Necrosis can be direct (direct destruction by a traumatic factor) or indirect (due to disruption of tissue nutrition).

Why does a dog have necrosis?

The reason that a dog has soft tissue necrosis can be an injury, wound, or lesion electric shock, exposure to high or low temperatures, chemical reagents (acids, alkalis). With indirect necrosis, there is a disruption in the supply of oxygen and nutrients to cells and tissues as a result of prolonged squeezing, squeezing, pinching, spasm blood vessels and nerves, thrombosis.

Necrosis is almost always accompanied by pathogens that cause necrotic infections. Necrosis of soft tissues includes: heart attack, gangrene, bedsores, dry and wet (appearance of pus) necrosis. The speed and extent of spread of dead cells depend on the duration of mechanical action, the infection that has joined, and also anatomical features damaged organ.

Symptoms: swelling, inflammation, pain reaction, discharge of pus, discoloration of the damaged area of ​​skin or limb, blistering, unpleasant odor from the wound. Subsequently, poisoning of the entire body occurs, which is accompanied by an increase in body temperature and weakness of the animal. If proper assistance is not provided, the dog will die.

Treatment

Treatment is carried out comprehensively: necrotic tissues and organs are surgically removed, and immunostimulants and drugs that have regenerative properties are prescribed in parallel. Painkillers and antibiotic therapy are also used. Surgically, necrotomy (dissection of necrosis), necrectomy (removal or amputation) can be performed.

Necrotomy is performed for necrosis that covers a large area, in particular on the limbs and chest. During this manipulation, necrotic tissue is cut into living tissue, due to which oxygen access is restored to it and nutrition is improved. Necrectomy is carried out within viable tissue after the boundaries of dead tissue are clearly defined. After removing the necrotic tissue, sutures are applied. Amputation of a limb or part of it is carried out only if necessary to ensure that the infection does not spread further and the animal does not die.

Since minor injuries - punctures, bruises, bites - can cause such a serious disease as necrosis, you need to carefully monitor your four-fingered friend, especially while walking. In the postoperative period, it is necessary to follow the rules of hygiene to prevent secondary infection. If dangerous symptoms appear, consult a specialist as soon as possible.

Without medical attention, the dog dies. The rate of development of necrosis depends on how long the mechanical impact on the tissue and further exposure to infection lasted, as well as on the anatomical features of the organ that is affected by necrosis.

Treatment

When treating necrosis, surgery cannot be avoided. Dead tissue and organs must be removed. There are two types of operations:

1. necrotomy (cutting through necrosis to remove dead soft tissue)
2. necrectomy (amputation or removal of a dead organ).

Necrotomy is performed for extensive necrosis, most often on the chest and limbs. During this manipulation, necrotic tissue is cut down to living tissue. This improves her nutrition and restores her access to oxygen.

Necrectomy is performed to prevent the infection from spreading further, that is, to save the life of the animal. In addition, treatment is carried out as a whole complex. Except surgical procedures therapy is also used.

As a rule, drugs that have regenerative properties and immunostimulants are prescribed. After surgery, antibiotics and painkillers are used. In case of bone necrosis after surgery, antibiotics are prescribed, which are administered by intraosseous injection.

Disease prevention

Often the cause of such a serious illness is quite minor injuries: bruises, injections, bites.

Therefore, in order to prevent tragic consequences, it is necessary to closely monitor the dog, especially during games and walks. Inspect all bruises, treat the slightest wounds with antiseptics, always show more serious wounds to a veterinarian, monitor bandages, and do not let the dog lick.

If an animal has undergone any surgery, it is necessary to strictly follow all hygiene rules so that neither primary nor secondary infection occurs. If the described symptoms of necrosis appear, you should consult a specialist as soon as possible.

May 19 2019

Folliculitis in dogs

Folliculitis- localized purulent inflammatory process of the tissue around the hair. A similar inflammation of only the hair opening is called ostiofolliculitis. The disease begins with the appearance of hyperemia of the skin around the hair with the formation on days 3-5 of a small pustule containing a small amount of yellowish-white pus with a thick consistency. Subsequently, the pustule may spontaneously open with the formation of a crust on the surface. However, under unfavorable conditions, folliculitis can be complicated by the development of a boil.

