Complications of Gynaecological Surgery

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Chapter 14 Complications of Gynaecological Surgery

Urinary tract injuries

Gynaecological surgery, in common with other surgical specialties, can be associated with complications. Most complications are minor, self limiting and have no long-term consequence for the patient, but they must still be avoided where possible, and actively managed where necessary, to make sure they do not become major complications.

Gynaecological surgery involves close dissection to viscera including the bladder, rectum, ureters as well as the great vessels of the pelvis. Complications can occur during difficult surgical dissections, especially when the anatomy is distorted (e.g. malignancy, endometriosis or infection).

Other complications, such as pulmonary embolus, myocardial infarction, pneumonia, or fluid or electrolyte imbalance are common to all surgery. For the purposes of this chapter, the most common complications related only to gynaecological surgery will be discussed.

Urinary tract injuries

Bladder Injuries

If a bladder injury is suspected intraoperatively, it can be localised by intravenous injection of indigo carmine, retrograde instillation of methylene blue through the urethral catheter or by opening the dome of the bladder and inspecting the mucosa. Subtle injuries can also be diagnosed using cystoscopy. Early involvement of an urologist is advised.

Primary closure of a cystotomy can be performed using a simple one or two-layered running closure with absorbable suture.

In general, it takes approximately 3–4 days for the bladder to re-epithelialise and about 3 weeks to regain its normal strength. A catheter can be left in situ for about 7 days with a cystogram performed just prior to its removal, to confirm healing.

In circumstances where a primary closure is difficult (e.g. vaginal surgery, unstable patient, history of pelvic irradiation) and there is a small injury (3 cm or less) in the bladder dome, a suprapubic catheter can be placed. A Foley catheter is placed through the cystotomy, with the bulb remaining in the bladder and the catheter exiting through a stab wound in the lower abdomen.

Women who have received prior lower pelvic radiation or have severe bladder injury require a stronger repair. A carefully dissected omentum, from the hepatic flexure to the splenic flexure, can be used over the two-layer closure to provide neovascularity.

After any repair to the bladder, it must be ensured that the ureteral orifices near the trigone are not compromised. This can be done by passing a stent, retrograde from the bladder toward the kidney or by dissection and visual identification of the distal ureter.

Injury to the ureter

The ureter will occasionally be damaged no matter how much skill and care are exercised. It is essential to directly visualise the ureters at surgery to check for peristalsis, gross dilation (obstruction) or urine leakage, in order to prevent ureteral damage.

The operating surgeon must have a thorough knowledge of the location of the ureter and where it is most susceptible to trauma. The three most common sites of ureteral injury, in the order of frequency of occurence are:

1. While dividing the infundibulopelvic ligament

2. During division of the uterine artery

3. When mobilising the bladder.

The ureter’s course is to some extent variable, and when under pressure, it will gradually change its position in the pelvis. A large tumour filling the pelvis will displace it laterally. A tumour in the broad ligament may displace the ureter outwards and upwards. Duplex (double) ureters are occasionally met with.

A ureter displaced by a fibroid which has occupied the broad ligament.

Radical surgery may destroy so much of the pelvic blood supply that the pelvic ureter becomes ischaemic, leading to fibrotic narrowing or fistula. Damage to the blood vessels may also be produced by pelvic irradiation.

Management of ureteric injury

Ureteric injury should be managed in consultation with a urologist, or a gynaecologist with subspecialty training in urogynaecology.

1. Types of ureteric injury identified at operation.

a. Crush injury from clamp or ligature. The clamp or ligature should be removed, and a ureteric stent inserted.

b. Ligation of the ureter.

The ligation of the ureter should be treated by an end-to-end anastomosis, reimplantation of the ureter into the bladder or by uretero-ureteric anastomosis into the opposite ureter.

