Lecture 11.
Acute purulent infections of serous cavities, blood vessels, bones, joints, peritonitis
Peritonitis – inflammation of the parietal and visceral peritoneum, which is accompanied by both local and general symptoms, impaired function of various organs and systems.
Peritonitis – one of the most serious diseases in abdominal surgery. The frequency of its occurrence – 5,5-6,0 per 10 000 population.
Despite the progress made in the diagnosis and treatment of peritonitis, mortality does not tends to decrease. Probably aware of this eminent scientist – a surgeon last century Wagner said, “I and my contemporaries brought up in the fear of God and the peritoneum.” Almost a hundred years KS Simonyan wrote that “… fear of God has passed, but before peritonitis remained.” Now, at the beginning of the new millennium, it is safe to say that the fear of God came, and before peritonitis – increased. The discovery of new antibiotics – antibiotics, antiseptics has given hope for a speedy curb this disease. But the enthusiasm of their performance changed disappointment – induced antimicrobial variability of microorganisms nullify advances in the development of new drugs. Improved results of treatment of peritonitis is possible only become prehensive approach to its early diagnosis, operative and postoperative treatment.
Etiology and pathogenesis.
Etiology and pathogenesis of acute peritonitis extremely complex and compound. Its development involved numerous mechanisms of damage and protection. In the pathogenesis of acute purulent peritonitis leading role played by the following factors:
pathogens;
intoxication;
hypovolemia;
profound metabolic disorders.
Bacterial invasion of the peritoneum is the leading pathogenetic link in the development of peritonitis. It hit microorganisms in the abdominal cavity is the trigger inflammatory response, consistent development of alteration, exudation and proliferation.
Research on the role of individual microorganisms in the etiology and clinical course of peritonitis received considerable attention in the literature. Conflicting data on the frequency of seeding microorganisms from peritoneal exudate resulting from our point of view, the use of inappropriate methods of collection of material and cultivation of microorganisms, especially anaerobic bacteria.
Numerous studies confirm that in most cases the infectious process in peritonitis has mixed aerobic-anaerobic nature. The dominant role played in the peritonitis Escherichia colli, Kkebsiella sp., Streptococcus faecalis, Staphylococcus aureus, and others. In recent years, increased frequency of sowing in peritonitis Proteus sp., Enterococus, Pseudomonas aeruginosa and fungi. Among anaerobes increasingly find clostridial forms: Bacteroides fragillis, Bacteroides melaninogenicus, Peptostreptococus sp. and others.Typical is a lot component associations, which include from 2-3 to 6-9 different types of aerobic and anaerobic microorganisms.
For causing inflammation in the peritoneum need a certain amount of microorganisms that are able to run their vital functions of the mechanisms of inflammation and time to support their implementation. That means etiologically-meal concentration is the presence of 1 ml of fluid 107-108 colony forming units / ml of microorganisms certain type. Lower concentrations of microorganisms caot long maintain the mechanisms of inflammation in relation to advance their rate of death during inflammation of reproduction.
When peritonitis occurs phasing of changes ionspecific resistance of the organism. Thus, for reactive peritonitis stage characteristic tension resistance factors – increasing of total serum bactericidal activity, reducing the titer of complement, increased phagocytic activity, intensity and completeness of phagocytosis, increased activity of acid phosphatase in neutrophilic leukocytes and decreased activity of alkaline phosphatase.
In toxic peritonitis stage is a reduction in the effectiveness of the mechanisms of natural protection, and end-stage watching the almost total failure of defenses.
For reactive peritonitis stage voltage characteristic immune system to combat the infection and toxins Nonbacterial origin. Determination of the content gammaglobulin fractions, indicating increased synthesis of specific antibodies that have tropism about toxins Nonbacterial origin.
Since the toxic stage, gradually developing state secondary immune deficiency. Reduced content of T-lymphocytes and their subpopulations activated, which is held in very low to the 7-15 day since the surgical treatment of peritonitis. Population of B lymphocytes changed during the course of peritonitis are less likely to detect and quantify the correlation of content with clinical status of patients is not always possible.
An important link in the pathogenesis of peritonitis is endogenous intoxication, which at certain stages of its development is leading, so that determines the severity of the patients.