Treatment begin with hair removal and antiseptic treatment of the skin with iodized or camphor alcohol. Then, using a sterile needle, carefully open the abscess and remove the pus with a swab. The affected areas of the skin are lubricated with a 2% formaldehyde solution, brilliant green, and methylene blue. If large areas of the skin are affected, irradiation is prescribed ultraviolet rays in suberythemal doses.

Furuncle in dogs

Furuncle (Furunculus)- purulent inflammation of the hair follicle, sebaceous jelly and adjacent loose fiber. The causative agent is most often staphylococcus. When the body's resistance to staphylococcus weakens, the disease can acquire a generalized form with the development of furunculosis. It usually begins with ostiofolliculitis, then the inflammatory process spreads to the loose tissue surrounding the hair follicle with the formation of a nodule of cellular infiltration, which turns into a dense lesion with tense, swollen and hyperemic skin above it. Subsequently, the nodule acquires a limited cone-shaped shape with severe pain. Due to inflammation, necrosis of the follicle and the surrounding loose connective tissue and skin occurs with the formation of a dead shaft with a hair in the center. Purulent demarcation inflammation, sequestration and melting of tissue elements develop around the rod. General reaction may manifest itself by the development of purulent-resorptive fever, especially in cases of generalized form of furunculosis.

Boils localized in the head area pose a great danger due to possible thrombosis of the external maxillary vein (V. maxillaris externa) with subsequent transfer of inflammation to the venous sinus, which is directly connected to the venous system of the brain.

Treatment carried out taking into account the stage of the disease, the nature of the lesion and the condition of the body. It must be comprehensive - local and general. During local treatment, they are removed hairline, the skin is washed warm water with soap, wipe the surrounding skin with 70% iodized alcohol, 1% solution of brilliant green, followed by exposure to dry heat (irradiation with Sollux, Minina lamps). At the stage of cellular infiltration, a short novocaine-antibiotic block is effective. When a purulent-necrotic rod forms, it is carefully removed without damaging the demarcation barrier (do not squeeze it out under any circumstances!). After removing the rod and exudate, antiseptic ointments (Vishnevsky, streptocidal) are used. At the same time, general antiseptic treatment (antibiotics) is carried out. For furunculosis, autohemotherapy, vitamin therapy, ultraviolet irradiation in erythemal doses.

Carbuncle in dogs

Carbuncle (Carbunculus). This name refers to acute purulent inflammation of several adjacent hair follicles, sebaceous glands with surrounding loose connective tissue. The disease is characterized by the development of a larger infiltrate than with a boil, followed by significant necrosis of the skin and subcutaneous tissue.

Etiology and pathogenesis are the same as with a boil, but differ in the more extensive nature of their development. Due to necrosis of the skin and subcutaneous tissue, cavities and niches containing necrotic tissue are formed in the thickness of the carbuncle tissue. The demarcation barrier is weakly expressed, its formation is slow, so carbuncles can be the cause of the development of general purulent infection(sepsis).

Clinical picture characterized by a dense consistency, a very painful inflammatory infiltrate with the presence of several pustules. The infiltrate gradually increases, acquires a dense consistency and a purple color. A few days after the formation of the infiltrate, the skin becomes thinner and becomes necrotic in several places, followed by the release of purulent exudate. It takes on the appearance of being pierced by many holes filled with purulent-necrotic plugs. Subsequently, these holes merge, forming an ulcer. The disease is usually accompanied by purulent-resorptive fever with an increase in body temperature up to 40°C.

Treatment is the same as for phlegmon, complex with the use of local and general effects, as well as symptomatic and pathogenetic agents(see treatment of phlegmon in this article).

Abscess in dogs

Abscess- limited acute purulent inflammation of loose connective tissue with the formation of a cavity filled with purulent exudate. People call this disease an abscess or an abscess. The abscess cavity is limited by the surrounding tissue by the membrane.

Etiology. There can be various reasons for the development of abscess formation in dogs. mechanical injuries skin and underlying tissues with the introduction of purulent or putrefactive infection into them. Infection can also occur hematogenously. Abscesses are classified according to their course: acute, subacute and chronic; by etiology - aseptic and infectious; according to the clinical manifestation - hot, cold and sintered according to the depth of occurrence - superficial and deep.

Clinical signs well expressed in superficial abscesses and are characterized by the formation of a hemispherical, fluctuating and painful swelling on palpation. At acute course inflammatory process there is an increase in local and general temperature, increased heart rate, breathing, depression of the animal, possible dysfunction of the affected organ. The diagnosis is confirmed by puncture.