2. Ureteric injury identified postoperatively.

Clinical Features

The signs and symptoms relate to the leakage of urine into the ureteric fistulae, and to ureteric obstruction, when the ureter has been ligated. If a ureteric fistula is present, urine leakage may be observed in an abdominal drain, or from the surgical incisions. The patient may develop lower abdominal pain and pyrexia. If the ureter has been ligated, the patient may develop loin pain and pyrexia.

Investigations

1. Ultrasound.

If ureteric obstruction is suspected, an ultrasound may be a useful initial test to identify hydronephrosis.

2. Computerised tomography (CT).

This is becoming another useful test with an increase in the widespread availability of CT scanning. It has the advantage of showing clear anatomical relationships as well as the site of any injury.

3. Intravenous urography.

Intravenous urography (IVU) is useful in the investigation both of ureteric fistulae and of ureteric obstruction. The urinary tract is outlined by radio-opaque dye and the site of leakage or obstruction of urine can be identified. Small fistulae may not be identified by this approach.

4. Percutaneous nephrostomy followed by antegrade pyelography.

This manoeuvre is both therapeutic and diagnostic. Percutaneous nephrostomy is carried out under an ultrasound or X-ray control. Using local anaesthesia, a catheter is passed through the skin and into the renal pelvis or ureter (percutaneous nephrostomy). This allows drainage of the kidney, and prevents further renal damage. Contrast medium can then be injected through the catheter (antegrade pyelography), and this gives further information on the extent of ureteric damage.

Treatment of Ureteric Injury

When ureteric injury is diagnosed, the principle of treatment, in the first instance, is to relieve the ureteric obstruction, thus preventing back pressure on the kidney and subsequent renal necrosis. Clearly, if both ureters have been damaged, and renal compromise/failure is already apparent, consideration should be given to renal dialysis. The following manoeuvres may be useful in the short term:

1. Percutaneous nephrostomy with or without antegrade stenting (see above).

2. Cystoscopy and retrograde insertion of ureteric stents.

In the longer term, formal repair of the ureter is necessary, and this may be achieved using one of the techniques outlined above. It should be emphasised again that these techniques are outside the areas of expertise of most gynaecologists.

Bowel injury

Serosal abrasions should be assessed and repaired where appropriate, particularly when it is a diathermy injury. Injuries involving the muscularis or both the muscularis and the mucosa should also be repaired.

For colonic injury, the lack of a preoperative bowel prep is not an indication for colostomy. After the bowel is repaired, the abdomen is copiously irrigated. Occasionally, a segment of the bowel must be resected, and if reanastomosis is performed, routine care can resume. If bowel reanastomosis cannot be performed due to extensive injury or pathology (i.e. dense adhesions or inflammatory changes), a diverting colostomy may be required.

Fistula formation

Urinary fistula

(L. fistula: a pipe) It is a pathological connection between the urinary tract and an adjacent structure through which urine escapes. A fistula between the bladder base and the vagina is the condition that is most often seen.

Aetiology

1. The exposed bladder wall is torn or penetrated during a vaginal operation, or during total abdominal hysterectomy. This is the commonest cause in this country.

A tear develops during mobilisation of the bladder.

Prolonged pressure of vertex on the vagina during obstructed labour. In a few days, a slough forms. (This should not occur with modern obstetrics in developed countries.)

2. The vaginal wall and bladder are torn during an obstetric operation, or pressure necrosis develops during a prolonged and difficult labour.

3. The ureter is damaged or made ischaemic during a pelvic operation, especially during radical hysterectomy. This produces a ureterovaginal fistula.Exposing ureter in radical hysterectomy

4. Radiation burns following treatment for carcinoma of the cervix. This fistula may appear several years after treatment.

5. Untreated or recurrent cancer of bladder or the genital tract. (This may also be complicated by radiation effects.)

6. Chronic tuberculosis or syphilis. Fistulae may complicate the surgical treatment of pelvic tuberculosis.

7. Congenital fistula. An accessory ectopic ureter may open into the vagina. This condition should be recognised in childhood.

