Lection 12.
Anaerobic surgical infection. Tetanus. Diphtheria wounds. Anthrax.
Terrible wound infection caused by pathogenic anaerobes and is characterized by rapid spread of necrosis with the formation of gas, severe general intoxication with primary injury of muscle and connective tissue.
The first mention of anaerobic infection is found in Hippocrates. Ambroise Pare described the disease in the form of hospital gangrene. Presented in sufficient detail the clinical picture of anaerobic gas infection in the works M.I.Pirogov who watched definite pathology during the Crimean War and called her “local stupor,” “mephitic gangrene”, “acute malignant edema”.
In 1899 Lidental Hihman and found that the main role in the occurrence of gas infection belongs Cl. perfringens, which opened seven years earlier. Later it was found that the main pathogens anaerobic gas infection are: Cl. perfringes (44-50%), Cl.oedomatiens (15-50%), Cl. septicum (10-30%), Cl. Hystolyticus (2-6%). All these organisms are spore-forming bacilli.
In the last decade, with the development of anaerobic technology in patients with gas gangrene were sown Cl. soldelli, faluh, sporogeneus. The idea of the genesis anaerorbnoyi infection fl “connected with the above mentioned microorganisms kept the 70-ies of XX century. At this moment with work of Faingold separated somewhat different to the clinic pathology with special course that caused unsporetic (clostridial) anaerobes.
Therefore, at the present stage of development of the doctrine of surgical infection separately allocate appropriate anaerobic clostridial and anaerobic clostridial infection.
Anaerobic clostridial infection is a disease of wartime. Indeed, the largest clinical material has been accumulated and summarized the experience of the Great Patriotic War, but nowadays when analyzing the results the Afghan war and large catastrophe (earthquake in Armenia, Turkey, California).
Floor “is originated from the fact that the implementation of clostridial, mainly in the soil which fall from the gastrointestinal tract of mammals requires certain conditions that in fact, occur at mass lesions:
– Large amounts of necrotic tissue and poorly oxygenation;
– Significant damage muscles and bones;
– A deep wound channel;
– Presence in the wound closed cavities, “pockets” and “heats”;
– Ischemic tissue damage due to major vessels or imposed on long plait.
Pathological-anatomical changes during anaerobic gas gangrene characterized by an acute inflammation of the serous-alternative, followed by progressive necrosis of tissues. In areas traumatic necrosis produced a large number of microbial exotoxins (hemolisine, myotoxins, neurotoxins) that cause progressive necrosis of muscle tissue. In Cases fascial swelling increases with subsequent stasis and thrombosis in the great vessels. As a result of exotoxins in the affected area develops hemolysis, which together with the decomposition products of muscle (myoglobin) perfuse the fat and skin, causing the appearance of typical anaerobic gangrene brown bronze and blue spots.
Pretty typical for definite pathology phenomenon is gassing. Gas bubbles infiltrate cellular tight spaces and cause expression of a number of symptoms.
In anaerobic clostridial infection quickly growing endotoxemia, accompanied by significant disturbance of water and electrolyte balance, depending on extremely large exudation in the area of injury. Because progressive endotoxemia and dehydration quickly death occurs.
Classification.
For anatomical features:
surface forms – epyfascial gangrene
deep forms – subfascial gangrene.
In pathological anatomical features: emphysematous, swelling and tissue lizing form.
Adrift: lightning, rapidly progressive and torpid forms.
Fulminant form usually manifests within a few hours.
Rapidly progressive – during the day.
When torpid course Clinic can develop within 2-3 days.
I give very demonstrative example lightning clinical course of anaerobic gas gangrene, which was observed in our clinic: the patient appealed to the district hospital with complaints of intense pain in the area arching right hand, which was 2 hours after injury shovel at work in the garden. When viewed in the district hospital suspected anaerobic gas infection and the patient ambulance was sent to our clinic. In the receiving department was delivered in 25 minutes, stated that the swelling had spread to the upper third of the arm. After 15 minutes, the patient brought to the operating room and in the performance of metameric cuts limbs from fastsiotomiyeyu, literally at hand surgeons observed an intensive dissemination gas on the front and back surfaces of the chest, first with the affected side, and then on the opposite side. Despite surgery and started intensive therapy the patient died on the operating table.
Clinic and diagnostics.
Initially when anaerobic gas gangrene manifest local symptoms. Very characteristic is the complaint of pain arching nature, occurrence of edema, which quickly spread to proximal direction. If the wounds it has areaktyvnyy appearance with minor mucous secretions ichorose character with an unpleasant odor. The skin on the periphery of the wound cyanotic, pale, or cyanotic with bronze and blue spots. Quite often we can determine thromb subcutaneous veins. Fiber swelling, soaked hemolyzed blood is “weak” look. Muscles as “cooked meat” swollen, grayish, protruding from a wound on the skin surface. When gassing in fluid bubbles last observed.