Under endogenous intoxication (endotoxemia) often understand the pathogenetic mechanisms of the disease association with the action on the body of toxic products formed as a result of violations of certain autonomic functions. Endotoxins exhibit a direct or indirect effect on the effector organs, cells and subcellular structures. In action at the cellular structures can be divided into:
a) those possessing cytolytic effect;
b) activators of lysosomal enzymes;
c) blockers mitochondrial bioenergetics;
d) initiators of free radical processes;
e) inhibitors of ribosomal protein synthesis.
When peritonitis manifestations of endotoxemia necessitated the selection of a toxic its stage and severity of intoxication, which can focus on this component of the pathological process, take appropriate measures to detoxify the body.
When peritonitis there are significant metabolic disturbances. The main reason dyscorellation in the metabolism in peritonitis is polypathogenetic hypoxia. The reason for the latter is a systemic disorder of blood circulation, respiratory, universal violation of membrane functions and mechanisms of disorders of tissue oxygen utilization due to rising trend advantages of anaerobic energy production routes. The relationship of these reasons causes an avalanche.
Violations of water-electrolyte metabolism in peritonitis is very significant. The inflammatory process in the abdomen accompanied by a progressive loss of water. Due to increased permeability of the walls of microvessels in the abdominal cavity, retroperitoneal space, perivascular tissue hollow and parenchymatous organs is sequestration of water, electrolytes and proteins with the formation of pathological “third space.” In addition, dysfunction of bowel advantage over its secretion increased absorption capacity “third space”, and the constant vomiting leads to large external losses of water and electrolytes. Losing such patients water per day may not exceed 30-50% of circulating blood volume, reach more than 3 liters. There have been hyponatremia and hypokalemia, steady decrease in the concentration of potassium ions in cells, especially red blood cells is caused by the dysfunction of the cell membrane and activation of potassium excretion from the body.
Violation of protein metabolism in peritonitis appears stable and progressive hypoproteinemia, dysproteinemia. Observe a significant decrease in the concentration of albumin and increased globulin concentration, which progresses in parallel increase the severity of the patients. Albumin-globulin ratio in peritonitis is less than one and decreases with the progression. There have been a growing concentration – and cc2-globulin and moderate decrease in globulin throughout the postoperative period.
Classification
According to etiology:
primary,
secondary.
The primary peritonitis occurs by ingestion of microflora in the peritoneum by hematogenous or lymphogenous.
Secondary peritonitis – a complication of various surgical diseases and injuries.
For causes of secondary peritonitis: traumatic, postoperative, perforated, inflammation – induced proliferation of inflammation of the organs and tissues of the abdominal cavity and extraperitoneal space.
For stages: reactive, toxic, terminal.
The nature of exudate: serous, fibrinous, purulent, putrid, hemorrhagic, mixed.
By the nature of microorganisms: aerobic (staphylococcus, streptococcus, E. coli, etc.).; Anaerobic (bacteroids, peptococcii etc..) Mixed (association of various microorganisms). Adrift: acute, chronic, subacute.
For prevalence: delimited; unlimited which is divided into local, diffuse, diffuse and total.
Delineated when inflammation distinguishable from the rest of the abdominal cavity anatomical structures – a large gland, intestinal loops. It is with good reactivity and low virulence microorganisms. An example would be infiltration of appendicitis, cholecystitis, pancreatitis, abdominal abscesses various locations.
Unlimited when inflammation of the place of occurrence may be distributed freely in the abdominal cavity.
Local covers 1 of 9 anatomical areas anterior abdominal wall, that is adjacent to the site of peritonitis: appendicitis – in the right iliac area, with cholecystitis – the right hypohondrium area.
In diffuse inflammation of the peritoneum covers not only at the point of origin, but also spread to adjacent areas (not more than from anatomical sites). For example, appendicitis, gynecological peritonitis in the inflammatory process involves the pelvic peritoneum, right, left iliac and suprapubic area.
In cases of diffuse peritonitis inflammation spreads more than 3 but not more than 6 anatomical sites. For example, signs of inflammation are found in the lower floor of the abdominal cavity with appendicitis, perforation of the sigmoid, intestinal obstruction.