Symptoms

Incontinence may immediately follow the injury, but, usually, the patient has several days of dysuria and haematuria with symptoms of urinary infection. A discharge appears followed by sloughing, and the patient finds that her vulva and perineum are constantly wet. This is soon followed by excoriation of the skin, accompanied by a strong ammoniacal smell and an incrustation of the vulva and vagina with urinary salts. The area becomes extremely tender.

Diagnosis

The fistula is localised by cystoscopy, an intravenous pyelogram and retrograde studies of the ureter. Further imaging with CT or magnetic resonance imaging (MRI), where available, can help to localise the fistulae.

Treatment

Simple vesicovaginal fistulae can be managed by prolonged bladder drainage to allow an opportunity for spontaneous healing. When healing fails to occur, surgical correction is necessary and this may be performed through a vaginal or transabdominal approach.

Simple ureterovaginal fistulae usually heal after being stented, preferably by percutaneous antegrade stents as they have higher success rates. If this fails, surgical repair will be necessary. Complex ureterovesicovaginal fistulae require stenting and drainage until inflammation and infection have resolved and surgical procedures may also be required for their resolution.

Adhesions

One function of the peritoneal surface of the pelvic and abdominal structures is to prevent adherence of these structures when they touch. If the peritoneum is injured as a result of surgery, the damaged areas may stick to each other and a permanent adhesion may form. This typically occurs within the first 5 days after surgery.

Postoperative adhesions occur in 60–90% of women undergoing major gynaecologic surgery. The incidence of adhesion-related intestinal obstruction after gynaecologic surgery is greater upon surgery for malignant conditions and pelvic radiation, compared to benign conditions. Symptoms may occur from weeks to several years after the procedure.

Lymphoedema and lymphocyst

Unilateral or bilateral lymphoedema of the lower extremities can occur after radical surgery, and the risk is greater when postoperative radiation is given.

This is a chronic problem for the resolution of which a referral to a specialist clinic can help. Support hosiery and leg wraps will minimise the oedema, elevation of the extremities while sitting and elevation of the foot of the bed also help to control the problem. Women with lymphoedema should be warned to take care of their skin and pay special attention to the development of erythema or tenderness, as these may indicate infection and a need for systemic antibiotics. Diuretics do not improve lymphoedema, and may lead to electrolyte abnormalities.

Lymphocysts are uncommon after pelvic lymphadenectomy, occurring in about 1–3% of women, 11–12 days after surgery. They are seldom symptomatic and are detected when radiologic studies are performed for the purpose of surveying the woman for recurrent neoplastic disease. Symptoms consist of vague, colicky, lower abdominal pain. Symptomatic lymphocysts and those causing hydronephrosis can be drained percutaneously. Recurrent lymphocysts should be re-drained by tetracycline instillation to sclerose the cavity.

Infectious morbidity

Fever within the first 48 h of surgery is almost always cytokine related. Fever-associated cytokines are released due to tissue trauma and do not necessarily signal infection. Fever due to the trauma of surgery usually resolves within 2–3 days.

Chest radiography, urinalysis, and blood and urine cultures are NOT indicated for all postoperative patients with fever. The need for laboratory testing should be determined from the findings of a careful history and physical examination. The febrile postoperative patient should be evaluated systematically, taking into account the timing of the onset of fever and its many possible causes.

Significant febrile morbidity after gynaecological surgery is usually attributable to infection of the urinary tract, wounds (including the vaginal cuff and necrotising fasciitis), or pelvic cellulitis and abscess. After the first two postoperative days, a thorough inspection of the wound and a good rectovaginal examination are the most important components of the fever work-up. Empiric broad spectrum antibiotics may then be started.

It may be appropriate to arrange further investigations to determine any septic source.

Hernia

Incisional hernia can occur in areas of weakness in incompletely healed surgical wounds. An approach to their prevention is the closure of the incision by incorporating a permanent suture of a length that is at least four times the length of the incision. Symptomatic or cosmetically unacceptable hernias are repaired surgically.