On the periphery of the wound swelling increases in the volume of certain segments of the limbs or the entire limb. The skin visual traces of superimposed bands. Progression of edema well detected by AV symptom Melnikov (ligature imposed on the limb at the most proximal level distribution of edema in 20-30 minutes crashes into the skin).
Palpation in the area of swelling is determined crepitation, with shaving skin wounds on the periphery bugged high “metallic” sound – a symptom blade, or a symptom of “spatula” (metallic sound with percussion spatula).
Gas accumulation in the wound when removing a tampon from the cavity latter accompanied by typical hlopayuchym sound – champagne cork symptom.When radiography of the affected limb visual band enlightenment that defoliate muscles – Symptom Krause.
Along with this, and sometimes even earlier than the local symptoms manifested severe clinical of intoxication. Patients complain of progressive general weakness, thirst, nausea, vomiting, lethargy, until he lost consciousness. On examination: the skin of patients with pale yellowish earthy shade, facial features sharp, dry tongue with massive gray-yellow layers. It is noted marked tachycardia, blood pressure falls, breathing rate to 40 for 1 min. It is noted oliguria.In blood, usually hyperleukocytosis with a shift to the left, accelerated ESR in urine protein appears and cylinders. In biochemical analysis of blood – hypoproteinemia, the increase in urea and creatinine.
General principles of treatment.
Treatment program of anaerobic gas infection should include simultaneous execution of radical surgical treatment with powerful multicomponent intensive therapy and hyperbaric oxygenation.
Radical surgical treatment is determined by excision of all nonviable tissue, especially muscles, because this is the best substrate for living of anaerobes and their distribution. The viability of muscle during surgical treatment can be identified macroscopically in appearance, the degree of bleeding, to reduce muscular fibers, and more precisely by determining the response to Electro stimulation.
All guidelines regarding of gas gangrene recommended implementation lampasnyh cuts, but not always highlighted feature of these cuts. And it is this feature is extremely important and that cuts have to be not only very long but also include mandatory fastsiotomiyu. Unfortunately neglect this feature rarely leads to the fact that surgeons cut through only the skin and subcutaneous tissue, limited drainage of these substrates and anaerobic infection while progressively distributed in the muscles, which remain in a closed fascial pouch.
After fasciotomy and determining the viability of muscle, if necessary, performed necrectomy, then washed the wounds antiseptic solutions (preferably oxidants) and drained big diameter tube drainage. This volume of surgical intervention may be radical in the early stages of gas gangrene.
Often, when there is total destruction of the soft tissue extremity only way to save the patient’s life is amputation.
There are three types of amputations that are recommended to perform during anaerobic gas infection:
– Amputation without suturing (the usual method three moment amputation by fascial cases held drains stump remains open seams imposed in the absence of progression of infection in 24-48 hours);
– Guillotine amputation (flush overlapping skin, fat, fascia, muscles and bones, supporters of the transaction believe that in this way we can stop the spread of infection, but experience shows that this method has no advantages, only further complicates treatment);
– Amputation stump with dissection (performed in cases where the surgeon is not completely convinced of the viability of the tissue stump, the latter is dissected medially and laterally, skin flap can be filed to the unchanged skin as a clutch, allowing greater aeration wound).
In cases of infection until the joint must perform disarticulation of limbs.
General principles of the treatment include:
a) the specific treatment that involves the application by antygangrene serum containing 50 thousand IU sera antiperfrinhens, antiseptics, antiedematiyens, only 150 thousand IU.
Since when intravenous infusion of sera rarely anaphylactic reactions occur, when they are introduced should follow these rules:
– Serum diluted with 300 ml of saline;
– Introduced slowly infusion rate of 20-40 drops per minute.;
– Solution must be heated to 36-380C;
– Infusion is performed under general anesthesia.
b) Nonspecific treatment includes powerful antibiotic therapy, preferably with the inclusion of a class of antibiotics imipinemiv (Tien) and imidazole (metrahil, flahil). The most expedient way of intravenous and intraarterial. Important place in the treatment of anaerobic infections should take detoxification therapy using detoxification solutions crystalloids (to 4-6 ml per day) and forced diuresis. A special place is occupied by extracorporeal detoxification methods (plazmophoresis, plazmosorbtion, splenoxenosorbtion). A symptomatic adjustment of all systems of homeostasis, especially cardiovascular and respiratory. Some attention should be given enteral nutrition as oral, and, in some cases, enteral probe.
