Anaerobic bacteria that invade muscle tissue during traumatic injury. In case of damage to the front of the head, they are very rare. Pathogeresis of gas gangrene. Most often, gas gangrene develops with gunshot wounds and injuries with extensive tissue proliferation and contamination with soil and scraps of clothing. A gas infection can also develop with other types of injuries, as well as with impaired blood circulation (pressing dressings, vascular injury, vascular ligation when a special tourniquet or pad is applied to the neck). In the area of extinguishing anaerobic infection, hemorrhagic edema, decay and melting of tissues are formed, in which gas bubbles accumulate and vascular thrombosis is possible. Gas gangrene clinic. Sharp start. Temperature up to 39-40 °, tachycardia, shortness of breath with deteriorating filling and pulse tension, blood pressure drops. Facial features are pointed. The skin is pale, yellowish-earthy, sometimes cyanotic. Appetite and sleep are severely disturbed. On the first day there are pains in the wound and along the vessels, clogged with blood clots. The wound is dry, its discharge is scanty, the color of meat slops (serous- hemorrhagic – ragic ). The muscles look like boiled or putrefactive meat. The wound often gives off a fetid, putrid odor. Gas in the tissues is detected by palpation (crepitus) and is visible on an x-ray. The skin over the affected area has a different color from white to bluish-purple and in places black, sometimes hemorrhagic blisters appear on the skin under the epidermis. Anemia, neutrophilic leukocytosis, a shift of the formula to the left, disappear, eosinophils disappear, toxic granularity of neutrophils, lymphopenia , monocytosis appear in the blood . Gas gangrene diagnosis. The described clinical picture of the disease plays the main role in recognition. It is necessary to differentiate with Ludwig’s angina. The course and complications of gas gangrene. The clinical picture develops rapidly, sometimes for several hours, complicated by extensive damage to the muscles and surrounding tissues, followed by their putrefactive decay. Severe intoxication can be fatal. Treatment of gas gangrene is surgical with wide incisions (usually in the submandibular region and in the neck) to provide aeration of the affected tissues. Subcutaneous injection of antigangrenous polyvalent serum. Antibiotics (up to 1 200 000 U of penicillin per day) and sulfa drugs at the same time. Drip infusion of blood. Intravenous — 5% glucose and saline, inside — ascorbic acid up to 1 g per day, drink plenty of fluids. The prognosis of gas gangrene is always serious. Prevention of gas gangrene. For all types of injuries to the facial part of the head, it is necessary to carry out a thorough surgical treatment, and in case of extensive crushing of tissues, antigangrenous sera and antibiotics should be administered.
HAYMORITIS ODONTOGENOUS ACUTE.
Etiology of sinusitis. The spread of the inflammatory process from the periodontium and peri-root cysts to the maxillary sinus (maxillary cavity). Pathogenesis of sinusitis. The mucous membrane of the maxillary cavity is affected as a result of the spread along the length of toxins and infection from a carious tooth with gangrenous disintegration of the pulp, complicated by acute or exacerbation of chronic periodontitis. The infection is transmitted to the mucous membrane of the maxillary cavity through the bone layer in a hematogenous way. Clinic of sinusitis. Pain and sensation of pressure, tension and a feeling of heaviness in both the buccal and zygomatic areas. The pains ” radiate to the zygomatic bone, to the frontal and temporal regions. From the nose on the sore side, mucous, mucopurulent and purulent discharge. Breathing is difficult, sometimes the cheek and lower eyelid swell. The temperature is elevated. There is a chill. Headache. The course and complications of sinusitis. . Acute odontogenic sinusitis lasts 2-3 weeks and ends with recovery or transition to a chronic form. Diagnosis of sinusitis. On palpation, pain in the anterior wall of the affected sinus, and sometimes the frontal. When rhinoscopy is visible hyperemic and swollen mucosa, especially in the middle “but sometimes and the lower nasal passage. The discharge on the mucous membrane of the middle nasal passage is visible in the form of a characteristic light strip. In order to obtain discharge, the opening of the maxillary sinus is expanded with 1-2% cocaine solutions or 2-3% ephedrine solution, then the patient’s head is tilted down and to one side , while the hole is at the bottom and the contents of the inflamed sinus easily flow out through it. and radiography gives a darkening of the affected sinus. With odontogenic sinusitis, there is a picture of acute periodontitis with characteristic changes in the periodontium on the roentgenogram. Differentiate with acute odontogenic periostitis, buccal abscess, tumors and syphilitic gum. Sinusitis forecast. With early intervention and removal of the causative tooth, the outcome is favorable. Sinusitis treatment. When the temperature rises – bed rest, antipyretic (aspirin, caffeine, pyramidon). With the phenomena of general intoxication – sulfonamides, antibiotics. For a better outflow of secretions into the nose, drops or aerosols of a 2-5% solution of ephedrine or 1-2% solution of cocaine with adrenaline are prescribed. Under stationary conditions, gauze tampons with these solutions are injected into the nose . Heat is prescribed on the affected side (heating pads, compresses, blue light, sollux, quartz), UHF, diathermy. Sometimes a sinus puncture is indicated through the nose or through the dog’s fossa with washing strips and the introduction of 100,000-200,000 U of streptomycin. Immediate removal of teeth with infection foci in the periodontium. If after tooth extraction there is a message through the socket, then the maxillary cavity can be washed through the socket with hydrogen peroxide, rivanol and penicillin. Prevention of sinusitis. Timely teeth sanitation.
