative period, as well as careful use of narcotics and sedatives.

SLEEP APNEASleep apnea has become a significant concern because the inci-dence of obese and morbidly obese patients has risen. Increasedfatty tissue in the neck may produce compression and narrowing of the airway, leading to intermittent apnea while a womansleeps. In addition, the chronic airway narrowing in obese pa-tients may also lead to hypoventilation. Increased chest wallthickness and adipose tissue in the abdominal wall and neck leadto a decrease in pulmonary compliance. The lowered PO2 may induce systemic as well as pulmonary hypertension. Patients willalso develop a chronically increased PCO 2 . Respiratory driveshifts from a CO2 -driven response to a response to low levelsof oxygen. When morbidly obese patients are given higher levels

of oxygen, as well as narcotics, they are at increased risk for ap-nea. These patients develop an increased sensitivity to narcoticsthat shuts down the respiratory drive. Patients with chronic hyp-oxia from any cause will often have an increased sensitivity tonarcotics, but it is particularly problematic in the obese patientwho is dependent on low levels of oxygen for respiratory stimu-lation. These patients should be given oxygen as needed. How-ever, during the postoperative period, when narcotics are given,continuous pulse oxymetry should be used to keep the oxygensaturation in the 94% range. At saturation levels of 96%to 99% these patients may lose respiratory drive and becomehypercarbic and acidotic.

CARDIOVASCULAR PROBLEMSHEMORRHAGIC SHOCK

Shock is defined as a condition in which circulatory insufficiency prevents adequate vascular perfusion of vital organs. Systemichypotension results in poor tissue perfusion and reduced capil-lary filling. If this pathophysiologic state is neglected, pro-longed hypotension results in oliguria, progressive metabolicacidosis, and multiple organ failure. Shock may be producedby hemorrhage, cardiac failure, sepsis, and anaphylactic reac-tions. Hypovolemic shock is the most common cause of acute

circulatory failure in gynecologic patients. Cardiogenic shockand septic shock are rare. Shock from postoperative hemorrhageis usually seen in the first several hours following surgery. In thperioperative period, hypovolemia may be secondary to severafactors, including preoperative volume deficiency, unreplacedblood loss during surgery, extracellular fluid loss during surgeryinadequate fluid replacement and, most commonly, continuedblood loss following the surgical procedure. Tachycardia is the

classic cardiovascular physiologic response to hypotension. Progressive hypovolemia results in diminished urine output.Thevast majority of perioperative cases of shock are related to

hemorrhage secondary to inadequate hemostasis. The develop-ment of shock from acute blood loss depends on the rate ofbleeding; for example, a slow venous ooze may produce a largamount of blood loss but not produce shock. Rapid loss of 20%of a woman’s blood volume produces mild shock, whereas a losof greater than 40% of blood volume results in severe shock. Actual measurement of intraoperative blood loss is imprecise, evenwith the extensive use of suction equipment. Studies have dem-onstrated that 15% to 45% of surgical blood loss is absorbed onthe drapes, laparotomy pads, and other areas. Thus, the level ofblood in the suction bottle does not accurately represent the true

loss from the procedure. Massive blood loss has been defined ahemorrhage that results in replacement of50% of the circulating blood volume in less than 3 hours.

Hypotension in the immediate postoperative period may besecondary to the residual effects of anesthesia or oversedationFor example, older patients often experience prolonged vasodi-lation secondary to the sympathetic blockade produced by epi-dural or spinal anesthesia. The most common cause ofpostoperative bleeding is a less than ideal ligature or hemorrhagefrom a vessel that has retracted during the operation. Bleedingmay come from an isolated artery or vein or may be more generalized when the bleeding is secondary to a clotting diathesisThe differential diagnosis of postoperative hemorrhagic shockincludes conditions such as pneumothorax, PE, massive pulmo-nary aspiration,myocardial infarction,and acutegastric dilation.The differential diagnosis of ineffective coagulation includessepsis, fibrinolysis, diffuse intravascular coagulation, and apreviously unrecognized coagulation defect, such as von Willebrand’s disease. Inadequate hemostasis sometimes developsfrom excessive transfusion. The progressive acidosis associatewith shock increases hemostatic problems. Hypothermia furthercomplicates hemostasis because it produces platelet dysfunctionand coagulopathy secondary to decreased activity of thrombox-anes. Thrombocytopenia, impaired platelet function, and a de-crease in factors V, VIII, and XI occur with massive transfusionsCoagulopathy begins with the transfusion of more than 5 unitsof blood. Hypofibrinogenemia is the first to develop, followedby deficiencies of other coagulation factors. Thrombocytopeniais the last recognized defect in the coagulopathy cascade. However, the timing of its development varies among individuals.Thus, transfusion of platelets should be determined by serialplatelet counts (Box 25-2). Similarly, preset formulas for thetransfusion of fresh-frozen plasma, such as 2 units of plasmafor every 5 units of packed cells, should be replaced by selectivtransfusion of plasma as needed to match a clotting deficiency.

Tachycardia and decreased urine output are two early signs ofhypovolemia caused by hidden internal bleeding. The body’sadrenergic response to hemorrhage includes perspiration, tachy-cardia, and peripheral vasoconstriction. Urine output decreases



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catheters may be necessary. It is important to measure the pres-sure with the woman at a 45-degree angle. Studies have demon-strated that a central venous pressure measurement in the supineposition will severely underestimate the volume of intravasculardepletion. A Foley catheter, with urometer, facilitates measure-ment of hourly urine outputs.

Returning a patient to the operating room to control hemor-rhage is often a difficult decision. However, this decision shouldnot be postponed. The woman should have an exploratory op-eration as soon as possible after volumereplacement.During thissecond operation, excellent anesthesia, a full selection of surgicalinstruments, and the value of good assistance cannot be overem-phasized. Proper exposure is paramount for the success of thisoperation. Initially the old clots are removed and further bleed-ing is reduced by direct pressure over the pelvic vessels. A system-atic search is conducted in an effort to identify the individualvessels that are bleeding. Often, the offending artery or vein can-not be identified, or friability of the tissues results in furtherbleeding.

In situations requiring reoperation, there is usually a need fortransfusion. There is a proven, time-honored surgical axiom:“The greater the blood loss, the more the surgeon underesti-mates.” Many clinicians will add 25% to 35% to their estimatedblood loss when hemorrhage occurs to be on the safe side whencalculating replacement. The ratio of 2 units of packed red bloodcells to 1 unit of fresh-frozenplasmais desirable. Forevery 6 unitsof packed red blood cells, a six-pack of platelets should be given.Each unit or pack of platelets will raise the platelet level by 15,000/mm3 . The platelet count should be maintained above50,000/mm3 in a woman who is bleeding. The importance of adequate transfusion is notonly support of intravascular volume,but supply of oxygen. The greater a woman’s comorbidities, thegreater the risks from perioperative anemia.