Treatment. At the initial stage of abscess formation, a short novocaine-antibiotic block is effective; to accelerate maturation, warming alcohol-ichthyol compresses and dressings with ichthyol ointment are effective. With the formation of a cavity, abscesses are opened after preliminary infiltration anesthesia, purulent exudate is removed and washed aqueous solutions antiseptics (hydrogen peroxide, furatsilin, ethacridine lactate, etc.). The cavity is drained and loosely filled with gauze drainage with A.I. ointment. Vishnevsky or emulsions of syntomycin, streptocide. Subsequent treatment is the same as for wounds in the second phase of healing.

Cellulitis in dogs

Phlegmon- Diffuse inflammation of loose connective tissue, accompanied by purulent-necrotic phenomena.

Etiology. The causes of phlegmon are various open mechanical damage with the introduction of purulent, putrefactive or anaerobic infection into them. This infection can penetrate hematogenously. Cellulitis can also occur as a result of complications of abscesses, boils, infected wounds, purulent arthritis, osteomyelitis, etc.

Depending on the location and inflammatory process, phlegmons are distinguished: subcutaneous, subfascial, intermuscular, retroperitoneal, pararectal and other organs in which there is loose connective tissue. The disease is very severe and is accompanied by severe depression of the animal, the manifestation of purulent-resorptive fever, and often the development of sepsis.

Clinical signs. The leading symptom of phlegmon is diffuse swelling spreading over a large area. There is severe pain, increased local temperature and tension in the swelling tissues. The general reaction of the body is characterized by a sharp increase in body temperature, depression of the animal, and decreased appetite. There is an increase in regional lymph nodes. In cases of putrefactive or anaerobic infection, gangrenous tissue breakdown occurs more intensely.

Treatment. The dogs are given rest. Antibiotics are administered intramuscularly in the form of a course, and sulfonamides are given orally. The site of infection is subjected to careful surgical treatment. In the initial period of development of phlegmon, short novocaine blockades, alcohol-ichthyol warming compresses, heating pads, thermal wraps, irradiation with Sollux and Minina lamps are used. However, resorption of phlegmon should only be done in combination with general antiseptic therapy.

If after the specified treatment there is no improvement and the swelling does not decrease, the phlegmon is immediately opened. The operation is carried out under local infiltration anesthesia, the resulting bleeding is stopped by torsion or ligation of the vessel. The wound is irrigated with a 3% solution of hydrogen peroxide prepared with a solution of furatsilin 1:5000, or hot (40-42°C) hypertonic solution sodium chloride. It is also advisable to drain the wound with gauze drainage soaked in the specified solution, followed by application of a suction bandage. Abscesses detected by palpation are also opened, necrotic tissue is removed, washed antiseptic solutions, then drains soaked in liquid ointment A.V. are inserted. Vishnevsky or other antiseptic agents. As the wound cavity fills with granulations and epidermization, in order to avoid the formation of a rough scar, dogs are prescribed walks, thermal procedures, tissue therapy.

Etiology. This disease occurs when, under the influence of certain chemicals and physical factors the following occurs: 1) the influx of arterial blood stops and the outflow of blood through the veins continues; 2) water easily evaporates from the surface of the skin, mucous membrane into the surrounding external environment; 3) the affected organ or area of ​​the body contains little moisture; 4) tissue damage is accompanied by dehydration - the loss of water from it (carbolic necrosis after applying a warming carbolic compress). Peripheral organs with a large area of ​​evaporation are most often affected by dry gangrene: ears, tail, lower limbs, in birds - comb and earrings.

The development of this disease is usually associated with damage vascular system in case of poisoning with uterine horns, or ergot (secali cornutum). As is known, the uterine horns act on the circular muscles of the vessels and the ganglia embedded in their walls, as a result of which vasomotor disorders arise - vasoconstriction, prolonged vasospasm, followed by ischemia and circulatory disorders, especially in small-caliber arterial vessels. Sphacelotoxin, chrysotoxin and se calin-toxin, contained in the uterine horns, have a necrobiotic effect on tissue, and cornutin causes vasospasm. Nutritional malnutrition increases toxic effect uterine horns and, therefore, contributes to the development of dry gangrene. Gangrene caused by ergot poisoning (Ergotismus gangraeiiosus) is observed in birds, pigs, cows, horses and other herbivores after feeding them bread or cereal plants containing a lot of ergot.

