surgical semeiology review

Surgical Semiology Review Guidelines for 1° semester Exam

(Based on Professor’s material and personal extras) Alessandro Motta, Medicine Class in English, 3rd Year, UVVG

Arguments included:

Antibiotics Asepsis Burns Frostbites Gas Gangrene Hemorrhages Infections Localized Acute Infections Phlegmons of Hand Semiology of muscle disease Tetanus Traumas Wounds

Tables of summary for bacteria and main classes of antibiotics:

Class Name

Gram + Aerobic

Staphylococcus aureus, penicillinase pozitive and negative, and methicillin resistant strains (MRSA), which are multi-‐resistant; Streptococcus pyogenes

(group A beta hemolytic). Also: -‐ Streptococcus pyogenes (group A beta hemolytic);

-‐ Streptococcus pneumoniae (pneumococcus); -‐ Enterococcus (Streptococcus) faecalis, multi-‐resistant;

-‐ Enterococcus faecium, multi-‐resistant; -‐ Bacillus anthracis

Gram – Aerobic

-‐N.Gonorrheae and N.meningitidis (cocci); -‐ The bacilli of the family Enterobacteriaceae (Escherichia coli, Klebsiella , Proteus , Citrobacter, Providencia spp, Enterobacter spp, Salmonella spp, Shigella spp, Yersinia enterocolitica, etc..) of which some strains of

Escherichia coli and Klebsiella pneumomiae are producing beta-‐lactamase with extended spectrum,multi-‐resistant.

-‐Bacillus Pseudomonas (Pseudomonas aeruginosa), also with multi-‐resistant strains;

-‐ Acinetobacter baumanii, multi-‐resistant strains; -‐ Other gram-‐negative bacilli: Pasteurella, Legionella pneumophila;

-‐ Helicobacter pylori (microaerophilic).

Gram + Anaerobic

-‐ Clostridium tetani, C. perfringens, C. botulinicum, C difficile, C.septicum of these C. difficile is multi-‐resistant;

-‐ Other species Peptococcus, Peptostreptococccus, Propionibacterium, Eubacterium, Actinomyces

Gram -‐ Anaerobic -‐ Bacteroides fragilis, multi-‐resistant strains;

Fusobacterium; Prevotella, Weilonella, Porphyromonas;

Mycobacteria -‐ M. tuberculosis (Koch bacillus), acidalcoholoresistant; -‐ M. leprae.

Spirochetes -‐ Treponema pallidum (syphilis agent); -‐ Leptospira colitis,L.interrogans.

Fungi -‐ Candida albicans, Cryptococcus neoformans, Histoplasma capsulatum, etc.

Protozoa -‐ Hystolitica Entamoeba, Giardia lamblia, Trichomonas vaginalis, Pneumocistis carinii, Toxoplasma gondii, etc.

Helmints -‐ Echinococcus granulosus (hydatidosis agent), Taenia, Ascaris lumbricoides, Trichinella spiralis, etc.

Main Class Sub-‐Class Reactive to Bacteria:

Penicillin’s Benzylpenicillins /Penicillin G

Gram-‐positive cocci, especially the streptococcus, staphylococcus aureus is

resistant. Gram-‐negative cocci, respectively gonococcus and meningococcus, Bacillus anthracis. Anaerobic bacteria such as Clostridium. In anaerobic infections is

necessary to associate with metronidazole.

Penicillin’s Phenoxymethylpenicillins /Penicillin V

Anti-‐staphylococcus penicillin (oxacillin, methicillin) excepting MRSA. . Ampicillin, Ampiplus (sulbactam). . Amoxicillin,

Amoxiplus, (clavulanic acid). Penicillins with Anti-‐Pseudomonas aeruginosa (bacillus Pseudomonas) include, among others, carbenicillin, ticarcillin and piperacillin.

Cephalosporin’s First Generation

Gram positive germs and some gram negative species. Names: cephalexin, cefazolin,

cephalotin and cephaclor.

Second Generation

Aerobic gram-‐positive and a large range of gram-‐negative Staphylococcus aureus

penicillinase secretor .There are not active against staphylococcus methicillin resistant

enterococcus and pseudomonas bacillus. Some names: Cefamandole,cefoxitin,

cefuroxime,cefotetan.

Third Generation

Have a very broad spectrum, including: • Gram-‐positive aerobes, including Staphylococcus penicillinase-‐secretor

• Aerobic gram-‐negative, including enterobacterias

• Some anaerobes, including Clostridium and Bacteroides species

• Clostridium difficile, Staphylococcus aureus metihcillin resistant, and Enterococcus faecium strains of Escherichia coli and Klebsiella pneumoniae producing ESBL are

resistant. Names: Cefoperazone, ceftazidime, ceftriaxone

and cefotaximul.

Fourth Generation

Acts on gram positive and some gram-‐negative anaerobes, such C.perfringens. Are useful in infections with ESBL multiresistant at generation cephalosporins I-‐III. Names:

CEFEPIMA and CEFPIROMA.

Carbapenem’s IMIPENEM+ CILASTATIN

• Gram-‐positive (streptococcus, staphylococcus, Enterococcus faecalis,

etc..)

-‐ Aerobic gram-‐negative (Enterobacteriaceae, Pseudomonas aeruginosa etc. Acinetobacter spp.)

-‐ Anaerobic gram positive (Clostridium spp, Actinomyces spp,

etc..) -‐ Gram-‐negative anaerobes

(Bacteroides spp, Fusobacterium spp, Weillonella spp, etc..).

-‐ Problem germs -‐ Bacteroides fragilis, Pseudomonas aeruginosa (bacillus Pseudomonas) and Enterococcus

faecalis. • Enterococcus faecium and some

strains of methicillin-‐resistant Staphylococcus aureus are not susceptible to imipenem.

• Imipenem is useful in severe infections in which are possible combinations of germs, including between aerobic and anaerobic.

Carbapenem’s Meropenemul Carbapenem’s Ertapenemul

Carbapenem’s Monobactam AZTREONAM is active against gram-‐negative aerobes, including Pseudomonas aeruginosa.

Aminoglycosides Gentamicin

Gram-‐negative as Enterobacteriaceae(E.coli, Klebsiella, Proteus, etc..) and Pseudomonas aeruginosa; gram-‐positive bacteria such as staphylococcus, including penicillinase

producing strains. Aminoglycosides Amikacin Aminoglycosides Kanamycin Aminoglycosides Streptomycin Tuberculosis

Neomycin

Aminoglycosides may be associated especially with beta-‐lactams; ampicillin-‐gentamicin combination may be useful in the field of

biliary infections.