Coagulation studies, prothrombin time, and activated pro-thrombin time should be obtained regularly during the bleeding episode. The term washout is used to describe the loss of clotting factors as a woman uses up her blood volume and is replacedwith packed cells and crystalloid. DIC (disseminated intravascu-lar coagulation) is an intravascular consumption and is differentthan washout. However, both conditions require replacementand ongoing evaluation. Importantly, with continued severebleeding, the use of recombinant factor VIIa (70 to 90 mg/kg)should be considered. Although expensive, factor VIIa initiates

a rapid burst of thrombin production and stimulates the entireclotting cascade. Many studies have shown it to be very effectivin situations of continued bleeding from small vessels in the faceof reoperation with washout.

Bilateral ligation of the anterior divisions of the hypogastricarteries distal to the posterior parietal branch is an effective op-eration to control persistent postoperative pelvic hemorrhage.This procedure results in a reduction of pulse pressure, whichallows a stable clot to form at the site where the pelvic vesselare injured. Classically, two ligatures are placed and tied aroundeach hypogastric artery (Fig. 25-3). The major potential compli-cation of this procedure is injury to the hypogastric vein. If thereis generalized oozing, thrombocytopenia, DIC, or factor VIII de-ficiency should be suspected. If these conditions are excludedvenous oozing from small vessels in the pelvis may be controlleby the local application of microfibrillar collagen compounds(e.g., Avitene, Gelfoam, Floseal).

Intraoperative rapid autologous blood transfusion is a tech-nique that is used extensively in cardiovascular and trauma sur-gery. Regretfully, it is underused or rarely performed bygynecologists. Grimes has described a simple device that can

Table 25-2 Indications for Administration of Various Blood Products

Product Content

Indication

Acceptable Unacceptable

Red blood cells Red cells To increase oxygen-carrying capacity inanemic women; for orthostatic hypotensionsecondary to blood loss

For volume expansion; to enhance woundhealing; to improve general well-being

Platelet concentrates Platelets Tocontrolor prevent bleedingassociated with

deficiencies in platelet number or function

In patients with immune thrombocytopenic

purpura (unless bleeding is life-threatening)Fresh-frozen plasma Plasma, clottingfactors

To increase the level of clotting factors inpatients with demonstrated deficiency

For volume expansion; as a nutritionalsupplement; prophylactically with massive bloodtransfusion

Cryoprecipitate Factors I, V, VIII,XIII, von Willebrandfactor, fibronectin

To increase the level of clotting factors inpatients with demonstrated deficiency of fibrinogen, factor VIII, factor XIII, fibronectin,or von Willebrand factor

Prophylactically with massive blood transfusion

From American Congress of Obstetricians and Gynecologists: ACOG Tech Bull 199:1, 1994.

Figure 25-3 Ligation of internal iliac artery. Double loop is beingdirected toward bifurcation of common iliac artery. (From Breen JL,Gregori CA, Kindzierski JA: Hemorrhage in gynecologic surgery.In Shaefer G, Graber EA [eds]: Complications in Obstetric andGynecologic Surgery. Hagerstown, physician, Harper & Row, 1981.)



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adapt this technique for use in any operating room. The majorcomplication of rapid autologous transfusion is a 10% hemolysisrate. The risks of air embolism or infusion of particulate matterare minimal. Obviously, autologous blood does not containplatelets or clotting factors, so platelets and fresh-frozen plasma will have to be given concurrently for severe hemorrhage. Rapidautologous transfusion is contraindicated in advanced pelvic in-fection or malignancy.

In many cases, angiographic embolization instead of explor-atory laparotomy is preferable (Fig. 25-4). Introduction of digital road mapping technology has improved the rapid identi-fication of bleeding vessels. Similarly, treatment of recurrentpostoperative hemorrhage or hemorrhage late in the postopera-tive course (7 to 14 days) may be performed with angiographicarterial embolization. Absorbable gelatin sponges, which pro-duce vascular occlusion for 10 to 30 days, or metal coils withDacron fibers, which produce permanent occlusion, may be used.

HEMATOMAS

This section will describe the management of wounds or pelvic

hematomas that develop slowly and are diagnosed after the firstpostoperative day. Proper management of postoperative hema-tomas is one of the most challenging and controversial subjectsin operative gynecology. The incidence of hematomas is in-versely related to the extent to which meticulous hemostasis isobtained intraoperatively. Women who are given low-dose hep-arin or who take aspirin chronically are at a slightly higher risk of hematoma formation. Hematomas result from intermittentor slow, continuous venous bleeding and are almost always

self-limiting. Eventually, the pressure of the expanding hematoma will exceed the venous pressure and a stable clot will form

The extent of the hematoma is determined partially by thepotential size of the compartment into which the bleeding occurs. Retroperitoneal or broad ligament hematomasmay containseveral units of blood. The diagnosis of a wound or pelvic hemtoma is usually suspected on the morning of the third postoperative day when the laboratory reports an unexpectedly low

hematocrit. The woman may have mild to moderate tendernessover the affected area. By the fifth postoperative day, the hematoma liquefies and is easier to outline during bimanual examination. Distinguishing between an uninfected hematoma and ahematoma that has become secondarily infected is difficult before incision and drainage. Both clinical situations produce tenderness and fever secondary to the inflammation surroundingthe hematoma. The diagnosis of most retroperitoneal hemato-mas may be made by physical examination. Most important ia careful rectovaginal examination. Radiologic imaging studieare indicated when the hematoma cannot be palpated.

Hematomas smaller than 5 cm in diameter may be treatedconservatively. Larger hematomas may be drained transcutaneously with CT or ultrasound direction as soon as they liquefy

If not treated, most large hematomas will become secondarilyinfected, even when the woman is treated with parenteral antibiotics. Effective drainage of most pelvic and broad ligamenhematomas usually can be accomplished vaginally or radiographically. Small subcutaneous hematomas or fascial hematomas usually resolve. However, they are associated with aincreased incidence of wound infection.

Any operation is accompanied by the potential risk of aunrecognized retained sponge or laparotomy pad. The exac

BAFigure 25-4 A, Anteroposterior digital subtraction pelvic angiogram in 37-year-old woman with persistent pelvic bleeding after surgicalmyomectomy for uterine leiomyomas demonstrates contrast pooling ( arrows) from branches of left uterine artery, consistent with activehemorrhage. B, Postembolization left uterine arteriogram shows occluded left uterine artery (long arrows) with no evidence of active bleeding.(From Vedantham S, Goodwin SC, McLucas B, Mohr G: Uterine artery embolization: An underused method of controlling pelvic hemorrhage.Am J Obstet Gynecol 176:938, 1997.)



