Хирургические болезни. Практикум = Surgical diseases. Practice book. Учебное пособие

1.4. FISTULA

Fistula is a pathological passage in tissues lined from the inside with the epithelium or granulations, connecting organ, natural or pathological cavity connected with each other and with the body surface.

Classification. Fistulas are classified according to:

•their causes:

congenital – caused by fetal malformations. The absolute number of cases has epitalized lining;

acquired – divided into:

−pathological (granulating or mixed);

−artificial, caused by surgical interventions;

•structure:

granulated – healing of such kinds of fistula does not occur due to the following reasons:

−chemically active ingredients of the content (gastric juice, secretion of the small intestine, chyme), bacterial toxins;

−accumulation of fistula discharge in the fistula cavity or in its additional passages;

−continuous discharge from the pathological focus;

epithelized – include a labial fistula in which the mucous epithelium of the hollow organ passes to the skin and eliminates the possibility of self-closing;

mixed (granulating and epithelized);

•character of discharge:

mucous;

pus;

urine;

fecal;

bile;

saliva;

cerebrospinal fluid;

•relevance to the body cavities:

external (including fistulas of the artificial origin, also called “stoma”). They may be complete or incomplete depending on the opening to the skin and preserving the partial transit along the gastrointestinal tract;

internal, including fistulas of the artificial origin, called “anastomosis”.

Etiology. Causes of internal fistulas are divided into:

•congenital;

•acquired;

•posttraumatic (caused by the open and closed penetrating wounds);

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•postoperative (after creating unloading stomas in separate portions of the gastrointestinal tract or for patient’s feeding);

•due to anastomotic leak from stitches; technical mistakes in the forma-

tion;

•inflammatory processes;

•pressure sores on hollow organs’ walls caused by foreign bodies;

•cancer.

Clinical picture. On examination of external fi stulas, it is possible to reveal the fistulous opening through which the content of the pathological focus is discharged. Over time, a channel, connecting the center (organ) with the skin, is formed, which is then internally coated with granulations or epithelium. A long term course of the pathological process is accompanied by an additional infection of surrounding tissues and results in the endogenous intoxication. In case of complete external fistula of the stomach and the small intestine loss of significant amounts of digestive juices leading to dysproteinemia, water and electrolyte disturbances are observed.

Internal fi stulas do not have specific symptoms and clinical signs are often associated with a particular organ lesion, usually occur against the background of the inflammatory infiltrate formation.

Treatment. Treatment of fistulas requires compulsory surgical treatment with the exception of granulation, which in some cases can be naturally closed. The condition for adequate surgical intervention in fistulas is their complete removal. The methods of thermal or chemical destruction of the fistula epithelium are generally ineffective.

Treatment of epithelial labial fistulas consists in pre-mobilization of a hollow organ involved in the process with subsequent resection performed within healthy tissues, rarely with a suturing of the defect.

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Chapter 2

VASCULAR DISEASES.

PERIPHERAL ARTERIAL DISEASES

2.1. ACUTE ARTERIAL OBSTRUCTION

Acute arterial obstruction (AAO) is a syndrome of a sudden onset of arterial blood flow disorders due to various causes, manifested by acute ischemia of the blood supply organ and creating a potential threat to its viability.

Etiology. The reasons of AAO are the following:

1.Embolism is an acute occlusion of arterial blood flow by a morphological substrate that has entered the vascular bed with a blood stream. In most cases, the morphological substrate of the embolism is a thrombus formed in the left parts of the heart (due to coronary artery disease or mitral malformations), above the sections of the large circle of circulation, rarely – pulmonary veins, trunk veins of the extremities. More rarely, emboli are fragments of atherosclerotic plaques, vascular catheters or stents, tiny fat particles (fat embolism), foreign bodies.

2.Acute thrombosis is a sudden occlusion of the arterial blood flow with a blood clot formed directly in the affected area due to diseases or injuries of the vascular wall.