Venous thrombosis

Deep vein thrombosis (DVT) of the lower limbs is a common disease and is often asymptomatic. Complications include pulmonary thromboembolism (PE) and post thrombotic leg syndrome (PLS).

Patients undergoing major general or gynaecological surgery, who are aged 40 years or more, or who have other risk factors (see below) have a significant risk of venous thrombosis. In many of these patients DVT remains asymptomatic, but, in others, it can cause serious morbidity and, potentially, mortality.

There is evidence that routine prophylaxis reduces morbidity, mortality and costs in hospitalised patients at risk of DVT and PE, as highlighted in national and international guidelines. In contrast, screening for asymptomatic DVT and its treatment, are expensive, insensitive and not cost-effective compared to routine prophylaxis in at-risk patients.

Risk factors for venous thrombosis

(SIGN Guidelines October 2002)

Age	Exponential increase in risk with age. In the general population: <40 years annual risk 1/10,000 60–69 years annual risk 1/1000 >80 years annual risk 1/100 May reflect immobility and coagulation activation
Obesity	3 × risk if obese (BMI ≥ 30 kg/m²) May reflect immobility and coagulation activation
Varicose veins	1.5 × risk after major general/orthopaedic surgery But low risk after varicose vein surgery
Previous VTE	Recurrence rate 5%/year, increased by surgery
Thrombophilias	Low coagulation inhibitors (antithrombin, protein C or S) Activated protein C resistance (e.g. Factor V Leidin) High coagulation factors (I, II, VIII, IX, XI) Antiphospholipid syndrome High homocysteine
Other thrombotic states	Malignancy 7 × risk Heart failure Recent myocardial infarction/stroke Severe infection Inflammatory bowel disease, nephrotic syndrome Polycythaemia, paraproteinaemia Bechet’s disease, paroxysmal nocturnal haemoglobinuria
Hormone therapy	Oral combined contraceptives, HRT, raloxifene, tamoxifen 3 × risk High dose progestogens 6× risk
Pregnancy, puerperium	10 × risk
Immobility	Bedrest >3 days 10× risk (increases with duration)
Hospitalisation	Acute trauma, acute illness, surgery, 10× risk
Anaesthesia	2× general vs. spinal/epidural

Pathology

Virchow’s triad encompasses the three broad categories of factors that are thought to contribute to the formation of venous thrombosis:

1. Changes in the vessel wall

Injury or trauma to the vascular endothelium encourages the platelets to adhere to the exposed collagen tissue and these then release substances which further facilitate platelet aggregation. Fibrin and leucocytes then adhere to the platelets. Recent work suggests that a balance is maintained between different groups of prostaglandins.

2. Changes in the pattern of blood flow (flow volume)

Venous flow in the legs is much reduced in the postoperative period and is a result of inactivity and poor muscle tone.

3. Changes in the constituents of blood (hypercoagulability)

Increased procoagulant activity, including elevated platelet count, platelet ‘stickiness’ and fibrinogen levels, contribute to hypercoagulability. Fortunately, there is also a compensating increase in fibrinolytic activity so that nearly all thrombi are naturally broken down.

Sites of thrombus formation

Common sites of thrombus formation include:

(1) The calf veins extending to the popliteal

(2) The long and short saphenous veins, especially those lateral to the knee

(3) The ilio-femoral segment extending to the vena cava

(4) Superficial thrombosis in the distal leg veins.

Clinical features of deep venous thrombosis

In many cases deep venous thrombosis (DVT) is asymptomatic. It is, therefore, imperative to carefully look for clinical features, particularly in the presence of any risk factors (see Risk Factors for Venous Thrombosis). The classical symptoms of DVT include swelling, pain and discoloration in the affected extremity. Physical examination may reveal the palpable cord of a thrombosed vein, unilateral oedema, warmth and superficial venous dilation. Other signs include the Homan’s test of dorsiflexion of the foot for eliciting pain in posterior calf (it should be noted that it is of little diagnostic value and is theoretically dangerous because of the possibility of dislodgement of a loose clot) and Pratt’s sign – the ability to elicit pain by squeezing the posterior calf.