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incidence of this worrisome complication is difficult to establishbut is estimatedto be from 1 in 1200 to 1500 laparotomies. Usu-ally, the sponge counts at surgery have been correct. When thiscomplication is discovered during the first postoperative week,the woman usually has a tender pelvic mass that is infected. When this mass is discovered after the immediate postoperativecourse, patients are often asymptomatic or exhibit minimal ten-derness. Thepossibility of a retained foreignbody should be con-

sidered in the differential diagnosis of pelvic hematomas andabscesses. A retrospective study of retained sponges by Gawandeand associates has noted that retained foreign bodies are morecommonly associated with a higher body mass index (BMI),emergency surgeries, and an intraoperative change in the typeof procedure to be performed.

THROMBOPHLEBITIS AND PULMONARY EMBOLUS

Surgery is a time of hypercoagulability secondary to the stress re-sponse. As such, the surgeon must be aware of the potential com-plications of thromboembolism throughout the postoperativecourse. Prophylaxis against deep vein thrombosis (DVT) is dis-cussed in Chapter 24 (Preoperative Counseling and Manage-

ment). However, prophylaxis needs to be continuedthroughout the hospital stay and, in certain high-risk cases, evenafter discharge. For example, patients with both a malignancy and a thrombophilia, or previous DVT and thrombophilia,and those who will have decreased ambulation may benefit from1 to 3 weeks of low-molecular-weight (LMW) heparin after leav-ing the hospital. Studies in patients with hip replacements andwith abdominal pelvic malignancies have shown significant re-ductions (50% to 66%) in the incidence of DVT with prolongedanticoagulation. Currently, there is insufficient evidence to makerecommendations for prolonged thromboprophylaxis for gyne-cology patients, except in high-risk situations. Without specificguidelines, the length of time for thromboprophylaxis should beindividualized. Prophylaxis will not prevent all DVTs; thus, partof daily rounds includes assessments for this complication.

Superficial ThrombophlebitisSuperficial thrombophlebitis is oneof themost frequently occur-ring postoperative complications and is most commonly associ-ated with IV catheters. Superficial thrombophlebitis is a benigndisease. However, it is associated with deep vein thrombophle-bitis in approximately 5% of cases. Superficial thrombophlebitisis frequently overlooked or disregarded as a cause of postopera-tive fever. Superficial tenderness anderythema outline the courseof the veins. Women with established superficial varicosities inthe lower extremities are especially susceptible because of local-ized stasis or pressure during the operative procedure and inac-tivity during the first 24 hours after operation. Patients withsuperficial thrombophlebitis of the legs also may have concom-itant deep venousdisease. Thus, the finding of superficial throm-bophlebitis does not eliminate the necessity to consider DVT aswell. Recurrent superficial phlebitis, in varying anatomic sites,may be a sign of occult malignant disease. Detailed basic inves-tigations have identified fibrin sheaths surrounding IV cathetersin 60% to 100% of patients studied. The exact fate of the severalinches of clot and fibrin sheath after the removal of the IV cath-eter is uncertain. Venography studies have found that these clotsand fibrin sheaths do not break up on catheter removal but ini-tially remain in situ. IV catheters are an important source of

nosocomial infections. Approximately 30% of all hospital-acquired bacteremias are secondary to IV lines. The most seriouscomplication of IV catheter use is infection of the thrombus,producing suppurative phlebitis or catheter sepsis.

The natural history of IV catheter-associated phlebitis wasdocumented by Hershey and colleagues. The classic symptomof phlebitis is inflammation of the subcutaneous tissue alongthe course of a vein or over the area of merging varicosities

The woman develops a painful, tender, erythematous induration(nodule or core). In most severe cases, there is associated feverThe duration of phlebitis is prolonged if the catheter is not im-mediately removed when the diagnosis of superficial phlebitis imade. I have recommended that all IV catheters be removed andreplaced at 48-hour intervals, regardless of whether signs orsymptoms of superficial phlebitis are present. In addition, theuse of an IV team decreased the incidence of catheter-associatedphlebitis from 32% to 15% in one series. Strict aseptic tech-niques should be used during catheter insertion. Cathetersinserted into the hand or forearm, through which antibioticsare infused, should be changed at least every 36 hours. Althoughnot all studieshave affirmed that recommendation,most authorshave suggested all IV lines be changed every 48 to 72 hours. Th

longer the catheter is left in place, the greater the risk of catheterrelated phlebitis (see Fig. 25-5). In one study, heparin flushes of IV catheters decreased the risks of phlebitis by an RR of 6 (95%CI, 4 to 8) over saline flushes. Recent series have documented theassociation of inherited thrombophilias with superficial phlebi-tis, increasing the risk by 4- to 13-fold. The more potent thethrombophilia, the higher the risk.

In summary, venous catheters should be removed at the firstsign of induration, erythema, or edema. Superficial phlebitis isthe leading cause of an enigmatic postoperative fever duringthe third, fourth, or fifth postoperative day.

The clinical management of mild superficial thrombophlebi-tis includes rest, elevation, and local heat. Moderate to severe superficial thrombophlebitis may be treated with a nonsteroidalanti-inflammatory drug (NSAID) such as ibuprofen or low-doseheparin. The rare case of proximal progression of the inflam-matory process should be treated with therapeutic doses of IVheparin and antibiotics.

Hours after insertion that phlebitis was diagnosed

% I

V c a

t h e

t e r s w

i t h p h

l e b i t i s

0 24 48 72 96 120 144 168

10

20

30

40

Figure 25-5 Intravenous catheters and development of infection.Phlebitis was diagnosed hours after insertion of catheter.(From Hershey CO, Tomford JW, Mclaren CE, et al: The natural historyof intravenous catheter–associated phlebitis. Arch Intern Med144:1374, 1984.)



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Deep Vein ThrombophlebitisThromboembolic complications generally occur early in the post-operative course, 50% within the first 24 hours and 75% within72 hours. Approximately 15% occur after the seventh postopera-tive day. Diagnosis of deep vein thrombophlebitis by physical ex-amination is insensitive. Thus, imaging studies are essential forestablishing the correct diagnosis. Venous thrombosis and PEare the direct causes of approximately 40% of deaths in gyneco-

logic cases. Theincidence of fatal pulmonary emboli followinggy-necologic operations is approximately 0.2%. Because womenoftendie within a few hours of theappearance of initialsymptoms,emphasis must be placed on prevention rather than treatment of this complication. PE is not the only major consequence of deepvenous thrombophlebitis. Many women develop chronic venousinsufficiency or postphlebitic syndrome of the legs as a major se-quela following thrombophlebitis. The resulting damage to valvesof the deep veins produces shunting of blood to superficial veins,chronic edema, pain on exercise, and skin ulceration.