Fluoroquinolones Ciprofloxacin

Has a broad spectrum, including: -‐ Gram-‐negative aerobes such as E. coli, Proteus, Klebsiella, including strains of

Acinetobacter and Pseudomonas aeruginosa; -‐ Gram positive, especially staphylococcus.

Fluoroquinolones Norfloxacin, Ofloxacin and PEFLOXACINA

Nitroimizadole Metronidazole

Anaerobic gram-‐positive as Clostridium (C. perfringens, C. botulinicum, C. tetany, including C. difficile), Peptococcus,

Propionibacterium, etc. Anaerobic gram-‐negative as Bacteroides (including B.fragilis), Fusobacterium, Veilonella, etc. Parasites like Trichomonas vaginalis, lamblia intestinalis,

Entamoeba hystolitica. Nitroimizadole Albendazole Indicated in hydatid cyst.

Lincosamide Lincomycin

-‐ Gram positive aerobes such as staphylococci and streptococci;

-‐ Anaerobic bacteria such as Propionibacterium, Fusobacterium and

Clostridium

Lincosamide Clindamycin

Glycopeptides Vancomycin

Clostridium difficile; Methicillino resistant Staphylococcus aureus

(MRSA); Enterococcus faecalis and Enterococcus faecium

Linezolid Linezolid

-‐Gram positive coccus, including problem germs like Staphylococcus aureus

meticilinoresistant ,Enterococcus faecalis, Enterococcus faecium, including strains resistant to vancomycin and penicillin-‐

resistant pneumococcal strains. -‐ Anaerobes, including Clostridium

perfringens and Bacteroides fragilis. Most gram-‐negative bacteria are resistant

Macrolides Erythromycin A and Clarithromycin

Antimycotics

Are useful in fungal reinfection, especially in immunodeficiency occurred after excessive

use of broad-‐spectrum antibiotics. The most commonly used antimycotics are fluconazole, ketoconazole, miconazole and

amphotericin B. Asepsis Vs. Antisepsis (main features) Asepsis: all measures, usually physical, which prevent contamination of wounds. Asepsis, removes infectious agents from the surfaces of objects in contact with tissues. Antisepsis: all measures, usually chemical, in which infectious agents are removed from living tissue. These measures are aimed destroying germs that have infected tissues. Disinfection: Disinfection is all measures to destroy pathogens (bacteria, viruses, fungi) on inert objects. The disinfection performed using chemical and physical means to destroy, in part, microbial populations. Disinfection is not equal with sterilization, because the surface of instruments after disinfection, still uncovered is subject to further contamination. Sterilizations: is the measure by which all-‐living organisms or spores are destroyed. Sterilization is done by physical and chemical methods and the sterilized material is sterile packaged in order to maintain this state until use. According to international practices, we talk about antiseptics for skin, mucouses, membranes and cavities of the body and talk about disinfectants for different areas for sanitary ware, furniture, and floors. Methods for sterilizations:

• Heat, both wet (boiling or autoclaving) or dry (Poupinel's oven, incinerator) • Radiations: ultraviolet, ionizing radiations and ultrasounds • Chemicals: with formaldehyde or gluterladehyde

Methods for antisepsis: Hydrogen Peroxide (H2O2): -‐ is an antiseptic widely used in surgical practice in recent wounds. Its effects are: -‐mechanical effect -‐ eliminates death tissues -‐oxidant effect by native O2 released; -‐hemostatic effect; -‐bactericidal effect. Use the solution of 3%. Boric acid is a white crystalline powder that is highly bactericidal. Potassium permanganate (KMnO4) is used in perianal lavage, vaginal (attention, stain!) Iodinated agents are containing iodine and used in the preparation of tincture of iodine 5% or 1% iodine alcohol. Iodofors are modern antiseptic solutions, which in addition to iodine contain detergents, being nontoxic and noniritative. Chlorates are antiseptic agents with sporocide effects, fungicides and virulicide by oxidation. It is used in wounds with pus. Chlorates chloramines are nitrogen compounds by releasing active chlorine. Most often used is chloramine B is the form of tablets 0.5 g The solution from 0.2 to 1% is used for aseptisation hands, and in 2-‐5% solution to disinfect laundry. Alcohols are widely used in surgery as alcohol concentration of 70%, mixed with methylene blue (rubbing alcohol). It is an antiseptic bactericide, but inactive against spores or fungi. Not applicable in wounds or mucous membranes. Use only aseptisation skin. In combination with iodine and chlorhexidine 0.5% it increases its effect. Aldehydes -‐ Formaldehyde gas is irritating to eyes. It is used as a solution of formalin to disinfect rooms and instruments. Phenol and cresol derivatives are historical, are mainly used in soaps or sputum disinfection (TB). Metal derivatives are bactericidal by enzyme inhibition. Colorants have cellular inhibiting effect by antiDNA or RNA action. Rivanol is a yellow solution, antiseptic, anti-‐inflammatory properties. It uses 2% solution for washing wounds. Methylene blue is used in dermatology and is a good urinary disinfectant. Detergents have bactericidal and bacteriostatic qualities.

Wounds Definition: it is a disruption of continuity of skin or mucous membranes. The wounds are therefore produced by external actions, affecting virtually any tissue or organ and can be mild, severe or fatal. Causes of wounds are: external (mechanical, thermal, chemical, radiant) or internal (intrinsic) which eventually will cause surface lesions (ulcers), Wound contamination with bacteria or foreign bodies can occur through mechanical damage (vulnerable external agents) which introduce a variety of germ tissue. Sometimes infection can occur by opening a naturally contaminated organ spreading its septic contents in adjacent tissues. Acute wounds are characterized by sudden onset, recently and will heal after a sequential algorithm with complete restoration of tissue Chronic wounds from different reasons are not staged on the same process of healing or stop at a certain stage of it without achieving full recovery. In case of mechanical wounds following the etiopathogenic characteristics of the vulnerable agent wounds are classified as: puncture wound, cut and bruise. In terms of pathology wounds are classified according to clinical evidence: puncture wound, cut, bruise, but specifying the depth (shallow, deep). Superficial wounds are limited to skin and fatty tissue till the fascia sheath, and the depth can be penetrable(involving internal organs) or impenetrable. According to the gravity they could be classified in Aseptic or Surgical, with minimum contamination or highly contaminated. It also varies due to the position of the wound (if affect the face could be more severe than another region). By the time we can classify two types of wounds: Recent (until 6 hours) and old (over 6 hours) Puncture wound (vulnus punctum) are caused by sharp objects, long, and penetrating deep into tissues. Sometimes they are superficial, sometimes deep, affecting cavities or organs. The danger is vascular damage, nerve or hollow, which sometimes are undetected.. Cut wounds (vulnus scissum) are produced by sharp objects (knife blades, knife, broken glass, etc.). The wounds have edges, smooth slopes and narrow base. The key feature of these wounds is from the surface to deep ,the tissues are not devitalized or crushed. They can be accidental (home, suicide) or operators. All surgical wounds fall into this category. Are wound with the best potential of healing. Contusion wounds have irregular edges, are devitalized, being produced by traumatic agents with irregular borders. These wounds are highly contaminated. Because blood irrigation disorders develops suppuration and serious anaerobic infections sometimes. Bite wounds are contusion wounds caused by animals or humans’ .The character of bitten wound depends on strength, on comprehension of the affected anatomical region on the particularities of the animal. Bitten wounds have a high infection potential by microbial flora inoculated by the animal. Rats can transmit serious diseases (rabies and spirochetoza).