Superficial dry necrosis - dry gangrene of the skin occurs very often in horses from circulatory disorders due to prolonged pressure (see “Bedsores”).

Clinical signs. Dry gangrene has characteristic clinical symptoms, on the basis of which a diagnosis can be made accurately. They consist of progressive drying, thinning and discoloration of the skin. The skin loses elasticity, becomes tight, insensitive and black. With dry necrosis of the lower extremities, the peripheral pulse disappears. The gangrenous area becomes numb and cold to the touch. Dry skin that has lost its elasticity (if it is not pigmented) turns pale, then takes on a blue-red color and finally turns black.

After 3-4 days, demarcation reactive inflammation is detected, through which sequestration of the dead area or organ occurs. At the border between living and dead tissues, a demarcation line appears in the form of a red stripe with a yellow border - the leukocyte zone. The latter, directly adjacent to dead tissue, clearly marks their boundaries. Subsequently, the line of demarcation is a belt of granulating tissue, covered with a small amount of thick yellowish-white pus, gradually increasing as the necrotic area is sloughed off.

Independent separation of a gangrenous area or organ through demarcation inflammation is called mutilatio (circumcision). The gradual drying of necrotic tissue is called mummification. Reactive inflammation serves as a reliable sign of stopping the further spread of tissue necrosis and rejection of the dead organ. When the tissues are inclined towards progressive necrosis, the demarcation line, the so-called reactive stripe of inflammation, has a vague appearance or is completely absent. It should be borne in mind that the demarcation line forms quickly in soft tissues and slowly in dense, poorly vascularized tissues - tendons, fascia, ligaments and aponeuroses.

Dry gangrene is usually not accompanied by symptoms of general intoxication and bacteremia, since mummifying tissues are not an environment favorable for the development of microbes, and the destruction of blood supply pathways prevents the absorption of tissue decay products. With the development of demarcation inflammation, a strong barrier is formed that eliminates the possibility of decay products and bacteria from the necrotic lesion penetrating into healthy tissues.

Treatment. It is necessary to take all measures to ensure that dry gangrene does not turn into wet gangrene. First of all, you should disinfect the skin with antiseptic and sealing agents: 3% alcohol solutions of pyoctanin, brilliant green or gentian violet, protect the affected area from mechanical damage by applying dry antiseptic dressings, handle tissues carefully and do not injure the demarcation line when bandaging. The use of baths, warming compresses, and wet dressings creates a real threat to the transformation of the dry form of gangrene into a wet one with all the ensuing bad consequences.

It is recommended to surgically remove the dead organ, the area is recommended after the formation of a demarcation line, so as not to leave (for example, during amputation) necrotic tissue.

WET GANGRENE

Gangraena humida

Etiology. Wet gangrene occurs more often in animals than dry gangrene. Its occurrence is associated with a delay venous blood in the absence of arterial blood flow in well-vascularized tissues. Such a circulatory disorder can be caused by severe bruises of soft tissues without violating the integrity of the skin, constriction with a tourniquet, elastic tube, annular foreign body of any organ, for example, a limb, penis, tongue, udder nipple, compressed intestinal loop in a hernial ring, frostbite and etc.

Rice. 42-43. Wet gangrene of the limb in a dog:

A - view of the affected limb before surgery; B - amputated limb; B - amputated stump (on the 10th day after surgery). ( Surgical clinic Moscow Veterinary Academy).

The impossibility of drying and evaporation of liquid from the surface of a dead organ, the presence of a large amount of liquid in it - blood and lymph - create very favorable conditions for softening, liquefying dead tissues, and introducing pathogenic microbes into them. The presence of microbes accelerates the melting of tissues and the spread of wet gangrene to healthy neighboring tissues. Usually it progresses so quickly that demarcation inflammation does not have time to develop, resulting in severe general intoxication of the body with very toxic products of tissue decay and bacterial activity.

Clinical signs. Wet gangrene begins with rapidly increasing congestion, swelling and coldness of the affected organ. The mucous membrane and non-pigmented skin, slightly cyanotic at the beginning of the disease, become purple-blue and then bluish-black within a few hours.

Rice. 44. Wet gangrene in the metatarsal region of a horse.