The reported incidence of DVT with gynecologic operationswithout prophylaxis varies from 7% to 45%, with an average of approximately 15%. Walsh and associates have found the inci-dence of DVT to be 7% after vaginal hysterectomy, 13% after

abdominal hysterectomy for benign disease, 25% after a Wertheim hysterectomy, and 45% after extensive gynecologiccancer surgery. The incidence of thrombophlebitis is directly de-pendent on risk factors such as the type and duration of opera-tion, age of the woman, thrombophilias, history of deep veinthrombophlebitis, peripheral edema,amount of blood lost at op-eration, restrictions in preoperative ambulation, obesity, immo-bility, malignancy, sepsis, diabetes, current oral contraceptive orhormone use, and conditions that produce venous stasis, such asascites and heart failure (Table 25-3). Older and obese womenhave an increased incidence of thrombophlebitis because of di-lation of their deep venous system. There is a two- to fourfoldincreased risk for venous thrombophlebitis in women taking postmenopausal estrogen therapy. The length of the surgicalprocedure also has an important influence on the developmentof thrombophlebitis. If the operation is 1 to 2 hours in duration,approximately 15% of women develop the disease; if the surgery is longer than 3 hours, the risk is greater (Table 25-4).

Table 25-3 Conditions Associated with Increased Risk for DeepVein Thrombosis

Active cancerAcute medical illness (e.g., acute myocardial infarction, heart failure,respiratory failure, infection)Advancing ageAntiphospholipid syndromeBehçet’s syndromeCentral venous catheterChronic care facility stayCongenital venous malformationDyslipoproteinemiaHeparin–induced thrombocytopeniaHormone replacement therapyImmobilizationInflammatory bowel diseaseIntravenous drug abuseLimb paresisLong–distance travelMyeloproliferative diseasesNephrotic syndromeObesityOral contraceptivesOther drugs

AntipsychoticsChemotherapeutic agentsTamoxifenThalidomide

Paroxysmal nocturnal hemoglobinuriaPregnancy, puerperiumPrevious venous thromboembolismProlonged bed restSuperficial vein thrombosisSurgeryTraumaVaricose veinsVena cava filter

From Kyrle PA, Eichinger S: Deep vein thrombosis. Lancet 365:1164, 2005.

Table 25-4 Risk Categories of Thromboembolism in Gynecologic Operations

Risk Category

Risk Level

Low Medium High

Age (yr) 40 40 50Contributing factorsOperation Uncomplicated

or minorMajor abdominal or pelvic Major, extensive

Weight Moderately obese—75 to 90 kg or> 20% above ideal weight

Morbidly obese— > 115 kg or > 30%aboveidealweightPrevious venous thrombosisVaricose veinsCardiac diseaseDiabetes (insulin-dependent)

Calf vein thrombosis (%) 2 10-35 30-60Iliofemoral vein thrombosis(%)

0.4 2-8 5-10

Fatal pulmonary emboli (%) 0.2 0.1-0.5 1Recommended prophylaxis Early ambulation Low-dose heparin or intermittent

pneumatic compressionLow-dose heparin or intermittent pneumaticcompression

From Mattingly RF, Thompson JD (eds): Te Linde’s Operative Gynecology, 6th ed. Philadelphia, JB Lippincott, 1985.



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The processof thrombosis most often begins in the deep veinsof the calf. It is estimated that 75% of pulmonary emboli orig-inate from a thrombus that began in the leg veins. If one leg isinvolved, the other leg has thrombophlebitis in approximately 33% of women. Usually, the thrombophlebitis remains local-ized, theclot lyses spontaneously, and thewoman is free of symp-toms. In approximately 1 in 20 cases the process extendscentrally to the veins of the upper leg and pelvis. Involvement

of the femoral vein often results in swelling caused by obstruc-tion of this large vein. Pulmonary emboli from calf veins aloneare rare, with only 4% to 10% of pulmonary emboli originating from this area. In contrast, there is a 50% risk of a PE if throm-bophlebitis of the femoral vein is not treated.

In 1854, Virchow described the three key predisposing orprecipitating factors in the production of thrombi: an increasein coagulation factors, damage to the vessel wall, and venous sta-sis. Subsequent studies have documented that all three events oc-cur with gynecologic operations. Blood flow in the iliac veindecreases by approximately 55% during an operation. During an operation, there are several normal physiologic changes thatproduce hypercoagulability, including increases in factors VIII,IX, and X, number of platelets, platelet aggregation and adher-

ence, fibrinogen, and lastly, thromboplastin-like substance fromtissue necrosis.Kakkar has described the cascade of events leading to the de-

velopment of thrombophlebitis. The initial event in the cascadeis stasis. Stasis leads to localized anoxia with subsequent gener-ation of thrombi at the anoxic site. This produces changes inthe lining of the vessel, with exposure of the basement mem-brane, platelet adhesion, and local coagulation. Thus, the mostimportant event in thrombophlebitis is the generation of thrombi in the presence of venous stasis. A thrombus may gen-erate in an area of stasis or it may generate wherever a vessel wallis damaged, with resultant exposure of the subendothelial colla-gen, to which platelets will adhere.

The site of initial formation of the thrombus is most oftennear the base of a valve cusp in the calf of the leg (Fig. 25-6).The thrombus propagates and grows by repetitive layers of plate-let aggregation and deposition of fibrin from fibrinogen. Themost recently formed portion of the propagating thrombi arefree-floating (not attached to the vein) and are most likely to be-come pulmonary emboli. Thebody attempts to repair the area of thrombosis through an invasion of fibroblasts from the vein wallto encompass the base of the thrombus. Eventually, the throm-bus is attached to the vein wall, the area is reepithelialized, orga-nization occurs, and symptoms resolve.

The signs and symptoms of deep vein thrombophlebitis de-pend directly on the severity and extent of the process. Many lo-calized cases of deep vein thrombophlebitis in the calf areasymptomatic and are only recognized by a screening proceduresuch as duplex ultrasonography. However, even extensive areasof deep vein thrombophlebitis may be asymptomatic; the firstsign may be the development of a PE. In a woman who is asymp-tomatic, the pathophysiologic process may not totally obstructthe individual vein and drainage is obtained via associated com-petent collateral circulation.