Bullets or fragments of shells produce concussion gunshot wounds. The force of impact of projectiles is very high and depends on speed and distance traveled by the projectile. These wounds have usually linear trajectories. Forward moving projectile will transmit kinetic energy to new tissue structures that will create cumulative destructive effects. These wounds are heavily contaminated by infected involvement of foreign bodies (earth, loose clothing, etc..) ,even the projectile itself is infected. The wounds caused by chemical agents are burns, producing lesions of grade 1-‐4. (after exposure to heavy acids or bases). Röntgen rays primarily produce radiation wounds. Depending on dose may occur dermatitis or erythema. Late consequences are fibrosis and ulcer. Wound healing at humans has a devolved matter and is produced by repairing the defect, which directly involves the appearance inflammation. Replacement of bone tissue and conjunctive is performed with the same tissue. All other damaged tissues are replaced by conjunctive tissue.

1. The first stage is the inflammation that occurs within 24 hours after the accident. Inflammatory signs appear (redness, swelling, local heat and pain).

2. Second stage (the stage of proliferation) occurs at 4-‐7 days after wound. At this stage the presence of fibroblasts and granulation tissue is crucial. This phase is at his best on days 5-‐7 and then decreases.

3. Stage three is the repair or healing phase, which begins on the 8th day. This phase is characterized by the appearance of increased fibrosis, which will produce a raised or depressed scar.

The scar is not identical with the skin that preceded wound because has no sebaceous glands, sweat glands, hair and pigment cells. If the wound was large with large destructions, the final scar will be larger. Therapeutic measures should provide a functional and aesthetic healing. First aid treatment of wounds involves hemostasis, a toilet, and disinfection of the wound edges, followed by sterile dressing. Hemostasis both temporary and permanent is done through specific maneuvers. Definitive treatment of the wound takes place in specialized services that are provided with opportunities to anesthesia, hemostasis, suture and sterile dressing. In a surgical treatment of recent wounds Anesthesia is very important. The toilet itself will be done with hydrogen peroxide 3%, at which time will remove clots and foreign corps by the wound. Mechanical cleaning can be accomplished by pressure washing with saline. Recent wounds (less than 6 hours) will be considered no infected and will be sutured first. Facial wounds will always be sutured.

Tetanus prophylaxis is required in the treatment of recent wounds. Best tetanus prophylaxis is the correct treatment of wounds. Tetanus prophylaxis is carried out with three doses of ATPase (purified and adsorbed tetanus toxoid) administered intramuscularly every two weeks.

Bitten wound treatment requires, in addition to general surgery of recent wounds, some special measures. Wound toilet after rigorous and hemostasis will be treated open.

Treatment of bitten wound by snake. In our country most venomous snake is the viper. Viper bites require treatment of urgency because of the danger of exitus (death).

Appearance of inflammatory infiltration in the case of sutured wounds requires cold compresses of rivanol and if complaints are increasing, it will be wide opened. After opening the wound will aspirate pus, necrotic tissue will be removed, and then will wash the wound thoroughly with hydrogen peroxide. Finally, the wound will be disinfected with Betadine, remaining open. Wound toilet is repeated several times a day. To the chronic wounds are added decubitus ulcers and venous or lymphatic stasis ulcers. The essential difference between acute and chronic wounds is that at healthy people heal acute wounds, whereas for chronic wound healing process stops at a certain stage. At one time these chronic wounds heal but can recur frequently.

Infection represents the local and general response of organism to invasion, multiplication, and metabolic activity of microorganisms. Surgical infection means the appearance of a septic collection, which needs surgery. The most common surgical procedures are: incision, drainage, wound cleaning. In surgery, infections include any kind of infections that appear at surgical patient. The enter gate is the penetration place of germs and it is represented by a skin or mucosal lesion. It could be apparent or not apparent, visible or invisible. Endogenous surgical infections are frequently contact infections, and secondary are produced by airborne and hematologic infections. The source for the endogenous surgical infections is the patient himself (infection of aseptic wounds) or the contamination is produced by the opening of septic cavities (bowel, gallbladder, etc.) Contamination represents the presence of living germs in tissues without multiplication. The infection produced in hospital are very serious because of the resistance of pathogens at drugs, and theirs virulence. Contamination is produced directly (hands, objects) or indirectly (air, saliva). Common pathogens of infections are: cocci Gram pozitive (stafilococcuc, streptococcus), coccus Gram negative, bacillus Gram pozitive (coal, diphtheria), bacillus Gram negative (coliforms, proteus, piocianicus, tiphicus), bacillus acidalcoholoresistant (bacillus Koch). Some microorganisms are defending with highly resistant capsules to phagocytosis (Candida Albicans, Piocianic, Streptococcus piogenes), others resist to phagocytosis (Bacillus Koch, Toxoplasma), others may produce exotoxins, that decrease immunity (Clostridium, Stafilococcus aureus). The association between aerobic and anaerobic microorganism enhances the effects. Resistance represents all the specific and nonspecific ways of organism whose work out to realize the natural ability of defense against microbial aggression. The nonspecific resistance includes all innate defense mechanisms of body. They are the microphages (leukocytes) and macrophages (RES cells). Phagocytosis is cellular defense factor. Humoral factors (complement, properdin, lysozyme, interferon) are very important in association with cellular factors.