In general peritonitis signs of inflammation are found throughout the abdominal cavity.
There are such severity peritonitis: I degree – light; II degree – moderate, III-A level – severe, III B -: very grievous; IV degree – terminal.
Clinical symptoms Clinical course of acute peritonitis depends on its type, shape, stage, number and virulence of the pathogen, immune responsiveness and resistance, the reasons that caused peritonitis, and other factors.
In the first stage, in violation of the integrity of the hollow organs of the gastrointestinal tract peritonitis begins abruptly with a sharp, barbed abdominal pain. In case of peritonitis as a consequence of progressive inflammation of abdominal pain increases and spreads throughout the abdomen gradually.
The pain is caused by irritation of nerve endings peritoneum. Changing the position of the body leads to a stretching of the affected area of parietal peritoneum, which intensifies the pain. To reduce the tension of the abdominal muscles and the parietal peritoneum ill try lying motionless on his back or side, bent legs to the abdomen.
There nausea, vomiting (sometimes multiple), after which he begins relief. Increases body temperature to 38 ° C. An objective examination reveal pale skin, tachycardia to 100-120 bpm, and sometimes bradycardia (“vagal pulse”) blood pressure in the normal range, rapid breathing, shallow. Abdomen retracted. Anterior abdominal wall throughout is not involved in breathing. When the superficial palpation determined diffuse tenderness throughout the abdomen, muscle tension – from minor to hard. Deep palpation impossible because of muscle tension and acute pain. Identify positive symptoms Shchetkin-Blumberg, Razdolsky, Resurrection. In the presence of large amounts of fluid in the abdominal cavity can be detected percussion dullness in the lateral abdomen. Peristalsis not listen. When researching finger through the rectum defined overhang of the anterior wall of the rectum and cutting her pain.
The second stage (toxic) – The main symptoms are common signs of intoxication. Feeling somewhat the severity of pain decreased, vomiting frequent, longer depart gases occurs anuria, the patient is euphoric, features exacerbated. Appears acrocyanosis, respiration frequent, shallow. Accelerated heart rate, lowers blood pressure. The abdomen becomes swollen, the anterior abdominal wall is not involved in breathing.
When the superficial palpation find that muscle tension anterior abdominal wall is less pronounced, watching her intense resistance (a symptom Mondor). Positive symptoms Shchetkin-Blumberg, the Resurrection, Razdolsky, percussion – reducing “liver dullness.” The symptoms of intestinal obstruction: Kivulya (tympanic sound with a metallic tint), “deathly silence” (disappearance bowel noises).
The third stage – terminal. It is characterized by the fact that the background of deepening functional intestinal failure and toxicity occur – deep metabolic and vital body functions. Clinically it is manifested abrupt tachycardia, shortness of breath, weakness, Hippocrates face, pale and dry skin. Tongue dry and coated with brown patina, it shows fingerprints teeth. It is noted centralization of circulation: low blood pressure, cold extremities. Patients in the mind, indifferent to his condition. Objective symptoms stomach is almost indistinguishable from that in the toxic stage. Instrumental methods of diagnosis
Plain radiography can detect:
a) free gas under the dome of the diaphragm;
b) pneumatosis intestinal bowl Kloybera.
Ultrasound scanning enables you to identify only certain forms of peritonitis, appendiceal infiltrate paraappendiceal, internal abscesses. The same applies to thermal imaging, which helps detect disease that can lead to peritonitis.
More informative are celiocentesis and laparoscopy.
Therapeutic tactics and choice of treatment. The presence of symptoms of peritonitis is an absolute indication for surgery, which must be made in the urgent procedure. Preoperative preparation is carried out only in patients with unstable hemodynamics is aimed at correction of cardiovascular and metabolic disorders, vital body functions, which will allow these patients to perform surgery.
The main components of surgical intervention in peritonitis
1. Eliminate sources of peritonitis.
2. Remediation of the abdominal cavity.
3. Drainage of abdomen.
The main access in the surgical treatment of peritonitis is a midline laparotomy. With abdominal fluid removed, set the cause peritonitis. If the reason it was acute appendicitis, appendectomy is performed, if acute cholecystitis – cholecystectomy, if strangulative intestinal obstruction with necrosis of intestine – resection of the bowel, in the case of perforation of the organ-stitching perforated hole.