3.Traumatic damage to the artery wall due to the intersection of the artery or compression by its hematoma, bone fragments; prolonged (more than 2 hours) application of a tourniquet to segments of the limb; more rarely as a result of accidental intraoperative dressing.

4.Tumors with secondary involvement of the wall (often have a myxomatous origin).

5.Prolonged arterial spasm (the main trunk vessel and secondary collaterals). Arterial spasm arises in the popliteal and brachial arteries, where the muscular layers are most pronounced, and therefore an active reaction to external (impact, compression) or internal stimuli (thrombophlebitis, thrombosis of distal parts of the peripheral arteries). Arterial spasm may be segmental or common (most often).

Currently, the absolute majority of AAO cases (more than 90%) occur in case of arterial thrombosis and embolism, they both are directly related to the improvement of diagnosis and the general increase in the number of patients of the elderly and senile age who have a history of coronary artery disease, heart defects with valve prosthetics.

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Clinical picture. Clinical manifestations of AAO depend on the stage of the process and the degree of acute ischemia (see Table 1):

Table 1. Dependence of the clinical manifestations of AAO on the stage of the process

and the degree of acute ischemia

Diagnosis. Diagnosis of AAO includes the following:

1.Data of laboratory diagnosis (including analysis of blood and urine, biochemical complex, defining PTI, INR).

2.Ultrasound Doppler study, which presents an auscultatory analysis of blood flow velocity, volume and regional systolic pressure at various segmental levels.

At stage II of AAO, there is no arterial inflow with preservation of venous outflow.

At stage III of AAO, a complete auscultatory absence of both arterial inflow and venous outflow is determined.

3.Ultrasound duplex angioscanning, which lets the doctors assess both the level of occlusion and the state of the vascular wall in the real time mode.

4.Radiopaque contrast angiography.

5.CT and MRI angiography by preliminary introduction of radiopaque preparations (ultravist, omnipak, otpireta) into the main bloodstream with further analysis of the reflected images (by blood vessels).

The main advantage of MRI angiography is the possibility of vascular structures visualization in 3-dimensional (3D) format with subsequent multi-cavity reconstruction.

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Treatment. Treatment of AAO should be performed when the diagnosis is determined, taking into account the confirmed stage of AAO and the degree of ischemia.

At the 1st degree an emergency surgery (within up to 24 hours) is recommended. In case of a stable condition, a complex of additional diagnostic measures is performed, and treatment begins with conservative therapy, which includes:

•administration of heparin (in a dose of 40–50 000 IU IV) or low-mo- lecular heparins (Fraxiparin, Kleksan, Fragim);

•introduction of plasma substitutes for hemorheological effect (rheopolyglucin, reogluman, reomacrodex, neorondex, rhodferrin), substrate antihypoxants (cytoflavin, reamberin);

•antiaggregants (tiklid, clopygoryl (plavix), suledoxid); pentoxifyl-

line);

•spasmolytics of myotropic effect (duspatalin, no-spa, drotaverin). At II-A degree treatment is supplemented with catheter thrombolysis

by activators of profibrinolysin (alteplase, streptokinase, celiaze, streptodecase). After thrombolysis, aspiration balloon thrombectomy or various endovascular interventions to correct blood flow (stenting, transluminal angioplasty, laser recanalization, etc.) are performed.

Beginning with II-B stage of the AAO, urgent interventions are undertaken to restore blood flow within a period of not later than 2–2.5 hours from the time of admission to the hospital. To do this, most often indirect (with the help of an inflating Fogarty balloon, connected with a catheter inserted into the lumen of the artery) and, less often – direct thrombembolectomy through the incision of the artery in the place of acute occlusion is performed.

At II-B degree AAO revascularization intervention is supplemented with fasciotomy to reduce subfascial edema of muscles, located in corresponding sheathes.

At III-B degree primary amputation is recommended without any attempts to restore blood flow, inevitably accompanied by a fatal outcome induced by the development of postischemic syndrome due to the penetration of an additional amount of metabolic acidosis products, enzymes and myoglobin in the bloodstream.

