Concept and classification of inhalation pneumonia
Inhalation of pneumonia can be classified as inhaled chemical and inhaled bacterial pneumonia. Inhalation chemical pneumonia is defined as lung chemical damage caused by sterile gastrointestinal content. Inhalation of bacterial pneumonia is defined as lung infections caused by inhalation of the insecticidal bacteria. Inhalation chemical pneumonia and inhalation bacterial pneumonia are likely to cause respiratory failure and ARDS (acute respiratory distress syndrome). The two differ in terms of cause, clinical performance and treatment. Inhalation of chemically transmitted pneumonia is non-infected at an early stage and does not require anti-infection treatment, and here we speak mainly about inhalation bacterial pneumonia. Clinical diagnostic criteria for bacterial inhalation pneumonia are: new or progressive immersion of pulmonary immersion after inhalation, combined with more than two clinical infections: (i) fever of 38°C; (ii) increased symptoms of emerging cough, cough or pre-respiratory diseases and sepsis; (iii) pulmonary degenerative signs, and/or wet tones; and (iv) impregnated leukemia 10 x 10° 9/L or 4 x 10° 9/L, accompanied or unaccompanied by a left transfer. It also excludes certain diseases that are similar to the clinical manifestations of pneumonia, such as tuberculosis, pulmonary oedema, non-infective interpulmonary disease, lung failure, lung tumours and infarction.
II. High risk factors for inhalation pneumonia
High-risk factors for inhalation pneumonia include: age, nervous system diseases (Pakinson’s disease, low mental state, Alzheimer’s disease, cerebral infarction/hemorrhage, epilepsy, etc.), difficulty of swallowing, retrogent diseases of the stomach, snout, bed rest, mechanical ventilation, medical effects (e.g. anaesthesia, sedatives, etc.):
Type 2 diabetes: high blood sugar increases plasma permeability pressure, sugar metabolism in white cells and reduced sugar fermentation, leading to a decrease in the ability of meso-particle cells to decompose, eat and kill. In addition, chronic high blood sugar facilitates the growth and reproduction of pathogenic microorganisms. Diabetes is affected by metabolic disorders in the body, accelerated decomposition of proteins, reduced synthesis, reduced immunoglobin and reagent capacity, and reduced lymphocyte cell conversion, leading to reduced cytology and body fluid immune response. Insulin receptors exist on insulin cells in the organism, and insulin contributes to the functioning of B and T cells both inside and outside the body, increasing the transmission of antigens. Insulin deficiency reduces immunosuppressive functions by reducing the ability of immunosuppressants, seropaths and cell immune functions.
2. Post-esophagus cancer (the cesophagus stomach): backwards of the stomach oesophagus: Patients are prone to retrovenant oesophagus after oesophagus, mainly in the form of pre-ecophagus or acidic liquids/food from the stomach oesophagus to the stomach or mouth when sleeping in bed at night. Functional gastric emptiness: the oesophagus cancer requires the removal of the stomach wall or part of the stomach, after which the stomach motion disorder occurs regularly, resulting in dysenteral emptiness and large amounts of gastrointestinal content. Impacts on respiratory function: oesophagus cancer operations damage the integrity of the patient ‘ s chest profile, damage the patient ‘ s rib muscles, in particular the muscular muscles, and to a certain extent the chest stomach affects lung expansion and the aerobic function of the patient.
Carbon monoxide poisoning: Carbon monoxide poisoning is the poisoning caused by respiratory inhalation of a product that occurs when carbon-containing substances are not fully burned. The intoxication mechanism is 200 to 300 times more closely associated with carbon monoxide and haemoglobin than with oxygen and haemoglobin, so that carbon monoxide can easily be combined with haemoglobin, creating carbon haemoglobins, depriving haemoglobins of oxygen capacity and function and suffocating tissue. It has toxic effects on whole body tissue cells, especially on the cortex of the brain.