Hyperbaric oxygenation.
At the present level of medicine proper treatment anaerobic clostridial infection is impossible without the use of hyperbaric oxygenation (HBO).
Research and B.V.Petrovskoho S.N.Efuni determined that a high concentration of oxygen paralyzes the formation of alpha-toxin clostridium further decreasing its concentration. In addition, increased oxygen tension in the tissues inhibits anaerobes livelihoods through oxidative inactivating of bacterial cells.
Sessions hyperbaric oxygenation is carried out at the level of compression of 3.2 atm. Number of sessions – 5-7.
Anaerobic unclostridial infection.
The said pathology is considered independently of the early 80-ies.Many clinicians in this period was noted that in some patients the clinical course of septic processes, as m “tissue and internal organs, ran distorted. There was an extremely rapid progression of endotoxemia with minimal early signs of local inflammation. Common approaches to surgical treatment resulted in relief of the patient. Many patients on a background of growing signs of immunosuppression manifest sepsis and they died.
With the development of anaerobic microbiological techniques were found to be major pathogens. that caused the aforementioned infectious processes were gram-negative bacillus genus Bacteroides.American scientist S. Finegold in a series of fundamental works (1977-1984.) Found that some groups of people who, because of various reasons, are immunosuppressive effects of exogenous or endogenous, are at increased risk of surgical infection caused asporogenous anaerobes. These include, besides the aforementioned Bacteroides, are gram-negative peptokocs. peptostreptocs, phuzobacteria. These microorganisms usually inhabit the gastrointestinal tract of man, and most of them vegetate in the colon. Usually they are facultative vegetative bacteria. Only in immunosuppression run their pathogenic mechanism. By the above risk groups S. Finegold took: patients with malignant tumors, especially those that are tsitostatychnu therapy, diabetics, drug addicts, alcoholics, people with AIDS.
Clinical picture.
For the diagnosis of clostridial anaerobic infections (ANI) is crucial correct interpretation of clinical signs. Locally emergence ANI preceding minor microscopic, abrasions, scratches sometimes surgery. The skin over the lesions, unlike the banal infections, not flushed, but rather cyanotic. Determined noticeable swelling on the periphery of the hearth. Pain in the center more often thaot determined, as stated around as a “rim.” When puncture typical manure caot be obtained. In the context of a scalpel if falls into underlying tissues. The wound looks like a conglomerate of “dirty flap” gray-brown color with a small amount of grayish-yellow fluid with drops of fat and unpleasant odor that most medical calls coli-bacillary. It should be noted that this odor is inherent Bacteroides and E. coli culture no odor. In the subsequent revision of the wound can establish that purulent necrotic process applies to the subcutaneous fascia basis and muscles, and the true distribution process is more extensive than its imaginary boundaries during the initial inspection and examination. Thus, we can diagnose clostridial anaerobic cellulitis, fasciitis, miositis. Any damage to the soft tissues often ascertained combined lesion of these substances.
With regard to changes in the general status, as already seen us, they appear much more intense than the banal aerobic infection. Rapidly growing temperature, common signs of intoxication, there is respiratory distress syndrome, showing signs of hepato-renal failure. Late and inadequate surgical treatment arises, as we have already noted, sepsis.
Verification of ANI can bacteriologically, with a special microbiological techniques, defining characteristic of this infection unsaturated volatile acids by chromatography and rapid method of staining of native material wounds Gram. The latter method gives a positive result in 75-85% of cases and draws its simplicity and speed, it is a significant step in building a treatment program ANI.
Principles of treatment.
As with any surgery, infection is a defining moment in treatment strategies ANI is radical debridement. It is different because the rate of invasion bacterial infection suggests that even small amounts of residue affected tissues leads to further progression. Therefore, in this situation, in any case caot follow the tenet of Hippocrates: “Where manure – it cut.” The surgeon who performs a radical surgical treatment should be guided by the idea to completely carve affected tissue, and in any case the idea of economical treatment for possible future closure of the wound. The latter point is solved by the elimination of signs of infection any plastic methods. Particular attention in the surgical treatment ANI should consider fasciitis, because the fascia is the least tolerant substance for bakteroyidnoyi infection and the process of “creeping” on them the fastest and furthest.
After radical surgical treatment of skin flap should turn out as clutches and hem them in unmodified skin. Thus, we increase the area of aeration wounds. The latter must be processed pulsating jet antiseptics and loosely fill drains with osmotically active ointments. Optimal completion of surgical treatment is treatment in a controlled environment abacterial that enables access by sterile air to minimize the possibility of vegetation clostridial anaerobes. In these circumstances, a 3-4 day appear young finely-granular granulation, which creates the opportunity for further plastic closure of wounds.