• Free ephitelial layers offers resistance by their resistance and acid pH. • Phagocytosis is the oldest defense by embedding, then enzymatic destruction of germs. • Complement, with the 9 C1-‐C9 fractions, has a role in: lysis of infected cells and viruses,

mycoplasmataceae and tumor cells, as in the increased formation of antibodies. • Interferon has potent inhibition of viral RNA synthesis and protein synthesis in

contaminated cells. • Inflammation is a nonspecific reaction of the body's defense, involving circulatory and

tissue mechanisms. Specific immune response is based on circulating antibodies that are produced by macrophages and B-‐lymphocytes. Cellular immunity is represented by neutrophils, macrophages and T lymphocytes and works by:

• Production of limfokine (enhances phagocytosis) • Destruction of damaged or infected cells (cytotoxic) • The action of K lymphocytes (killer) on cells was fixed on Ig.G.

Bacteremia is the presence of viable bacteria in the blood stream. The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly accomplished by blood cultures) is always abnormal. Septicemia is a related medical term referring to the presence of pathogenic organisms and toxines in the bloodstream, leading to sepsis. Sepsis is a potentially deadly medical condition characterized by a whole body inflammatory state (called a systemic inflammatory response syndrome or SIRS) caused by a severe suspected or proven infection. Severe sepsis or the septic syndrome is defined as sepsis with one or more organ dysfunction signs like: oliguria, hypotension, metabolic acidosis, ARDS, acute alteration of mental status. (the chapter continues with septic shock…)

Acute localized infections are characterized by the presence of purulent collection and necrotic processes, limited at a topographic region requiring surgical treatment. The most common location of these infections is the skin. The most common causative agents are: Staphylococcus aureus and group A β-‐hemolytic streptococci, anaerobes, Escherichia coli. Through small skin lesions, sometimes unapparent, are entering to produce located necrotic and purulent collections . Case by case: Folliculitis: Is inflammation of the hair follicle caused most commonly by Staphylococcus aureus. Occurs often in regions with increased body hair (legs, sacral region). Is manifested by minute erythematous follicular pustules without involvement of the surrounding skin, the primary lesion is a white to yellow follicular pustule, flat or domed. In sycosis barbae (barber's itch), the primary lesion is a follicular pustule pierced by a hair. Bearded men may be more prone to this infection than shaven men. It occurs due to infection by contact of several hair follicles during shaving. Treatment consists of: dressings with tincture of iodine, possibly hair removal. Boil Furuncle Skin Abscess: Furuncle is an infection of the hair follicle and sebaceous gland caused by Staphylococcus aureus. Etiopathogenesis: it is caused by Staphylococcus aureus, commonly appears on the neck , arms or legs as a red nodule up to 1 cm in size, and usually after some time opens and drains pus. Furuncles may be itchy and painful and low-‐grade fever may be present. It usually heals on its own. Occurs at patients with immunodeficiency, after a wrong treated folliculitis, microtraumas, poor hygiene. General signs: pruritus, local pain after that intense pain, itching, fever. Local signs: rash around a hair follicle, followed by local cianosis. A furuncle may begin as a tender, pinkish-‐red, swollen nodule but ultimately feel like a water-‐filled balloon. Pain gets worse as it fills with pus and dead tissue. Pain improves as it drains. It may drain on its own. More often the patient or someone else opens the furuncle.

• Is usually pea-‐sized, but may be as large as a golf ball • May develop white or yellow centers (pustules) • May join with another furuncle or spread to other skin areas • May grow rapidly • May weep, ooze, crust

Carbuncle is made up of several skin boils (furuncles). The infected mass is filled with fluid, pus, and dead tissue. Fluid may drain out of the carbuncle, but sometimes the mass is so deep that it cannot drain on its own. Carbuncles may develop anywhere, but they are most common on the back and the nape of the neck. Men get carbuncles more often than women. Most carbuncles are caused by the bacteria staphylococcus aureus. The infection is contagious and may spread to other areas of the body or other people. Intense hyperemia overlying skin may create confusion with cellulitis, but the underlying purulent mass that

breaks through the holes of skin clear diagnosis. General signs are: fever, chills, headache, and insomnia. Evolution is to cure or to septic complications that may even lead to death. Treatment: painkillers, antibiotics, dressings with rivanol and betadine. Surgical treatment: extraction of pustules or large incision in form of H letter or in form of a cross. Hydradenitis Suppurativa: is an acute inflammation of the sweat glands (apocrine furunculosis). Caused by Staphylococcus aureus, appearing in armpits, groin, and anal area or under the breasts and inner thighs -‐ areas that are often rubbed and are rich in the sweat and oil glands. Initially produces sweat glands inflammation then moves deeper in hypodermis. Clinical signs: inflammatory induration around a node that is affected gland, local intense pain , lymphadenitis occurs as a result of local infection dissemination, fever, chills. Positive diagnosis is determined by: -‐ Favorite location for the development (axillary disease); -‐ Pseudotumoral characters in its infancy; -‐ Lack of pustule. Evolution is chronic with successive relapses and successive glands attachments . It has three stages: inflammation, fistulization and scarring. Local treatment in the first phase, involves shaving hairiness, followed by antiseptic dressings. Advanced stage requires surgery, consisting of incision, drainage. General treatment requires antibiotics. Abscess: is a localized collection of pus in any part of the body that is surrounded by swelling (inflammation). Abscesses occur when an area of tissue becomes infected and the body's immune system tries to fight it. White blood cells move through the walls of the blood vessels into the area of the infection and collect within the damaged tissue. During this process, pus forms. Pus is the build up of fluid, living and dead white blood cells, dead tissue, and bacteria or other foreign substances. Abscesses can form in almost every part of the body and may be caused by infectious organisms, parasites, and foreign substances. Abscesses in the skin can be easily seen, and are red, raised, and painful. Abscesses in other areas of the body may not be obvious, but if they may cause significant organ damage. Clinical Forms:

• Breast, Germs enter in tissue through small continuity solutions or lesions produced by breastfeeding in unhygienic conditions. Another cause of the abscess is the Montgomery glands infection. Tissue infection spreads in depth, producing suppurative collections.

• Post-‐injection, occurs due to poor hygienic injections performing. Most commonly occur after intramuscular injections.

• Bartholin’s, abscess is the buildup of pus that forms a lump (swelling) in one of the Bartholin's glands, which are located on each side of the vaginal opening. This kind of abscess forms when a small opening (duct) from the gland gets blocked. Fluid in the gland builds up and may become infected. Fluid may build up over many years before an abscess occurs.

• Peri-‐anal, is a collection of pus that appears in perianal region;is caused by infection of the anal glands and crypts. Infection develops in the anal wall, then in perianal adipose tissue, reaching the skin, which manages fistulising. Path can be straight up or tortuous between an anal gland abscess and the cavity of the perianal abscess; from here the abscess can expansion to skin, to ischio-‐rectal fossa.