Dressler’s postinfarction syndrome . Diagnosis and treatment of post-infarction syndrome Dressler .
Dressler’s postinfarction syndrome (late pericarditis) usually develops with extensive, complicated, or recurrent myocardial infarction with a frequency of 1-3%. Currently, this syndrome is becoming less common, as the quality of treatment for patients with MI has improved significantly. So, with timely TLT, Dressler’s syndrome does not form at all. The decrease in the incidence of this syndrome is also facilitated by drugs prescribed for ischemic heart disease (AB), statins , clopidogrel ). Dressler’s postinfarction syndrome is the second illness that occurs at 2-8 weeks of MI. The basis of this syndrome is an autoimmune aggression (antibody-mediated response to release and resorption of cardiac antigens and components necrotic myocardium after infarction) and after subsequent development hyperergic reaction sensitizer Wann body with benign lesions serositis GOVERNMENTAL membranes (including the pericardium). The course of this syndrome can be acute, protracted, or recurrent. The classic triad of Dressler’s syndrome : pericarditis with discomfort or pain in the heart (reminiscent of pleural) and pericardial rubbing noise (more common “dry” (usually fibrinous at autopsy), then often transformed into exudative), pleurisy (more often fibrinous), pneumonitis (less common ), manifested by the clinical picture of focal pneumonia in the lower lobes (cough, rales and crepitus), resistant to AB. This is complemented by the malaise of patients, fever and ESR, eosinophilia and leukocytosis, various skin changes (more often exanthema). It takes several months for late pericarditis to resolve.
Possible following atypical forms of this syndrome due to neuro-reflex and neuro- tropic editor: • articulate – are affected more often the upper limbs of the type of poly- or monoarthritis (syndromes “shoulder”, “brush”, “the front of the chest” or grudino- defeat costal joints). Some clinicians distinguish these manifestations as independent complications of myocardial infarction; • cardiopulmonary – pain and trophic changes in the shoulder joint with a violation of its function; • low-specific ( oligosymptomatic ) – with prolonged moderate fever, leukocytosis, increased ESR and eosinophilia in half of the cases; • “abortive” – ESR is accelerated, only weakness and tachycardia are noted. • ophthalmic – there are descriptions by foreign authors of edema of the eyeball, sometimes contact lenses cause a similar symptom complex . However, it should be understood that contact lenses have nothing to do with Dressler’s syndrome . This syndrome always proceeds as a complication of myocardial infarction. Diagnostics of the postinfarction Dressler syndrome . The diagnosis of Dressler’s syndrome is verified by echocardiography and chest x-ray. So, if a patient who has undergone myocardial infarction develops HF and chest X-ray shows an increase in the shadow of the heart (due to pericardial effusion), along with pleurisy, joint pain and fever, this syndrome should be excluded. Pathognomonic for Dressler’s syndrome and rapid effect of GCS. Treatment of Dressler’s postinfarction syndrome . In case of MI (especially in the first 4 weeks), long-term use of NSAIDs (especially ibuprofen, which causes thinning of the postinfarction scar) and GCS are not indicated due to the fact that they inhibit the healing of the myocardium, promote the formation of aneurysms and can cause heart ruptures. If 4 weeks have passed after myocardial infarction and the patient has only severe pericarditis, then he is prescribed oral aspirin (500 mg every 4 hours) or indomethacin (200 mg / day ) and analgesics. In the absence of effect and the presence of complete Dressler’s syndrome , individual patients (with severe relapses of symptoms) are prescribed oral corticosteroids – prednisolone at 20-40 mg / day ( dexamethasone at 8 mg) in a short course of 2-3 weeks with a gradual dose reduction over 5-6 weeks (the dose is reduced by 2.5 mg every 5 days) as symptoms improve.