2.2. CHRONIC ARTERIAL OBSTRUCTION

Chronic arterial obstruction (insufficiency) (CAO) is a complex of syndromes that unites various diseases according to etiopathogenesis based on gradually increased arterial blood circulation pathology (chronic ischemia).

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CAO occurs in 2–3% of the adult population, about 600–800 new cases per 1 million population are reported annually. They are accompanied by 10–20 cases of amputations per year per 100,000 adults. In most cases CAO occurs 3–5 years after the onset of the first symptoms.

Classification. Obliterating diseases of the lower extremity vessels (ODLEV) are divided into 2 types:

1.Functional diseases of arteries (synonyms – angiotrophoneurosis, angiospasm, trophoparalysis of vessels, neurocirculatory dystonia). This group of diseases occurs in people with hyperactivity of the sympathetic part of the nervous system, mainly in young women with increased emotional lability. Background factors are the following: repeated stresses, smoking, repeated cold.

2.Organic diseases of the arteries. Accompanied by the development of organic (structural) impairments of the arterial wall, such diseases result in subsequent chronic tissue ischemia.

Currently, the clinical classification of AAO of the lower extremities, proposed by R. Fontaine (1954) and A.V. Pokrovsky (1979), with the ad-

ditions of V.S. Saveliev and V.M. Kohkin (1997), is generally accepted:

• Stage I or asymptomatic stage is characterized by the appearance of

the symptom of “intermittent claudication” (clandicatio intermitetns – a symptom of Charcot) when walking of more than 1000 m;

•Stage II-A – pain during exercise and “intermittent claudication”, which occurs while walking 200–1000 m;

•Stage II-B – the appearance of “intermittent claudication” while walking a distance of up to 200 m;

•Stage III – ischemic pain in the limb, arising at rest (more often at night):

Stage III-A – pain at rest in the absence of ischemic edema and the possibility of keeping the horizontal position of the leg in the bed for more than 2 hours;

Stage III-B – pain at rest, attachment of ischemic edema, absence of the possibility of keeping the foot in the horizontal position for more than 2 hours;

•Stage IV – the stage of trophic disorders (appearance of ulcers, necrosis or gangrene). Assessing the ability to handle NDT, this stage is divided into:

Stage IV-A – appearance of gangrene of the fingers, part of the foot with the possibility of maintaining the supporting function of the limb; сases of “critical ischemia”;

Stage IV-B – progressive gangrene of the limb without the possibil-

ity of maintaining the ability to support the lower limb.

Etiology. CAO is usually caused by the development of inflammatorydegenerative or atherosclerotic processes, leading to obliteration (narrowing) of the lumen of the arterial vessel. This narrowing, called stenosis or

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complete closure of the artery lumen (occlusion), can occur in any kinds of main vessels – carotid, coronary, mesenteric, renal. However, for general surgical practice, the lesions of the arteries of the lower extremities are of paramount importance.

The prevalence of obliterating diseases of the lower extremity vessels is about 5% of the total population and significantly increases by age 60– 70. Among the localization of the ODLEV, the femoropopliteal segment is affected in 50–55% of cases, the aorto-iliac is affected in 25–30% of cases, the tibial artery in 12–20%.

The risk factors of CAO are:

•belonging to the male sex (occurs 2 times more often than in women of the corresponding age);

•elderly and senile age;

•smoking (in case of smoking for more than 20 years, the risk increases by 3 times);

•diabetes mellitus (increases the risk by 4 times);

•arterial hypertension;

•excess weight and lipid metabolism disorders (increases the risk by 2 times).

Among the nosological forms of ODLEV 80–90% are obliterating atherosclerosis of the lower extremity vessels (OALEV), 10–20% – other diseases; obliterant thromboangiitis (OTp), nonspecific aorto-arteritis (NAA or Takayasu’s disease), and diabetic macroangiopathy of NK (DA). Lesions of the arteries of the upper limbs are much less common and account for only about 1% of all cases of ODLEV.