Studies using 125 I-labeled fibrinogen to screen the legs havedocumented that approximately one of two women who developdeep vein thrombophlebitis following gynecologic surgery is to-tally free of symptoms. Among women who develop signs andsymptoms, approximately 68% have induration of the calf

muscles, 52% have minimum edema, 25% have calf tenderness,and 11% develop a difference of more than 1 cm in diameter of the leg. Homans’ sign is present in 10% and differential painover the calf with a blood pressure cuff is present in approxi-mately 40%. The clinical diagnosis of iliofemoral thrombosisis much easier—the woman usually develops severe symptomcaused by obstruction of venous return. Usually, there is an acuteonset of severe pain, swelling, and a sensation that the leg wilburst.

The clinician must maintain a high degree of suspicion to be-gin the diagnostic workup for deep vein thrombophlebitis. Theclinical symptoms and signs of DVT are nonspecific. A clinicaclue is the persistence of a low-grade fever with unexplainedtachycardia. The tachycardia is often more rapid than one wouldexpect with a low-grade fever. The finding of a definite difference in leg circumference is supportive evidence of DVT. Phys-ical examination of the legs produces false-positive findings inapproximately 50% of cases. At the time of the initial bedsideexamination, the physician will develop a level of suspicionfor DVT based on physical findings and clinical characteristicsIf the likelihood is low, the next step would, in nonsurgical pa-tients, be a D-dimer level; however in the postoperative patient,D-dimer is not reliable. D-Dimer is a protein from cross-linkedfibrin after it has been degraded by plasmin in the fibrinolyticprocess. Thus, D-dimer may be elevated because of trauma, sur-gery, intravascular hemolysis, pregnancy, and other inflamma-tory states. If the signs and symptoms are suggestive, or thewoman is at high risk, the next step should be imaging. Interest-ingly, the more symptomatic the disease, the more adherent the

A

B

C

DFigure 25-6 Stages in development of thrombus in valve pocket of deep veins of leg. A, Stasis in valve pocket results in thrombingeneration. B, Platelet aggregation and fibrin formation. C,Propagation of platelet-fibrin nidus. D, Blockage of venous flow withresultant retrograde extension. (From Bloom AL, Thomas DP [eds]:Haemostases and Thrombosis. Edinburgh, Churchill Livingstone,1981, p 684.)



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thrombus. The greater the symptoms, the less likely the develop-ment of a PE.

Ascending contrast venography (phlebography) is the mostaccurate method for detecting deep vein thrombophlebitis,but is rarely if ever used. Duplex ultrasound , the combinationof Doppler and real-time B-mode ultrasound, and colorDoppler are the preferred methods for diagnosing deep veinthrombophlebitis. The diagnostic accuracy of venography is

more than 95% for peripheral disease and more than 90% foriliofemoral thrombophlebitis. Contrast venography is more ex-pensive, painful, and time-consuming. Duplex ultrasonography has remarkably high sensitivity and specificity in symptomaticwomen. Real-time ultrasound imaging provides visualizationof the larger veins and sensitive Doppler ultrasound is focusedsimultaneously on the suspicious vessel. The technology dependson changes in venous flow for a positive diagnosis. A meta-analysis from White and coworkers has documented that thesensitivity of duplex ultrasonography in detecting proximalthrombi is 95% (95% CI, 92% to 98%) and the specificity is99% (95% CI, 98% to 100%).The advantages of this methodare that it is noninvasive, easy to use, highly accurate, objective,simple, and reproducible. Color Doppler ultrasonography

may improve the diagnostic accuracy in larger veins. The maindisadvantage of duplex ultrasound is its limited accuracy wheninvestigating small vessels in the calf. The inability to compressthe deep vein by moderate pressure with the ultrasound probe isthe most widely used criterion for the positive diagnosis of DVT.

Lensing and colleagues, in a prospective study of 220 pa-tients, used compressibility of the vein as the sole criterion fordiagnosis of DVT. For all patients in their study, including bothproximal vein and calf vein thrombosis, the sensitivity was 91%and the specificity was 99%.

The objectives of the clinical management of deep veinthrombophlebitis associated with gynecologic surgery are early detection and early therapy. In reality, antithrombotic therapy is preventive medicine, because the therapeutic agent interruptsprogression of the disease (thrombus formation) butdoes not ac-tively resolve the disease process. Anticoagulation with heparin

(unfractionated or LMW heparin) is the treatment of choicefor the initial diagnosis of DVT (Table 25-5). LMW heparinis as effective and is safer than unfractionated heparin. LMWheparin, although more expensive than unfractionated heparin,has several advantages and has effectively replaced unfractionateheparin as the gold standard for treatment of DVT. LMW hep-arin may be given subcutaneously once or twice daily. It does norequire monitoring in women with normalandstable renal func-

tion. It induces significantly less heparin-induced thrombocytopenia and has a lower risk of inducing bleeding. Because bloolevels are more reproducible, there is actually a lower incidencof complications noted in some studies in terms of progressiofrom DVT to pulmonary emboli. Additionally, studies compar-ing LMW heparin with unfractionated heparin have shown agreater effect with thrombus regression within the veins themselves. Testing of levels of LMW heparin is based not on thactivated partial thromboplastin time (aPTT), but on the anti-factor Xa activity level. Levels are calculated specifically for eLMW heparin. An aPTT of 1.5 times normal corresponds ap-proximately to an antifactor Xa activity level of 0.2. Therapeutilevels are found between 0.4 and 0.8. Bleeding usually occurwhen levels of the antifactor Xa activity level rise more tha

1.0 to 1.2. If needed in patients with unstable renal status, levelmay be checked approximately 4 hours after dosing.If unfractionated heparin is desired as an IV infusion, the

initial loading dose is 5,000 to 10,000 IU, followed by a continuous infusion of 1000 to 1500 IU/hr. The dosage of unfractio-nated IV heparin should be adjusted to prolong an aPTT to2.5 times control values. Continuous heparin infusion is pre-ferred over periodic bolus injections because there are fewehemorrhagic complications (6% versus 14%). The averaghalf-life of heparin is 1 to 2 hours after IV injection. Failurto achieve adequate anticoagulation in the first 24 hours otherapy increases the risk of recurrent venous thromboembolism15-fold. Heparin should be continued for 5 to 7 days. Oral war-farin (Coumadin), 15 mg daily, should be initiated within thefirst 48 hours of heparin therapy. Following 2 to 3 days o10 to 15 mg of warfarin daily, the international normalized ratio

Table 25-5 Options for Initial Anticoagulant Treatment of Deep Vein Thrombosis

DrugMethod of Administration Dosage *

Reported Risks (no./total no. [%])

Heparin-InducedThrombocytopenia {

MajorBleeding

Unfractionated heparin IV Loading dose, 5000 U or 80 U/kg of bodyweight with infusion adjusted to maintainaPTT within therapeutic range

9/332 (2.7) 35/1853 (1.9)