Sutures are placed in peritonitis, requiring additional consolidation and protection from the harmful effects of peritoneal exudate. This line of stitches cover the greater omentum streak on the stem (if the gland is not involved in the inflammatory process) or protect them with auto-graft or geterotissue that record over the line of stitches.
Remediation of the abdominal cavity with common forms of peritonitis performed by washing her antiseptic solution and subsequent drying. Choice of antiseptic solution depends on the nature of fluid isolated microflora. Priority should be given an antiseptic with a broad spectrum of antimicrobial activity.
Complete abacterial abdominal cavity with common forms of peritonitis achieve usually fails. However, 3-4-fold washing it with antiseptic solutions exposed for 10-15 minutes reduces bacterial contamination of more than 75%.
After rehabilitation abdomen perform intubation of the small intestine intestinal probe to decompression proximal gastrointestinal tract, removal of toxic substances from the intestinal lumen.
Postoperative treatment must be carried out with consideration of pathogenesis of peritonitis and depends on the severity of its course.
Complex treatment of postoperative peritonitis include:
a) antibiotic therapy: antibiotics, sulfonamides (drugs better administered intravenously and endolymphatic – as in parietal lymph vessels by catheterization lymphatic vessels of lower limb and invisceral link the lymphatic system by intraoperative catheterization visceral lymph nodes;
b) anti-inflammatory, anti-histamines, which strengthen the vascular wall, improve the rheological properties of blood;
c) immunocorrection;
d) correction of violations of water-electrolyte balance of protein, fat, carbohydrate metabolism;
e) detoxification therapy: its volume depends on the degree of severity of peritonitis.
f) recovery of the gastrointestinal tract;
g) symptomatic treatment in violation of the cardiovascular and respiratory systems;
h) parenteral nutrition and tube;
i) hyperbaric oxygenation.
Prevention of peritonitis is the timely diagnosis and effective treatment of diseases that can cause peritonitis.
Pleurisy
Pleurisy – inflammation of the pleura.
In most cases the effusion is not an independent disease and is a pathological process that complicates the course of disease:
– Lung
– Mediastinal
– Diaphragm,
– Chest wall,
– Subdiaphragmatic spaces.
Classification:
There pleurisy:
– Infectious,
– Noninfectious (aseptic).
Infectious depending on the type and nature of the infectious agent:
– Staphylococcal,
– Pneumococcal,
– Putrefactive,
– Anaerobic,
– TB and. etc.
Noninfectious depending on the nature of the underlying disease manifestation or complication which it is:
– Rheumatic,
– Carcinouse,
– Post-traumatic. etc.
Depending on the nature of tissue changes distinguish pleurisy:
– Dry
– fibrous,
– Transudate
– exudative.
Transudate pleurisy, depending on the nature of the effusion is divided into:
– Serous,
– Serous – fibrinous,
– Purulent,
– Purulent,
– Bleeding,
– Heloise.
In the case when the purulent exudate gets gas (usually air in the pleural cavity gets the breakout lung abscess, cavity) occurs pneumoempyema.
The clinical course distinguish pleurisy:
– Sharp
– Subacute,
– Chronic.
Depending on the presence or absence of distant separation effusion pleural cavity pleurisy distinguished:
1. diffuse (total)
2. delimited (encysted)
Etiology and pathogenesis.
Since the vast majority of pleurisy is a complication or manifestation of various, mainly lung disease, etiological factor should be considered a disease of pleurisy which led to pleurisy.
The source of infection is usually different lung diseases (pneumonia, abscess, gangrene, suppuratioonparasitogenic echinococcus cysts or cysts, collapse cancerous tumors, breakthrough tuberculous cavity). Sometimes the infection gets into the pleura lymphatics from distant foci of inflammation (cholecystitis, appendicitis, paranephritis, carbuncles, boils, etc.)..In penetrating wounds microflora directly enters the pleural cavity. Very often there is a purulent pleurisy, when injury is accompanied by hemothorax.
Pathogens pleurisy in adults more often streptococci, rarely – staphylococcus and pneumococcus, and the children – mostly pneumococci.