Algorithm for the treatment of pulmonary hypertension. Primary prevention of PE.
Algorithm for the treatment of pulmonary hypertension:
• diltiazem (900 mg / day ); • anticoagulant therapy;
• inotropic agents – dopamine (with refractory pancreatic insufficiency) or norepinephrine (with hypotension);
• diuretics – for edema in the presence of pancreatic insufficiency;
• analogs of prostaglandin I2, causing regression of hypertrophy of the pulmonary vasculature – intravenous epoprostenol , inhalation of iloprost ;
• atrial septostomy (palliative surgery);
• inhalation of NO;
• phosphodiesterase inhibitors ;
• antagonists of serotonin receptors.
Patients with high PH due to recurrent PE may be bed-ridden with severe dyspnea at rest. They should undergo embolectomy (median sternotomy followed by dissection of both PAs and removal of organized blood clots), which can reduce or even relieve severe PH.
PE prevention is the goal of preventing further episodes of PE (which are difficult to treat). Two approaches are used to prevent fatal PE. Primary prevention is the use of drugs (heparin, AKND) or physical methods that effectively prevent DVT and PE. Thus, preoperative prophylaxis of SVTE according to Kakar is carried out : 5000 units of UFH subcutaneously 2 hours before surgery and every 8 hours after for 7-14 days. Sometimes UFH is injected subcutaneously at a dose of 80 U / kg of body weight every 12 hours. It is better to use LMWH, which are administered once a day and are more effective – dalteparin subcutaneously 2500-5000 IU every 24 hours (1-2 hours before surgery and after 24 hours after it). Doses of heparin depend on the risk of PE (for example, large orthopedic operations are associated with a high risk of PE – in these cases, maximum doses of heparin are used); individual properties of the patient (body weight, presence of RF ETS) and the risk of bleeding. In patients at high risk of PE, moderate doses of warfarin are used . Effective and safe primary prevention of pulmonary embolism is carried out in high-risk patients. This prophylaxis is preferable, it is more effective in preventing mortality and complications from pulmonary embolism, and is less costly than treatment of emerging pulmonary embolism. NVMG (subcutaneously 1 time per day for 6-14 days) should be prescribed to patients with severe CHF (FC 3-4 NYHA) who are assigned to bed rest. Aspirin is not used for prophylaxis, as it is not very effective in preventing venous thrombosis.
Preparing the patient for cardiac catheterization
Prior to admission to the cardiac catheterization laboratory, the cardiologist responsible for the procedure should give the patient all information about the upcoming examination, including risks and benefits, and answer questions from the patient and / or family. The pre-catheterization examination includes a history, physical examination, and ECG. Routine laboratory tests include a complete blood count with platelet count, blood electrolyte levels, creatinine and glucose, prothrombin time as INR, and partial thromboplastin time for patients receiving heparin. It is necessary to clarify important details of the anamnesis, namely the presence of diabetes mellitus (insulin-dependent or not), kidney disease, to determine the anticoagulant status and peripheral vascular disease, as well as to collect an allergic history for contrast agents and latex. The physician needs to be aware of any previous major interventions, including cardiac catheterization, PCI, surgical, peripheral, and cardiac surgery.
The patient should not eat for at least 6 hours before the study. Intravenous access must be provided. Usually used per os or IV sedation (eg, benzodiazepines ). When prescribing these drugs, pulse oximetry should be used to monitor respiratory function. In some laboratories, premedication with antihistamines, such as difeningidramin (25 mg / in), as antiallergy agents and for prolongation sedation. To reduce the risk of bleeding, oral anticoagulants should be discontinued and the INR should be <1.8. Aspirin and other oral antiplatelet agents are not canceled before the procedure. Patients with diabetes taking metformin should stop taking the drug in the morning before catheterization and not resume until renal function has returned to normal (at least 48 hours after the procedure). All patients need to undergo pre-procedure and post-procedure hydration. Its degree depends on heart function and fluid balance. However, if possible, it is advisable to inject at least 1 liter of liquid. Patients with a history of allergic reactions to a contrast agent require per os or IV prophylaxis before the study. It is recommended to take 60 mg of prednisolone per os or 100 mg of hydrocortisone intravenously 12 hours before catheterization. You can also enter the non-selective histamine blocker cimetidine (300 mg i.v. ) and dipheninehydramine (25-50 mg i.v. ). A history of urticaria does not predispose to contrast agent reactions.