• Cold, Is a collection of pus, usually propagated from a bone or lymph node infection source with tuberculosis etiology.

Phlegmon is a spreading diffuse inflammatory process with formation of suppurative and purulent exudate or pus. This is the result of acute purulent inflammation, which may be related to bacterial infection. Etiology: commonly by bacteria -‐ streptococci, spore and non-‐spore forming anaerobes. Factors affecting the development of phlegmons are virulence of bacteria and immunity strength. Depending on the location is: superficial (subcutaneous,) deep, mixed.

Are distinguished four phases in evolution of phlegmons: Invasion phase: with edema and cellulitis; takes 1-‐2 days. Acute-‐phase of inflammation: the pus appears in small quantities, uncollected, and

blistering; takes 2-‐4 days. Suppuration-‐phase: with pus and death tissues (disseminated necrosis gray-‐green),

ulceration and vascular thrombosis; takes 5-‐6 days. Repair stage: removal of death tissues, healing appearance.

Cellulitis is an infection of the underlying skin tissue, appearing as a red, swollen, warm, tender skin patch of various sizes. An infection usually starts when Staphylococcus aureus (or group A streptococci, or rarely other bacteria) enter through the skin wound and spreads under the skin. The legs and arms are most commonly affected. Fever is usually present and the local lymph nodes may be swollen. Cellulitis always needs to be treated – oral antibiotics are usually given. Extremity immobilization and lifting diminish swelling and pain. Erysipelas is a pyodermitis , a type of skin infection. Group A Streptococcus usually causes bacteria erysipelas. The condition may affect both children and adults. Risk factors include:

• A cut in the skin • Problems with drainage through the veins or lymph system • Skin sores (ulcers)

In the past, the face was the most common site of infection. Now it accounts for only about 20% of cases. The legs are affected in up to 80% of cases. Erysipeloid is inflammation of the skin (dermatitis) due to bacteria. This is an infection caused by the bacteria, Erysipelothrix rhusiopathiae insidiosa. This type of bacteria is found in fish, birds, mammals, and shellfish. It usually affects people who work with these animals (such as farmers or butchers). Bursitis is inflammation of the fluid-‐filled sac (bursa) that lies between a tendon and skin, or between a tendon and bone. The condition may be acute or chronic. Bursae are fluid-‐filled cavities near joints where tendons or muscles pass over bony projections. They assist movement and reduce friction between moving parts. Bursitis can be caused by chronic overuse, trauma, rheumatoid arthritis, gout, or infection. Sometimes the cause cannot be determined. Bursitis commonly occurs in the shoulder, knee, elbow, and hip. Other areas that may be affected include the Achilles tendon and the foot. Chronic inflammation can occur with repeated injuries or attacks of bursitis.

Finger infection-‐panaritium is an infection is localized at the fingers. Increased frequency of these infections is determined by using hands without hands protection measures. Etiology -‐ germs involved are pyogenic cocci (streptococcus, staphylococcus, etc..), and gram negative coliforms. Entering gate can be a little scratch, sometimes unnoticed by the patient. In relation with localization the infection can be in proximal, middle or distal phalange lodge. Depending on the depth of the infectious process panaritium are classified in the next clinical forms:

1. Erythematous redness 2. Blistering pus 3. Paronychial (nails) at the edges of the fingernail 4. Sub-‐ungual usually by foreign body aggression

Other Forms:

• Felon (subcutaneous) • Infectious flexor tenosynovitis • Osteal • Articulate • Ingrown Toenail

Lymphangitis is the inflammation of the lymphatic vessels and channels. This is characterized by certain inflammatory conditions of the skin caused by bacterial infections. The most common cause of lymphangitis in humans is Streptococcus pyogenes (Group A strep), although it can also be caused by the fungus, staphylococcus or gonococcus. Thin red lines may be observed running along the course of the lymphatic vessels in the affected area, accompanied by painful enlargement of the nearby lymph nodes. Inflammation of a lymph node is called lymphadenitis. Pathologically are described five stages of evolution:

1. Congestive adenitis-‐without skin involvement. 2. Suppurative adenitis -‐micro abscesses in lymph nodes with conglomeration of nodes

and an abscess formation. 3. Phlegmon is formed around the lymph nodes. 4. Fistulization-‐pus is seen through multiple tracks. 5. Sclerosis of the suppurative process with severe scar formation.

Clinically, there is a hypertrophy of lymph nodes accompanied by spontaneous pain or at palpation. In advanced stages appears a conglomeration of nodes with the formation of an abscess and skin fistulization.

Necrotizing fasciitis is a rare but very severe type of bacterial infection. Many types of bacteria can cause necrotizing fasciitis (e.g., Group A streptococcus (Streptococcus pyogenes), Staphylococcus aureus, Clostridium perfringens,Bacteroides fragilis, Aeromonas hydrophila). Such infections are more likely to occur in people with

compromised immune systems. Is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. Infectious process is not interested in muscle, and the name of the disease is given by Wilson (1952). The infection begins locally at site of trauma, which may be severe (such as the result of surgery), minor, or even non-‐apparent. Patients usually complain of intense pain that may seem excessive given the external appearance of the skin. With progression of the disease, often within hours, tissue becomes swollen. Diarrhea and vomiting are also common symptoms. Traumas are defined as energy transfer produced by external or internal agents on different parts of the body. Abdominal trauma (AT) includes all injuries parietal and visceral caused by traumatic agents. These are frequently associated with thoracic trauma, cranio-‐cerebral, pelvic, and so on. Depending on the involvement of abdominal organs, both abdominal bruises and wounds can be: with or without organic lesion. The pathogenesis of AT is targeting all road accidents, sports and domestic accidents, the traumatic agent acts on the surface of the abdomen. The producing mechanism can be direct when the causative agent acts on a static body, or the contrary, a moving body collides with a fixed object. The producing mechanism is indirect, when the contact with the traumatic agent occurs to another segment.(fall on feet with cervical spine fractures and and splenic rupture). Through this mechanism occur ruptures, organ desinsertion, snatching the ligaments of the intra abdominal organs, due to inertial motion. By morphopathology:

Parietal lesions interested abdominal wall. They are represented by hematoma, muscle rupture allowing herniation of intra-‐abdominal organs.

Cavitary organs lesions: hematoma or large tissue destructions. On the other side and in the same time, is produced mesenteric lesions and is installed a hemoperitoneum. It should be noted that some times are formed true eschar of the visceral wall. (stomach, intestine), which by detachment at a certain time will cause severe peritonitis by perforation.