Principles of antibiotic therapy ANI is not particularly different from the above-mentioned principles of treatment of anaerobic infections in general. It should only be kept in mind that asporogenous anaerobes most susceptible group imidasoles (trihopol, tinidazol, metronidazole, metrogil, flahil) because these drugs in combination with cyphalosporines III-IV generation and klindamicine most appropriate to apply for ANI. All other points detoxification immunocorrective and symptomatic therapy are similar to those used in the treatment of generalized infection.
Tetanus.
Epidemiology, etiology and pathogenesis. Causative agent of tetanus is tetanus bacillus (Vas.tetani), which has three characteristics: there are anaerobes, forms spores and release a toxin.It is found in soil, and its spores are in the digestive tract of sheep, horses and other animals. In an environment coli comes from human and animal feces.
The causative agent of tetanus is very stable. He for one hour withstands heating to 80° C. In dried form can maintain its viability without light for 10 years. Tetanus spores are not always die after boiling for 30-60 min. In the external environment, they can be stored for a long time (years).
Gateway to tetanus bacillus are random wound mechanical and thermal surface skin damage, frostbite, burns. Tetanus bacillus may enter the body by criminal abortion, surgery of the colon, removal of foreign bodies, etc..
Contact with sticks in the wound does not necessarily lead to the development of tetanus. Sometimes wounds determined tetanus bacillus without clinical signs of disease. To the presence of a microbe developed tetanus, required under its virulence, local favorable conditions, hypoxia, presence of hematoma, foreign bodies (crushed wound of necrotic tissue without oxygen) and lowered body resistance.
The incubation period for tetanus ranges from a few days to 3 months, often it is 10-14 days. What a shorter incubation period, the heavier the disease. Once in the wound, tetanus bacillus begins to produce strong exotoxin that has two factions-tetanospazmin (causes convulsive muscle contractions) and tetanolizyn (causes hemolysis of red blood cells).
Tetanospazmin – a neurotoxin that affects the central nervous system. Concerning his actions there are several opinions. Some believe that the toxin from the wound axial cylinders of peripheral nerves (in the front, motor, roots) moves in the spinal cord, which affects the anterior horn cells. Part of the toxin enters the lymph and blood, and with them – at the end of motor nerves and further in anterior horn cells of the spinal cord and motor nuclei of the brain stem. From here formed cells arousal reflex affects the muscles, causing a typical symptom of tetanus – their rigidity.
According to other researchers, the toxin from the injury immediately into the blood and lymph and from there only affects motor centers and neuromuscular connection.
Toxin damage and some internal organs (heart muscle, liver, lungs). It affects higher autonomic centers of the brain stem that the results in tachycardia, hypotension, severe sweating.
Classification. In place of penetration of the pathogen into the body distinguished: wound, postinjection, post burning, postoperative tetanus and tetanus after frostbite, electrical. Separately isolated neonatal tetanus and mothers.
With the spread of it is classified as follows. Overall tetanus: the ascending form more often in animals, descending – often observed in humans. In this form first appear muscle tension head, neck, general stiffness. Later in the process involved all the muscles of the trunk and limbs, there are general clonic convulsions.
Mixed form characterized by uniform signs uplink and downlink tetanus. There are still local (limited) tetanus, which is characterized by limited lesions muscles localized in the area of injury. Local tetanus is usually preceded by a general, but not promptly recognized.
The clinical course distinguish four forms of tetanus: a rapid, acute, subacute and chronic.
According to the severity of the process distinguish very severe, moderate and mild forms of tetanus.Clinical picture. Overall tetanus begins with slightly expressed
Prodrome: weakness, irritability, rapid onset of fatigue, headache, sweating, pain and slight twitching of muscles in the wound. After the prodromal period, there is first a formidable sign of disease – muscle stiffness. With an upward revision it occurs first in the muscles near the wound, while descending – captures the chewing muscles (lockjaw – trismus). They are not antagonists, as previously frantically cut. The patient experiences difficulty during mouth opening, short-term cramps and pain in masticatory muscles (“locked jaw”). Signs of these steadily increasing.
Patients concerned about pulling pain and stiffness in the neck muscles, neck, back, lumbar region. Having difficulty while walking, heaviness in the back and lumbar region. Sometimes there are abdominal pain and muscle tension anterior abdominal wall, which may cause misdiagnosis of acute surgical pathology of the abdominal cavity. Tetanus often begins with swallowing difficulties and pain in the throat, which is the reason for the referral of patients to consult a ENT. In connection with the reduction of facial muscles of the face of the patient acquires a characteristic appearance – “sardonic smile” (risus Sardonicus).