The nature of fluid distinguish serous, sero-fibrinous, purulent, putrid and hemorrhagic pleurisy.
Serous and sero-fibrinous pleurisy observed in tuberculosis, lobar pneumonia, abscesses and other lung diseases.
Purulent and putrid pleurisy develops the breakout purulent foci in the pleural cavity, the festering blood that poured out, and sepsis.
Hemorrhagic pleurisy occurs malignant tumor lung and pleura.
Sometimes hemorrhagic exudate is tuberculous process and injuries. Localization of pus in the pleural cavity pleurisy distinguish pervasive, medium, small, encysted (apical, basal, parietal, paramediastynitis), single and multi.
Clinic. In case of pleurisy appear stabbing pains in the chest, aggravated during breathing and coughing. Temperature 39-40°, pulse quickens and becomes soft. Patient half chest stuck out, behind when breathing, intercostal spaces smooth and extended. Palpation marked weakening trembling voice, percussion determined voiceless. Placing upper limit effusion, which causes voiceless sound, looks like the curve, the so-called line of Ellis – Damuazo – Sokolov. The upper limit of fluid coming from the spine outwards and upwards to the inner edge of the blade, then descends. In the middle axillary line curve increases, dropping to the nipple line.
Thus, the maximum height of fluid formed at the inner edge of the shoulder and underarm area. This placement of fluid in the pleural cavity due to the negative intrapleural pressure difference and elastic force for each of the lungs. Above and medial revealed clear percussion sound on the surface, resembling a triangle. This – Zone of compressed lungs. Purulent exudate leads to a shift of the mediastinum to the healthy side, so on the other side near the spine marked triangular muting. Auscultatory zone muting respiratory noise there. Above muting auscultation weakened breathing and the sound of pleural friction.
When X-ray eclipse visible homogeneous pleural cavity, the fluid level and shift of the mediastinum. From the blood marked leukocytosis with a left shift, accelerated ESR. When puncture the pleural cavity, which in these cases is conducted in VIII intercostal space along the mid axillary line, receive manure.
Treatment. Acute suppurative pleurisy treated by conservative and surgical means. At the onset of the disease taking steps to evacuate pus and smoothing lungs, improve heart and eliminate hypoxia. Purulent exudate suck repeated puncture followed by administration of antibiotics in the pleural cavity, depending on the sensitivity of microflora to them. Simultaneously prescribe antibiotics intramuscularly, camphor, korglikon, oxygen, hot compress sollux, UHF. Recently, in connection with the use of antibiotics these measures is enough, and most (75%) of the patients recovering. If the process progresses, resorting to surgery and drainage of the pleural cavity. Introduction drainage often conducted closed method – through a small incision in the intercostal spaces or through bed resected rib. Around drainage soft tissue layers sewn. Drainage through a system of tubes connecting with the device for continuous, active aspiration of pus. If a suction device is not ready, you can temporarily lower the drain in a bottle or a bank filled with antiseptic fluid.
In the presence of encysted purulent pleurisy with massive pleural make a wide incision pleural cavity with its subsequent drainage. This wound is gradually filled with granulation and healing. Consequences of treatment of purulent pleurisy through the use of antibiotics and timely operations improved. Mortality is 4-6%.
Osteomyelitis
Among purulent diseases of bones and joints:
1) severity of the course
2) difficulty of diagnosis
3) bad consequences highlights acute hematogenous osteomyelitis
Coverage problems osteomyelitis caused by:
1) insufficient study of the pathogenesis
2) a high percentage of diagnostic errors
3) late hospitalization
4) lack of unanimity of the choice of diagnostic methods, the volume of transactions
5) postoperative care.
Hematogenous osteomyelitis term coined in 1831 Reynaud.
TP Krasnobaev (1925) proposed a classification:
1) toxic form
2) septic
3) locally lobular form.
According to the International Classification of Diseases, Injuries and Causes of Death osteomyelitis classified:
1. For reasons (for agents):
a) monoculture (staphylococcus, streptococcus);
b) mixed, or associated culture (double, triple association);
c) the agent was not found;
2. Clinical forms of osteomyelitis
1) acute hematogenous osteomyelitis:
a) generalized form (septykotoksychna, septykopiyemichna);
b) local (focal) form;
2) posttraumatic osteomyelitis:
a) after fracture;
b) firearm;
c) post;
d) X-Ray.