The affected organ is sharply increased in volume; his sensitivity completely disappears. Then softening and disintegration of the tissue occurs with the release of a bloody-gray liquid, often with a putrid odor. Disintegrating soft fabrics are very swollen and take on a yellowish, gray or brown color. Necrotic fascia, tendons and aponeuroses are also swollen, disintegrated and often have a dark brown color. Necrotic bones are rough and porous. If a putrid infection occurs, the disintegrating tissues are colored chocolate brown and emit a stench (putrid gangrene - Garigraena putrida). The demarcation line is absent or very weakly expressed. All these local changes are accompanied by a sharp increase in general temperature and depressive state animal.

The prognosis is guarded or poor. Since necrosis (liquation necrosis) of tissues occurs faster than the development of granulation tissue, a general putrid infection often occurs, and the animal dies from sepsis.

Treatment. It is necessary to limit the necrotic process and strive to turn wet gangrene into dry, accelerate the rejection of soft tissues or remove them surgically, without waiting for the formation of a demarcation line. At wet gangrene the intestinal loop is subjected to resection, the limb (in small animals), and the penis are amputated. For wet gangrene of soft tissue, dead tissue is removed and then applied sulfa drugs(white streptocide with potassium permanganate or iodoform) (90: 10), sulfacyl (albucid) or turpentine. Also shown are cardiac drugs and intravenous infusions alcohol, Kadykov's liquid.

ULCERS

An ulcer is a tissue defect that does not have a tendency to heal due to the molecular breakdown of cellular elements and the development of pathological granulations. An ulcer should also be called a granulating wound if it does not tend to scar and epidermize. They can be of different depths, sizes, shapes and locations. Very different periods of their formation.

An ulcer that occurs due to any infectious disease is called symptomatic or infectious.

Etiology. The reasons for the formation of ulcers are varied. They can be divided into two groups.

The first includes general disorders: 1) weakening or exhaustion of the body due to heavy blood loss and infections, poor feeding and maintenance; 2) general diseases of the body, accompanied by a decrease in the ability of tissues to regenerate and hypersensitivity to infection (diabetes); 3) reduced resistance of tissues against infection with hypovitaminosis A and C; 4) infectious diseases(enzootic lymphangitis, necrobacillosis, tuberculosis, glanders, leptospirosis); 5) abnormal blood composition and the resulting decreased tissue resistance to mechanical insults and infectious influences (chronic anemia); 6) metabolic disorders; 7) trophic disorders that occur after damage to the central nervous system; 8) chronic poisoning; 9) endocrine disorders; 10) thrombophlebitis and 11) stable microflora.

The second group of reasons contributing to ulcer formation include various factors local significance: 1) frequent contamination of a granulating wound or defect; 2) mechanical damage - friction, pressure, stretching; 3) large size of the defect itself; 4) foreign bodies, fabric sequesters, fragments of grenades, mines, artillery shells and aerial bombs; 5) density, inflexibility of tissues; 6) insufficient blood supply to the tissues of the defect, granulating wound (embolism, vascular thrombosis); 7) trophic disorders due to neuromas and damage to peripheral nerves; 8) irrational choice and use of antiseptics; 9) the influence of specific agents (actinomycosis, botryomycosis); 10) phlegmonous processes accompanied by skin necrosis; 11) prolonged suppuration, which caused reduced resistance of the cellular elements of local tissue due to poisoning by toxic products and impaired lymph and blood circulation; 12) tissue poisoning with persistent chemical agents; 13) thermal and thermochemical extensive burns; 14) irritation of tissues with secretions and excreta - gastric juice, feces, urine and saliva.

SIMPLE ULCER

A simple ulcer most often occurs after the opening of abscesses, boils, abscessing phlegmons, festering hematomas, due to scratching, burns and after bedsores. Any ulcer, when the regeneration of granulation tissue and skin (horny) epithelium is restored, turns into a simple ulcer.

With a simple ulcer, the defect is covered with healthy granulations. They have a pink-red color, uniform granularity, a fairly dense consistency and are covered with a thin layer of thick mucopurulent exudate of a yellowish-white color. Released in small quantities, the exudate does not extend beyond the ulcer; It usually dries on its surface and forms easily removable crusts. Swelling of the skin and subcutaneous tissue around the circumference of a simple ulcer is barely noticeable. There is no pain.

Epidermization around the circumference of the ulcer is well expressed or somewhat slowed down. Young skin epithelium has the appearance of a pale red stripe, sometimes with a purple tint, increasing towards the center of the defect. The skin epithelium sometimes grows not only along the periphery of the ulcer, but also on various areas its surface, forming epithelial islands. The latter increase in size and then merge with each other and with the marginal epidermal strip.