All these phenomena are accompanied by a sense of fear, sleep disturbance, general weakness, and sometimes irritability, sweating, fever. Subsequently tonic convulsions cover all the muscles of the trunk. Since the back muscles are stronger than muscles of the anterior surface of the body, while reducing their patient arch, lies on the heel and neck. The provisions of this was called Opisthotonus – opisthotonus. Limbs at this time bent at the elbow and hip joints. Stiff intercostal muscles severely restricts breathing movements of the chest, which becomes inactive. When convulsive contractions of the diaphragm is covered, it may be sudden respiratory failure until asphyxia. Seizures occur under the influence of the smallest hearing or visual stimuli. A drop of water that falls from the tap, sunbeam, creaking beds – all of which can lead to their appearance. Originally seizures are rare, but if the disease progresses, they become more and more frequent, and there are already spontaneously.Duration minor court did not exceed 1-2 with intervals of several hours, medium – 2-5 sec intervals for 10-15 minutes. Seizures are accompanied by severe pain. They are sometimes so strong that lead to the breakdown of muscle and fracture.Because tonic muscles perineum violated acts of defecation and urination. In some cases, tonic (characterized by prolonged spasm) and clonic (muscle spasm alternates with their relaxation) may include muscle spasms only certain parts of the body (local form of tetanus). Consciousness in tetanus preserved, making the patient’s condition even more difficult. Reduces blood pressure, tachycardia and arrhythmia appear, decreased urine output (oliguria). The clinical picture of severe tetanus increases downward to 2-3rd week. With favorable course all these phenomena gradually die down: the frequency and strength of the court reduced the body temperature decreases, decreases trismus, improves swallowing. Spasmodic muscle contractions disappear in the following sequence, which were: chewing, facial muscles, neck, trunk, and extremities.
Each of the clinical forms of tetanus has its own characteristics. Yes, lightning forms symptoms develop rapidly, within 12-24 hours. The disease runs hard, seizures occur, often accompanied by threatening asphyxia. Body temperature rises to 39-40° C, accelerated heartbeat. After 1 – 2 days dies. In case of severe forms symptoms develop within 24-48 hours. (All symptoms). Seizures court repeated several times an hour. Often within 4-5 days the patient dies.
Slower growing clinic in case of an acute form (incubation period lasts 4-6 days). Expressed mild symptoms, seizures are rare, several times a day. Other symptoms are moderate. Often the disease ends recovery.
Chronic tetanus is rare and is characterized by less severe. With him there is limited muscle damage localized in the area of injury. There are still late and recurrent tetanus. The first may develop several months or even years after getting sick injury. The reason it is the activation of latent infection under the influence of triggering factors: trauma, surgery (especially late removal of foreign body). The cause of recurrent tetanus is also activation of latent infection. When you have the classic triad of symptoms (trismus, dysphagia, neck stiffness), the diagnosis of tetanus is not complicated. The presence of only one component of the triad is the basis for the diagnosis of tetanus. Trismus may be a manifestation of dental disease, and isolated dysphagia or muscle stiffness in the neck – the result of nervous and mental disease. During this period of treatment, begun at a typical clinical picture, we can consider late. It is important to establish the diagnosis in the early stages of the disease. The main feature is a symptom of increased reflex excitability. You can check with your fingertips lightly on the parotid region, accompanied by spasm of the facial muscles. Lorin and Epstein offered to investigate reflex masticatory muscles by tapping on the spatula assigned to the lower teeth. In patients with tetanus, in the absence of overt clinical signs observed apnea, prolonged contraction of masticatory muscles. By the early signs of tetanus are also pulling pain and muscle twitching in the wound, excessive sweating, which does not correspond to body temperature, pain in the back.
The diagnosis is confirmed by detection tetanus in material necrotic tissue thin bacilli with similar disputes to drumsticks and detection tetanus toxin in cultures with tests “toxin – antitoxin” in mice.
Treatment of patients with tetanus aims to maximize pathogen destruction tetanus toxin neutralization that circulates in the blood, ensuring the free passage of respiratory depression reflex excitability of striated muscles and prevent complications.
Therefore, treatment of tetanus should be conducted in the following areas:
1) the specific therapy,
2) anticonvulsant therapy,
3) improve the overall condition, correction of protein, fluid and electrolyte balance and acid-base status,
4) surgery,
5) other methods.