3. For localization process: osteomyelitis of long bones:
a) epiphyseal;
b) metaphyseal;
c) diaphyseal;
d) total
Osteomyelitis of flat bones
a) Pelvic;
b) blade;
c) iliac;
d) skull.
4. Stages and phases of hematogenous osteomyelitis:
1) Acute phase:
a) intramedullary phase;
b) extramedullary phase;
2) subacute stage:
a) phase of healing;
b) phase continue.
3) chronic phase:
a) acute phase;
b) the phase of remission;
c) phase of healing.
5. Morphological forms
a) diffuse;
b) lobular;
c) diffuse lobular.
6. Complications:
1) local
a) pathological fracture
b) pathological dislocation
c) false joints
d) contracture;
e) ankylosis
2) general:
a) amyloidosis
b) destructive pneumonia
Variants of acute hematogenous osteomyelitis (for Doletskym SJ):
1. breakwire (49%) – healing occurs in the first 2-3 months of onset;
2. prolonged (36%) – also ends by healing, but requires a longer (6-8 months) treatment;
3. lightning (2%) – usually fatal and happens when toxic and septic forms;
4. chronic (13%) – is characterized by the formation of sequester, fistulas, lesions of the extremities, marked recurrent exacerbation in terms of more than 6 months.
Etiology.
Every microbe can cause osteomyelitis. However, the main causative agent is Staphylococcus aureus. In monoculture aureus is at 61%.Lately often planted along with aerobes and clostridial anaerobes.
High pathogenicity of selected crops. Plasma cougulative activity detected in 95% of cases. Also expressed gialuronidase and hemolytic activity.
Viral infections, against which in 40-50% of cases develop disease.
Viruses contribute:
1) lower the body’s defenses
2) increase the virulence of microorganisms
3) create favorable conditions for development.
Pathogenesis. Acute hematogenous osteomyelitis develops on the background of altered reactivity and accompanied by a violation of homeostasis.
Theories of pathogenesis
1. Vascular (embolic) founder A.A.Bobrov (1888). Bone vessels ending blindly in the metaphysis forming an extensive network (E. lexer, 1884). This structure occurs mainly in young age (in children).
2. Allergic theory (S.M.Derizhanov, 1940). On the basis of sensitization of the organism occurs in the bone fire aseptic inflammation that leads to vasoconstriction of circulatory disturbance bone.
3. Nervously reflex theory (N.N.Yelanskyy, 1954). Reflex spasm of blood vessels with blood circulation due to various external stimuli. Do not rule out the role of sensitization and the presence of covert infection.
4. M.V.Hrynov (80 years of the twentieth century.) At the heart of osteonecrosis is not intravascular circulatory disorders (embolism) and external compression of vascular inflammatory infiltrate.
Predisposing factors of acute hematogenous osteomyelitis.
1) endogenous microflora fire – promotes allergic reaction
2) non-specific stimuli (trauma, hypothermia, exhaustion, illness, paralyze the body
Immune mechanisms of pathogenesis. In patients with depressed cellular immunity.
1. The number of T lymphocytes reduced
2. Reduced the amount of IgG
3. Increasing the number of B-lymphocytes.
Acute hematogenous osteomyelitis develops on the background:
1) reduction of nonspecific resistance
2) prior sensitization
3) under the influence of an infectious agent.
Pathological Anatomy.
In the bone marrow appear.
On the first day:
1) effects of reactive inflammation
2) congestion
3) vasodilatation
4) blood stasis exit form elements
5) intercellular infiltration.
At 3-5 days: accumulation of eosinophils, segmented neutrophils.
At 10-15 days:
1) purulent infiltration progresses
2) necrosis of bone marrow
3) focal hemorrhage
4) accumulation of fluid
At 20-30 days:
1) focus on detritus
2) accumulation of segmented neutrophils and lymphocytes.
At 35-45 days – necrosis extends to all elements of bone, there curtailment.