We observed this type of epidermization in horses when thermal burns flame and in several cases after extirpation of the spinal cartilage with resection of the horny wall. Epidermal islands can occur if throughout the defect there are remains of sebaceous and sweat glands or remnants of hair follicles, which are known to be located deep in the skin, as well as if epidermal cells are accidentally implanted into the wound during a particular operation.

How smaller sizes ulcers, the sooner the skin epithelium envelops and, conversely, the larger the area of ​​ulceration, the slower epidermization occurs.

A simple ulcer heals by forming a scar. It should be borne in mind that a fresh, recently formed scar easily stretches and tears, forming long-lasting cracks - rhagades - in places of greatest mobility.

Treatment. The main task in the treatment of a simple ulcer comes down to the following: 1) maintain the integrity of the granulation tissue; 2) eliminate the possibility of damage; 3) promote its proper development; 4) speed up the process of epidermization. To do this, it is necessary to carefully handle granulation tissue during dressings. You cannot roughly remove crusts of dried exudate, wipe the surface of the ulcer with gauze compresses, tear off the dressing if it has dried, roughly remove and introduce drainage, or use potent antiseptic agents that destroy living cells.

To protect the surface of the ulcer from secondary infection, it is necessary to shave or cut the hair well around its circumference, wipe the skin with an alcohol solution of iodine 1: 3,000 or a solution of iodine in gasoline 1: 800, apply dressings or apply a frame bandage. If the skin in the area of ​​ulceration is very dirty, you should first wash it with soap and water and then dry it with a clean towel. If there is pus covering the entire surface of the ulcer, it is carefully removed with a damp gauze compress.

The crusts are removed with tweezers or a gauze compress, trying to avoid damage to the granulations. Pus from granulations should not be completely removed, since this is associated with the danger of damaging their most delicate surface layer and leads to a decrease in the protective bodies produced by the body itself. The pyogenic layer, through which the ulcer is cleared, at the same time stimulates the proliferation of cellular elements and, consequently, the regeneration process.

If it is necessary to accelerate epidermization, drying, gently disinfecting, enhancing regeneration are prescribed. skin epithelium ointments - xeroform with digitalis, zinc with the addition of 2-4% salicylic acid, 8% scharlamouth ointment or Vitaderm.

EDEMAUS ULCER

Ulcus oedematosum

An edematous ulcer occurs most often in horses due to tissue malnutrition due to a disorder of blood circulation in the area of ​​the granulating defect. For example, compression of venous vessels by the scarring edge of an ulcer can lead to stagnation of venous blood and pathological growth of granulations. A weakening of cardiac activity, accompanied by stagnation of venous blood, has a particularly dramatic effect on the development of edematous granulations.

An edematous ulcer is characterized by the development of pale, very flabby granulation tissue. It is usually pinkish-gray in color, swollen, and has a consistency similar to thick mucus that spreads easily when pressed with a finger. The tissue around the circumference of the ulcer is also swollen and, after palpation, easily leaves a mark in the form of a pit that slowly levels out. The bottom of the ulcer is covered with serous-mucous discharge; epidermization is absent.

Treatment of edematous ulcers should be local and general. The use of any antiseptic agents that stimulate the growth of granulations gives negative results, since diseased granulation tissue does not tolerate any irritation. Therefore, only dressings with sunflower oil or fish oil, blood dressings and careful asepsis.

All attention should be focused on the work of the heart. First of all, eliminate anything that makes the heart work harder or tires it. The animal is provided with complete rest and easily digestible food. It is also necessary to eliminate constipation, if any, and increase cardiac activity by administering an infusion of digitalis with calcium chloride orally. With this method of treatment, after a few days the granulations become dense and acquire a pink-red tint; the discharge becomes mucopurulent; epidermization appears.

INFLAMMED ULCER

Ulcus inflammatorium

Inflamed ulcers are observed relatively often in animals. It is a consequence of the development of local infection, prolonged mechanical irritation, the action of chemical irritants, physiological secretions and excreta ( gastric juice, urine, feces), retention of pus or ichorous fluid.

With an inflamed ulcer, there is a pronounced inflammatory infiltrate. The edges and bottom of the ulcer are covered with bright red granulations. Sometimes granulations acquire a yellowish tint due to their fatty degeneration. Purulent exudate is released in large quantities. The tissue around the circumference of the ulcer is swollen, compacted, inactive and painful on palpation.