Specific therapy involves the use of tetanus toxoid (DCA). Dose of serum for adults is 100 000-150 000 AO for children – 20 000-80 000 AO, Baby – 10 000-20 000 AO. Before the introduction of therapeutic doses spend intradermal and subcutaneous tests for Bezredkom. Originally administered 0.1 ml of diluted (1:100) serum intradermally in 20 minutes – 0.1 ml undiluted serum subcutaneously. A negative result (induration diameter less than 0.9 cm) heated serum remainder injected intramuscularly and intravenously. Half doses of serum injected intravenously (diluted in isotonic sodium chloride solution at a ratio of 1:10), the second half – one time intramuscularly.
Serum was administered 2-3 days in a row, gradually reducing the dose. Course dose serum – 200 000 – 350 000 AO. Today abroad some authors refuse to enter because of the risk of serum hypersensitivity, possible allergic reactions including anaphylaxis.
We must remember that whey is effective as a prophylactic because it neutralizes a toxin that circulates freely in the blood. At fixed nervous tissue toxione of the current medications is not valid. Therefore, the serum should be introduced in the first 2-3 days.
Specific therapy includes intravenous administration of not less than 10,000 IU of human tetanus immunoglobulin diluted isotonic sodium chloride solution. The literature highlights the beneficial therapeutic effect of homologous antitoxin, ie serum obtained from immunized donors or hyper immunized toxoid. Introduction antitoxin should be combined with antibiotic therapy (intramuscular or intravenous) and rectal introduction as suppositories metronidazole 1 g every 8 hours, destroying all living microorganisms and prevents future development of toxin.Important role in treatment of tetanus is active anticonvulsant therapy. In milder forms of the disease incubation period of 2 weeks, occasional bouts of court a good therapeutic effect give input neyroplehichnyh drugs, 25% magnesium sulfate solution (20-30 ml intramuscular) use hloralhidratovyh enemas. With neyropleptic drugs used chlorpromazine, which produces a calming, anticonvulsant, analgesic effect (4 ml of 2.5% solution 4-5 times a day intramuscular).
The average degree of tetanus severity with frequent severe seizures, breathing disorders showing administering large doses neyroplehichnyh (50 mg aminazine after 6 h), antihistamines (diphenhydramine, suprastin) drugs in combination with drugs or chloralgidrat enemas. In case of heavy flow tetanus expressed breathing disorder that threatens asphyxia, often painful cramps used muscle relaxants and produce mechanical ventilation. Patient intubuyut, injected him muscle relaxants, connect the device to mechanical ventilation and exercise superficial anesthesia nitrous oxide. If you want to continue this therapy for a long time, perform tracheostomy. It uses muscle relaxants antydepolarised action (tubaryn, tubocurarine). Artificial ventilation may be a long time (sometimes up to 14 days).
To correct protein, fluid and electrolyte balance and acid-base status conduct corrective infusion therapy.
Surgical treatment of tetanus is the wide opening wounds (especially blind wounded), excision of necrotic tissue, removal of foreign bodies (fragments, splinters of wood, scraps of clothing, etc.), providing good outflow of wound, locally administered antibiotics. The wound was thoroughly washed with hydrogen peroxide and loosely tamponuyut. For large lesions with massive limbs, crushed fabrics shown amputation.
A role in the treatment of tetanus play HBO and antibiotics. We must remember that most bakterial microorganisms resistant to antibiotics, and planting often results should wait a few days. In this case, shows broad-spectrum antibiotics.
A patient with tetanus requires a special care. First of all, it should be placed in an isolated, quiet and darkened room to avoid any irritants to care for patients allocated special middle and junior medical staff that operates under the direction of a physician.
Great attention should be paid to patients’ diet (food should be high, fortified with plenty of fluids). If TRIZ patient to feed fluid food with rubber tip or via nasogastric tube.In case of delay urinary catheterization demonstrated a soft catheter in case of constipation – cleansing enemas. The vessel must be rubber. From the epidemiological point of view, patients with tetanus is not contagious and danger to the environment is not. Necessary daily patient laboratory and radiological examination (for timely diagnosis of pulmonary atelectasis).
Preventing tetanus. Preventive measures in tetanus divided into nonspecific and specific.
Nonspecific prevention of tetanus is to conduct timely and complete debridement, cleaning it from foreign bodies, necrotic tissue, bacteria, blood clots, which is complemented by the introduction of antibiotics.
Specific prophylaxis of tetanus include active immunization regardless of injury and active-passive for suspected disease tetanus. Active immunization is pertussis-diphtheria-tetanus (DPT) and adsorbed diphtheria-tetanus vaccines to all children under 1 year (1st and 2nd injections at intervals of 6.8 weeks, 3rd – 4-6 months), and tetanus toxoid over the population living in areas with incidence of tetanus 1 or more per 100 000 population, all agricultural workers, builders, workers and employees of railway transport, water supply, sewage and sewage treatment plants, peat development and logging, laboratory workers who work with tetanus culture workers vivarium, athletes.