Investigations for deep venous thrombosis

Diagnostic imaging (venography, ultrasound) should be performed expeditiously (within 24 h if possible) in patients with suspected DVT. In all patients with clinically suspected DVT, the diagnosis should be confirmed or excluded by diagnostic imaging, either by non-invasive testing by ultrasound (compression or Duplex scanning) followed by contrast venography, if negative (to detect calf and non-occlusive proximal DVT) or contrast venography (to detect both calf and proximal DVT). It may be necessary to carry out serial (repeat after 7 days) ultrasound examinations to detect a proximal extension of a calf DVT. A single negative ultrasound may be sufficient to exclude DVT in patients with low clinical pre-test probability and/or a normal fibrin D-dimer assay.

Fibrin D-dimer assay

Plasma D-dimers are specific cross-linked derivatives of fibrin that are produced when fibrin is degraded by plasmin, so its concentration is raised in patients with venous thromboembolism. Although sensitive for venous thromboembolism, high concentrations of D-dimers are insufficiently specific for making a positive diagnosis because they occur in other disorders such as a malignancy, pregnancy and after operations. Nevertheless, D-dimer tests generally have a high negative predictive value and are useful rule-out tests that reduce the need for imaging when used in conjunction with clinical probability, plethysmography and the ultrasound.

Ultrasound

This is the best non-invasive technique for diagnosing venous thrombosis. It has a better sensitivity and specificity (97%) in diagnosing of proximal DVT compared to the distal calf vein thrombosis (approximately 75% sensitivity).

Colour flow duplex ultrasonography evaluates blood flow characteristics within the vessel using a pulsed Doppler signal.

Methods of thromboprophylaxis

General Measures

(1) Early ambulation – immobility increases the risk of DVT by about 10 fold and, hence, early mobilisation and leg exercises should be encouraged in postoperative patients.

(2) Postoperative physiotherapy – the physiotherapist encourages the patient to perform deep breathing and exercises to restore muscle tone.

(3) Hydration – haemoconcentration increases blood viscosity and reduces blood flow, especially in the deep veins of the leg in immobile patients; hence adequate hydration should be ensured in immobilised patients.

Mechanical Methods

Mechanical thromboprophylactic methods have been shown to increase mean blood flow velocity in the leg veins and to reduce venous stasis. Unlike pharmacological methods, they do not increase the risk of bleeding. Mechanical methods are contraindicated in patients at risk of ischemic skin necrosis, for example those with critical limb ischemia or severe peripheral neuropathy. Mechanical methods include:

(1) Graduated elastic compression stockings (GECS) – these reduce the pooling of blood in the leg veins. Graduated static compression stockings exert a greater pressure at the ankle than at the thigh.

(2) Pneumatic stockings – inflatable lower leg stocking device that applies intermittent pneumatic pressure to the legs during an operation.

Methods of thromboprophylaxis

Unfractionated and low molecular weight heparins

Unfractionated heparin (UFH) and low molecular weight heparins (LMWHs – dalteparin, enoxparin, reviparin and tinzaparin) are effective in the prophylaxis of VTE in both surgical and medical patients.

The risk of wound haematomas can be minimised by avoiding injection sites close to wounds.

Treatment of dvt

The goals of treatment for DVT are to stop clot propagation and to prevent clot recurrence, pulmonary embolism (PE), and pulmonary hypertension (a potential complication of multiple recurrent PEs). These goals are usually achieved with anticoagulation therapy using heparin followed by warfarin, according to local protocols.

Pulmonary embolism

An embolism arises from a thrombus which was non-occlusive in the vessel in which it was formed and it is therefore symptomless. This then travels to the lung, causing occlusion of the pulmonary vessels.

Peripheral pulmonary embolism

Small emboli are lysed rapidly and are symptomless unless an infarction occurs. They often precede a major embolism, unless treatment is given.