Parenchymal organ lesions are frequent and can be punctiform, subcapsular hematoma or partial and complete ruptures. The consequence of these injuries will be: internal bleeding or peritonitis, the lesions are more interested by the hilum organs or major vessels, as much the installation and evolution of hypovolemic shock will be much faster.

In liver Injuries: internal bleeding may occur like: interstitial hematoma, retroperitoneal, mesenteric hematoma, or peritoneal cavity one. Peritoneal contamination in the first phase has a chemical character, after 6 hours will be replaced by a microbial peritonitis. Hemoperitoneum will produce hypovolemia. If bleeding is important and take time to be installed quickly will appear the hypovolemic shock. Morel-‐Lavalle effusion: occurs especially in tangential blows of the sidewall, on which occasion small vascular rupture will produce the exit of plasma from the vessels in the tissues or interstitial spaces when an edema is produced ; sometimes is important, with the formation of a hematoma above the aponeurosis. Are recognized in the form of bulging of the region, fluctuant

and puncture blood draw. Treatment is removal by aspiration puncture or incision, and then if infection appears drainage is needed. The hematoma above the aponeurosis are blood collections posttraumatic, situated above the aponeurosis usually caused by direct internal trauma . Symptomatology is dominated by pain. The collection is fixed, usually in the sheath of straight abdominal muscle. Puncture extracts blood. Echography or CT scan established the diagnosis. Treatment consists in evacuatory puncture or drainage and haemostasis. Hernias and eventrations postcontusion are caused by strongest trauma including the ones at the level of preexisting hernias, but asymptomatic, or at the level of postoperative scars. Following this contusions appear hematomas and muscle tears, through which herniates abdominal contents. An open Abdominal Trauma occur more frequently with criminal purpose (suicide or homicide) with white weapons or firearms. Is relatively common in work, accidents or sports. The high frequency of traffic accidents has increased the AT especially in polytrauma. Abdominal wounds are penetrative or non-‐penetrative. Wounds caused by white weapons can cause multiple organ damage, especially if the traumatic agent is twisted in the wound. Injuries caused by firearms are complex with a small hole at the entrance and a bigger hole at the exit Emergency surgery should be performed on a patient hemodynamic and respiratory balanced sedated and with balanced functional parameters. Hemorrhages, first of all a classification as well reported by professor’s slides…

Hence is basically the same material we studied for physiopathology so it won’t be a problem…

Bleeding could be either internal or external… those internal may be categorized as:

• Seen exteriorly: o From upper digestive tract

(UDH) hematemesis, melena, rare hematochezia

o From lower digestive tract (LDH) hematochezia, melena, proctoraggia

o Not from digestive tract: hemoptysis, hematuria, menorrhagia, metrorrhagia

• Not seen from the outside: o Hemothorax o Hemopericardium o Interstitial hemorrhages (hematomas)

Types of vessels involved may be venous, arterial, capillaries or mixed. Hemostasis is the attempt of stop the bleeding, may be medical, surgical or combined. Bleedings are major emergencies, in which the para-‐clinic investigations should not delay the application of therapeutic measures. THE GOLDEN RULE OF HEMOSTASIS IS THE MAKING OF THE COMPRESSION BANDAGE.

Burns are injuries of skin or other tissue caused by thermal, radiation, chemical, or electrical contact. Cutaneous burns are caused by the application of heat, cold, or caustic chemicals to the skin. When heat is applied to the skin, the depth of injury is proportional to the temperature applied, duration of contact, and thickness of the skin. Along with burn size and patient age, the depth of the burn is a primary determinant of mortality. Burn depth is also the primary determinant of the patient’s long-‐term appearance and functional outcome.

Epidermal burns (first-‐degree)-‐as implied; these burns involve only the epidermis. They do not blister, but become erythematous because of dermal vasodilation, and are quite painful. Over 2–3 days the erythema and pain subside. By about the fourth day, the injured epithelium desquamates in the phenomenon of peeling, which is well known after sunburn.

Superficial partial-‐thickness (second-‐degree)-‐burns includes the upper layers of dermis, and characteristically form blisters with fluid collection at the interface of the epidermis and dermis. When blisters are removed, the wound is pink and wet. The wound is hypersensitive, and the burns blanch with pressure.

Deep partial-‐thickness (second-‐degree)-‐. Deep partial-‐thickness burns extend into the reticular layers of the dermis. They also blister, but the wound surface is usually a mottled pink-‐and-‐white color immediately after the injury because of the varying blood supply to the dermis.The patient complains of discomfort rather than pain.

Full-‐thickness (third-‐degree)-‐involve all layers of the dermis and can heal only by wound contracture, epithelialization from the wound margin, or skin grafting.

Fourth-‐degree burns involve not only all layers of the skin, but also subcutaneous fat and deeper structures. These burns almost always have a charred appearance, and frequently only the cause of the burn gives a clue to the amount of underlying tissue destruction. Electrical burns, contact burn some immersion burns, and burns sustained by patients who are unconscious at the time of burning may all be fourth-‐degree.