LMW heparin 0/333 (0) 20/1821 (1.1)Dalteparin Subcutaneous 100 U/kg every 12 hr or 200 U/kg daily;

maximum, 18,000 U/day

Enoxapar in Subcutaneous 1 mg/kg every 12 hr or 1.5 mg/kg daily;maximum, 180 mg/day

Tinzaparin Subcutaneous 175 U/kg daily; maximum, 18,000 U/dayNadroparin Subcutaneous 86 U/kg every 12 hr or 171 U/kg daily;

maximum, 17,100 U/day

*Doses vary in patients who are obese or who have renal dysfunction. Monitoring of antifactor Xa levels has been suggested for these patients, with dose adjustment to atarget range of 0.6-1.0 U/mL 4 hr after injection for twice-daily administration or 1.0-2.0 U/mL for once-daily administration. Even though there are few supporting data,most manufacturers recommend capping the dose for obese patients at that for a 90-kg patient.{The therapeutic range of activated partial thromboplastintime correspondsto heparin levelsof 0.3-0.7 U/mL,as determinedby antifactorXa assay. Highlevels of heparin-binding proteins and factor VIII may result in so-called heparin resistance. In patients requiring more than 40,000 U/day to attain a therapeutic aPTT, the dosage can beadjusted on the basis of plasma heparin levels.From Bates SM, Ginsberg JS: Treatment of deep-vein thrombosis. N Engl J Med 351:271, 2004.



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(INR) will usually be 1.5 to 2. This therapeutic level—an INRof 2—should be maintained by appropriate adjustment of the war-farin dosage. The biologic half-life of warfarin is 2 to 3 days. Anticoagulation with warfarin should be continued for 6 to9 months for adequate secondary prophylaxis. A meta-analysisfrom Ost and colleagues has evaluated the duration of anticoa-gulation following venous thromboembolism. Studies of 3 months of therapy were compared with studies of 6 months

or longer. The risks of bleeding (the major complication) weresimilar between short- and long-term therapy. However, the rel-ative risk of recurrent thromboembolism was 0.21 (95% CI,0.14 to 0.31) comparing long-term with short-term heparinuse. Some patients with large DVT, antiphospholipid antibody syndrome, or malignancies may require extended therapy be-yond 6 to 9 months because of increased risks of recurrence(Table 25-6).

Theprimary risk of chronic anticoagulation therapy is thepo-tential for major bleeding complications. Major bleeding occursin approximately 4% woman-years of therapy. Thus, it is impor-tant to follow these women carefully with serial coagulationstudies. Approximately 1% of patients on full-dose heparindevelop thrombocytopenia (platelet count < 100,000/mm3 ).

If thrombocytopenia develops, heparin should be discontinuedbecause of the potential risk of paradoxic thrombosis.Rarely, patients will not be candidates for anticoagulation. In

these patients, inferior vena caval filters may be used to protectagainst pulmonary emboli. Temporary vena caval filters may beplaced with fluoroscopic guidance. In some patients with largeDVT and other risk factors, such as compound thrombophiliasand malignancy, consideration may be given to both anticoagu-lation and filter placement.

Many clinicians will obtain laboratory studies to identify thrombophilic states when a DVT occurs. These tests shouldbe obtained with any idiopathic DVT. However, there is lesssupport for the cost-benefit ratio in obtaining this informationfora surgically related DVT. If management decisions, including the duration of therapy or the use of estrogens in the future,might be changed, thrombophilia studies should be obtained. Additionally, in a woman with a family history of thrombosis,it would be reasonable to obtain these studies.

There is no evidence that bed rest is helpful for patients withDVT or that immobilization will prevent pulmonary embolism.Patients with confirmed DVT may receive NSAIDs, becausecoagulation factors will be monitored. Patients should also be

prescribed support stockings, which should be worn for severalmonths to 2 years. The use of support stockings decreases therisks of post-thrombotic syndrome. In their systematic review,Segal and associates summarized trials that noted that womenwho used stockings up to 2 years after DVT had reductions inthe incidence of post-thrombotic syndrome of more than 50%.

Pulmonary Embolism

The accurate diagnosis of PE is essential for the prevention ofmorbidity from lack of treatment or unnecessary anticoagulationtherapy. Autopsy studies have documented that pulmonary em-boli are undiagnosed clinically in approximately 50% of womenwho experience this complication. Approximately 10% ofwomen with a PE die within the first hour. The mortality of women with correctly diagnosed and treated pulmonary emboliis 8%, in contrast to approximately 30% if the disease is not trea-ted. Most pulmonary emboli in gynecologic patients originatefrom thrombi in the pelvic and femoral veins. Predisposing riskfactors are found in most women with PE. Anticoagulationtherapy is also dangerous, because heparin is one of the leadingcauses of drug-related deaths in hospitalized patients.

No combination of symptoms or signs is pathognomonic for

PE. The signs and symptoms of PE are nonspecific, and similarsymptoms are caused by many other forms of cardiorespiratorydisease. Many patients with PE will be asymptomatic. Commonconditions considered in the differential diagnosis of pulmonaryembolism include pneumonia, cardiac failure, atelectasis, aspira-tion, acute respiratory distress syndrome, and sepsis. Althoughthe differential diagnosis is broad in scope, the symptoms shouldalert the physician to the possibility of a PE, thus allowing aproper diagnostic workup to establish or rule out the disease. A national study of 327 patients with angiographically provenPE found that chest pain, dyspnea, and apprehension are themost common symptoms. The dyspnea is often of abruptonset. The classic triad of shortness of breath, chest pain, andhemoptysis is seen in less than 20% of women with provenPE. Tachycardia, tachypnea, rales, and an increase in the secondheart sound over the pulmonic area are the most frequently found signs of pulmonary emboli (Table 25-7). Approximately 15% of women with pulmonary emboli have an unexplainedlow-grade fever associated with a PE. A high fever is rarelassociated with a PE but definitely may occur. The clinical man-ifestations of PE are produced primarily by occlusion of thelarge branches of the pulmonary arteries by embolic material.