With a secondary infection of an inflamed ulcer, necrosis of the superficial layers of granulation tissue and exacerbation of inflammatory phenomena around the circumference of the ulcer may occur. In such cases, a dirty gray coating appears on the surface of the granulations, the purulent discharge becomes more liquid, and the ulcer itself increases in size. An inflamed ulcer thus turns into a progressive ulcer.

Treatment. It is necessary to eliminate the underlying cause and avoid the use of irritating antiseptics, open the pockets if there is retention of pus. To limit the absorption of microbes and toxins, it is necessary to apply a suction dressing and provide the animal with complete rest. For progressive ulcers, it is recommended to use dressings with a hypertonic water-glycerin solution of magnesium sulfate and sodium hypoiodite or with a hypertonic 20% solution of sodium sulfate in an equal mixture with a 2% solution of chloramine or shiny green, reversible streptocide-sulfidine emulsion, novocaine therapy.

There is evidence that dogs that licked purulent exudate suffered from severe gastroenteritis, accompanied by smelly diarrhea and severe exhaustion. Improvement in general condition animals and recovery occurred after applying bandages.

GANGRENOUS ULCER

Ulcus gangraenosum

A gangrenous ulcer occurs most often after severe frostbite, with general blood infection (sepsis), diabetes, gangrenous dermatitis and wet gangrene. The most common causative agents of gangrenous ulcers are B. putrificus, B. necrophorus and B. perfringens.

A gangrenous ulcer can also develop in a horse after incorrect cauterization.

Most characteristic features Gangrenous ulcers are characterized by the speed of its formation and progressive tissue necrosis. The surface of the ulcer is covered with a soft, dirty, structureless mass of tissue decay, saturated with fetid, ichorous fluid. The latter is contained not only in the decaying tissue, but is also partially released outside. The animal has a fever. Sometimes jaundice of visible mucous membranes is observed.

Treatment. It is necessary to pay attention to the main suffering and carry out general therapeutic measures that increase the activity of the heart and the hepatic-renal barrier (subcutaneous camphor oil, intravenous alcohol, calcium chloride with methenamine, sulfidine, etc.).

Local treatment consists of early removal (with scissors) of dead tissue, the use of agents that increase tissue resistance to infection, stimulate the growth of granulations, inhibit the activity of microbes and limit the absorption of their waste products. For this purpose, dressings with white streptocide powder and potassium permanganate, 2% Schaufler's chloracide, 2% Skvortsov's chloride, 5% potassium permanganate, turpentine or iodoform are most often used.

After the rejection of dead tissue and the appearance of granulations, it is recommended to periodically lubricate the surface of the ulcer with a 5% aqueous or silver nitrate solution prepared in 40° alcohol, followed by applying a dressing with fish oil, petroleum jelly or Vishnevsky’s liquid ointment.

/ Hepatocutaneous syndrome in dogs and cats (superficial necrolytic dermatitis)

Hepatocutaneous syndrome in dogs and cats (superficial necrolytic dermatitis)

Text of the article and photos 1-10 from the SMALL ANIMAL DERMATOLOGY A COLOR ATLAS AND THERAPEUTIC GUIDE 2017

Translation from English: veterinarian Vasiliev AB

Peculiarities

Hepatocutaneous syndrome/superficial necrolytic dermatitis is a unique skin disorder in animals with chronic liver disease or glucagon-secreting pancreatic tumors. The exact pathogenesis of hepatocutaneous syndrome is unknown, but increased gluconeogenesis triggered by hyperglucagonemia (pancreatic tumor) or increased amino acid catabolism in the liver (chronic liver disease) is thought to cause low plasma amino acid concentrations and epidermal protein depletion, which causes superficial necrolytic dermatitis.

It is uncommon in dogs and rare in cats, with most high frequency occurrence in older animals. Dogs that may be predisposed are Sheltie, West Highland White Terrier, Cocker Spaniel and Scottish Terrier. Skin lesions are characterized by minimal to intense itching, bilateral symmetrical erythema; scales, crusts; erosions; and ulcers on the distal parts of the extremities and around the mouth and eyes. Lesions may also involve the ears, elbows, hocks, external genitalia, ventral trunk and oral cavity. The fingertips typically have mild to severe hyperkeratosis, fissures, and ulcers.