Burn patients with or without inhalation injury commonly manifest an inflammatory process involving the entire organism; the term systemic inflammatory response syndrome (SIRS) summarizes that condition. SIRS with infection (i.e., sepsis syndrome) is a major factor determining morbidity and mortality in thermally injured patients. Metabolic responses to burn injuries may be hyper metabolism, lipolysis, proteolysis, neuroendocrine and an elevation in catecholamine. The immune status of the burn patient has a profound impact on outcome in terms of survival and major morbidity. Many mediators are released from both injured and uninjured tissues at the wound site where they exert local and systemic effects. The timetable of induction/suppression and physiologic sequel are similar in patients suffering thermal and non-‐thermal trauma. Proper fluid management is critical to survival following major thermal injury. An aggressive approach to fluid therapy has led to reduce mortality rates in the first 48 hours post burn. Frostbites are traumas produced by cold cause local and general disturbances, which must be considered by the interrelation cold-‐reactivity of body. Cryo-‐aggression can lead to: hypothermia, freezing, "Slow freezing" ("trench foot"). At or below 0 °C (32 °F), blood vessels close to the skin start to constrict, and blood is shunted away from the extremities. The same response may also be a result of exposure to high winds. This constriction helps to preserve core body temperature. In extreme cold, or when the body is exposed to cold for long periods, this protective strategy can reduce blood flow in some areas of the body to dangerously low levels. This lack of blood leads to the eventual freezing and death of skin tissue in the affected areas. There are four degrees of frostbite. Each of these degrees has varying degrees of pain. First degree: This is called frostnip and only affects the surface of the skin, which is frozen. On the onset, there is itching and pain, and then the skin develops white, red, and yellow patches and becomes numb. The area affected by frostnip usually does not become permanently damaged as only the skin's top layers are affected. Long-‐term insensitivity to both heat and cold can sometimes happen after suffering from frost nip. Second degree If freezing continues, the skin may freeze and harden, but the deep tissues are not affected and remain soft and normal. Second-‐degree injury usually blisters 1–2 days after becoming frozen. The blisters may become hard and blackened, but usually appear worse than they are. Most of the injuries heal in one month, but the area may become permanently insensitive to both heat and cold. Third and fourth degrees If the area freezes further, deep frostbite occurs. The muscles, tendons, blood vessels, and nerves all freeze. The skin is a hard, feel waxy, and use of the area is lost temporarily, and in severe cases, permanently. The deep frostbite results in areas of purplish blisters which turn black and which are generally blood-‐filled. Nerve damage in the area can result in a loss of feeling. This extreme frostbite may result in fingers and toes being amputated if the area becomes infected with gangrene. If the frostbite has gone on untreated, they may fall off. The extent of the damage done to the area by the freezing process of the frostbite may take several months to assess, and this often delays surgery to remove the dead tissue. General causes: inadequate blood circulation when the ambient temperature is below freezing leads to frostbite. This can be because the body is constricting circulation to extremities on its own to preserve core temperature and fight hypothermia. In this scenario the same factors than can lead to hypothermia (extreme cold, inadequate clothing, wet clothes, wind chill) can contribute to frostbite. Or poor circulation can be due to other factors such as tight clothing or boots, cramped positions, fatigue, certain medications, smoking, alcohol use, or diseases that affect the blood vessels, such as diabetes. (I did not liked the way the argument was exposed on Professor’s material, thanks god exists wiki…!)

The Gaseous Gangrene Usually occurs in severe dirty wounds with an associated injury of major blood vessels and is characterized as a fulminating infection associated with profound toxemia and high mortality. Found, fortunately, very rare in surgical practice. It is characterized by necrosis of infected tissues (muscle, fatty tissue), followed by the production of gas. Are used various names as: streptococcal gangrene, bacterial synergistic gangrene, and Fournier gangrene. Is a disease with multiple bacterial etiologies, the relative incidence of the various anaerobes varies in the reports from different eras and geographical locations. The condition is most often caused by bacteria called Clostridium perfringens, septicum, histoliticum. However, it also can be caused by Group A streptococcus, Staphylococcus aureus and Vibrio vulnificus can cause similar infections. Essential condition is hypoxia who is present in wounds. Gas gangrene generally occurs at the site of trauma or a recent surgical wound. Exogenous gangrene developed in open fractures, wounds contaminated with soil. Iatrogenic gangrene occurs after surgery, on the digestive tract, through accidental contamination of surgical wounds. Patients who develop this disease in this manner often have underlying blood vessel disease (atherosclerosis or hardening of the arteries), diabetes, or colon cancer. Clostridium bacteria produce many different toxins, four of which (alpha, beta, epsilon, iota) can cause potentially deadly syndromes. The toxins cause damage to tissues, blood cells, and blood vessels. The debut is sudden, after a short incubation period (from several hours to several days), intense pain, feeling pressure at wound site. After removing the dressing the wound is dirty with ragged edges, possibly with retention of foreign bodies. Wound edges are swollen, dry bottom, with minimal, brown, fetid secretion and mixed gas. The site of infection becomes inflamed with a pale to brownish-‐red and very painful tissue swelling. If you press on the swollen tissue with your fingers, you may feel gas as a crackly sensation. The edges of the infected area expand so quickly that changes can be seen over a few minutes. The involved tissue may be completely destroyed. Muscle disease Semiology Muscles could undergo several kinds of traumas, such as:

1. Contusion 2. Stupor 3. Bruising 4. Hematoma 5. Hernias 6. Wound 7. Rupture

Muscle contusion is most often caused by the action of external traumatic agent. There are internal mechanisms of muscle contusion production by bone injury (broken bone or dislocated bone fragment). Act on intensity of traumatic agent may cause different consequences from fibrotic changes to partial or total muscle rupture. The changes are depending on the destructive force of traumatic agent and the condition of muscle contraction.

Stupor muscle is resulting of minimal bruising, producing a state of temporary inactivity of muscle. Clinically there was a transient reduction in force of muscle contraction. The lesion is microscopic and healing is spontaneous. Treatment includes rest, cold applications. Muscle bruising is small vascular break expression, producing little bleeding of fibers, with restitutio ad integrum. Treatment: rest, wet applications, cold. Intramuscular hematoma is the result of big trauma with major vascular injuries, which will lead to blood collections in the muscles. These hematomas are common features with other hematomas (see postoperative complications), but sometimes being intraaponeurosical hematoma can produce compression and ischemic disorders (box tibial). Muscle hernia occurs secondary to aponeurosis rupture. In this case the underlying muscles herniates aponeurosis gap, which is compressed by the fascia. Clinic is a soft tumor in a relaxed muscle. During contraction the hernia disappears or decreases substantially. The most commonly occurs in the brachial biceps muscle, but may form at forearm and calf muscles. Treatment is surgical and is aimed to restore continuity of aponeurosis. Muscle wound is a muscle fiber continuity solution produced by cutting, puncture, and crush. Is followed by severe heads retirement. As the muscle injury is greater, as the motor sequel will also be more pronounced. Cut wounds heal with less sequels, but contusion wound is healing sometimes with important scars. Infectious component increases as the wound is more contaminated (wounds of war). Muscle rupture is a consequence of external trauma (hitting), or a consequence of strong muscle contraction (athletes). Another cause is the muscle pathological changes, which may produce at minimal efforts, muscle rupture. Muscle rupture is the muscle contractions result of a violent, uncontrollable one. The most commonly occurs at athletes' unwarmed “in cold and humid climate. Significant ruptures produce intense pains, sometimes syncope, the feeling of rupture during muscle contraction. Pain is accompanied by functional impotence and analgesic position of member. Superficial bruises or hematomas characterize the contusion. Inflammatory Myopathies: Primitive acute myositis occurs more frequently during the septic development, with a suppurative character. Shows a diffuse phlegmonous form, with increased general phenomena, and a localized form with suppuration muscle (circumscribed). Diagnosis of these infections is difficult due to depth. Pyomyositis is a bacterial infection commonly caused by Staphylococcus aureus. Blood cultures are negative and staphylococcal secondary releases are rare. It is a common disease in tropical areas or in immigrants from these countries. Psoas abscess: the most commonly is inoculated by vertebral osteomyelitis, pyogenic or tuberculous. Suppurative process spreads to the groin, with exteriorization under the inguinal ligament, or Scarpa triangle. Another way of producing is from a septic source intra or retroperitoneal (perikidney abscess, and colic cancer or diverticulitis) that spreads to the muscles. Suppurative myositis of right abdominal is secondary to transverse abdominal wall opening in surgery. Sowing occurs from abdominal septic processes, or enteric fistulas in training. Clinical manifestations are common to suppurative collections and the treatment is antibiotic and surgical. CLOSTRIDIAN ACUTE MYOSITIS is rapidly progressive necrotic infection of skeletal muscle produced by clostridia (perfringens). These infections are secondary to faecal or soil contamination of wounds (see gas gangrene).