Tetanus toxoid introducing 0.5 mL (2 vaccinated and 2 booster). From the completeness active immunization depends on further active and passive immunization in case of injury (Emergency Prevention). It is open for all injuries, burns, frostbite, gangrene and tissue necrosis, animal bites, criminal abortion, birth, which took place not in a hospital, abscesses, penetrating wounds of the digestive system, removing foreign bodies.
Active immunization spend tetanus toxoid and human tetanus immunoglobulin, at least – of tetanus toxoid. Scheme emergency specific prevention of tetanus depending on the conditions and situations contained in the special instructions.
Weather in tetanus depends on the duration of the incubation period (it is shorter, the heavier the disease), the clinical forms of tetanus, reactivity, specific and nonspecific timely prevention, complete treatment.
ANTHRAX
Anthrax – specific acute infectious disease caused by the penetration of the body sporohennoyi anthrax bacillus (Bac. anthracis).
Etiology. Sources and factors of transmission of anthrax is primarily domestic animals, as well as leather, fur, horns, hooves and food of animal origin (milk and dairy products, meat, etc.). Sometimes it can be a source of infection and other animals – a cat, bear, gray rat, birds, dogs, white mouse.
Human anthrax infection can occur contact, aerogenic, nutritional and transmissibility ways. Most often infection occurs during slaughtering, skinning the animals, cutting meat animals who suffered from anthrax. Usually the disease occurs warm seasons.
Depending on the pathways of spores of the pathogen into the body distinguish the following clinical forms of the disease: pulmonary (occurs when microbes entering the respiratory tract when inhaled), intestinal (if eating contaminated food) and cutaneous. It is cutaneous anthrax, which manifests the formation of specific ulcers – anthrax (pustule maligna, carbunculus malignus), has the greatest value in surgery, so we consider it in more detail.
The pathogenesis of anthrax is specific toxemia, which is due sybirkovym exotoxin, some fraction of which causes coagulation proteins, tissue swelling, leading to the development of toxic-infectious shock.
Infection with cutaneous anthrax occurs by ingestion of spores of the pathogen on damaged skin. Infection by sticks is much less. The incubation period lasts from several hours to several days, an average of 2-3 days.
In the pathogenesis of cutaneous disease are the following types of damage: carbunkul, edematouse, bullous and eryzypelas form. Each of these forms in case the generalization process can lead to anthrax sepsis. In the area of penetration of the pathogen occurs anthrax – a fire hemorrhagic necrotic inflammation with development of edema and tissue necrosis. Skin lesions in sybirtsi depend on specific waste products wand so-called death factor. When in the area of penetration it is not enough, the changes on the part of the skin with a small, limited. If in the primary cell of a large number of pathogens, they can invade the bloodstream and settle in areas of secondary localization. The originator of the place can be entered mobile penetration macrophages in the next regional lymph nodes, which typically occurs without significant inflammation disorders barrier function, resulting in the generalization process or does not occur, or occurs in the later stages of infection.
Clinical picture. Clinical picture of cutaneous anthrax depends on its type. Carbunkul form occurs most often (99.1%). Most often affects the cheeks, eyelids, forehead, neck, wrist and forearm. On hands and pinna anthrax does not happen.
Local changes in anthrax begins with a slight itch, then a seal skin and mihurets in place pathogen invasion. After pulling or scratching vesicles formed ulcer with a dark bottom, which begins to rapidly increase in size. After the formation of ulcers itching goes, but there are phenomena of intoxication: fever, headache, insomnia, nausea, decreased appetite. Fever occurs in parallel to increase the size of anthrax. Around the ulcer is formed with inflammatory roller with raised edges. At this time there is soft tissue swelling around the ulcer, which spreads to the surrounding area. The bottom of the ulcer penetrates and becomes purple with the release of serous or sero-hemorrhagic fluid. Near ulcers formed subsidiaries vesicles, which eventually merged with each other, increasing the area of injury.
Usually there are single carbuncles, but sometimes can form 2-3 and more. However, the size and number of carbuncles not aggravate the severity of the disease. Anthrax, unlike from ather carbuncles, not painful. It is often accompanied by regional lymphadenitis. Enlarged lymph nodes are a bit sensitive, but not painful.
Shortly exudation of ulcers decreases necrotising areas becomes dry. The central part of carbuncle becomes darker and uneven. Body temperature at this time is reduced. Carbuncle covered with scabs, swelling gradually decreases. Scab land separated from the skin and begins to act on its surface. At the end of the 3rd week crust completely away and formed granulating ulcer with a slight discharge, which later rumen. Duration of scarring, as well as the severity and nature of scarring depends on the depth of tissue necrosis and localization carbuncle.