4. Acute carbon monoxide (CO) poisoning delayed brain disease: is the sudden occurrence of neuro-system diseases dominated by dementia, mental symptoms and cones after a period of sane dementia after acute CO poisoning. In general, between 2 and 60 days after acute CO poisoning, 87 per cent of patients are reported to have been infected within one month after acute CO poisoning. Many patients as well as their families undervalued follow-up treatment because of an improvement in their acute CO poisoning, resulting in disability and even death. High pressure oxygen is effective for acute and delayed brain disease, and most patients can return to life-care or better if they insist on high pressure oxygen treatment.
III. Inhalation of bacterial pneumonia
1. Actively treat cases of primary illness.
Dilution of slurry: dilution of sluice with a drug such as aminobromosole; transformational position and mechanical vibrations to facilitate excretion of the genre, if no autonomous cough capacity requires snorting and, if necessary, the bronchic lens attracts and washes.
3. Correction of low oxygen haemorrhagic disorders: constant low flow of oxygen and mechanical ventilation if necessary; dynamic monitoring of blood and gas analysis, preferably keeping oxygen subpressure above 60 mmHg.
4. Treatment and care of the disease: body temperature > 38°C deheating (pharmaceutical or physical cooling), rehydration of liquids, coughing, asthma. Time-lapse and oral care, etc.
5 Nutritional support: maintenance of hydrolytic balance for digestible, nutritious foods or nutrients. Those who cannot eat through mouth should feed. Those who cannot have intestines can have intestines.
6. Uplifting the patient ‘ s bed (30° ~ 45°) prevents abscess and misuse of the stomach content. Thus, when feeding a patient who has a high risk of misuse, the patient should be in a sitting or half-bedroom until one or two hours after eating. There is also a need for proper management of nasal catheters; attention is paid to the monitoring of gastrophs, which should stop feeding if they exceed 50 ml.
Clean mouth can also play an important role in the prevention of inhalation pneumonia.
8. Other preventive measures: Reduction of drugs that can increase the incidence of misdose (e.g. sedatives, choline receptor retardants, anti-anxiety drugs, etc.), enhancement of the exercise of the disease ‘ s eating and cough function, enhancement of the management of artificial airbags, etc.
IV. Antibiotic treatment principles for inhalation pneumonia
The initial empirical anti-infection treatment proposal: “Physics with anti-aerobic effects, such as amazole silin Shubatan and potassium amosilin Kravite, or a combination application of methazole, clinicillin, etc., may also be selected for respiratory noonone-type drugs such as Mosisa. However, for joint use, such as nitroglycerin, clinicin, etc., it is not used routinely, but only for patients with severe dental dysentery, stench, or chest imaging that confirms the presence of necrosis or pulmonary sepsis.
2. Access to anti-pneumococcal drug options at the Moderate Hospital: second and third generations of sepsis (not necessarily including anti-falsifying single-cell activity), β-nimide/betamide inhibitor; penicillin allergies opt for quinone or clinicillin + achicin. Recommended antibacterial drugs for pseudosyncs: “Use of β-neamamine drugs (e.g., thalamus, thalamus, thorone quambatan, thalasilin, carbon carcylene) + cyclopropa or thoroxyfluorosaltron; or above-mentioned β-neamide drugs + Amino sugar + Achicillin; or the above-mentioned β-neamide + aminoquinone (aminotrinams are used to replace the above-mentioned β-endomamines for penicillin allergies) or carbon methacne if the condition is serious.
3. Method of delivery and course of treatment: The recommended initial treatment should be an intravenous formulation, converted to an oral formulation once clinical symptoms have improved and the gastrointestinal function is normal, with an average of 7-10d, or an average of 7-10d, or 10-21d, of golden venomella, copper-coloured hysteria and non-activism. The assessment of therapeutic efficacy and the adjustment of the empirical antibiotic treatment programme: general white cell count, body temperature, etc., determine the clinical reduction of pneumonia and provide comprehensive analysis to guide clinical use. Improvements in video science often lag behind clinical indicators and have limited judgement value. After effective treatment, inhalation of bacterial pneumonia is usually marked by clinical improvement within 48-72h. Antibiotic programmes should not be adjusted at this time. If a pathogen examination has been performed, 72h may then consider the use of narrow spectrum antibiotics based on pathogen results.