Diagnosis. To assess the indices of macrohemodynamics in AAO noninvasive investigation methods are applied, including:

•ultrasound dopplerography with the definition of segmental pressure at various levels (including finger arteries) and ankle-brachial index (in case of “critical ischemia” and LPI less than 0.4 conv. units). The arteries of the upper limbs are affected in less than 1% of cases and according to the sound flow in the projection of the brachial artery, it will always remain unchanged, its speed is taken as the standard (or “1”), on the lower extremity (LE) arteries to “1” (the standard). LPI can be measured in the direction of a significant decrease in tests with physical activity: a treadmill test at the speed of

3.2Kph for 5 minutes. In this test, the time of the first manifestation of the pain syndrome (the so-called minimum distance of walking) is established, as well as the time of the patient’s stop because of severe pain (or the maximum distance of walking);

•duplex scanning of lower extremities arteries (including the vessels of the shin and foot), iliac vessels, aorta, allowing to establish the level of stenosis of these vessels;

•rheovasography – the method of graphical recording of oscillations due to the resistance of the blood flow to the alternating electric current of

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high frequency. It is recorded after longitudinal application of electrodes: in the zone of the lumbar ligament – popliteal fossa – rear of the foot. It is based on the detection of pulse waves in the ascending (anacrotic-α) and descending (kakrota-β) parts, allowing to estimate the ratio of the height of their amplitude to the height of the calibration pulse (called the rheovasographic index);

•oscillography is a technique for determining the magnitude of the pulse oscillations of the arterial wall depending on the level of pressure in the mange superimposed on a certain segment of the lower extremities (LE).

Invasive methods of investigation, including:

•radiopaque angiography of the aorta, iliac arteries and vessels of the lower limbs;

•computer tomography angiography, consisting of:

spiral CT with rotation of the radiographic unit around the patient and continuous movement of the table along a spiral;

electro-beam therapy (EBT), which scanning the motion of the bolus of contrast medium at a high speed (140 cm / sec) in the direction of the blood flow along large arteries;

CKT (EBT) – to receive reconstruction of slices in the 3D image;

•magnetic resonance angiography (MRA), which the specialists to analyze reflected signals from blood moving along blood vessels and acting as a natural contrast medium. In some cases, to eliminate various artifacts, MRA is carried out with contrast enhancement by a paramagnetic complex (gadolinium).

The methods of microhemodynamics (microcirculation) assessment in AAO are the following:

•video capillaroscopy;

•finger plethysmography;

•radioisotope scintigraphy;

•laser doppler flowmetry (a technique to estimate the linear and volume velocity of blood flow, based on the capture of a beam of ultrasound oscillations reflected from the surface moving in the main arterial blood). It allows the doctors to confirm the localization of the level of the vessel occlusion;

•transcutaneous oximetry (in critical ischemia, the transcutaneous oxygen tension in the foot tissues is less than 30 mm Hg).

Treatment. Conservative therapy in ODLEV includes the following:

•elimination of pain syndrome;

•dealing with angiospasm (the use of antispasmodics in this case is recommended only in case of the spastic form of the disease and at its initial stage or in the absence of persistent ischemia and trophic disorders);

•correction of rheological and hemocoagulation. It is achieved by the introduction of:

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anticoagulants based on low molecular weight heparin (clexane, fragmine, fraxiparin) for 8–10 days with the further administration of anticoagulants of indirect effect;

antiplatelet agents (trental, ticlopid (ticlid), clopidogrel (plavix), and others;

complex drugs, including synthetic analogue of prostaglandin E1 – alprostadil (vasaprostan); it improves microcirculation, blood flow of tissues, which has antiaggregatory and antisclerotic effect;

•stabilization of oxidative processes by inhibiting the processes of lipid peroxidation and activation of antioxidant protection. It is achieved by using:

substrate antioxidant drugs (reamberin, cytofl avin, mexidol, emoxipin);

tissue metabolism activators (gliatilin, solcoseryl, actovegin), improving aerobic glycolysis by utilization of glucose, oxygen and activation of Krebs cycle enzymes, stimulating the synthesis of ATP and normalizing the energy metabolism of cells.