Osteomyelitis begins from:
1) inflammatory foci in the metaphysis
2) reactive inflammation of bone marrow
3) disturbance of microcirculation, increase perfusion of vessels with the release of cellular elements of blood
4) leukocyte infiltration of the bone marrow
5) raising the pressure in the bone medullary canal
6) compression of venous channels
7) blood stasis, thrombophlebitis shallow vessels bone
8) necrosis
9) intramedullary, periosteum, intramuscle, subcutaneous phlegmon
10) Breakthrough pus through the skin
11) pus spreads metaphysis to epiphysis
12) Breakthrough pus in the joint
13) spread manure oeighboring bone
Sequestration of bone.
Sequestration:
1) cortical
2) central
3) penetrating (in a certain sector of a circle)
4) pervasive (segmental or tubular).
The formation of sequester – from 4 weeks to 4 months.
On the border of healthy tissue bone is:
1) the demarcation line
2) proliferating granulation forming pyogenic membrane and prevent the spread of the pathological process in the periphery.
Sequestration is in a cavity filled with pus.
The cavity is covered sequestration capsule (box) of bone.
On radiographs capsule can be seen in 4-6 weeks from the onset.
Sequestration prevent:
1) healing of osteomyelitis focus
2) non-absorbable
3) not implantable.
Clinic
Semiotics is diverse and depends on:
1) the virulence of microbes
2) reactivity
3) localization process
4) patient age
5) presence of complications.
The local (focal) form. The most common and is characterized by local suppurative inflammatory changes. It starts suddenly, sharply, often after trauma, hypothermia.
Prodromal period of 1-2 days:
1) weakness
2) illnesses
3) mild fever
4) the temperature to 400C
5) pain in the injured limb, intense, arching, permanent
6) in the affected area 2-3 days edema of tissue.
1. Swelling of the thigh
2. Severe pain on percussion bones
3. Flexion contracture
Generalized form. a) toxic (lightning) – extremely difficult. Complicated by septic shock.
Starts:
1) hyperthermia with fever
2) excitation
3) delirium
4) cramps
5) symptoms of severe intoxication
6) collaptoid status
7) oliguria.
Diagnosed extremely hard on the background of the critical condition of the patient. Patients often die in the coming hours or days. Autopsy – multiple shallow cavity in the sponge bone, filled with blood “herbaceous exudate.
Heart. Borders expanded, tone deaf, systolic murmur, tachycardia to 120 bpm. the ECG – degenerative changes in the myocardium, blood pressure decreased. When septic shock – a collapse.
Lungs. Breathing frequent, shallow, dry and moist rales. Complications – secondary suppurative destructive pneumonia.
The liver and spleen were enlarged, indicating the presence of septic condition.
Kidneys. Changes in urine positive symptom Pasternatsci.
b) septycopyemia form.
Getting sharp, rapid, severe intoxication. Complications as other purulent foci (multiple osteomyelitis) and organs (lungs, kidneys, liver). Vomiting, diarrhea.
The appearance of ulcers in other organs due to bacterial dissemination.
Methods of test. Morphological composition of blood:
1) leukocytosis, left shift
2) suppressed hematopoiesis and function – developed hypochromic anemia
3) toxic granularity
4) ESR more 30mm/h.
Further leukocytosis may change leukopenia.
Biochemical studies
1) reducing the amount of protein and 55 g / l by albumin (hepatic dysfunction)
2) globulins increased by α 1 and α 2. Confirming the activity of the inflammatory process
Electrolyte metabolism:
1) hypokalemia
2) hyponatremia
3) hypercalcemia
Rheovasography: assesses the extent and nature of circulatory
Arterial osciography: register inflammatory hyperemia of the soft tissues.
Ultrasonic echolocation – confirms osteomyelitis fire and its limits.
Skin thermometry – over the fire skin temperature at 2-40C higher.
Color contact thermography – registration of thermal energy in the form of infrared radiation. Accuracy of the method ± 0,10 C.
Temperature drop over the fire ignition is from 0.2 to + 0.4 0C.Puncture bone – 1) promotes timely verification of diagnosis (search manure) 2) is a therapeutic manipulation (evacuation of pus).
Intraosseous thermometry. Determination intraosteal pressure – the higher pressure (400 mm H2O), the transition often chronic.