Table 25-6 Recommendations for Duration of Anticoagulant Therapy for Patients with Deep Vein Thrombosis

Characteristics of Patient * Risk of Recurrence in Year after Discontinuation (%) Duration of Therapy

Major transient risk factor 3 3 moMinor risk factor, no thrombophilia < 10 if risk factor avoided

> 10 if risk factor persistent

6 mo

Until factor resolvesIdiopathic event; no thrombophilia or low-riskthrombophilia

< 10 6 mo {

Idiopathic event; high-risk thrombophilia > 10 IndefiniteMore than one idiopathic event > 10 IndefiniteCancer; other ongoing risk factor > 10 Indefinite

*Examples of major transient risk factors are major surgery, major medical illness, and leg casting. Examples of minor transient risk factors are the use of an oralcontraceptive and hormone replacement therapy. Examples of low-risk thrombophilias are heterozygosity for factor V Leiden and G20210A prothrombin gene mutations.Examples of high-risk thrombophilia are antithrombin, protein C, and protein S deficiencies, homozygosity for factor V Leiden or prothrombin gene mutation orheterozygosity for both, and presence of antiphospholipid antibodies.{Therapy may be prolonged if the patient prefers to prolong it or if the risk of bleeding is low.From Bates SM, Ginsberg JS: Treatment of deep-vein thrombosis. N Engl J Med 351:273, 2004.



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comparing urokinase and recombinant human tissue-type plas-minogen activator. The latter was found to act more rapidly andto be safer than urokinase. Thrombolytic therapy is the methodof choice in patients with massive pulmonary emboli (angio-graphically, > 50% obstruction of the pulmonary arterial bed)with associated moderate to severe hemodynamic embarrass-ment, lobular obstruction, or multiple segmental profusion de-fects. Random trials of heparin versus thrombolytic therapy haveshown that emboli clear more rapidly with initial thrombolytictherapy.

The MAPPET-3 trial (Management Strategies and Prognosisof Pulmonary Embolus-3) found that in severely affected pa-tients (but not those in shock), thrombolytic therapy was supe-rior to heparin. However, for all patients, particularly those withsmall emboli, the increased risks of intracranial bleeding mayoutweigh the benefits (1% to 3% of patients). Trials have eval-uated thrombolytic therapy with heparin and found the combi-nation superior to heparin alone.A thrombolytic agent is infusedIV for the first 12 to 24 hours and heparin therapy is continuedfor 7 to 10 days. The clinical assumption is that approximately

Figure 25-7 Helical CT of pulmonary embolism. The letters on the cube help orient the viewer as the three-dimensional image is rotated.A, Anterior; F, foot; H, head; L, left. (Courtesy of Dr. Charles McGlade, Sacred Heart Medical Center, Eugene, OR.)



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7 days are needed for the intravascular venous thrombus to be-come firmly attached to the vein’s side wall. In patients who haveheparin allergies, or develop heparin-induced thrombocytopenia (HIT), thrombin inhibitors are an alternative therapy.

An adjunct for treatment is vena caval filters. The most widely accepted indication for vena cava filters is failure of medicalmanagement or a contraindication to heparin therapy. Approx-imately 35% of vena cava filters are placed for prophylacticindications. A randomized trial reported by Decousos and co-workers compared vena cava filters with LMW or unfractionatedheparin. They concluded that the initial beneficial effect of vena cava filters for the prevention of PE is counterbalanced by anexcess of recurrent DVT, without any difference in mortality rates. Treatment of a massive PE in an unstable womaninvolves a choice of thrombolytic therapy, pulmonary artery embolectomy, transvenous catheter embolectomy, or filterplacement in the inferior vena cava.

All patients with pulmonary emboli should have warfarintherapy after heparin treatment for 3 to 9 months. The risk of a woman developing a subsequent fatal PE during the 3 monthsof anticoagulation therapy is approximately 1 in 70 to 100.Trials from Canada and from Sweden have found better long-term survival with extended anticoagulation, 18 months to2 years. Some authors believe that if there are additional risk factors, such as very potent thrombophilias, indefinite anticoa-gulation is indicated.

URINARY TRACT PROBLEMS

INABILITY TO VOID

Many women experience an inability to void or an incompleteemptying of the bladder during the postoperative period. Thecause is complex, but the inability to void is more frequentand lasts longer after an operation that involves the urethra orbladder neck. The major pathophysiologic change is the direct

trauma and edema produced by the surgical procedure to theperivesical tissues. Other factors that contribute include the potential of overdistention from excessive hydration and dyssynchronous contractions from the bladder neck. The differentialdiagnosis includes anxiety, mechanical interference, obstructionby swelling and edema, neurologic imbalance, and drugassociated detrusor hypotonia.

The woman’s initial attempts at voiding should be made in asitting position. Obviously, privacy is important to minimizeperformance anxiety. It is best not to remove the Foley catheteuntil the woman is ambulatory. Most women have difficulty inemptying their bladder completely on a bedpan or in a semirecumbent position during the first 24 hours after abdominal hys-terectomy. Catheter drainage keeps the bladder at rest andavoidsacute bladder distention with resulting detrusor dysfunction andpossibly retrograde reflux of urine. The age-old tradition of intermittent clamping and releasing of the Foley catheter to regainbladder tone is counterproductive and is not based on soundphysiologic principles.

Most problems with voiding resolve without medication andwith time. If mechanical obstruction is not suspected to be a ma jor factor, intermittent straight catheterization is indicated. Thiswill result in a lower incidence of UTI and a more rapid return tonormal function than periodic replacement and removal of aFoley catheter for the evaluation of residual urine volume Although bacteriuria occurs secondary to intermittent catheter-ization, development of pyelonephritis is rare unless the womahas concomitant vesicoureteral reflux. Bacteriuria may occumore frequently with indwelling catheters. Most women prefeself-catheterization. They especially appreciate intermittent selfcatheterization because it gives them control over part of theipostoperative care. Routine culture of the urine with removaof a catheter in an asymptomatic woman is not necessary. Rarelymedications may be given to patients who experience prolongeperiods of inability to void. Reflex urethral spasm is common after plastic surgery to repair an enterocele or rectocele. Urethraspasm may be diminished by an a -adrenergic receptor blocking

Hemodynamically unstable

Thrombolysis contraindicated

Consider: catheter embolectomy orsurgical embolectomy

Anticoagulate: intravenousunfractionated heparinor subcutaneous low

molecular weight heparinplus warfarin started day 1–3

Anticoagulation contraindicated

Hemodynamically stable

No No YesYes

Inferior vena cavafilter

Recurrentpulmonaryembolism

Pulmonary embolism

Thrombolysis + ?inferior vena cava filter

Figure 25-8 Algorithm for treatment of pulmonary embolism. (From Taj MR, Atwal AS,Hamilton G: Modern management of pulmonary embolism. Br J Surg 86:853, 1999.)



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agent such as phenoxybenzamine (Dibenzyline). However,hypotension may be associated with this drug. Bladder hypoto-nia may occur as a result of overdistention, prolonged inactivity,or use of medications such as beta blockers. Bladder hypotonia may be treated with bethanechol (Urecholine), 25 to 50 mg every 8 hours. Urecholine effectively produces detrusor contrac-tions. However, this is rarely prescribed in the postoperativesetting.