2.3. OBLITERATING ATHEROSCLEROSIS OF THE LOWER EXTREMITY VESSELS

It is a vascular disease, caused by primary infiltration of the vascular wall with high-density lipid complexes against the background of changes in cholesterol metabolism. Activation of the process is facilitated by hypertension, adynamia, diabetes mellitus, chronic intoxications, hormonal disorders, overweight, chlamydial infection.

Further diffuse impregnation of the intima of the vessels with lipids is accompanied by a secondary thickening of the wall, propagating distally and leading to the atrophy of the muscle fibers (the middle layer of the arteries). Often in the distal segments of the arteries, due to a slowdown in blood flow, clots arise, thus completely blocking the lumen.

Due to the occlusion or stenosis of the artery lumen, perfusion pressure of peripheral tissues is reduced, with the threshold value of 25–30 mm Hg.

The decrease in perfusion pressure in tissues below this value triggers a number of pathological mechanisms including:

•hyperproduction of inflammatory mediators: cytokines, biologically active kinins; products of POL (aldehydes, ketones, hydroperoxides), nitric oxide (NO ), platelet activating factor (PAF) against the background of a significant inhibition of the mechanisms of antioxidant protection;

•opening of arteriovenous shunts;

•development of ischemic edema;

•attachment of destructively necrotic tissue changes with their secondary inflammation and infection.

Clinical picture. The following types of clinical course of OALEV are distinguished:

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•chronic stable (duration of the process is more than 10–15 years);

•chronic with slow progression;

•chronic with exacerbations (called subacute with the appearance of dry gangrene, necrosis, formation of trophic ulcers, detected in 40% of patients);

•acute, manifested by acute arterial insufficiency and “critical ischemia” against a background of previous relatively favorable condition.

“Critical ischemia” (Jaminson, 1982) is understood as a condition characterized by:

•constant pain at rest, which determines the prescription of analgesics for more than 2 weeks;

•a decrease in LIP less than 0.4 units or transcutaneous oxygen tension in foot tissuesless than 30 mm Hg;

•appearance of trophic ulcers, gangrene of fingers or feet (sometimes wet gangrene or mummification of tissues with signs of necrotic areas selfrejection).

Appearance of “critical ischemia” stipulates the need for urgent correction of the main blood flow.

Treatment. Operative treatment of OALEV includes the following groups of interventions:

1. Operations to restore or reconstruct the main blood flow. Restorative operations include interventions, aimed at restoring the ar-

terial blood flow achieved by: thromboembollectomy, endarterectomy, percutaneous balloon dilatation, endoprosthetics or stenting.

Reconstruction is the operations aimed at creating by-pass of blood flow by removing, substituting or shunting the occluded area (below or above the occlusion).

Endarterectomy is a kind of intervention aimed at removing the inner membrane (intima) together with atherosclerotic masses (intimendarterectomy). It is used for local occlusion with a length of up to 5–7 cm; in a number of cases it has the nature of palliative intervention due to the high risk of planned reconstruction.

For the purpose of the blood flow reconstructing in a multilevel lesion, the following procedures are used: prosthetics, shunting of the affected vascular segments with allo-, auto-, xenografts; aorto-femoral prosthesis, profundoplasty – stitching of an autovenous patch in the femoral artery to stimulate blood flow in case of its stenosis (deep femoral artery), femoralpopliteal or femoral-tibial types of shunting.

2. Operations for indirect vascularization of the ischemic limb include interventions that contribute to indirect increase in the blood flow in tissues in systemic lesions of the main arteries by:

•resection of posterior tibial veins with ligation of arteriovenous anastomoses (V.M. Koshkin, 1993);

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