Cytological method.
X-ray methods (12-15 days).
Allows you to:
1) confirm or reject the diagnosis
2) to identify the foci
3) the degree of severity
4) the prevalence changes.
Most early on radiographs revealed changes m “tissue (edema)Changes in bone:
1) the disappearance of trabecular structure and cortex
2) the emergence of foci of osteoporosis and destruction.
Pathognomonic signs:
1) periostitis
2) curtailment.
Computed tomography – the possibility of serial sections with a minimum distance between them (to 0.5 cm)
Densitometry – the degree of bone demineralization.
Osteomedulography – normally contrast resolves after 10-30 min. In contrast osteomyelitis delayed for a long time.
Radioisotope scan (radioactive gold) – in the acute phase is marked most of his savings.
Treatment
1) complex
2) etiopathogenetic
Effects of treatment depend on:
1) the timeliness
2) adequacy.
Most effective when it begins in the first 24 hours.
The treatment program based on the principles T.P.Krasnobayeva:
1) impact on Macro-organism
2) the microorganism
3) local treatment centers.
Generalized form can be accompanied by:
1) dehydration
2) deterioration of the peripheral circulation
3) the development of septic shock:
a) the admission of exo-and endotoxins
b) biologically active substances from decay and bacteria cells.
Impact on Macro-organism:
1) removal of intoxication
2) reduce or eliminate the dysfunction of vital organs
3) improve the body’s defenses
Intensive care:
1) correction of homeostasis:
a) water and electrolyte balance
b) hypovolemia
c) intoxication
d) disturbance of microcirculation
2) therapy dysfunction of vital organs
3) maintenance of energy balance and increase immune resistance of body.
In the most severe patients – Transfusion therapy.
In septic conditions – hemosorbtion (extracorporal blood purification)
Infusion Therapy – glucose with insulin (60% of daily volume “volume). Regulation of water and electrolyte balance – ions of sodium and potassium.
Protein preparations – albumin, plasma amino Dextran – reopolyglukine, polyglukin Low molecular polymers – neokompensan, polidez. Preparations starch – stabizol, rehydron. Correction of vital functions – shown symptomatic therapy. Activated proteolytic system – the use of inhibitors of proteolytic enzymes (kontrikal, trasylol, tsalol):
1) reduce the proteolytic activity
2) reduce the severity of inflammation
Allergy body – desensitizing agents (diphenhydramine, tavegil, pipolfen, calcium chloride, Telfast).
Maintaining energy balance:
1) full oral feeding
2) intravenous parenteral nutrition:
a) facilitate the protein synthesis
b) acceleration terms regenerative processes.
Increasing immune resistance of body Nonspecific immunotherapy(Metatsyl, pentoxyl, levamisole, timalin, splenin, Nukleinat sodium).
Immunostimulators improve:
1) metabolic processes
2) leucopoiesis
3) increase the phagocytic activity of leukocytes
4) production of gamma-globulin5) accelerate regeneration.
Specific immunotherapy – the use of drugs modulating active or passive immunity.
Active immunization:
1) in the subacute or chronic stage of the disease
2) in protracted of healing
3) the resistance of microorganisms to antibiotics.
Passive immunity (input immune plasma or hammaglobulin) in the acute stage of the disease.
Effect on microorganisms. Generally accepted is to use antibiotics since the first hours of the disease. The sensitivity of microbes to antibiotics is a major criterion for its purpose.
The need for long-term antibiotic therapy (up to 6 weeks) is determined by:
1) poor diffusion of drugs in bone
2) risk of early relapse
3) transition to the chronic stage.
Support optimal concentrations of antibiotics. Indications for discontinuation of antibiotics are:
1) satisfactory condition of the patient
2) stable normalization temperature for 10-14 days
3) leukocyte reaction
4) Regression ESR.
Premature cancellation of antibiotics –
1) relapse
2) transition to the chronic form.
Chronic osteomyelitis.
1) secondary chronic osteomyelitis, as result of acute hematogenous osteomyelitis
2) chronic osteomyelitis that develops after traumatic injury
3) atypical forms of chronic osteomyelitis (cause of these forms is considered low virulence of microbes with high reactivity)