Chronic Myositis This group of disorders is characterized by chronic muscle inflammation that arise after the development of acute inflammation as chronic abscess. Evolution is long, with clinical symptoms cleared, benign, with the appearance of tumors or progressive muscle induration. The cause of these chronic inflammations is germs nonspecific and / or specific with lower virulence. One of the forms of chronic nonspecific myositis is ossifying myositis. We know two such forms: progressive and circumscribed form. Progressive ossifying chronic myositis is genetically determined, with autosomal dominant character. The disease affects muscle structures, aponevrozele, tendons, which undergoes progressive induration, while loss of contractile capacity. Circumscribed ossifying chronic myositis occurs following muscle trauma with hematoma, which in time is reorganized becoming bone. Clinically appears a bone formation intramuscularly complying on muscle matrix, moving to adjacent bone structures. Chronic tuberculous myositis secondary has its outbreaks from bone tuberculosis, from which infection spreads to muscle tissue. The disease is manifested by the formation of tuberculoms, which gradually turns into cold abscesses. Pathology shows a cross-‐sectional gray rodent intramuscular tumor, or a tumor containing yellowish pus. Treatment is primarily general (TB) and local-‐excision and drainage Syphilis myositis. Muscle manifestations occur during secondary syphilis in the form of rheumatic pain and induration accompanied by contraction (neck, arms) and in the tertiary stage of syphilis appears accumulated gums. Gums evolve into processes of muscular sclerosis. Chronic parasitic myositis may occur after various parasites, the most common being the echinococcus (hydatic). Inoculation is made by blood, and the evolution is following the classic stages. Most commonly affects the limbs muscles and paravertebral muscles. Clinically: occurrence of tumors, intramuscular, painless, mobile to surrounding tissue. Thyphic Myositis occurs during development of typhoid fever, from day-‐7th. Muscles’ tumors: Leiomyoma is a tumor of smooth muscle. The most commonly develops in the hairs erector muscles, or muscles of the vascular wall. Can rarely develop in the intestinal wall muscles. Clinically manifest as tumors with features of benign and treatment is surgical. Cavernous muscle angioma appears as painful tumors, soft, and vaguely defined. Treatment is surgical. Rabdomyoma develops from striated muscle with tumor character. Often is an intraoperative surprise. Treatment of choice is resection of the tumor. Muscular lipoma is fatty tissue developed in the interstitial. It is round or oval. Rhabdomyosarcoma -‐ tumor soft, yellow, turns in striated muscles, and on section shows numerous hemorrhagic areas. Have two forms: embryonic rhabdomyosarcoma (in children) and pleomorphic rhabdomyosarcoma (in adults). Treatment is surgical, with wide ablation and radiotherapy. Leiomyosarcoma develop from smooth muscle. Clinical tumor is in the form of increased consistency, relatively well defined, but infiltrating surrounding tissues. Treatment consists of wide excision.

Tetanus is a toxic infection caused by anaerobic tetanus bacillus, characterized by muscle contraction and profound alteration of homeostasis. Anaerobic tetanus bacillus is the causative agent of the disease. The vegetative form is less resistant. Sporulated form is particularly resistant to high temperatures (120 'to 90 ° C and 15' to 110 ° C). It is a ubiquitously germ, being met on the ground in the animal excrement and street dirt in the vegetative form, and especially in sporulated form. Entering gates are contusion wounds, open fractures or deep puncture, burns or umbilical wounds (newborns). Tetanospasmina produce muscle fiber contraction,and tetanolysina and a neurotoxin have modest neural effects. Infection begins when the spores enter the body through an injury or wound. The spores release bacteria that spread and make a poison called tetanospasmin. This poison blocks nerve signals from the spinal cord to the muscles, causing severe muscle spasms. The spasms can be so powerful that they tear the muscles or cause fractures of the spine. The time between infection and the first sign of symptoms is typically 7 to 21 days. Most cases of tetanus in the United States occur in those who have not been properly vaccinated against the disease. Three phases of symptoms:

1) Incubation is made in 2-‐20 days and depends on the amount of exotoxin produced,respectively the location of the wound to the CNS(central nervous system). Period from 7-‐8 days occurs most often fatal development.

2) The invasion is characterized by the appearance of anxiety, sweating, neck pain,

fotofobia. Later maxillo-‐facial neuritis occurs trismus, rizus sardonicus, then general signs: insomnia, nausea.

3) The status period -‐manifestations includes muscle contractures. Firstly tonic

contractions occur; occur then paroxysmal crises triggered by light, sound or mechanical excitation. In the terminal phase, pharyngeal muscle contraction will lead to asphyxia and death by respiratory failure

Clinical forms:

Mild -‐ with trismus, opisthotonus and mild muscle stiffness; Medium form -‐ muscular contracture manifests with moderately tendency to

paroxysmal crises and early dyspnea; Serious form -‐ with generalized contractions, paroxysmal generalized crises, respiratory

failure, circulatory failure, fever Treatment for blocking specific exotoxin or eliminate fixed exotoxins not exists. Prophylactic treatment is made for wound with tetanous potential. Tetanus prophylaxis is mandatory for all doctors and carried out with ATPA. Curative treatment aims the excision of the wound reducing the production of exotoxins. Open wound will be treated with antiseptic solutions (H2O2). Treatment is tetanus serum and tetanus human immunoglobulin 5000-‐10000 UT for blocking toxins. Active immunization with tetanus ATPA is indispensable. Antibiotics indicated: Penicillin G in large doses. Prognosis: mortality is 30-‐50%. The incubation time is shorter the disease severity it's much higher. The prognosis is more serious when the time elapsed until the first signs of crisis triggering muscle contraction is shorter That’s it folks! Hope it is good enough to pass this exam! “May the force be with you”

Alessandro Motta

surgical semeiology review

Documents