Lameness may occur due to damage to the pads of the toes. Polydipsia or polyuria may be present if both diabetes. On the other side, systemic symptoms underlying metabolic disease is rarely obvious when initial examination, but usually become obvious after a few months.

Differential diagnoses

Diagnosis

1 Complete blood count: neutrophilia or normocytic, normochromic, non-regenerative anemia may be present.

2 Biochemical analysis blood ( liver failure): Findings typically include mild to moderate increases in serum alkaline phosphatase and alanine aminotransferase, total bilirubin, and bile acids. Hypoalbuminemia and decreased urea levels are common. Hyperglycemia may be present.

3 Plasma concentrations of amino acids are sharply reduced (hypoaminoacidemia).

4 Serum glucagon concentrations: increased in glucagenoma, may be elevated or normal in hepatopathy.
5 Ultrasonography abdominal cavity: evidence of chronic liver disease (small liver with a hyperechoic, reticular pattern surrounding hypoechoic honeycomb areas), pancreatic tumor, or liver metastases (hyperechoic or hypoechoic foci in the liver parenchyma).

6 Histology (liver biopsy): Chronic liver disease is usually characterized by a distinct vacuolar hepatopathy with parenchymal collapse or extensive liver fibrosis (cirrhosis).
7 Dermatohistopathology: early lesions demonstrate diagnostic findings of pronounced diffuse parakeratotic hyperkeratosis with intercellular and intracellular edema, degeneration of keratinocytes in upper layers epidermis and hyperplastic basal cells, which give rise to the characteristic “red, white and blue” histological appearance of strionigral degeneration. A mild superficial perivascular dermatitis with evidence of bacterial, dermatophyte, or yeast infection may be present. Chronic changes usually reveal nonspecific changes that are rarely diagnostic.

Treatment and prognosis

1 Any secondary or yeast skin infection should be treated with appropriate antimicrobial therapy.

2 If the underlying cause is resectable glucagenoma, then surgical removal tumors lead to recovery.

3 If the underlying cause is liver disease, this cause should be identified and corrected (eg hepatotoxicity due to anticonvulsant therapy). In order to symptomatically improve liver function, therapy with one of the following antioxidants may be useful:

• S-adenosylmethionine (sAME) denosyl 18–22 mg/kg orally once daily (90 mg for small animals, 225 mg for larger animals)
• Urzodiol (Actigall) 10 mg/kg orally once a day
• Vitamin E 400 IU orally every 12 hours

4 In dogs with liver fibrosis, colchicine 0.03 mg/kg orally given once daily may help slow the progression of fibrosis. Potential side effects long-term use of colchicine include vomiting, increased peristalsis, and diarrhea.

5 Parenteral amino acid support is the symptomatic treatment of choice to reduce the severity of skin lesions in animals with chronic disease liver and can increase life expectancy by several months. A 10% amino acid solution (Aminosyn; Abbott Laboratories, Abbott Park, IL) 25 mL/kg IV can be given through a jugular catheter over 6-8 hours, or a 3% amino acid and electrolyte solution (ProcalAmine; Braun Medical, Bethlehem, PA) 25 mL/kg IV can be given through a peripheral venous catheter over 8 hours. Treatment can be repeated every 7-10 days or as long as needed. Significant improvement in skin condition should be observed within 1-3 weeks.
6 Oral administration of amino acid solutions works well. Alternatively, oral support of 3-6 raw egg yolks per day, zinc and essential fatty acids may help improve skin conditions in some animals, but these treatments are usually not as effective as intravenous administration amino acids.

7 Treatment with anti-inflammatory doses of prednisone may temporarily improve the skin condition, but some dogs are susceptible to diabetes and additional disease liver after the use of glucocorticoids.

8 Symptomatic local therapy(keratolytic or moisturizing shampoos) can improve skin condition.

9 The prognosis for animals with chronic liver disease or metastatic pancreatic neoplasia is poor and survival time from the onset of skin lesions may be only a few months.

Severe bacterial and yeast pododermatitis often complicates clinical picture this syndrome.

Type of distribution of lesions in canine and feline hepatocutaneous syndrome

Photo 1. Hepatocutaneous syndrome in dogs and cats. Cortical dermatitis with alopecia on the nasal planum and muzzle.

Photo 2. Hepatocutaneous syndrome in dogs and cats. Close-up view of the dog in Photo 1. Cortical dermatitis with alopecia on the lips and nasal planum is similar to the lesions seen in autoimmune diseases skin.