INFECTION

The most commonly acquired infection in the hospital and themost frequent cause of gram-negative bacteremia in hospitalizedpatients is catheter-associated UTI. Approximately 40% of nos-ocomial infections are UTIs, and 60% of these are directly re-lated to an indwelling urethral catheter. Of patients withinfections from bladder catheters, 1% will develop bacteremia.However, patients without catheters may develop overdistentionand bladder atony as a result of postoperative pain. Overdisten-tion produces a temporary paralysis of the detrusor activity thatmay take several days to resolve. The atonic bladder is also proneto UTI. Thus, after a gynecologic operation, the woman is sus-ceptible to UTI, with or without a catheter in place.The normal uroepithelium inhibits adherence of surface bac-teria to the walls of the urethra and bladder. A bladder catheterdisrupts this property andsurface bacteria areable to colonize thelower urinary tract. Additionally, bacteria form a sheet or bio-film of microorganisms and bacterial bioproducts that adheresto the catheter. These biofilms protect bacteria from antibiotics.This characteristic of biofilms explains why antibiotic suppres-sion is ineffective for patients with chronic catheterization andwhy replacement of a catheter is necessary in the treatment of systemic infection secondary to a colonized urinary tract. Theincidence of a positive culture increases dramatically with time. After a Foley catheter has been in place for 36 hours, approxi-mately 20% of women have bacterial colonization and, after72 hours, more than 75% have positive cultures. If the catheterdrains into an open system for longer than 96 hours, 100% de-velop bacteriuria. Women with an indwelling catheter in placewith a closed drainage system develop UTIs at the rate of approx-imately 5%/24 hours; this increases to 50% of women after7 days of continuous catheterization.

Catheter-related UTIs are related to the patient’s age. In onestudy,30% of women older than 50 years developed an infection,compared with 16%of postoperativewomen younger thanage 50.Diabetes increased the incidence of catheter-related UTIs three-fold. The incidence of infection is directly related to how long the catheter is in place. The incidence of a positive urine cultureafter a single in-and-out catheterization is approximately 1%.

Sterile technique used during insertion, strict aseptic cathetercare, and maintenance of a closed drainage system are all impor-tant steps forreducingthe incidenceof infection through reducedcolonization. Bacteria ascend from the exterior to the bladder via the lumen of the catheter or around the outside of the catheter. A meta-analysis by Saint and colleagues has noted that silveralloy–coated urinary catheters are significantly more effectivein preventing UTIs than silver oxide catheters. The silveralloy–coated catheters are more expensive than standard Foley catheters. However, they reduce nosocomial UTIs by approxi-mately 50%. A sterile, closed drainage system is another prophy-lactic measure to reduce the incidence of UTIs. In one study,

strict closed drainage reduced the rate of infection from 80%to 23%. Studies have documented a lower risk of infectionwith a suprapubic, transabdominal urinary catheter. The lattertechnique also decreases patient discomfort and permits earlierspontaneous voiding. Systemic prophylactic antibiotics exert ashort-term effect, decreasing the initial incidence of infection.However, the negative effect of prophylactic antibiotics has beenan increased emergence of antibiotic-resistant bacteria. There-

fore, prophylactic antibiotics are not used to cover a catheter, ex-cept in immunocompromised patients. With catheterization forlonger than 3 weeks, all patients have bacterial colonization, re-gardless of theuseof prophylactic antibiotics anda closedsystem.

The symptoms of UTI usually develop 24 to 48 hours afterthe Foley catheter is removed. Of interest, the signs and symp-toms associated with a catheter-acquired lower UTI are notnearly as pronounced or as specific as those associated with cystitis unrelated to catheter use. Patients with lower UTIs usuallydo not have fever butexperience urinary frequency andmild dys-uria, which are difficult to distinguish from normal postopera-tive discomfort. As noted, older women may manifest mentalstatus changes as the first sign of problems. Women with upperUTIs usually have a high fever, chills, and flank pain. If urinary

tract symptoms persist after appropriate antibiotic therapy, oneshould obtain imaging studies to evaluate the possibility of ob-struction in the urinary tract. Obstruction of the ureter withoutassociated infection may be asymptomatic or produce only mildflank tenderness. No appreciable change will be noted in urinaryoutput with an isolated unilateral ureteral obstruction.

The diagnosis of UTI is established by urinalysis and urineculture. Women with high-volume urine outputs may demon-strate minimal findings on urinalysis but have a positive urineculture. Stark andMaki have emphasized that a bacterial concen-tration of 102 organisms/mL in a catheterized specimen is signif-icant. In their studies, more than 95% of patients with 102

colony-forming units (CFU)/mL subsequently developed thestandard criterion of infection, which is 100,000 CFU/mL fora midstream culture.

A minimum of 3 days of antibiotic therapy for a woman whohas developed cystitis after catheter use is the recommendedtreatment. One-day, single-dose antibiotic treatment is not aneffective treatment for UTI.

To reduce the incidence of UTI, the Foley catheter should beused judiciously. When possible, use of a suprapubic catheter orintermittent in-and-out catheterization is preferable to continuousdrainage with a Foley catheter. If a Foley catheter is used, retro-grade flow of urine from thebag to thebladder during ambulationshould be avoided. Preventivemeasures, such as aseptic care of thecatheteranda closed, sterile drainage system,are also important. Itis not necessary to treat catheter-associated urinary tract colonizationunlessthe patientbecomes febrile(develops infection). If signsand symptomsof infection occurwith a Foley in place, the womanshouldbe treatedwith systemicantibiotictherapyfor10 days.Pro-phylactic antibiotics are not used unless the patient is immuno-suppressed, because they often result in a UTI with a Proteus orPseudomonas sp. rather than the more common Escherichia coli.

URETERAL INJURY AND URINARY FISTULA

Vesicovaginal and ureterovaginal fistulas are infrequent yet significant complications of operations for benign gynecologic condi-tions. In the United States, gynecologic operations are found to



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be the cause of approximately 75% of urinary tract fistulas.Surprisingly, it is not the difficult cancer operation but ratherthe simple total abdominal hysterectomy for benign disease, suchas myomas or abnormal bleeding, that is most frequently associ-ated with this complication. Fistulas following gynecologic sur-gery are secondary to abdominal hysterectomy in 75% of casesand to vaginal surgery in the remaining 25%. The exact incidenceof injury to the ureter associated with gynecologic surgery is

unknown because many patients do not exhibit symptoms. How-ever, it has beenestimated that ureteral injury occurs as frequently as 1/200 abdominal hysterectomies. The ratio of injuries to theurinary bladder to ureteral injuries in nonlaparascopic surgeriesis approximately between 3:1 and 5:1. Ibeanu an

pos opt care

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