Symptoms	Signs
Fever	Pyrexia
Tachypnoea	Pleural rub
Pleural pain	Crepitations
Haemoptysis (40%)	Perhaps opacity on lung X-ray

Central pulmonary embolism

A large embolus impacting the main pulmonary artery will be immediately fatal, but if it is a little more peripheral, circulatory obstruction will be incomplete and there is a chance of survival.

Symptoms	Signs
1. Collapse

– vasoconstriction

– hypotension

– distended neck veins

– Gallop rhythm

3. Respiratory distress

The cardiac output drops at once and there is intense reflex vasoconstriction leading to tachycardia, hypotension and syncope if the patient is sat up. The respiratory distress is very severe and pulmonary cyanosis may be aggravated by a right-to-left shunt through a patent foramen ovale which exists in 25% of the individuals.

Pulmonary embolism management

1. Remember the risk factors for thromboembolism.

2. Suspect PE in all women presenting with a sudden onset of shortness of breath, chest pain, unexplained tachycardia or cardiovascular collapse.

3. Involve senior medical staff.

4. Assess and ensure adequate airway, breathing and circulation. Commence cardiopulmonary resuscitation if the patient is in cardiac arrest.

5. Transfer the patient to the high-dependency area when appropriate and commence monitoring: non-invasive blood pressure, pulse oximetry, ECG, urine output.

6. Send samples for a full blood count, clotting studies, urea and electrolytes, liver function tests and thrombophilia screen.

7. Request ECG, arterial blood gas and chest X-ray.

Investigations

ECG

ECG is non-specific for the diagnosis of a PE. Right axis deviation and right ventricular strain pattern may be present with a large PE. S waves in lead 1, Q wave in lead 3 and inverted T waves in lead 3 (s1Q3T3) patterns are very rare.

Chest X-Ray

This will help to exclude a pneumothorax and pneumonia. The non-specific radiological changes in PE include segmental collapse, a raised hemi diaphragm, consolidation and unilateral pleural effusion. A wedge-shaped infarction is a rare finding.

Arterial Blood Gases

With massive PE, PaO₂ may be reduced with and a normal or low PaCO₂.

Ventilation/Perfusion (V/Q) Scans

V/Q scanning is the most useful initial test in patients with suspected PE. They are interpreted using standardised criteria and, based on the extent of ventilation-perfusion mismatches, the scan is interpreted as normal, low probability, intermediate probability or high probability for a PE. A normal scan reliably excludes PE and a high-probability V/Q scan is considered as sufficient evidence for the diagnosis of a PE in a patient with a high clinical suspicion. Perfusion scan alone can be performed with a ventilation scan being performed only if the perfusion scan is abnormal.

Duplex Doppler Leg Ultrasound

Bilateral Doppler ultrasound leg studies should be performed in all cases of suspected PE.

CT Pulmonary Angiography

CT, after contrast injection, permits excellent visualisation of the pulmonary arteries and a direct visualisation of pulmonary arterial clots in larger vessels – all during a single breath hold.

Treatment of pulmonary embolus

In most cases, anticoagulant therapy is the mainstay of the treatment. Heparin or LMWHs (such as enoxaparin and dalteparin) are administered initially, while warfarin therapy is commenced.

Massive PE causing haemodynamic instability is an indication for thrombolysis, the enzymatic destruction of the clot with medication. The aim of this therapy is to dissolve the clot, but there is an attendant risk of bleeding or stroke.

Surgical management of acute PE (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes.

Chronic PE leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated by a surgical procedure known as a pulmonary thromboendarterectomy.

If anticoagulant therapy is contraindicated and/or ineffective, or to prevent new emboli from entering the pulmonary artery and combining with an existing blockage, an inferior vena cava filter may be implanted.

Mortality

A retrospective study of 1.45 million gynaecology inpatients in England reported a mortality rate of 0.2% within 30 days of admission and 0.5% within 90 days. The 30-day death rate in patients with cancer was higher than for patients without cancer (5.1% vs. 0.1%).

Related

Gynaecology Illustrated