Edematouse form of anthrax occurs very difficult. Her first feature is the occurrence of a slight itching in the area of pathogen invasion. Then there is a progressive swelling of the tissues, which precedes the development of skin necrosis. Temperature for 2-3 days reaches its maximum (400 C) and lasts until the end nekrotyzatsiyi and early scab formation. There are phenomena of intoxication (delirium, brain disorders, convulsions, vomiting) that may result in this period to the death of the patient. Swelling is painful, tight and can be extended to large areas of the body. He then covered with small blisters filled with serous fluid, and areas of necrosis. In the third, the fourth day blisters burst and begins to stand out in a large number of serous fluid. On the 8th – 10th day blisters and areas of necrosis covered crust and the disease becomes current as at carbunkul form.Bullous form of anthrax is characterized by development at the site of pathogen invasioot vesicles and large bladder (bull), under which is in the process of tissue necrosis. After a period of bladder wall fall and necrotising.
When eryzypelas form of anthrax on the face and hands, a lot of white walled vesicles of different sizes, which are located in congested swollen but not painful skin. A few days later revealed vesicles and in their place ulcers are formed with a dark bottom and large serous secretions. Deep necrosis usually not formed, the formation of scabs is quick and after their rejection scarring was observed. This type of anthrax is characterized by mild and favorable prognosis.
Diagnosis. Diagnosis of anthrax is on the basis of epidemiological history (nursing animals dividing of animals drinking infected food and so on.), Clinical presentation, results of intra-dermal tests with antraxyn and laboratory studies. Internally allergic skin test with antraxyn is the introduction to the inner surface of the forearm 0.1 ml antraxyn – antigen, which is released from Bac. Anthracis. Patients from 3-4 days of the disease in 24-48 hours after administration antraxyn there hyperemia and infiltration in diameter not less than 8 mm.
Besides conducted bacteriological investigation of the vesicles, carbuncles, ulcers or discharge from the scab that fell, highlighting and determined pathogen diseases.
Blood samples (1 ml) was taken from a vein, preferably during fever. Her sown directly in culture medium and make smears on a slide.Treatment of cutaneous anthrax – should only be conservative. Not permitted to active surgical measures (conduct autopsies, probe, vyshkribaty ulcer). Divide bubble only to fester.Treatment should begin with the rest of the affected area. The major role played by specific therapy, antibiotics, chemotherapy
Diphtheria of wound
Diphtheria – an acute infectious disease caused by germs Lyefflyera. It affects the mucous membranes of the throat, tonsils, sinuses, larynx, trachea, genitals. From a surgical point of view of greater interest is the diphtheria bacillus infection of wounds (diphteria vulnerum).
Etiology and pathogenesis. Diphtheria bacillus common in the environment, but is also found in the human body. In a saprophyte parasite is in the throat, intestines, surface wounds. Bacillus does not form spores. When heated to 60° C quickly dies. Infection of wounds occurs during contact with patients with diphtheria (coughing, sneezing, through dishes, etc.). Diphtheria bacillus produces a strong toxin that damages the cardiovascular system and causes paralysis of certaierve disorder that manifests accommodation, paresis of the muscles of the pharynx. Getting in wound diphtheria bacillus causes it specific inflammation.
Clinical picture. When diphtheria wound has a specific form: on the surface appear gray-yellow fibrinous raids, firmly soldered to the underlying tissues. During fibrinous films observed tissue necrosis. With wounds allocated serous and serous and bloody fluid. The skin around the wound is hyperemic edematous tissue. Regional lymph nodes are enlarged. When connecting banal infection increased body temperature.Infection of wound diphtheria bacillus accompanied by the general reaction of the organism, which is typical for diphtheria: paralysis of certain nerves toxic lesion of the heart muscle that can lead to sudden death.
Accurate diagnosis of diphtheria wounds can be placed only on the basis of the results of biological research. Feature diphtheria infection of wounds is that they heal very poorly and there is a risk of germs getting into the bloodstream.Treatment. When diphtheria am patient becomes a source of infection and should be isolated. Treatment should begin immediately after diagnosis. Subcutaneous, intra-muscular or intravenous antitoxic serum antidiphtheritic – 20 000 – 40 000 AO (after preliminary tests of the method Bezredka). The wound was covered with bandages soaked with antiseptic or antidiphtheritic serum.In the case of diphtheria bacilli association with banal microflora within 6-8 days spend adequate antibiotic therapy.Surgery is not performed and shown only in the presence of purulent nodules, phlegmon.Along with the above mentioned activities carried symptomatic therapy.
